Stages of breast cancer
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:{caption:"Highly Cited",originalUrl:"/media/original/117"}},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"9280",leadTitle:null,fullTitle:"Underwater Work",title:"Underwater Work",subtitle:null,reviewType:"peer-reviewed",abstract:"Underwater work is work done underwater, generally by divers during diving operations. It also includes work done underwater by remotely operated vehicles (ROVs) and manned submersibles. The versatility and multifarious skills of underwater work mean that it is possible to operate over a wide range of activities, working in hyperbaric conditions or in confined spaces. This book exposes and discusses the inner workings of underwater work along with its challenges and opportunities.",isbn:"978-1-78985-229-5",printIsbn:"978-1-78985-222-6",pdfIsbn:"978-1-78985-230-1",doi:"10.5772/intechopen.83282",price:100,priceEur:109,priceUsd:129,slug:"underwater-work",numberOfPages:88,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"647b4270d937deae4a82f5702d1959ec",bookSignature:"Sérgio António Neves Lousada",publishedDate:"March 31st 2021",coverURL:"https://cdn.intechopen.com/books/images_new/9280.jpg",numberOfDownloads:1721,numberOfWosCitations:0,numberOfCrossrefCitations:2,numberOfCrossrefCitationsByBook:1,numberOfDimensionsCitations:2,numberOfDimensionsCitationsByBook:2,hasAltmetrics:0,numberOfTotalCitations:4,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"September 20th 2019",dateEndSecondStepPublish:"March 2nd 2020",dateEndThirdStepPublish:"May 1st 2020",dateEndFourthStepPublish:"July 20th 2020",dateEndFifthStepPublish:"September 18th 2020",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"248645",title:"Dr.",name:"Sérgio",middleName:null,surname:"Lousada",slug:"sergio-lousada",fullName:"Sérgio Lousada",profilePictureURL:"https://mts.intechopen.com/storage/users/248645/images/system/248645.jpg",biography:"Sérgio António Neves Lousada has an international Ph.D. in Civil Engineering (Hydraulics). He teaches Hydraulics, Environment, and Water Resources and Construction at the University of Madeira, Portugal. He has published articles and books and participated in events mainly in the areas of hydraulics, urban planning, and land management. Furthermore, he collaborates with the Environmental Resources Analysis Research Group (ARAM), University of Extremadura (UEx); VALORIZA - Research Center for the Enhancement of Endogenous Resources, Polytechnic Institute of Portalegre (IPP), Portugal; CITUR - Madeira - Centre for Tourism Research, Development and Innovation, Madeira, Portugal; and Institute of Research on Territorial Governance and Inter-Organizational Cooperation, Dąbrowa Górnicza, Poland. 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However, in this paper, we have utilized only standard deviation of CCF as estimation parameter to estimate the population size. We utilized four acoustic sensors and considered chirp sound which is commonly generated by damselfish (Dascyllus aruanus), humpback whales (Megaptera novaeangliae), dugongs (Dugong dugon), etc., species to accomplish the simulations. 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From collecting samples to protecting underwater cultural heritage sites scientific divers need to address issues concerning scientific methodology, diving safety, professional acknowledgement, training, legal implications etc. All of these matters are handled in different ways depending on factors like region, organizations involved, legal framework, diving philosophy etc. producing a diverse framework on scientific diving as a distinct type of underwater work. The ScienceDIVER project’s main objective is to study and analyze this fragmented landscape, in order to provide insight and suggestions towards a commonly accepted framework that will promote scientific diving as a means of forwarding knowledge both within the scientific community and its interaction with the public.",signatures:"Alexandros Tourtas, Kimon Papadimitriou, Elpida Karadimou and Ralph O. 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An approach called Corridor SLAM (C-SLAM) was developed for this purpose. It implements a global exploration strategy that consists of first creating a trunk corridor on the seabed and then branching as far as possible in different directions to increase the explored region. The system guarantees the safe return of the vehicle to the starting point by taking into account a metric of the corridor lengths that are related to their energy autonomy. 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Limerick",institutionURL:null,country:{name:"Ireland"}}},{id:"269578",title:"Dr.",name:"Gabriel",middleName:null,surname:"Leen",fullName:"Gabriel Leen",slug:"gabriel-leen",email:"Gabriel.Leen@ul.ie",position:null,institution:null},{id:"269579",title:"M.Sc.",name:"Fintan",middleName:null,surname:"McGuinness",fullName:"Fintan McGuinness",slug:"fintan-mcguinness",email:"Fintan.McGuinness@ul.ie",position:null,institution:null},{id:"269580",title:"Dr.",name:"Gerard",middleName:null,surname:"Dooly",fullName:"Gerard Dooly",slug:"gerard-dooly",email:"Gerard.Dooly@ul.ie",position:null,institution:null}]},book:{id:"8271",title:"Applications of Optical Fibers for Sensing",subtitle:null,fullTitle:"Applications of Optical Fibers for Sensing",slug:"applications-of-optical-fibers-for-sensing",publishedDate:"April 24th 2019",bookSignature:"Christian Cuadrado-Laborde",coverURL:"https://cdn.intechopen.com/books/images_new/8271.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"220902",title:"Dr.",name:"Christian",middleName:null,surname:"Cuadrado-Laborde",slug:"christian-cuadrado-laborde",fullName:"Christian Cuadrado-Laborde"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},ofsBook:{item:{type:"book",id:"11722",leadTitle:null,title:"New Perspectives of Asthma",subtitle:null,reviewType:"peer-reviewed",abstract:"\r\n\tAsthma is the most common chronic lower respiratory disease in children worldwide. Asthma usually starts at an early age, progresses differently, and the phenotype is fluid, which may worsen or disappear over time. At the same time, childhood asthma faces additional challenges due to the maturation process of the respiratory and immune systems, the natural history of the wheezing disease, the lack of good evidence-based medical evidence, the difficulty of establishing diagnostic and drug delivery pathways for disease, and the variable and often unpredictable response to treatment. The search is on for better ways to guide the diagnosis and treatment of asthma and even predict its occurrence. Therefore, non-coding RNAs have come into people's vision and play a great role in the occurrence and development of asthma through immune regulation and signal pathways. We have gained a lot of valuable experience in the continuous search for its relationship with asthma, and may even become a new target for the treatment of asthma in the future. So in this book, we will also mention the relationship between non-coding RNAs and asthma in the hope that more people will take notice.
\r\n\t
Breast cancer is the leading cause of cancer death in women, the second most common cancer worldwide, and the fifth most common cause of cancer-related deaths [1-3]. Not only are the incidence rates of breast cancer increasing, partly due to improved screening and detection techniques, but also the global burden of breast cancer exceeds all other cancers. So it is imperative to improve the quality of life of these patients.
Our knowledge of the process of tumorigenesis has increased significantly over the last decade thanks to continued funding from federal and private organizations, improved technologies enabling affordable sequencing of the entire genome, analysis of large data sets as well as gene expression profiles of human tumor samples, and improved animal models that attempt to resemble tumor formation in humans. The predisposing risk factors, precancerous lesions, and disease progression vary significantly across the tissues of origin. However, common themes have been described that drive a normal cell to undergo transformation and generate a tumor. We plan to lay the groundwork for our discussion utilizing the widely recognized models of colorectal cancer by Bert Vogelstein, the two hit hypothesis by Alfred Knudson, and the common characteristics of cancer cells described by Doug Hanahan and Robert Weinberg.
Furthermore, in this chapter we aim to discuss the early events that cause a normal breast epithelial cell to initiate the process of tumor formation and delineate them from later stage insults to the cell that cause it to progress to advanced metastatic disease. We particularly plan to focus on the role of oxidative stress and one major environmental agent i.e. ionizing radiation inducing DNA damage and chromosomal instability. At the same time we will discuss the cell cycle changes that ensue and the implications of loss of a tumor suppressor gene. Concurrently, there are morphological changes that can be witnessed in experiments performed with cancer cells in vitro which we will tie in with the underlying molecular mechanisms. We will trace the damaged cell along its course to metastasis by focusing on the molecular mechanisms that cause loss of cell-cell adhesion, loss of cellular polarity, ability to migrate through the stroma and gain access to the vascular or lymphatic system, resistance to anoikis and ability to seed a tumor in a new environment. A myriad of hypotheses exists in literature that attempts to explain the process of cancer formation and progression.
Next, we will classify breast tumors as malignant or non-malignant while describing the subtypes of each in a concise manner. Since the therapeutic options available in the clinic are targeted to particular genetic subtypes such as BRCA1 positive, estrogen receptor (ER) positive or triple negative (Her2-/-, ER -/-, PR -/-) etc., we will also discuss these molecular signatures. The clinical diagnosis criteria and imaging modalities will be mentioned concisely. A limited number of clinical trials that have a promising premise behind the study and considered to be ground breaking will be described.
Therapeutic options for breast cancer have expanded in the past 10 years to improve the survival outcomes for the disease. Existing FDA approved pharmacologic agents, small molecule inhibitors in clinical trials and drugs shown to have efficacy in preclinical studies will be methodically described in the final section. In the process, we hope to summarize where we are now with respect to this potent disease that affects millions.
As a cell achieves a neoplastic phenotype, its genetic sequence is usually vastly altered and multiple genes are mutated, amplified, or lost. Several models have been proposed regarding what leads to tumorigenesis. One of the models proposed by Dr. Bert Vogelstein proposes the loss of function of tumor suppressors [4-7]. According to his model, loss of function of tumor suppressors such as p53 leads to genomic instability which eventually leads to tumorigenesis via alterations in metabolism, loss of sensitivity to apoptotic signals, and increased invasiveness [8, 9]. Loss of function of the tumor suppressor, p53, is associated with the development of most, if not all, tumor types [10-12]. An inactivating mutation in a tumor suppressor not only leads to hyper-proliferation of epithelial cells, it may also inactivate DNA repair genes. Mutations in proto-oncogene can either create an oncogene or lead to a cascade of inactivation of several more tumor suppressor genes before resulting in cancer. Figure 1 shows this model for colon carcinogenesis.
The cascade of events that lead to oncogenesis.
An alternate theory that accounts for both hereditary and non-hereditary cancer is the two-hit theory of cancer causation proposed by Dr. Alfred Knudson [13, 14]. Normal cells have two undamaged chromosomes, one inherited from each parent. People with a hereditary susceptibility to cancer inherit a damaged gene on one of the chromosomes at conception which is their ‘first hit’ or mutation. Others receive the ‘first hit’ in their lifetime. Damage to the same gene on the second chromosome in their lifetime may lead to cancer. An overview of this model is given in Figure 2 and is seen in cancer such as retinoblastoma.
Weinberg and Hanahan have proposed the hallmarks of cancer which helps explain oncogenesis. These are biological capabilities acquired during the complex multistep development of cancer. Figure 3 summarizes the 8 hallmarks of cancer. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction [15]. All these hallmarks lead to genomic instability and persistent inflammation, possibly fueling further genetic diversity, as well as propagation, acquisition and fostering of multiple hallmark functions.
The two-hit model of carcinogenesis.
The 8 possible hallmarks of cancer.
A possible contributing factor that hasn’t gained much attention is the role of fragile sites. Common fragile sites (CFSs) are regions of the genome with a predisposition to DNA double-strand breaks in response to intrinsic (oncogenic) or extrinsic replication stress. CFS breakage is a common feature in carcinogenesis from its earliest stages and through its evolutions. In a recent article the association of several fragile sites stability with key DNA damage response (DDR) and DNA repair proteins like breast cancer type 1 susceptibility protein (BRCA1), Ataxia telangiectasia and Rad3 related (ATR), and Ataxia telangiectasia mutated (ATM) opens another possibility for the induction and/or acceleration of instability in breast tissue [16]. For example
A proto-oncogene is a normal gene that can convert to an oncogene due to mutations (generally dominant mutations) or increased expression [18-20]. Proto-oncogenes function in promoting cell division and inhibiting cell differentiation. Oncogenes, however, promote all the markers of a cancer cell such as increased cell division and replication stress, decreased cell differentiation, and inhibition of cell death (usually apoptosis). A proto-oncogene can convert into an oncogene due to various reasons including chromosomal translocation (such as BCR-ABL that is seen in leukemia), gene amplification, point mutations, deletions, alterations in promoter region leading to increased transcription, and insertions that lead to a hyperactive gene product. Human epidermal growth factor receptor 2 (HER2) is a proto-oncogene that is amplified in about 30% of breast cancer [18]. This is discussed in detail in a subsequent section. To balance the effect of oncogenes, tumor suppressors are present as well to regulate cell growth and cell death but mutations in them can lead to tumor formation. The guardian of the genome, p53, is the most commonly mutated tumor suppressor gene in human cancer [21, 22]. It is involved in multiple pathways including maintenance of genomic stability by causing cell cycle arrest as the cell attempts to repair the damaged DNA, apoptosis, tumor progression, and metastasis [23]. Not surprisingly, a lot of breast cancers harbor mutations in this transcription factor as well. Since p53 has been linked to how BRCA1 dictates DNA repair and cell death, it may have a role in tumor response to treatment as well [24].
Checkpoints are present throughout the cell cycle that halt further progression of DNA replication and cell division, either permanently (senescence) or transiently, when damaged DNA is detected. This activates specific DNA repair pathways (discussed below). ATM and ATR are key proteins in the DNA damage response pathway. ATM is recruited to and activated by DNA double strand breaks while ATR is recruited to and activated by replication protein A-coated double stranded DNA. Two of the best studied ATM/ATR targets are the protein kinases checkpoint kinase 1 (CHK1) and checkpoint kinase 2 (CHK2). Together with ATM and ATR, these proteins reduce cyclin dependent kinase (CDK) activity which slows down or arrests cell-cycle progression at the G1–S, intra-S and G2–M cell cycle checkpoints allowing more time for DNA repair before progression of replication or mitosis. Moreover, ATM/ATR can promote DNA repair by a variety of methods including induction of DNA repair proteins transcriptionally or post-transcriptionally, by recruiting repair factors to the damage-site, and by activating DNA-repair proteins by modulating their post-transcriptional modifications such as phosphorylation, acetylation, ubiquitylation or SUMOylation.
Continuous DNA damage checkpoint activation may lead to selective suppression of the DNA-damage response-induced antitumor barriers. This may be due to inactivating mutations. This process promotes genomic instability and tumor progression [25-28]. Prolonged overexpression of licensing factors such as hCdt1 and hCdc6 prevent cell death and lead to a more aggressive phenotype. Overexpression of the replication licensing factor Cdc6 led to phenotypic changes with mesenchymal features and loss of E-cadherin. Analysis in various types of human cancer revealed a strong correlation between increased Cdc6 expression and reduced E-cadherin levels [29]. Cells possessing re-replicated DNA above a critical threshold are typically neutralized by cell death mechanisms but cells with re-replicated elements below a critical threshold are prone to recombination processes leading to genomic instability. As a result these cells are much more resistant to therapy [30].
DNA can be damaged spontaneously during replication stress and cell division as well as due to exogenous/environmental agents. This leads to thousands of DNA lesions/cell per day. In some cases of high oxidative or environmental stresses, repair resistant complex DNA damage can be induced as analytically discussed in a recent review by Kryston et al. 2011 [31]. As little as one unrepaired DNA double strand break can be lethal to the cell. Thus, the DDR and DNA repair pathways are in place to maintain the genomic integrity. This response pathway detects the DNA damage, signals their presence to recruit repair factors and halt cell cycle progression, and promote DNA repair. DNA lesions can block genomic replication and transcription and lead to mutations. Most of the time, cells undergo death in the form of apoptosis or necrosis when there is unrepaired DNA. Cells defective in DNA repair are hypersensitive towards DNA damaging agents. For example, breast cancer cells with defective BRCA proteins are sensitive to poly ADP ribose polymerase (PARP) inhibitors. This is an active area of research with promising results thus far. This is discussed further in a later section. DNA repair pathways include base excision repair (BER), nucleotide excision repair (NER), double strand break repair via homologous recombination (HR) or non-homologous end joining (NHEJ), and mismatch repair (MMR) [32-34]. Frequently, multiple proteins are involved in the repair of the damaged DNA. The repair pathways are briefly described below.
In MMR-mediated repair, nuclease, polymerase and ligase enzymes fix a single-strand cut that is induced upon detection of mismatches and insertion/deletion loops. DNA glycosylase detects a damaged base in BER-mediated repair. This is subsequently removed before nuclease, polymerase and ligase proteins complete the repair. NER-mediated repair recognizes helix-distorting base lesions. The damage is excised as a 22–30-base oligonucleotide, producing single-stranded DNA that is a substrate for DNA polymerases and associated factors. The process ends with ligation. There are 2 major DNA double strand break repair pathways. NHEJ is predominantly used in the repair of radiation induced DNA damage. It is highly efficient but error-prone. The Ku proteins recognize and bind to the damaged site and activate the protein kinase DNA-PKcs, leading to recruitment and activation of end-processing enzymes, polymerases and DNA ligase IV. In contrast, HR uses sister-chromatid sequences as the template to mediate faithful repair. It is used in repair of replicative stress-induced lesions, stalled replication forks, and inter-strand DNA crosslinks. HR starts with single strand DNA generation, which is promoted by various proteins including the MRE11–RAD50–NBS1 (MRN) complex. In events catalyzed by RAD51 and the breast-cancer susceptibility proteins BRCA1 and BRCA2, the single strand DNA then invades the undamaged template and, following the actions of proteins mentioned above such as polymerases, nucleases, helicases, etc., the DNA is repaired.
One of the most famous mutations in cancer is the BRCA family of genes which are critical for HR-mediated repair of DNA double strand breaks [35, 36]. Mutations in the BRCA genes lead to an increased risk for breast cancer as part of the hereditary breast-ovarian cancer syndrome. Women with mutated BRCA1 or BRCA2 gene have up to a 60% risk of developing breast cancer [37, 38]. Hypermethylation of the BRCA1 promoter may be an inactivating mechanism for BRCA1 expression [39, 40]. Many of the mutations in BRCA1 or BRCA2 that predispose to breast cancer cause premature termination of the amino acid coding sequences, resulting in a truncated, dysfunctional protein.
Mutations in ATM, a critical DNA repair protein, lead to Ataxia Telangiectasia (AT). As mentioned above, ATM is a serine/threonine protein kinase that is recruited and activated by DNA double strand breaks and phosphorylates proteins that initiate activation of the DNA damage checkpoint, leading to cell cycle arrest, DNA repair or apoptosis. Several of these targets, including p53, CHK2 and H2AX are tumor suppressors which explains why AT sufferers are predisposed to breast cancer and are hypersensitive to radiation [41, 42]. Another example is the Werner syndrome which is marked by mutations in Werner syndrome ATP-dependent helicase (WRN) and Rad51 genes leading to deficiency in HR- and NHEJ mediated DNA double strand break repair which, as expected, leads to increased incidence of breast cancer.
Breast cancer often metastasizes to bones, lungs, liver and brain [43-47]. The metastatic cascade is a series of biological steps that tumor cells must complete to exit the primary tumor and develop a new tumor at a distant site. One of the most critical steps involves invasion of the basement membrane and surrounding tissue and enter the bloodstream or lymphatic system. Cells that survive, eventually move into the tissue and establish a new colony that may form a tumor down the line. The host defense system is able to fend off millions of cancer cells that enter the blood stream but a few may escape nonetheless. Invasion involves the loss of cell-cell adhesion which may be mediated by matrix metalloproteinases and urokinases which break down integrins which attach tumor cells to their microenvironment and plasminogen respectively [48-54]. Cadherins are an intricate part of cell-cell adhesion and so downregulation of e-cadherin and upregulation of n-cadherin, involved in epithelial and mesenchymal phenotypes respectively, can promote metastasis [55-60].
Circulating tumor cells (CTCs) which like breast cancer is a heterogeneous population on cells, have a crucial role in the metastatic cascade, tumor dissemination and progression. Epithelial-to-mesenchymal transition (EMT) has an important role in the generation of CTCs and the acquisition of resistance to therapy [61-63]. Fibroblasts and myofibroblasts represent the majority of stromal cells within breast cancer. These cells promote the growth of cells by creating the perfect environment for cell survival and proliferation including enhanced angiogenesis. Tumor cells can express chemokine receptors that not only help direct migrating tumor cells to specific sites, they also determine if the cells will thrive and colonize at those sites. The bloodstream is highly unfavorable to tumor cells owing not only to the presence of immune cells, but also physical forces and anoikis, which combats metastasis. Interestingly, binding of tumor cells to coagulation factors, including tissue factor, fibrinogen, fibrin and thrombin, creates an embolus and facilitates arrest in capillary beds followed by the establishment of metastasis [64].
EMT is an important process in metastasis. Here, epithelial cells lose cell-to-cell contacts and cell polarity, downregulate epithelial-associated genes, upregulate mesenchymal-genes, and undergo major changes in their cytoskeleton. This confers greater motility and invasiveness. Expression of stem-cell markers and acquisition of stem-cell characteristics are important processes in this pathway as well. Once the tumor cells seed at the secondary site, they undergo redifferentiation to an epithelial phenotype [65]. One of the factors involved in EMT is epithelial derived growth factor (EGFR) which induces tissue factor which in turn promotes tumor seeding via the process described above. The transcription factor Twist-related protein 1 (TWIST1), the receptor ligand tumor derived growth factor β (TGFβ), Hypoxia-inducible factor 1 (HIF1), HER2, and Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/ Protein kinase B (AKT) signaling pathways have also been implicated in metastases. In preclinical models, expression of TWIST reduces metastasis and number of CTCs. CTCs often express NOTCH1 which confers self-renewal abilities. Some cells also express Aldehyde dehydrogenase 1 (ALDH1), another gene associated with stem cell like properties. Interleukin 6 (IL6) and Interleukin 8 (IL8) attract CTCs while Matrix metalloproteinase-1 (MMP1)–collagenase 1 and the actin cytoskeleton component fascin 1 help CTCs infiltrate into tumors. Overexpression of the chemokine receptor C-X-C chemokine receptor type 1 (CXCR1) in CTCs is associated with decreased metastases and may be a therapeutic target.
Risk factors for malignant breast tumors include increased estrogen exposure which can be due to a number of reasons. For example, a woman can be exposed to increased estrogen due to increased total number of menstrual cycles, older age at 1st live birth, and obesity (increased estrogen exposure as adipose tissue converts androstenedione to estrone). BRCA1 and BRCA2 gene mutations also increase the risk of breast cancer and much research has been done in this avenue. Interestingly, increased incidence of triple negative breast cancer is seen in the African American population. Breast cancer risk is also increased with increased alcohol intake. Research suggests alcohol stimulates tumor growth by fuelling the production of growth factors that promote angiogenesis and by suppressing the immune system [66].
The breast is an organized organ and diseases may arise at any of its structural subunits. The stroma provides a supporting environment and this is where fibroadenoma and phyllodes tumor can arise. The smallest subunit is the lobule where we can see lobular carcinoma. Lobules give rise to terminal ducts where we can see tubular carcinoma. Next are major ducts where fibrocystic changes, DCIS, and invasive ductal carcinoma are often seen. These join to form the lactiferous sinus where intraductal papilloma may arise. Finally, Paget disease can be seen at the nipple. Figure 4 summarizes the different breast pathologies.
Pathologies that can affect the different breast tissues.
Not all breast tumors are malignant. Fibroadenoma are small, mobile, firm mass with sharp edges. They are most common in those <35 years old and increase in size and tenderness in response to estrogen as is seen in pregnancy and prior to menstruation. As mentioned, it does not lead to breast cancer. Similarly, intraductal papillomas are small benign tumors that grow in lactiferous ducts, typically beneath the areola. They can cause serous (faintly yellow and thin) or bloody nipple discharge. Of note, they do increase the risk for carcinoma be approximately 2-fold [67]. Phyllodes tumor are large bulky mass of connective tissue and cysts with leaf-like projections. They are most common in the 6th decade of life and similar to intraductal papilloma, can become malignant.
Malignant breast tumors are more common in postmenopausal women. They usually arise from terminal duct lobular unit. Overexpression of different proteins such as HER2 and EGFR are often seen. As discussed in a later section, receptor status can affect the therapy and prognosis. Since approximately 70% of the breast is drained by the axillary lymph node, involvement of this node indicating metastasis is the single most important prognostic factor. Since there is more tissue in the upper outer quadrant of the breast, tumors often arise here.
Malignant breast tumors can be subdivided into noninvasive and invasive tumors. Noninvasive tumors include ductal carcinoma in situ (DCIS), Paget disease, and comedocarcinoma. Comedocarcinoma is a subtype of DCIS where ductal caseous necrosis is seen. DCIS fills the ductal lumen and arises from ductal atypia. They are often seen as microcalcification on mammography due to necrosis. Paget disease results from underlying DCIS and results in eczematous patches on the nipple. Invasive breast tumors include invasive ductal and lobular cancer. A firm, fibrous mass with sharp margins and small, glandular, duct-like cells are seen in invasive ductal tumors. They are the worst and most invasive of the tumors as well as the most common, comprising of over 70% of all breast cancer. Invasive lobular cancer often presents bilaterally with multiple lesions in the same location. Pathologically, they present as an orderly row of cells. Fleshy, cellular lymphocytic infiltrate is seen with medullary breast carcinoma and it has a good prognosis. Finally, inflammatory breast tumor presents with dermal lymphatic invasion and has approximately 50% survival at 5 years. Due to blockage of the lymphatic drainage, Peau d’orange is often seen with this condition.
The classification is important because treatment varies based on the type of cancer. When a tumor is diagnosed as benign, it is often left alone. With malignant tumors, biopsy is performed to determine the severity and aggressiveness of the tumor.
Molecular subtypes of breast cancer may be useful in planning treatment and developing new therapies and so a lot of research is being conducted in this field. Figure 5 depicts some of the more common subtypes. Most studies divide breast cancer into six major molecular subtypes:
Luminal A
Luminal B
Triple negative/basal-like
HER2 positive
Claudin low
Normal-like
Subtypes of breast cancer.
Some of the less common subtypes include apocrine molecular type. Molecular apocrine breast cancers are aggressive estrogen receptor negative tumors overexpressing either HER2 or gross cystic disease fluid protein-15 (GCDFP15) [68]. Breast cancers that do not fall into any of these subtypes are often listed as unclassified.
Most breast cancers are luminal tumors. Luminal tumor cells look the most like the cells of breast cancers that start in the inner (luminal) cells lining the mammary ducts. Luminal A tumors tend to be ER+ and/or PR+, HER2-, and tumor grade 1 or 2. Less than 15% of luminal A tumors have p53 mutations. Hence, luminal A tumors tend to have the best prognosis, with fairly high survival rates and fairly low recurrence rates. Since luminal A tumors tend to be ER+, treatment often includes hormonal therapy which is discussed in a subsequent section.
As mentioned above, luminal tumors have cells that look like those of breast cancers that start in the inner (luminal) cells lining the mammary ducts. Luminal B tumors tend to be ER+ and/or PR+. Since they have highly mitotically active cells, they are positive for Ki67. They are often HER2+ as well. Interestingly, women with luminal B tumors are often diagnosed at a younger age than those with luminal A tumors and have a poorer prognosis due to poorer tumor grade, larger tumor size and lymph node involvement. About 30% of the tumors also have mutations in p53.
Triple negative breast cancers are: ER-, PR-, and HER2-; hence the name triple negative. There are several subsets of triple negative breast cancer. One subset is referred to as basal-like because the tumors have cells with features similar to those of the outer (basal) cells surrounding the mammary ducts. Most basal-like tumors have mutations in p53. About 15 to 20% of breast cancers are triple negative or basal-like. These tumors tend to occur more often in younger and African American women. Of note, most BRCA1 breast cancers are both triple negative and basal-like. Triple negative/basal-like tumors are often aggressive and have a poorer prognosis. These tumors are usually treated with some combination of surgery, radiation therapy and chemotherapy.
The molecular subtype HER2 type is not the same as HER2+ and is not used to guide treatment. Although most HER2 type tumors are HER2+ (and named for this reason), about 30 percent are HER2-. HER2 type tumors tend to be ER-, PR-, with lymph node involvement and poor tumor grade. About 10% to 15% of breast cancers fall under this category and about 75% of HER2 type tumors contain p53 mutations. HER2 type tumors have a fairly poor prognosis and are prone to early and frequent recurrence and metastases. Women with HER2 type tumors appear to be diagnosed at a younger age than those with luminal A and luminal B tumors. HER2/neu-positive tumors can be treated with the drug trastuzumab (Herceptin) and this is discussed in further detail in a subsequent section.
Claudin low is often triple-negative, but distinct in that there is low expression of cell-cell junction proteins including E-cadherin and frequently there is infiltration of lymphocytes. It is also enriched in mesenchymal and stem cell features [69].
About 6 to 10% of all breast cancers are classified as normal-like. These tumors are usually small and tend to have a good prognosis.
Breast cancer is divided into different stages. Table 1 summarizes these stages.
The extent of cancer can be used to stratify patients. Patients with clinical stage I, IIA, or a subset of stage IIB disease (T2N1 where T= tumor, N= node) are classified as having early-stage breast cancer. Patients with a T3 tumor without nodal involvement or stage IIIA to IIIC disease are classified as having locally advanced breast cancer. Stage IV is when there are distant metastases present and is seen in about 5% of newly diagnosed patients.
\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t
\n\t\t\t\t | \n\t\t\tRestricted to membrane of the milk duct (DCIS, LCIS) | \n\t\t
\n\t\t\t\t | \n\t\t\t<2cm tumor restricted to the breast | \n\t\t
\n\t\t\t\t | \n\t\t\t2-5 cm tumor +/- metastasis to draining lymph node | \n\t\t
\n\t\t\t\t | \n\t\t\tMetastasis to the lymph nodes +/- superficial skin and surrounding muscles | \n\t\t
\n\t\t\t\t | \n\t\t\tMetastasis to other parts of the body | \n\t\t
Stages of breast cancer
The surgical approach to the primary tumor depends on the size of the tumor, whether or not multifocal disease is present, and the size of the breast. Options include breast-conserving therapy or mastectomy and both have similar outcomes.
The risk for metastatic disease in the regional nodes is related to tumor size, histologic grade, and the presence of lymphatic invasion within the primary tumor. As mentioned above, the axillary nodes drain most of the breast tissue. Tumor characteristics are used to select adjuvant treatment for patients with breast cancer. Patients with hormone receptor-positive breast cancer should receive adjuvant endocrine therapy. For patients with triple-negative breast cancer, treatment option includes adjuvant chemotherapy if the tumor size is >0.5 cm. Patients with HER2-positive breast cancer >1 cm in size typically receive a combination of chemotherapy plus HER2-directed therapy. Following chemotherapy, patients with ER-positive disease generally receive adjuvant endocrine therapy.
Most patients with locally advanced, inoperable breast cancer should receive neoadjuvant systemic therapy rather than proceeding with primary surgery in an attempt to shrink the tumor. Typically, these patients are usually not candidates for breast conservation. Neoadjuvant treatment improves the rate of breast conservation without compromising survival outcomes and so most patients get chemotherapy in the neoadjuvant setting rather than endocrine therapy. Due to its greater toxicity to cancer cells, chemotherapy is associated with higher response rates in a faster time frame. As mentioned earlier, HER2-directed agent (ie, trastuzumab) should be added to the chemotherapy regimen for tumors that are HER2-positive. Following surgery, all patients who undergo breast-conserving surgery generally undergo adjuvant radiation therapy (RT) to maximize locoregional control. Some patients treated by a mastectomy should receive postmastectomy RT in order to kill any cancer cells that may have escaped during the procedure.
Patients with hormone receptor-positive breast cancer should receive adjuvant endocrine therapy. The selection of endocrine therapy is made according to menopausal status. In patients with ER-positive breast cancer, in whom surgery is not an option or life expectancy is limited, primary hormonal treatment with either tamoxifen or an aromatase inhibitor without surgery is generally used.
The heterogeneity of breast cancers makes it a challenge to diagnose and treat this solid tumor.
The main types of treatment for breast cancer are:
Surgery
Radiation therapy
Chemotherapy
Hormone therapy
Targeted therapy
Treatments can be classified into broad groups (Figure 6), based on how they work and when they are used.
Different treatments available for breast cancer.
As the name implies, local therapy is intended to treat a tumor at the site without affecting the rest of the body. Examples include surgery and radiation therapy. Systemic therapy refers to drugs which can be given by mouth or directly into the bloodstream to reach cancer cells anywhere in the body. Chemotherapy, hormone therapy, and targeted therapy are systemic therapies that are widely used.
Since even in the early stages of breast cancer, cancer cells may break away from the primary breast tumor and begin to spread, adjuvant therapy is often given to patients with no detectable cancer after surgery. A small number of cells can\'t be ‘felt’ on a physical exam or seen on X-rays or other imaging tests, and they cause no symptoms until they reach a certain number but, menacingly, they can go on to become new tumors in nearby tissues, other organs, and bones. Hence, adjuvant therapy is a mainstay following surgery. Both systemic therapy like chemotherapy, hormone therapy, and targeted therapy, and radiation can be used as adjuvant therapy.
In neoadjuvant therapy, patients are treated with chemotherapy or hormonal therapy prior to surgery. The goal of this treatment is to shrink the tumor in the hope it will allow a less extensive operation to be done. This also lowers the chance of the cancer coming back later.
For both DCIS and early-stage invasive breast cancer, doctors generally recommend surgery to remove the tumor. To make sure that the entire tumor is removed, the surgeon will also remove a small area of normal tissue around the tumor until a negative margin is achieved. A lumpectomy is the removal of the tumor and a small cancer-free margin while a mastectomy is the removal of the entire breast. It is important to lower the risk of recurrence and to get rid of any remaining cancer cells that can lead to both local and distant recurrence of cancer. Adjuvant therapies include radiation therapy, chemotherapy, targeted therapy, and/or hormonal therapy which are described below. Surgical treatment for breast cancer involves removal of the lymph nodes and can also include resection of the surrounding axillary nodes.
This involves killing the cancer cells by inducing clustered DNA damage using ionizing radiation. By overwhelming the cell with DNA damage, the cell undergoes apoptosis. As little as one DNA double strand break can be lethal to the cell. By giving multiple doses of radiation broken up into fractions, the hope is to prolong survival. Some of the side effects include dermatologic issues, fibrosis, nausea etc. due to the radiation. Although most side effects usually go away after radiation therapy has been concluded, some long-term side effects may occur months or even years after treatment ends. These late effects which usually associate with persistent inflammation and oxidative stress may include developing a secondary primary cancer. However, we must mention that the risk of developing a second cancer because of radiation therapy is relatively low, and this risk is generally outweighed by the benefit of treating the primary, existing cancer and offering survival to the patient.
This involves using drugs and small molecules to selectively kill the cancer cells. Examples include: carboplatin, cisplatin, cyclophosphamide, docetaxel, doxorubicin, fluorouracil (5-FU), gemcitabine, methotrexate, paclitaxel, etc. A patient may receive one drug at a time or combinations of different drugs at the same time. Research has shown that combinations of certain drugs are sometimes more effective than single drugs for adjuvant treatment and so combinations are often used. Carboplatin and cisplatin are alkylating agents and belong to the group of platinum-based antineoplastic agents. They interact with DNA to interfere with DNA repair. These drugs cross-link with the DNA strands, mostly to guanine groups. This causes intra- and inter-strand DNA cross-links, resulting in inhibition of DNA, RNA and protein synthesis. Antimetabolites, such as methotrexate, are more active against S-phase cells where they block DNA synthesis whereas vinca alkaloids are more active in the M-phase where they inhibit spindle formation and alignment of chromosomes. Antimetabolites are compounds that bear a structural similarity to naturally occurring substances such as vitamins, nucleosides or amino acids. They compete with the natural substrate for the active site on an essential enzyme or receptor. Methotrexate competitively inhibits dihydrofolate reductase, which is responsible for the formation of tetrahydrofolate from dihydrofolate. This plays an important role in the synthesis of, among others, purines and methionine. Anthracyclines such as doxorubicin intercalate with DNA and affect the topoisomerase II enzyme. This DNA gyrase splits the DNA helix and reconnects it to overcome the torsional forces that would interfere with replication. The anthracyclines stabilize the DNA topoisomerase II complex and thus prevent reconnection of the strands. Paclitaxel promotes assembly of microtubules and inhibits their disassembly which interferes with cell division.
One of the more recent treatment options for breast are PARP inhibitors which showed initial promise in patients with tumors that have BRCA1 or BRCA2 mutations and therefore deficient double strand break repair. PARP inhibitors achieve an enhanced or synthetic lethality for tumor cells by blocking DNA repair pathways. PARP, which has multiple family members, detects single strand DNA breaks and participates in BER. It forms poly (ADP-ribose) polymers on itself and a number of substrates which can alter a number of pathways including DNA repair. Inhibition of PARP leads to persistent single strand break which converts to a double strand break as the cell attempts to replicate the DNA. Normal cells have an intact HR-mediated repair pathway and so are able to repair the DNA double strand break. However, in the absence of intact HR-mediated repair pathway which can happen with loss of or mutation in BRCA proteins, the cell is unable to repair the double strand break. As a result, typically, the cell undergoes apoptosis. A phase II study of the PARP inhibitor olaparib in patients with advanced breast cancer with BRCA1 or BRCA2 mutations has shown promising results with a response rate of 11/27, a progression-free survival of 5.7 months, and a median objective response duration of 144 days [70]. Phase III trials are currently in progress to evaluate olaparib in breast cancer [71]. TNBC also demonstrates BRCAness and so PARP inhibitors may be useful in this setting as well. Data from clinical trials have not been conclusive in this regard thus far.
Phosphatase and tensin homolog (PTEN) regulates RAD51 mediated DNA repair to maintain genomic stability. PTEN mutations, which occur in 30–50% of breast cancers, cause genomic instability similar to that seen in BRCA-deficient cells and so may be targets of PARP inhibitors as well [72].
Hormonal therapy is widely used in breast cancer treatment. These are used in the setting of ER+ and PR+ tumors. Since these tumors use hormones to fuel their growth, blocking the hormones can help prevent or at least slow down the growth of the tumor.
Selective estrogen receptor modulators (SERMs) are a class of compounds that act on the estrogen receptor. Tamoxifen blocks estrogen from binding to breast cancer cells. It is effective for not only lowering the risk of recurrence in the breast that had cancer, it also reduces the risk of developing cancer in the other breast, and the risk of distant recurrence. It is also approved to reduce the risk of breast cancer in women at high risk for developing breast cancer and for lowering the risk of a local recurrence for women with DCIS who have had a lumpectomy. Tamoxifen is also an effective treatment for metastatic hormone receptor-positive breast cancer. However, chronic Tamoxifen use has been linked with some toxicity and adverse effects like persistent oxidative stress and others as reviewed in [73].
Aromatase inhibitors (AIs) decrease the amount of estrogen made by tissues other than the ovaries in postmenopausal women by blocking the aromatase enzyme, which converts androgens into estrogen. These drugs include anastrozole and exemestane. Similar to Tamoxifen, AIs are also an effective treatment for metastatic hormone receptor positive breast cancer.
Fulvestrant, a SERM, is an additional hormonal therapy approved for patients with metastatic breast cancer. Fulvestrant is an estrogen-receptor targeting therapy that is used for the treatment of advanced-stage breast cancer in postmenopausal women with endocrine-sensitive cancer [74-77].
Targeted therapy is a treatment that targets specific genes or proteins. One of the advantages of this is that it limits damage to healthy cells. Trastuzumab, a monoclonal antibody, is approved for both the treatment of advanced breast cancer and as an adjuvant therapy for early-stage HER2+ breast cancer. Trastuzumab does have cardio toxic effects. Pertuzumab is a monoclonal antibody marketed by Genentech for the treatment of HER2+ breast cancer, in combination with trastuzumab and docetaxel. It inhibits the dimerization of HER2 with other HER receptors, which reduces tumor growth. Lapatinib, a dual tyrosine kinase inhibitor which interrupts the HER2/neu and epidermal growth factor receptor (EGFR) pathways, is commonly used for women with HER2-positive metastatic breast cancer when trastuzumab and pertuzumab in combination with docetaxel are no longer effective at controlling the cancer’s growth. Lapatinib decreases tumor-causing breast cancer stem cells and inhibits receptor signal processes by binding to the ATP-binding pocket of the EGFR/HER2 protein kinase domain, preventing auto-phosphorylation and subsequent activation of the signal mechanism.
Table 2 lists some of the current trials evaluating different therapies for breast cancer.
\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t
\n\t\t\t\t | \n\t\t\tCompare the efficacy of Faslodex (fulvestrant) to Aromasin (exemestane) in hormone receptor positive postmenopausal women with advanced breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tCompare whole breast radiation therapy to partial breast radiation therapy in treating women who have undergone surgery for ductal carcinoma in situ or stage I or stage II breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluate epirubicin (an anthracycline) together with vinorelbine (an anti-mitotic drug) in treating patients with stage II, stage III, or stage IV breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluate the efficacy and safety of bevacizumab when combined with standard chemotherapy compared with chemotherapy alone in subjects with previously treated metastatic breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluate the safety and efficacy of zoledronic acid (a bisphosphonate) when added to standard therapies in breast cancer patients with metastatic bone lesions. | \n\t\t
\n\t\t\t\t | \n\t\t\tExamine combination therapy with Trastuzumab, Cyclophosphamide, and an allogeneic Granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting whole cell breast cancer vaccine in patients with stage IV HER2/neu-overexpressing breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tAssess the toxicity, maximum tolerated dose, safety and preliminary efficacy of BZL101, an aqueous extract from herba Scutellaria Barbata D. Don of the Lamiaceae family, for the treatment of advanced metastatic breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tDetermine whether RAD001 can inhibit growth of tumor cells and/or stop the formation and activity of bone degrading osteoclasts. | \n\t\t
\n\t\t\t\t | \n\t\t\tTo see if the drug KU 0059436 (olaparib) is effective and well tolerated in treating patients with measurable BRCA1- or BRCA2-positive advanced breast cancer and for whom no curative therapeutic option exists. | \n\t\t
\n\t\t\t\t | \n\t\t\tHow well does erlotinib work in treating women undergoing surgery for stage I, stage II, or stage III breast cancer? | \n\t\t
\n\t\t\t\t | \n\t\t\tEfficacy of Anastrozole with fulvestrant in treating postmenopausal women with stage II or stage III breast cancer that can be removed by surgery. | \n\t\t
\n\t\t\t\t | \n\t\t\tEfficacy and safety of IPI-504 (heat shock protein 90 inhibitor) with Trastuzumab in pretreated, locally advanced or metastatic HER2+ breast cancer | \n\t\t
\n\t\t\t\t | \n\t\t\tEfficacy of Dasatinib in locally advanced triple negative breast cancer patients | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluate cisplatin and paclitaxel together with everolimus and to see how well it works in treating patients with metastatic breast cancer | \n\t\t
\n\t\t\t\t | \n\t\t\tAssess the safety and efficacy of BKM120 (PI3K inhibitor) in combination with trastuzumab in patients with relapsing HER2 overexpressing breast cancer who have previously failed trastuzumab. | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluate the efficacy and safety of combination chemotherapy with DoceTaxel (Detaxel) and Oxaliplatin (Oxalitin) in recurrent or metastatic breast cancer | \n\t\t
\n\t\t\t\t | \n\t\t\tAssess the response to treatment with fulvestrant at a dose of 500 mg/month with a loading dose of 500 mg, in terms of progression free survival, overall survival, and clinical benefit rate, in post-menopausal women with advanced breast cancer and estrogen receptor positive, who were treated with this medicinal product and at said dose after having progressed with a previous anti-estrogen therapy. | \n\t\t
\n\t\t\t\t | \n\t\t\tCompare the efficacy and tolerability of two dose-schedules of eribulin (a ketone analog) plus lapatinib in HER2-positive breast cancer, pre-treated with trastuzumab in the adjuvant and/or metastatic setting. | \n\t\t
\n\t\t\t\t | \n\t\t\tEvaluating the treatment of bevacizumab in association with pre-operative chemotherapy, followed by surgery, adjuvant chemotherapy and radiotherapy in patients with inflammatory breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tCompare the safety and efficacy of nab-paclitaxel in combination with either gemcitabine or carboplatin to the combination of gemcitabine and carboplatin as first line treatment in female subjects with triple negative metastatic breast cancer or metastatic triple negative breast cancer. | \n\t\t
\n\t\t\t\t | \n\t\t\tAssess the efficacy and safety of single agent olaparib, a PARP inhibitor, vs standard of care based on physician\'s choice of capecitabine (that is converted to 5-FU during metabolism), vinorelbine (anti-mitotic drug) or eribulin (a ketone analog) in metastatic breast cancer patients with germline BRCA 1/2 mutations. | \n\t\t
\n\t\t\t\t | \n\t\t\tDetermine whether lucitanib, a potent tyrosine kinase inhibitor, is safe and effective in the treatment of patients with fibroblast growth factor aberrant metastatic breast cancer. | \n\t\t
Current clinical trials evaluating therapies for breast cancer
Breast cancer continues to be a threat and a challenge to treat. While a lot has been accomplished in the past decade, there is more that can be done. Further understanding of tumor evolution will lead to the eradication and effective prevention of this disease. At the same time delineating the breast oncogenic mechanisms like DNA damage response, conversion of DNA lesions to mutations, etc. will help us target initiating events and further optimize personalized therapies and possibly develop new ones. Therefore we believe that it is the ‘DNA’ which plays the dominant role and holds the key for effective treatment of the whole phenomenon of breast carcinogenesis.
5-FU: Fluorouracil
AI: Aromatase inhibitor
AKT: Protein kinase B
ALDH1: Aldehyde dehydrogenase 1
AT: Ataxia telangiectasia
ATM: Ataxia telangiectasia mutated
ATR: Ataxia telangiectasia and Rad3 related
BER: Base excision repair
BRCA1: Breast cancer type 1 susceptibility protein
CDK: Cyclin dependent kinase
CFS: Common fragile sites
Chk1: Checkpoint kinase 1
Chk2: Checkpoint kinase 2
CTC: Circulating tumor cells
CXCR1: C-X-C chemokine receptor type 1
DCIS: Ductal carcinoma in situ
DDR: DNA damage response
EGFR: Epidermal derived growth factor
EMT: Epithelial-to-mesenchymal transition
GCDFP15: Gross cystic disease fluid protein-15
GM-CSF: Granulocyte-macrophage colony-stimulating factor
HER2: Human epidermal growth factor receptor 2
HIF1: Hypoxia-inducible factor 1
HR: Homologous recombination
IL6: Interleukin 6
IL8: Interleukin 8
MMP1: Matrix metalloproteinase-1
MMR: Mismatch repair
MRN: MRE11–RAD50–NBS1
NER: Nucleotide excision repair
NHEJ: Non-homologous end joining
PARP: Poly ADP ribose polymerase
PI3K: Phosphatidylinositol-4,5-bisphosphate 3-kinase
PTEN: Phosphatase and tensin homolog
RT: Radiation therapy
SERM: Selective estrogen receptor modulator
TGFβ: Tumor derived growth factor β
TWIST: Twist-related protein
WRN: Werner syndrome ATP-dependent helicase
Somaira Nowsheen and Khaled Aziz thank the Mayo Clinic Medical Scientist Training Program for fostering an outstanding environment for physician-scientist training. Somaira Nowsheen was supported by the Laura J. Siegel Breast Cancer Fellowship Award from the Foundation for Women’s Wellness. Dr. Georgakilas was supported by an EU Marie Curie Reintegration Grant MC-CIG-303514, Greek National funds through the Operational Program Educational and Lifelong Learning of the National Strategic Reference Framework (NSRF)-Research Funding Program: THALES (Grant number MIS 379346) and COST Action CM1201 Biomimetic Radical Chemistry.
Primary liver cancer represents an enduring global threat as the fifth most common cancer worldwide and the second highest global cause of cancer-related mortality [1]. The most common form of liver cancer is hepatocellular carcinoma (HCC), which makes up over 90% of primary hepatic malignancies and independently represents the fourth most common cause of cancer-related death worldwide [2, 3]. Hepatotropic viruses such as hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are the most common causes of HCC, accounting for at least 80% of cases. HCC is also prevalent in individuals with underlying cirrhosis with other risk factors being alcohol use, non-alcoholic fatty liver disease (NAFLD), diabetes mellitus, obesity, aflatoxin exposure, hereditary hemochromatosis, tobacco use, oral contraceptive use, and other inherited metabolic disorders including tyrosinemia and glycogen storage disease type 1 (Von Gierke disease) [4, 5, 6, 7].
The American Association for the Study of Liver Disease (AASLD) recommends that adults with cirrhosis undergo screening for HCC given the overall observed mortality benefit. Surveillance consists of abdominal ultrasonography every six months either with or without alpha fetoprotein (AFP) measurement. Patients who have a lesion ≥ 1 cm or AFP measurement ≥ 20 ng/mL are recommended to undergo further diagnostic evaluation with multiphasic computed tomography (CT) scan or magnetic resonance imaging (MRI) of the abdomen [8, 9]. In some instances, HCC can be diagnosed radiographically via LI-RADS criteria (LR-5 is diagnostic), which consists of imaging findings of washout, enhancing capsule, and threshold growth in addition to overall size diameter increase over the course of months [10]. In instances in which lesions are indeterminate or cannot be diagnosed radiographically, patients typically undergo either biopsy or close interval repeat imaging [8].
Solid tumor oncological staging is usually based on the tumor (T), node (N), and metastasis (M) classification system. This system does not take into account the degree of liver dysfunction or patient performance status and is less useful for predicting the course of HCC [9]. The Barcelona Clinic Liver Cancer (BCLC) staging system is the most universally accepted staging system for HCC as it takes into account tumor burden, liver functional status, and patient performance status. In the BCLC system, patients are classified into different stages, including very early (BCLC stage 0), early (BCLC stage A), intermediate (BCLC stage B), advanced (BCLC stage C), and terminal (BCLC stage D). Very early to early-stage HCC (BCLC stage 0 or A) cancers are treated with curative intent through resection, ablation, or even liver transplant (LT); overall survival is as high as 75% at 5 years. The standard of care for patients with intermediate stage HCC (BCLC stage B) is transarterial chemoembolization (TACE) or transarterial radioembolization (TARE). Patients with advanced HCC (BCLC stage C) often present with cancer-related symptoms but usually have moderately preserved liver function (Child-Pugh A or B). These patients receive systemic therapy, though other treatment modalities are under investigation. BCLC stage D HCC is considered terminal and is usually managed with best supportive care [11, 12].
Unfortunately, over 80% of HCC are diagnosed at the advanced stage (BCLC stage C or D). Therapy options such as TACE and tumor resection are often not appropriate in these patients, and 5-year survival is as low as 18% [13, 14]. Researchers and physicians have been investigating potential effective treatment options in these patients in the past decade and have made great advances. In this systemic review, we summarize the latest strategies and upcoming methods of managing advanced (BCLC stage C) HCC.
HCC has been historically considered a chemotherapy-resistant tumor. Most chemotherapy agents require hepatic metabolism and cannot be used in the setting of severely impaired liver function [15]. Overall survival is often dictated by underlying hepatic function rather than extensive tumor burden. Despite these challenges, researchers have applied targeted immunotherapy for advanced HCC treatment and, at least in certain clinical scenarios, have found benefit [16].
Multi-agent combination therapy with atezolizumab and bevacizumab has recently replaced sorafenib as first line treatment for advanced HCC. Atezolizumab and bevacizumab are monoclonal antibodies that target program death ligand 1 (PD-L1) and vascular endothelial growth factor (VEGF), respectively [17, 18]. When used together, these medications inhibit both T cell apoptosis and angiogenesis. The combination of these medications was compared to sorafenib in patients with treatment naïve advanced HCC in the IMbrave150 trial. The trial showed that patients treated with atezolizumab and bevacizumab had significantly improved overall survival (OS) and progression free survival (PFS) when compared to those treated with sorafenib [17]. Adverse events occurred at similar rates among the two groups, with the most common adverse effects in patients given atezolizumab with bevacizumab being hypertension and proteinuria. Following systemic review of nine randomized control trials, the American Society of Clinical Oncology (ASCO) has deemed combined atezolizumab/bevacizumab as the first line treatment for advanced HCC applicable to those with Child-Pugh A liver disease, Eastern Cooperative Oncology Group Performance Status (ECOG PS) no higher than one and treated esophageal varices (EV) [18]. Recent updates from Finn and colleagues on the IMbrave150 trial reported that median OS was 19.2 months in those taking atezolizumab and bevacizumab vs. 13.4 months in those taking sorafenib (HR, 0.66 [95% CI, 0.52, 0.85]; P=0.0009). At 18 months, those treated with atezolizumab and bevacizumab had an OS of 52% while patients on sorafenib has an OS of 40%. Atezolizumab and bevacizumab combination therapy has demonstrated the longest OS in a front-line phase III clinical study for advanced HCC to date and remains the standard of care for treatment-naïve, advanced HCC [19].
Tyrosine protein kinase inhibitors (TKIs) had been at the forefront of advanced HCC treatment for quite some time. The first TKI approved by the Food and Drug Administration (FDA) for treatment of advanced HCC was sorafenib, which was first approved for treatment of unresectable HCC in 2007 (Table 1). This TKI targets VEGF, platelet derived growth factor (PDGF), and others molecular pathways to inhibit angiogenesis [20]. The Sorafenib Hepatocellular Carcinoma Assessment Randomized Protocol (SHARP) study was the first multi-center, placebo-controlled, phase III clinical trial in untreated, Child-Pugh A advanced HCC patients, and demonstrated a 2.8-month overall survival (OS) in those treated with sorafenib versus placebo (10.7 vs. 2.9 months) [21]. Further clinical trials and subset analysis showed that sorafenib provides survival benefit in patients with HCC not amendable to loco-regional therapy, though the benefit appears to be greater for patients with Child Pugh A cirrhosis than Child Pugh B cirrhosis [22]. Cheng et al. performed a randomized, double-blind, placebo control trial of sorafenib in the Asian Pacific region in patients with advanced HCC. Following six weeks of therapy, patients treated with sorafenib had significantly higher median OS (6.5 months vs. 4.2 months; [HR] 0.68 [95% CI 0.50–0.93]; p=0.014) and time to progression (2.8 months vs. 1.4 months; HR 0.57 [0.42–0.79]; p=0.0005) [23]. Despite the clinical benefits of sorafenib, many patients are unable to tolerate the significant side-effects, which include diarrhea, hand and feet skin irritation, weight-loss, and electrolyte derangements [21, 24, 25]. With its OS benefits and effects on disease progression, sorafenib remains a first-line option for advanced HCC [18].
Regimen | ASCO recommendations | Criteria for use |
---|---|---|
Atezolizumab + Bevacizumab | First-line | ECOG PS ≤ 1, Child-Pugh A, following EV treatment |
Sorafenib | First-line | When there are contraindications to Atezolizumab – Bevacizumab therapy |
Lenvatinib | First-line | |
Nivolumab | First-line or Second-line | |
Cabozantinib | Second-line or Third-line | |
Regorafenib | Second-line | Those who failed Sorafenib |
Ramucirumab | Second-line | AFP ≥ 400 |
Pembrolizumab | Second-line | |
Nivolumab + Ipilimumab | No recommendations |
American Society of Clinical Oncology (ASCO) recommendations for systemic therapy in advanced (BCLC stage C) HCC [18].
Following the success of Sorafenib, several other TKIs were developed as potential treatment options in advanced HCC patients. Lenvatinib is a TKI that targets multiple pathways within angiogenesis including VEGF receptors, fibroblast growth factor (FGF) receptors, platelet derived growth factor (PDGF) alpha as well as RET and KIT [26]. An open-label, multicenter, phase III clinical trial known as the REFLECT trial showed lenvatinib to be non-inferior to sorafenib in advanced HCC patients with respect to OS. In the same trial, patients treated with lenvatinib had a higher incidence of hypertension, decreased appetite, and weight loss, while those treated with sorafenib had a higher incidence of hand-foot skin reaction (HFSR) and diarrhea. Patients treated with lenvatinib had significantly better progression-free survival (PFS) (7.4 months vs. 3.7 months, p < 0.001), time to progression (8.9 months vs. 3.7 months, p < 0.001), and objective response rate (24.1% vs. 9.2%, p < 0.001) [25, 27]. Vogel et al. analyzed prognostic factors of the REFLECT trial and reported that baseline liver function tests such as albumin-bilirubin grade and Child-Pugh score were predictive of OS. These markers may be used to monitor overall safety and efficacy of lenvatinib treatment. Regardless of baseline liver function, lenvatinib led to longer OS than sorafenib [28]. Given this data, the ASCO now considers lenvatinib a reasonable first-line treatment option for advanced HCC [18].
Ongoing studies are being conducted on the use of lenvatinib alongside nivolumab, an anti-PD-1 monoclonal antibody often used as second line therapy for HCC, in patients with unresectable, advanced HCC. Early results from the phase 1b trial of this open label study show that lenvatinib combined with nivolumab is well tolerated in BCLC stage C HCC with multiple patients demonstrating partial or complete response [29].
Other agents have been investigated for advanced HCC for patients with disease resistant to first-line therapy. Cabozantinib is a TKI that targets mesenchymal-epithelial transition (MET) factor to disrupt hepatocyte growth factor pathway, a pathway that is often important for HCC oncogenesis [30]. A phase III clinical study known as the CELESTIAL trial showed that for patients who had suffered disease progression while on sorafenib, cabozantinib led to longer OS and PFS than placebo [31, 32, 33]. Although adverse effects such as diarrhea, HFSR, hypertension, nausea, and decreased appetite, were found to be twice as high in the cabozantinib group than in the placebo group, the effects were generally mild and considered manageable [31, 32, 33]. Given its clinical benefit, the ASCO has classified cabozantinib as a second-line therapy for advanced HCC [18].
Regorafenib is another TKI that has been utilized as a second-line agent in advanced HCC [18, 34, 35]. The RESORCE trial along with other studies support the use of regorafenib in treatment-resistant advanced HCC with active investigations focusing on applying the use of regorafenib in combination with other medications against advanced HCC [36]. When comparing cabozantinib and regorafenib as second line therapy in patients who had failed sorafenib therapy, the side effect profile of these medications was similar (with only increased incidence of diarrhea in patients taking Regorafenib), and both therapies provided similar benefits in regard to OS and PFS [37].
The latest TKI to show efficacy in advanced HCC is a VEGF receptor inhibitor called apatinib. This medication had been implemented in patients with hepatitis B infection in the past. Li et al. performed a multi-center, double blind, randomized phase III control trial in China in patients with advanced HCC refractory to at least one systemic agent [38]. The median OS was significantly higher in those treated with apatinib compared to placebo (8.7 months vs. 6.8 months, p < 0.05). The most common adverse effects of apatinib were hypertension, thrombocytopenia, and HFSR [38].
Clinicians have also applied the use immunomodulatory checkpoint inhibitors as treatment for advanced HCC. Nivolumab is an immunoglobulin (IgG) 4 antibody that targets program death 1 (PD-1) on the surface of T cells to promote the antitumor properties of T cells [39]. Clinical trials have shown nivolumab to be a safe treatment option for advanced HCC with non-comparison studies showing durable and effective clinical response to treatment [40]. Multicenter phase III clinical trials comparing nivolumab to sorafenib are currently underway [41, 42]. Interim results of the CheckMate 459 trial, a randomized, multicenter phase III study, have shown no significant difference in median OS between nivolumab and sorafenib; however, the objective response rate was as high as 15% in those taking nivolumab vs. 7% in those taking sorafenib [41, 42]. Additionally, nivolumab was associated with superior health-related quality of life with patients reporting fewer side effects [43].
Pembrolizumab is another monoclonal antibody directed against PD-1 that has been used as therapy for patients with advanced HCC [44]. The KEYNOTE trials were conducted to evaluate the efficacy of pembrolizumab and were expanded to compare the use of pembrolizumab following disease progression while on sorafenib to best supportive care. Despite pembrolizumab reducing the risk of death by 22%, there was no significant difference in OS between the two groups [44, 45]. Continued research is ongoing regarding the use of this anti-PD-1 agent for advanced HCC treatment.
Ramucirumab is a monoclonal antibody directed against vascular endothelial growth factor receptor 2 (VEGFR-2) that is approved for advanced HCC therapy in patients with alpha-fetoprotein (AFP) levels ≥400 ng/mL. Ramucirumab was initially compared versus placebo in a double-blind, multicenter, randomized control phase III trial known as REACH-1; unfortunately, there was no statistically significant difference in OS for those given ramucirumab or placebo in those who had failed first line sorafenib therapy [46]. Following subgroup analysis of the REACH-1 trial, the REACH-2 trial showed that ramucirumab had a statistically significant survival benefit compared to placebo in patients with AFP ≥400 ng/mL [47, 48]. The side-effect profile of ramucirumab is mild, with only reported increased frequency of hypertension and proteinuria, making it a second-line therapy for advanced HCC by the ASCO for patients with AFP ≥400 ng/mL [18, 46, 47]. Given its specific target population, ramucirumab is not routinely used in HCC patients with AFP <400 ng/mL.
Ipilimumab is a monoclonal antibody that targets cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) to downregulate immune function. The Checkmate 040 trial assessed the use of ipilimumab alongside nivolumab for advanced HCC patients and demonstrated combination therapy to have an object response rate twice as high as nivolumab monotherapy (31% vs. 14%) This combination therapy was also well tolerated with an acceptable side effect profile when compared to similar systemic therapy [49, 50].
The Checkmate 040 trial was expanded to investigate triple combination therapy consisting of nivolumab, ipilimumab, and cabozantinib altogether [51]. When compared to the combination of just nivolumab and ipilimumab, those on triple therapy had a longer period of progression-free survival (6.8 months vs. 5.5 months). Treatment related adverse events were higher in those taking triple therapy with a discontinuation rate of 20% in the triple therapy group and 3% in the double therapy group [51].
Therapies in the form of embolization fall under the category of locoregional therapy and are typically contraindicated in patients with advanced HCC with underlying vascular invasion, extrahepatic spread, or poor performance status. However, some patients with advanced HCC classified as BCLC stage C have benefited from locoregional therapies [52].
Advanced HCC patients with tumor invasion off a branch of the portal vein or limited extrahepatic disease involvement have been trialed with TACE therapy [53]. TACE consists of injecting an emulsified chemotherapeutic agent into the hepatic artery flowing towards the underlying tumor, followed by embolization of the vessel to contain the drug and localize cell death within the malignancy [52, 53]. TACE has historically been more successful in localized disease without extrahepatic or diffuse vascular involvement and serves as the first-line treatment for intermediate (BCLC stage B) HCC. Consensus regarding the overall clinical utility of TACE in advanced HCC when compared to systemic therapy remains under discussion [54]. Certain studies have shown TACE to be clinically safe and feasible in select advanced HCC patients with good collateral blood flow, and a meta-analysis reported TACE to be associated with higher treatment responses in advanced HCC when compared to other more conservative treatment approaches [54]. However, a retrospective analysis by Pinter and colleagues demonstrated no significant difference in OS between patients treated with TACE versus sorafenib, with Child-Pugh class predicting OS in these patients [55]. Meanwhile, Choi et al., reported through retrospective analysis that TACE in addition to sorafenib is associated with significantly increased time to progression when compared to sorafenib therapy alone, though no difference was seen with regard to OS [56]. Other retrospective studies including the TACTICS trial also found that combining TACE with sorafenib in advanced HCC improved progression-free survival when compared to sorafenib therapy alone [57, 58, 59, 60, 61].
Y-90 trans-arterial radio-embolization (TARE) is a therapy modality by which the isotope yttrium90 is delivered in in small vector beads to malignancy areas through branches of the hepatic artery [62]. TARE has been applied to treatment of advanced HCC in tumors that invade discrete segmental areas of the liver. Additionally, TARE has been shown to decrease overall portal vein tumor thrombus load [62]. Recent data indicates that when comparing the efficacy of TARE vs. sorafenib in advanced HCC patients, those who underwent TARE had a significantly higher tumor response rate, though there was no significant difference in OS [63]. Studies have also been conducted on combining TARE with systemic therapy in advanced HCC. No clear benefit was seen when combining TARE with sorafenib [64]; however, there have been case reports or series of positive outcomes in combining TARE with different systemic modalities [65, 66].
Most recently, a multicenter, single-arm, retrospective study conducted at three separate medical centers called the LEGACY study assessed the clinical efficacy of TARE therapy in unrespectable HCC [67]. Chemoembolization served as a primary treatment for 72.2% of the cohort with advanced disease. The three-year OS rate for the entire cohort was 86.6% with 62.2% of patients experiencing a duration of response of greater than six months [67]. This study led to the FDA approval of TheraSphere Y-90 Glass Microsphere for treatment of advanced HCC [68].
Garin et al. conducted research on the dosimetry of TARE therapy through a randomized, multicenter, open-label phase II trial known as DOSISPHERE-01 [69]. Patients received either a standard dose of Y-90 to the perfused lobe or a personalized dose of Y-90 targeted to the index lesion. Results showed that personalized dosimetry significantly improved response rates when compared to standard dosimetry in cases of locally advanced HCC (71% vs. 35%, p < 0.01) [69].
Hepatic artery infusion chemotherapy (HAIC) has been used in the treatment of advanced HCC to directly delivery high concentrations of chemotherapeutic agents [70]. Studies on advanced HCC lesions that were unresectable, refractory to TACE, or associated with portal vein thrombus (PVT) have demonstrated positive responses to HAIC within patient cohorts. Groups in Korea and Japan have implemented HAIC with agents including cisplatin, 5-fluororuacil (5-FU), and pegylated interferon α-2b [70]. A randomized trial comparing interferon therapy coupled with 5-FU HAIC to sole interferon therapy in advanced HCC patients showed a significantly higher response rate (45.6% vs. 24.6%, p < 0.05) and longer median progression free survival (6.5 months vs. 3.3 months, p=0.0048) in the patients who received HAIC [71]. In their study comparing HAIC and sorafenib in advanced HCC patients, Song and colleagues reported that the median overall survival was significantly longer in the patients who received HAIC (OS: 7.1 months vs. 5.5 months, p < 0.05) [72].
As medical and surgical expertise continue to improve, surgery is no longer contraindicated in some advanced HCC patients [73]. Surgical resection of advanced HCC, either in the form of hepatectomy or en-bloc resection, has been revisited as a potentially efficacious way of increasing OS. Data has shown that the overall median survival time in advanced HCC patients with PVT who undergo surgical resection to be between 8 and 22 months, with OS between 21.7% to 69.6% at one year [74]. Given the high incidence of post-operative recurrence, multi-disciplinary approach to surgical planning on a case-by-case basis is needed [74, 75]. Liang and colleagues performed a meta-analysis and found that patients who underwent surgical resection of advanced HCC with PVT had longer OS than those who were treated with TACE therapy [76].
The combination of systemic therapy with surgical resection has also been applied to advanced HCC patients. Takeyama et al. studied the use of sorafenib as a potential neo-adjuvant therapy prior to surgical resection. Patients who underwent surgical resection following treatment with sorafenib had a significantly increased three-year survival than patients who underwent therapy with sorafenib alone [77]. Incorporating surgical resection with other treatment modalities including TACE and radiofrequency ablation have also promoted positive prognostic outcomes in select patients [74, 75]. Overall, the indication for surgical therapy in advanced HCC patients with or without PVT requires a multi-disciplinary approach and may entail utilizing systemic or locoregional therapy during treatment planning.
Several systemic agents have been trialed for treatment of advanced HCC over the past decade. As newer agents are approved for use in advanced HCC, combined treatment options remain intriguing topics for investigation. Gosain et al. have hypothesized that sorafenib and pembrolizumab may have synergistic effects and are currently conducting a trial to evaluate the efficacy of these drugs when used in combination [78]. Given the favorable response rates of nivolumab that were seen in the Checkmate 040 trial, Welling et al. are conducting a phase II, randomized control of nivolumab combined with HuMax-IL8 and cabiralizumab (an anti-CSF1R antibody) in advanced HCC patients. HuMax-IL8 (now known as BMS-986253) is a novel, fully human monoclonal antibody that inhibits interleukin-8 (IL-8) [79]. Combining locoregional with systemic therapy is also under investigation [80]. Among multiple studies being conducted, the EMERALD-1 trial is a randomized, double-blind, placebo-controlled phase III study assessing anti-PD-1 agent durvalumab alongside TACE therapy with or without bevacizumab [81].
Alternative molecular targets are also being evaluated. El-Khouiery et al. are currently working on an advanced HCC phase I trial of humanized agonist IgG2 monoclonal antibodies to a specific tumor necrosis factor receptor known as OX40. Underlying safety and pharmacodynamic dose-dependent response are now being investigated [82]. Another phase I trial currently underway involves a small activating RNA (saRNA) known as MTL-CEBPA that targets transcription factor C/EBP-α, which is involved in hepatic homeostasis and cell-cycle control. The preliminary results showed that it is relatively safety and can have potential synergistic efficacy with tyrosine kinase inhibitors in HCC [83]. Like new combinations of locoregional-systemic combinations and new uses of systemic agents, novel molecular-targeting agents offer hope for improved outcomes in advanced HCC.
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\\n\\nOpenness - We communicate honestly and transparently. We are open to constructive criticism and committed to learning from it.
\\n\\nDisruptiveness - We are eager for discovery, for new ideas and for progression. We approach our work with creativity and determination, with a clear vision that drives us forward. We look beyond today and strive for a better tomorrow.
\\n\\nIntechOpen is a dynamic, vibrant company, where exceptional people are achieving great things. We offer a creative, dedicated, committed, and passionate environment but never lose sight of the fact that science and discovery is exciting and rewarding. We constantly strive to ensure that members of our community can work, travel, meet world-renowned researchers and grow their own career and develop their own experiences.
\\n\\nIf this sounds like a place that you would like to work, whether you are at the beginning of your career or are an experienced professional, we invite you to drop us a line and tell us why you could be the right person for IntechOpen.
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Integrity - We are consistent and dependable, always striving for precision and accuracy in the true spirit of science.
\n\nOpenness - We communicate honestly and transparently. We are open to constructive criticism and committed to learning from it.
\n\nDisruptiveness - We are eager for discovery, for new ideas and for progression. We approach our work with creativity and determination, with a clear vision that drives us forward. We look beyond today and strive for a better tomorrow.
\n\nIntechOpen is a dynamic, vibrant company, where exceptional people are achieving great things. We offer a creative, dedicated, committed, and passionate environment but never lose sight of the fact that science and discovery is exciting and rewarding. We constantly strive to ensure that members of our community can work, travel, meet world-renowned researchers and grow their own career and develop their own experiences.
\n\nIf this sounds like a place that you would like to work, whether you are at the beginning of your career or are an experienced professional, we invite you to drop us a line and tell us why you could be the right person for IntechOpen.
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His studies in robotics lead him not only to a PhD degree but also inspired him to co-found and build the International Journal of Advanced Robotic Systems - world's first Open Access journal in the field of robotics.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"441",title:"Ph.D.",name:"Jaekyu",middleName:null,surname:"Park",slug:"jaekyu-park",fullName:"Jaekyu Park",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/441/images/1881_n.jpg",biography:null,institutionString:null,institution:{name:"LG Corporation (South Korea)",country:{name:"Korea, South"}}},{id:"465",title:"Dr",name:"Christian",middleName:null,surname:"Martens",slug:"christian-martens",fullName:"Christian Martens",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"479",title:"Dr.",name:"Valentina",middleName:null,surname:"Colla",slug:"valentina-colla",fullName:"Valentina Colla",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/479/images/358_n.jpg",biography:null,institutionString:null,institution:{name:"Sant'Anna School of Advanced Studies",country:{name:"Italy"}}},{id:"494",title:"PhD",name:"Loris",middleName:null,surname:"Nanni",slug:"loris-nanni",fullName:"Loris Nanni",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/494/images/system/494.jpg",biography:"Loris Nanni received his Master Degree cum laude on June-2002 from the University of Bologna, and the April 26th 2006 he received his Ph.D. in Computer Engineering at DEIS, University of Bologna. On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. 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From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. 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After finishing his P. hD degree in 1992, he served in the Industry as a Scientific Officer and continued his academic career as a visiting scholar for a number of educational institutions. In 1996 he joined National University of Science & Technology Pakistan (NUST) as an Associate Professor; NUST is one of the top few universities in Pakistan. In 1999 he joined an International Company Lineo Inc, Canada as Manager Compiler Group, where he headed the group for developing Compiler Tool Chain and Porting of Operating Systems for the BLACKfin processor. The processor development was a joint venture by Intel and Analog Devices. In 2002 Lineo Inc., was taken over by another company, so he joined Aalborg University Denmark as an Assistant Professor.\nProfessor Akbar has truly a multi-disciplined career and he continued his legacy and making progress in many areas of his interests both in teaching and research. 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These reactions occur through a regular radical chain causing growth of polymer by three steps, namely, initiation, propagation, and termination. To understand ionizing radiation-induced polymerization, the water radiolysis must be taken into consideration. This chapter explores the mechanism of water molecules radiolysis paying especial attention to the basic regularities of solvent radicals’ interaction with the polymer molecules for forming the crosslinked polymer. Water radiolysis is the main engine of the polymerization processes, especially the “free-radical polymerization.” The mechanisms of the free-radical polymerization and crosslinking will be discussed in detail later. Since different polymers respond differently to radiation, it is useful to quantify the response, namely in terms of crosslinking and chain scission. A parameter called the G-value is frequently used for this purpose. It represents the chemical yield of crosslinks, scissions and double bonds, etc. For the crosslinked polymer, the crosslinking density increases with increasing the radiation dose, this is reflected by the swelling degree of the polymer while being immersed in a compatible solvent. If crosslinking predominates, the crosslinking density increases and the extent of swelling decreases. If chain scission predominates, the opposite occurs. A further detailed discussion of these aspects is presented throughout this chapter.",book:{id:"6149",slug:"ionizing-radiation-effects-and-applications",title:"Ionizing Radiation Effects and Applications",fullTitle:"Ionizing Radiation Effects and Applications"},signatures:"Mohamed Mohamady Ghobashy",authors:[{id:"212371",title:"Dr.",name:"Mohamed",middleName:null,surname:"Mohamady Ghobashy",slug:"mohamed-mohamady-ghobashy",fullName:"Mohamed Mohamady Ghobashy"}]},{id:"53504",doi:"10.5772/66925",title:"Applications of Ionizing Radiation in Mutation Breeding",slug:"applications-of-ionizing-radiation-in-mutation-breeding",totalDownloads:3478,totalCrossrefCites:9,totalDimensionsCites:13,abstract:"As a predicted result of increasing population worldwide, improvements in the breeding strategies in agriculture are valued as mandatory. The natural resources are limited, and due to the natural disasters like sudden and severe abiotic stress factors, excessive floods, etc., the production capacities are changed per year. In contrast, the yield potential should be significantly increased to cope with this problem. Despite rich genetic diversity, manipulation of the cultivars through alternative techniques such as mutation breeding becomes important. Radiation is proven as an effective method as a unique method to increase the genetic variability of the species. Gamma radiation is the most preferred physical mutagen by plant breeders. Several mutant varieties have been successfully introduced into commercial production by this method. Combinational use of in vitro tissue culture and mutation breeding methods makes a significant contribution to improve new crops. Large populations and the target mutations can be easily screened and identified by new methods. Marker assisted selection and advanced techniques such as microarray, next generation sequencing methods to detect a specific mutant in a large population will help to the plant breeders to use ionizing radiation efficiently in breeding programs.",book:{id:"5451",slug:"new-insights-on-gamma-rays",title:"New Insights on Gamma Rays",fullTitle:"New Insights on Gamma Rays"},signatures:"Özge Çelik and Çimen Atak",authors:[{id:"147362",title:"Dr.",name:"Özge",middleName:null,surname:"Çelik",slug:"ozge-celik",fullName:"Özge Çelik"},{id:"147364",title:"Prof.",name:"Çimen",middleName:null,surname:"Atak",slug:"cimen-atak",fullName:"Çimen Atak"}]},{id:"32846",doi:"10.5772/36950",title:"Current Importance and Potential Use of Low Doses of Gamma Radiation in Forest Species",slug:"current-importance-and-potential-use-of-low-doses-of-gamma-radiation-in-forest-species",totalDownloads:5277,totalCrossrefCites:2,totalDimensionsCites:13,abstract:null,book:{id:"1590",slug:"gamma-radiation",title:"Gamma Radiation",fullTitle:"Gamma Radiation"},signatures:"L. G. Iglesias-Andreu, P. Octavio-Aguilar and J. Bello-Bello",authors:[{id:"110581",title:"Dr.",name:"Lourdes",middleName:null,surname:"Iglesias-Andreu",slug:"lourdes-iglesias-andreu",fullName:"Lourdes Iglesias-Andreu"}]},{id:"58410",doi:"10.5772/intechopen.72074",title:"Radiation-Induced Degradation of Organic Compounds and Radiation Technologies for Purification of Aqueous Systems",slug:"radiation-induced-degradation-of-organic-compounds-and-radiation-technologies-for-purification-of-aq",totalDownloads:1415,totalCrossrefCites:8,totalDimensionsCites:12,abstract:"Environmental application of radiation technologies is an important part of radiation processing. Radiation treatment of aqueous systems contaminated with organic compounds is a promising method of water and wastewater purification and corresponding technologies are being developed. In this chapter, the following aspects of radiation treatment process are considered: sources of contamination and major contaminants of water and wastewater; primary processes in aqueous systems initiated by ionizing radiation; principal ways of contaminant conversion as consequences of primary processes (complete mineralization of organic compounds, partial decomposition of organic molecules resulted in detoxification, decolorization, disinfection of polluted water, and improvement in biological degradation of contaminant, polymerization of monomers’ contaminants, oxidation-reduction processes, and coagulation of colloids); sources of ionizing radiation; and main equipment applied in radiation technologies of aqueous system purification.",book:{id:"6149",slug:"ionizing-radiation-effects-and-applications",title:"Ionizing Radiation Effects and Applications",fullTitle:"Ionizing Radiation Effects and Applications"},signatures:"Igor E. Makarov and Alexander V. Ponomarev",authors:[{id:"213652",title:"Dr.",name:"Igor",middleName:null,surname:"Makarov",slug:"igor-makarov",fullName:"Igor Makarov"},{id:"213657",title:"Dr.",name:"Alexander",middleName:null,surname:"Ponomarev",slug:"alexander-ponomarev",fullName:"Alexander Ponomarev"}]}],mostDownloadedChaptersLast30Days:[{id:"32842",title:"Sterilization by Gamma Irradiation",slug:"sterilization-by-gamma-irradiation",totalDownloads:74766,totalCrossrefCites:37,totalDimensionsCites:85,abstract:null,book:{id:"1590",slug:"gamma-radiation",title:"Gamma Radiation",fullTitle:"Gamma Radiation"},signatures:"Kátia Aparecida da Silva Aquino",authors:[{id:"102109",title:"Dr.",name:"Katia",middleName:"Aparecida Da S.",surname:"Aquino",slug:"katia-aquino",fullName:"Katia Aquino"}]},{id:"32837",title:"Environmental Gamma-Ray Observation in Deep Sea",slug:"environmental-gamma-ray-observation-in-deep-sea-",totalDownloads:2917,totalCrossrefCites:4,totalDimensionsCites:6,abstract:null,book:{id:"1590",slug:"gamma-radiation",title:"Gamma Radiation",fullTitle:"Gamma Radiation"},signatures:"Hidenori Kumagai, Ryoichi Iwase, Masataka Kinoshita, Hideaki Machiyama, Mutsuo Hattori and Masaharu Okano",authors:[{id:"108174",title:"Dr.",name:"Hidenori",middleName:null,surname:"Kumagai",slug:"hidenori-kumagai",fullName:"Hidenori Kumagai"},{id:"108237",title:"Dr.",name:"Masa",middleName:null,surname:"Kinoshita",slug:"masa-kinoshita",fullName:"Masa Kinoshita"},{id:"137650",title:"Dr.",name:"Ryoichi",middleName:null,surname:"Iwase",slug:"ryoichi-iwase",fullName:"Ryoichi Iwase"},{id:"137656",title:"Dr.",name:"Hideaki",middleName:null,surname:"Machiyama",slug:"hideaki-machiyama",fullName:"Hideaki Machiyama"},{id:"146918",title:"Dr.",name:"Mutsuo",middleName:null,surname:"Hattori",slug:"mutsuo-hattori",fullName:"Mutsuo Hattori"},{id:"146919",title:"Dr.",name:"Masaharu",middleName:null,surname:"Okano",slug:"masaharu-okano",fullName:"Masaharu Okano"}]},{id:"58998",title:"Ionizing Radiation-Induced Polymerization",slug:"ionizing-radiation-induced-polymerization",totalDownloads:1784,totalCrossrefCites:8,totalDimensionsCites:17,abstract:"Ionizing radiation can induce some kinds of reactions, other than polymerization, such as dimerization, oligomerization, curing, and grafting. These reactions occur through a regular radical chain causing growth of polymer by three steps, namely, initiation, propagation, and termination. To understand ionizing radiation-induced polymerization, the water radiolysis must be taken into consideration. This chapter explores the mechanism of water molecules radiolysis paying especial attention to the basic regularities of solvent radicals’ interaction with the polymer molecules for forming the crosslinked polymer. Water radiolysis is the main engine of the polymerization processes, especially the “free-radical polymerization.” The mechanisms of the free-radical polymerization and crosslinking will be discussed in detail later. Since different polymers respond differently to radiation, it is useful to quantify the response, namely in terms of crosslinking and chain scission. A parameter called the G-value is frequently used for this purpose. 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A further detailed discussion of these aspects is presented throughout this chapter.",book:{id:"6149",slug:"ionizing-radiation-effects-and-applications",title:"Ionizing Radiation Effects and Applications",fullTitle:"Ionizing Radiation Effects and Applications"},signatures:"Mohamed Mohamady Ghobashy",authors:[{id:"212371",title:"Dr.",name:"Mohamed",middleName:null,surname:"Mohamady Ghobashy",slug:"mohamed-mohamady-ghobashy",fullName:"Mohamed Mohamady Ghobashy"}]},{id:"53780",title:"Gamma-Ray Spectrometry and the Investigation of Environmental and Food Samples",slug:"gamma-ray-spectrometry-and-the-investigation-of-environmental-and-food-samples",totalDownloads:2501,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Gamma radiation consists of high‐energy photons and penetrates matter. This is an advantage for the detection of gamma rays, as gamma spectrometry does not need the elimination of the matrix. The disadvantage is the need of shielding to protect against this radiation. Gamma rays are everywhere: in the atmosphere; gamma nuclides are produced by radiation of the sun; in the Earth, the primordial radioactive nuclides thorium and uranium are sources for gamma and other radiation. The technical enrichment and use of radioisotopes led to the unscrupulously use of radioactive material and to the Cold War, with over 900 bomb tests from 1945 to 1990, combined with global fallout over the northern hemisphere. The friendly use of radiation in medicine and for the production of energy at nuclear power plants (NPPs) has caused further expositions with ionising radiation. This chapter describes in a practical manner the instrumentation for the detection of gamma radiation and some results of the use of these techniques in environmental and food investigations.",book:{id:"5451",slug:"new-insights-on-gamma-rays",title:"New Insights on Gamma Rays",fullTitle:"New Insights on Gamma Rays"},signatures:"Markus R. 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Some candidates of the GeV counterpart of gamma-ray bursts, observed by Tupi telescopes, are also presented.",book:{id:"5451",slug:"new-insights-on-gamma-rays",title:"New Insights on Gamma Rays",fullTitle:"New Insights on Gamma Rays"},signatures:"Carlos Navia and Marcel Nogueira de Oliveira",authors:[{id:"189908",title:"Dr.",name:"Carlos",middleName:null,surname:"Navia",slug:"carlos-navia",fullName:"Carlos Navia"},{id:"243084",title:"MSc.",name:"Marcel",middleName:null,surname:"De Oliveira",slug:"marcel-de-oliveira",fullName:"Marcel De Oliveira"}]}],onlineFirstChaptersFilter:{topicId:"227",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:32,numberOfPublishedChapters:318,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:15,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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He is currently appointed as the Voigt Chair in Data Science in the Department of Industrial Engineering, with a joint appointment as Professor in the Computer Science Division, Stellenbosch University. Prior to his appointment at Stellenbosch University, he has been at the University of Pretoria, Department of Computer Science (1998-2018), where he was appointed as South Africa Research Chair in Artifical Intelligence (2007-2018), the head of the Department of Computer Science (2008-2017), and Director of the Institute for Big Data and Data Science (2017-2018). 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Travieso-González received his MSc degree in Telecommunication Engineering at Polytechnic University of Catalonia (UPC), Spain in 1997, and his Ph.D. degree in 2002 at the University of Las Palmas de Gran Canaria (ULPGC-Spain). He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. He is the founder of The IEEE IWOBI conference series and the president of its Steering Committee, as well as the founder of both the InnoEducaTIC and APPIS conference series. He is an evaluator of project proposals for the European Union (H2020), Medical Research Council (MRC, UK), Spanish Government (ANECA, Spain), Research National Agency (ANR, France), DAAD (Germany), Argentinian Government, and the Colombian Institutions. He has been a reviewer in different indexed international journals (<70) and conferences (<250) since 2001. He has been a member of the IASTED Technical Committee on Image Processing from 2007 and a member of the IASTED Technical Committee on Artificial Intelligence and Expert Systems from 2011. \n\nHe has held the general chair position for the following: ACM-APPIS (2020, 2021), IEEE-IWOBI (2019, 2020 and 2020), A PPIS (2018, 2019), IEEE-IWOBI (2014, 2015, 2017, 2018), InnoEducaTIC (2014, 2017), IEEE-INES (2013), NoLISP (2011), JRBP (2012), and IEEE-ICCST (2005)\n\nHe is an associate editor of the Computational Intelligence and Neuroscience Journal (Hindawi – Q2 JCR-ISI). He was vice dean from 2004 to 2010 in the Higher Technical School of Telecommunication Engineers at ULPGC and the vice dean of Graduate and Postgraduate Studies from March 2013 to November 2017. 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His research interests include computer/machine vision, machine learning, pattern recognition, computational intelligence. \nDr. Papakostas served as a reviewer in numerous journals, as a program\ncommittee member in international conferences and he is a member of the IAENG, MIR Labs, EUCogIII, INSTICC and the Technical Chamber of Greece (TEE).",institutionString:null,institution:{name:"International Hellenic University",institutionURL:null,country:{name:"Greece"}}},editorTwo:null,editorThree:null},{id:"25",title:"Evolutionary Computation",coverUrl:"https://cdn.intechopen.com/series_topics/covers/25.jpg",isOpenForSubmission:!0,annualVolume:11421,editor:{id:"136112",title:"Dr.",name:"Sebastian",middleName:null,surname:"Ventura Soto",slug:"sebastian-ventura-soto",fullName:"Sebastian Ventura Soto",profilePictureURL:"https://mts.intechopen.com/storage/users/136112/images/system/136112.png",biography:"Sebastian Ventura is a Spanish researcher, a full professor with the Department of Computer Science and Numerical Analysis, University of Córdoba. 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He is an academic staff member of the Department of Reproduction and Artificial Insemination, Selçuk University, Turkey. He manages several studies on sperms and embryos and is an editorial board member for several international journals. His studies include sperm cryobiology, in vitro fertilization, and embryo production in animals.",institutionString:"Selçuk University, Faculty of Veterinary Medicine",institution:null},{id:"90846",title:"Prof.",name:"Yusuf",middleName:null,surname:"Bozkurt",slug:"yusuf-bozkurt",fullName:"Yusuf Bozkurt",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/90846/images/system/90846.jpg",biography:"Yusuf Bozkurt has a BSc, MSc, and Ph.D. from Ankara University, Turkey. He is currently a Professor of Biotechnology of Reproduction in the field of Aquaculture, İskenderun Technical University, Turkey. His research interests include reproductive biology and biotechnology with an emphasis on cryo-conservation. He is on the editorial board of several international peer-reviewed journals and has published many papers. Additionally, he has participated in many international and national congresses, seminars, and workshops with oral and poster presentations. He is an active member of many local and international organizations.",institutionString:"İskenderun Technical University",institution:{name:"İskenderun Technical University",country:{name:"Turkey"}}},{id:"61139",title:"Dr.",name:"Sergey",middleName:null,surname:"Tkachev",slug:"sergey-tkachev",fullName:"Sergey Tkachev",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/61139/images/system/61139.png",biography:"Dr. Sergey Tkachev is a senior research scientist at the Institute of Fundamental Medicine and Biology, Kazan Federal University, Russia, and at the Institute of Chemical Biology and Fundamental Medicine SB RAS, Novosibirsk, Russia. He received his Ph.D. in Molecular Biology with his thesis “Genetic variability of the tick-borne encephalitis virus in natural foci of Novosibirsk city and its suburbs.” His primary field is molecular virology with research emphasis on vector-borne viruses, especially tick-borne encephalitis virus, Kemerovo virus and Omsk hemorrhagic fever virus, rabies virus, molecular genetics, biology, and epidemiology of virus pathogens.",institutionString:"Russian Academy of Sciences",institution:{name:"Russian Academy of Sciences",country:{name:"Russia"}}},{id:"310962",title:"Dr.",name:"Amlan",middleName:"Kumar",surname:"Patra",slug:"amlan-patra",fullName:"Amlan Patra",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/310962/images/system/310962.jpg",biography:"Amlan K. Patra, FRSB, obtained a Ph.D. in Animal Nutrition from Indian Veterinary Research Institute, India, in 2002. He is currently an associate professor at West Bengal University of Animal and Fishery Sciences. He has more than twenty years of research and teaching experience. He held previous positions at the American Institute for Goat Research, The Ohio State University, Columbus, USA, and Free University of Berlin, Germany. His research focuses on animal nutrition, particularly ruminants and poultry nutrition, gastrointestinal electrophysiology, meta-analysis and modeling in nutrition, and livestock–environment interaction. He has authored around 175 articles in journals, book chapters, and proceedings. Dr. Patra serves on the editorial boards of several reputed journals.",institutionString:null,institution:{name:"West Bengal University of Animal and Fishery Sciences",country:{name:"India"}}},{id:"53998",title:"Prof.",name:"László",middleName:null,surname:"Babinszky",slug:"laszlo-babinszky",fullName:"László Babinszky",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/53998/images/system/53998.png",biography:"László Babinszky is Professor Emeritus, Department of Animal Nutrition Physiology, University of Debrecen, Hungary. He has also worked in the Department of Animal Nutrition, University of Wageningen, Netherlands; the Institute for Livestock Feeding and Nutrition (IVVO), Lelystad, Netherlands; the Agricultural University of Vienna (BOKU); the Institute for Animal Breeding and Nutrition, Austria; and the Oscar Kellner Research Institute for Animal Nutrition, Rostock, Germany. In 1992, Dr. Babinszky obtained a Ph.D. in Animal Nutrition from the University of Wageningen. His main research areas are swine and poultry nutrition. He has authored more than 300 publications (papers, book chapters) and edited four books and fourteen international conference proceedings.",institutionString:"University of Debrecen",institution:{name:"University of Debrecen",country:{name:"Hungary"}}},{id:"201830",title:"Dr.",name:"Fernando",middleName:"Sanchez",surname:"Davila",slug:"fernando-davila",fullName:"Fernando Davila",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/201830/images/5017_n.jpg",biography:"I am a professor at UANL since 1988. My research lines are the development of reproductive techniques in small ruminants. We also conducted research on sexual and social behavior in males.\nI am Mexican and study my professional career as an engineer in agriculture and animal science at UANL. Then take a masters degree in science in Germany (Animal breeding). Take a doctorate in animal science at the UANL.",institutionString:null,institution:{name:"Universidad Autónoma de Nuevo León",country:{name:"Mexico"}}},{id:"309250",title:"Dr.",name:"Miguel",middleName:null,surname:"Quaresma",slug:"miguel-quaresma",fullName:"Miguel Quaresma",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/309250/images/9059_n.jpg",biography:"Miguel Nuno Pinheiro Quaresma was born on May 26, 1974 in Dili, Timor Island. He is married with two children: a boy and a girl, and he is a resident in Vila Real, Portugal. He graduated in Veterinary Medicine in August 1998 and obtained his Ph.D. degree in Veterinary Sciences -Clinical Area in February 2015, both from the University of Trás-os-Montes e Alto Douro. He is currently enrolled in the Alternative Residency of the European College of Animal Reproduction. He works as a Senior Clinician at the Veterinary Teaching Hospital of UTAD (HVUTAD) with a role in clinical activity in the area of livestock and equine species as well as to support teaching and research in related areas. He teaches as an Invited Professor in Reproduction Medicine I and II of the Master\\'s in Veterinary Medicine degree at UTAD. Currently, he holds the position of Chairman of the Portuguese Buiatrics Association. He is a member of the Consultive Group on Production Animals of the OMV. He has 19 publications in indexed international journals (ISIS), as well as over 60 publications and oral presentations in both Portuguese and international journals and congresses.",institutionString:"University of Trás-os-Montes and Alto Douro",institution:{name:"University of Trás-os-Montes and Alto Douro",country:{name:"Portugal"}}},{id:"38652",title:"Prof.",name:"Rita",middleName:null,surname:"Payan-Carreira",slug:"rita-payan-carreira",fullName:"Rita Payan-Carreira",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRiFPQA0/Profile_Picture_1614601496313",biography:"Rita Payan Carreira earned her Veterinary Degree from the Faculty of Veterinary Medicine in Lisbon, Portugal, in 1985. She obtained her Ph.D. in Veterinary Sciences from the University of Trás-os-Montes e Alto Douro, Portugal. After almost 32 years of teaching at the University of Trás-os-Montes and Alto Douro, she recently moved to the University of Évora, Department of Veterinary Medicine, where she teaches in the field of Animal Reproduction and Clinics. Her primary research areas include the molecular markers of the endometrial cycle and the embryo–maternal interaction, including oxidative stress and the reproductive physiology and disorders of sexual development, besides the molecular determinants of male and female fertility. She often supervises students preparing their master's or doctoral theses. She is also a frequent referee for various journals.",institutionString:null,institution:{name:"University of Évora",country:{name:"Portugal"}}},{id:"283019",title:"Dr.",name:"Oudessa",middleName:null,surname:"Kerro Dego",slug:"oudessa-kerro-dego",fullName:"Oudessa Kerro Dego",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/283019/images/system/283019.png",biography:"Dr. Kerro Dego is a veterinary microbiologist with training in veterinary medicine, microbiology, and anatomic pathology. Dr. Kerro Dego is an assistant professor of dairy health in the department of animal science, the University of Tennessee, Institute of Agriculture, Knoxville, Tennessee. He received his D.V.M. (1997), M.S. (2002), and Ph.D. (2008) degrees in Veterinary Medicine, Animal Pathology and Veterinary Microbiology from College of Veterinary Medicine, Addis Ababa University, Ethiopia; College of Veterinary Medicine, Utrecht University, the Netherlands and Western College of Veterinary Medicine, University of Saskatchewan, Canada respectively. He did his Postdoctoral training in microbial pathogenesis (2009 - 2015) in the Department of Animal Science, the University of Tennessee, Institute of Agriculture, Knoxville, Tennessee. Dr. Kerro Dego’s research focuses on the prevention and control of infectious diseases of farm animals, particularly mastitis, improving dairy food safety, and mitigation of antimicrobial resistance. Dr. Kerro Dego has extensive experience in studying the pathogenesis of bacterial infections, identification of virulence factors, and vaccine development and efficacy testing against major bacterial mastitis pathogens. Dr. Kerro Dego conducted numerous controlled experimental and field vaccine efficacy studies, vaccination, and evaluation of immunological responses in several species of animals, including rodents (mice) and large animals (bovine and ovine).",institutionString:"University of Tennessee at Knoxville",institution:{name:"University of Tennessee at Knoxville",country:{name:"United States of America"}}},{id:"251314",title:"Dr.",name:"Juan Carlos",middleName:null,surname:"Gardón",slug:"juan-carlos-gardon",fullName:"Juan Carlos Gardón",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/251314/images/system/251314.jpeg",biography:"Juan Carlos Gardón Poggi received University degree from the Faculty of Agrarian Science in Argentina, in 1983. Also he received Masters Degree and PhD from Córdoba University, Spain. He is currently a Professor at the Catholic University of Valencia San Vicente Mártir, at the Department of Medicine and Animal Surgery. He teaches diverse courses in the field of Animal Reproduction and he is the Director of the Veterinary Farm. He also participates in academic postgraduate activities at the Veterinary Faculty of Murcia University, Spain. His research areas include animal physiology, physiology and biotechnology of reproduction either in males or females, the study of gametes under in vitro conditions and the use of ultrasound as a complement to physiological studies and development of applied biotechnologies. Routinely, he supervises students preparing their doctoral, master thesis or final degree projects.",institutionString:"Catholic University of Valencia San Vicente Mártir, Spain",institution:null},{id:"125292",title:"Dr.",name:"Katy",middleName:null,surname:"Satué Ambrojo",slug:"katy-satue-ambrojo",fullName:"Katy Satué Ambrojo",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/125292/images/system/125292.jpeg",biography:"Katy Satué Ambrojo received her Veterinary Medicine degree, Master degree in Equine Technology and doctorate in Veterinary Medicine from the Faculty of Veterinary, CEU-Cardenal Herrera University in Valencia, Spain. She is a Full Professor at the Department of Medicine and Animal Surgery at the same University. She developed her research activity in the field of Endocrinology, Hematology, Biochemistry and Immunology of horses. She is a scientific reviewer of several international journals : American Journal of Obstetrics and Gynecology, Comparative Clinical Pathology, Veterinary Clinical Pathology, Journal of Equine Veterinary Science, Reproduction in Domestic Animals, Research Veterinary Science, Brazilian Journal of Medical and Biological Research, Livestock Production Science and Theriogenology. Since 2014, she has been the Head of the Clinical Analysis Laboratory of the Hospital Clínico Veterinario from the Faculty of Veterinary, CEU-Cardenal Herrera University.",institutionString:"CEU-Cardenal Herrera University",institution:{name:"CEU Cardinal Herrera University",country:{name:"Spain"}}},{id:"309529",title:"Dr.",name:"Albert",middleName:null,surname:"Rizvanov",slug:"albert-rizvanov",fullName:"Albert Rizvanov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/309529/images/9189_n.jpg",biography:'Albert A. Rizvanov is a Professor and Director of the Center for Precision and Regenerative Medicine at the Institute of Fundamental Medicine and Biology, Kazan Federal University (KFU), Russia. He is the Head of the Center of Excellence “Regenerative Medicine” and Vice-Director of Strategic Academic Unit \\"Translational 7P Medicine\\". Albert completed his Ph.D. at the University of Nevada, Reno, USA and Dr.Sci. at KFU. He is a corresponding member of the Tatarstan Academy of Sciences, Russian Federation. Albert is an author of more than 300 peer-reviewed journal articles and 22 patents. He has supervised 11 Ph.D. and 2 Dr.Sci. dissertations. Albert is the Head of the Dissertation Committee on Biochemistry, Microbiology, and Genetics at KFU.\nORCID https://orcid.org/0000-0002-9427-5739\nWebsite https://kpfu.ru/Albert.Rizvanov?p_lang=2',institutionString:"Kazan Federal University",institution:{name:"Kazan Federal University",country:{name:"Russia"}}},{id:"210551",title:"Dr.",name:"Arbab",middleName:null,surname:"Sikandar",slug:"arbab-sikandar",fullName:"Arbab Sikandar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/210551/images/system/210551.jpg",biography:"Dr. Arbab Sikandar, PhD, M. Phil, DVM was born on April 05, 1981. He is currently working at the College of Veterinary & Animal Sciences as an Assistant Professor. He previously worked as a lecturer at the same University. \nHe is a Member/Secretory of Ethics committee (No. CVAS-9377 dated 18-04-18), Member of the QEC committee CVAS, Jhang (Regr/Gen/69/873, dated 26-10-2017), Member, Board of studies of Department of Basic Sciences (No. CVAS. 2851 Dated. 12-04-13, and No. CVAS, 9024 dated 20/11/17), Member of Academic Committee, CVAS, Jhang (No. CVAS/2004, Dated, 25-08-12), Member of the technical committee (No. CVAS/ 4085, dated 20,03, 2010 till 2016).\n\nDr. Arbab Sikandar contributed in five days hands-on-training on Histopathology at the Department of Pathology, UVAS from 12-16 June 2017. He received a Certificate of appreciation for contributions for Popularization of Science and Technology in the Society on 17-11-15. He was the resource person in the lecture series- ‘scientific writing’ at the Department of Anatomy and Histology, UVAS, Lahore on 29th October 2015. He won a full fellowship as a principal candidate for the year 2015 in the field of Agriculture, EICA, Egypt with ref. to the Notification No. 12(11) ACS/Egypt/2014 from 10 July 2015 to 25th September 2015.; he received a grant of Rs. 55000/- as research incentives from Director, Advanced Studies and Research, UVAS, Lahore upon publications of research papers in IF Journals (DR/215, dated 19-5-2014.. He obtained his PhD by winning a HEC Pakistan indigenous Scholarship, ‘Ph.D. fellowship for 5000 scholars – Phase II’ (2av1-147), 17-6/HEC/HRD/IS-II/12, November 15, 2012. \n\nDr. Sikandar is a member of numerous societies: Registered Veterinary Medical Practitioner (life member) and Registered Veterinary Medical Faculty of Pakistan Veterinary Medical Council. The Registration code of PVMC is RVMP/4298 and RVMF/ 0102.; Life member of the University of Veterinary and Animal Sciences, Lahore, Alumni Association with S# 664, dated: 6-4-12. ; Member 'Vets Care Organization Pakistan” with Reference No. VCO-605-149, dated 05-04-06. :Member 'Vet Crescent” (Society of Animal Health and Production), UVAS, Lahore.",institutionString:"University of Veterinary & Animal Science",institution:{name:"University of Veterinary and Animal Sciences",country:{name:"Pakistan"}}},{id:"311663",title:"Dr.",name:"Prasanna",middleName:null,surname:"Pal",slug:"prasanna-pal",fullName:"Prasanna Pal",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/311663/images/13261_n.jpg",biography:null,institutionString:null,institution:{name:"National Dairy Research Institute",country:{name:"India"}}},{id:"202192",title:"Dr.",name:"Catrin",middleName:null,surname:"Rutland",slug:"catrin-rutland",fullName:"Catrin Rutland",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/202192/images/system/202192.png",biography:"Catrin Rutland is an Associate Professor of Anatomy and Developmental Genetics at the University of Nottingham, UK. She obtained a BSc from the University of Derby, England, a master’s degree from Technische Universität München, Germany, and a Ph.D. from the University of Nottingham. She undertook a post-doctoral research fellowship in the School of Medicine before accepting tenure in Veterinary Medicine and Science. Dr. Rutland also obtained an MMedSci (Medical Education) and a Postgraduate Certificate in Higher Education (PGCHE). She is the author of more than sixty peer-reviewed journal articles, twelve books/book chapters, and more than 100 research abstracts in cardiovascular biology and oncology. She is a board member of the European Association of Veterinary Anatomists, Fellow of the Anatomical Society, and Senior Fellow of the Higher Education Academy. Dr. Rutland has also written popular science books for the public. https://orcid.org/0000-0002-2009-4898. www.nottingham.ac.uk/vet/people/catrin.rutland",institutionString:null,institution:{name:"University of Nottingham",country:{name:"United Kingdom"}}},{id:"283315",title:"Prof.",name:"Samir",middleName:null,surname:"El-Gendy",slug:"samir-el-gendy",fullName:"Samir El-Gendy",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRduYQAS/Profile_Picture_1606215849748",biography:"Samir El-Gendy is a Professor of anatomy and embryology at the faculty of veterinary medicine, Alexandria University, Egypt. Samir obtained his PhD in veterinary science in 2007 from the faculty of veterinary medicine, Alexandria University and has been a professor since 2017. Samir is an author on 24 articles at Scopus and 12 articles within local journals and 2 books/book chapters. His research focuses on applied anatomy, imaging techniques and computed tomography. Samir worked as a member of different local projects on E-learning and he is a board member of the African Association of Veterinary Anatomists and of anatomy societies and as an associated author at local and international journals. Orcid: https://orcid.org/0000-0002-6180-389X",institutionString:null,institution:{name:"Alexandria University",country:{name:"Egypt"}}},{id:"246149",title:"Dr.",name:"Valentina",middleName:null,surname:"Kubale",slug:"valentina-kubale",fullName:"Valentina Kubale",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/246149/images/system/246149.jpg",biography:"Valentina Kubale is Associate Professor of Veterinary Medicine at the Veterinary Faculty, University of Ljubljana, Slovenia. Since graduating from the Veterinary faculty she obtained her PhD in 2007, performed collaboration with the Department of Pharmacology, University of Copenhagen, Denmark. She continued as a post-doctoral fellow at the University of Copenhagen with a Lundbeck foundation fellowship. She is the editor of three books and author/coauthor of 23 articles in peer-reviewed scientific journals, 16 book chapters, and 68 communications at scientific congresses. Since 2008 she has been the Editor Assistant for the Slovenian Veterinary Research journal. She is a member of Slovenian Biochemical Society, The Endocrine Society, European Association of Veterinary Anatomists and Society for Laboratory Animals, where she is board member.",institutionString:"University of Ljubljana",institution:{name:"University of Ljubljana",country:{name:"Slovenia"}}},{id:"258334",title:"Dr.",name:"Carlos Eduardo",middleName:null,surname:"Fonseca-Alves",slug:"carlos-eduardo-fonseca-alves",fullName:"Carlos Eduardo Fonseca-Alves",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/258334/images/system/258334.jpg",biography:"Dr. Fonseca-Alves earned his DVM from Federal University of Goias – UFG in 2008. He completed an internship in small animal internal medicine at UPIS university in 2011, earned his MSc in 2013 and PhD in 2015 both in Veterinary Medicine at Sao Paulo State University – UNESP. Dr. Fonseca-Alves currently serves as an Assistant Professor at Paulista University – UNIP teaching small animal internal medicine.",institutionString:null,institution:{name:"Universidade Paulista",country:{name:"Brazil"}}},{id:"245306",title:"Dr.",name:"María Luz",middleName:null,surname:"Garcia Pardo",slug:"maria-luz-garcia-pardo",fullName:"María Luz Garcia Pardo",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/245306/images/system/245306.png",biography:"María de la Luz García Pardo is an agricultural engineer from Universitat Politècnica de València, Spain. She has a Ph.D. in Animal Genetics. Currently, she is a lecturer at the Agrofood Technology Department of Miguel Hernández University, Spain. Her research is focused on genetics and reproduction in rabbits. The major goal of her research is the genetics of litter size through novel methods such as selection by the environmental sensibility of litter size, with forays into the field of animal welfare by analysing the impact on the susceptibility to diseases and stress of the does. Details of her publications can be found at https://orcid.org/0000-0001-9504-8290.",institutionString:null,institution:{name:"Miguel Hernandez University",country:{name:"Spain"}}},{id:"350704",title:"M.Sc.",name:"Camila",middleName:"Silva Costa",surname:"Ferreira",slug:"camila-ferreira",fullName:"Camila Ferreira",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/350704/images/17280_n.jpg",biography:"Graduated in Veterinary Medicine at the Fluminense Federal University, specialist in Equine Reproduction at the Brazilian Veterinary Institute (IBVET) and Master in Clinical Veterinary Medicine and Animal Reproduction at the Fluminense Federal University. She has experience in analyzing zootechnical indices in dairy cattle and organizing events related to Veterinary Medicine through extension grants. I have experience in the field of diagnostic imaging and animal reproduction in veterinary medicine through monitoring and scientific initiation scholarships. I worked at the Equus Central Reproduction Equine located in Santo Antônio de Jesus – BA in the 2016/2017 breeding season. I am currently a doctoral student with a scholarship from CAPES of the Postgraduate Program in Veterinary Medicine (Pathology and Clinical Sciences) at the Federal Rural University of Rio de Janeiro (UFRRJ) with a research project with an emphasis on equine endometritis.",institutionString:null,institution:null},{id:"41319",title:"Prof.",name:"Lung-Kwang",middleName:null,surname:"Pan",slug:"lung-kwang-pan",fullName:"Lung-Kwang Pan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/41319/images/84_n.jpg",biography:null,institutionString:null,institution:null},{id:"201721",title:"Dr.",name:"Beatrice",middleName:null,surname:"Funiciello",slug:"beatrice-funiciello",fullName:"Beatrice Funiciello",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/201721/images/11089_n.jpg",biography:"Graduated from the University of Milan in 2011, my post-graduate education included CertAVP modules mainly on equines (dermatology and internal medicine) and a few on small animal (dermatology and anaesthesia) at the University of Liverpool. After a general CertAVP (2015) I gained the designated Certificate in Veterinary Dermatology (2017) after taking the synoptic examination and then applied for the RCVS ADvanced Practitioner status. After that, I completed the Postgraduate Diploma in Veterinary Professional Studies at the University of Liverpool (2018). My main area of work is cross-species veterinary dermatology.",institutionString:null,institution:null},{id:"291226",title:"Dr.",name:"Monica",middleName:null,surname:"Cassel",slug:"monica-cassel",fullName:"Monica Cassel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/291226/images/8232_n.jpg",biography:'Degree in Biological Sciences at the Federal University of Mato Grosso with scholarship for Scientific Initiation by FAPEMAT (2008/1) and CNPq (2008/2-2009/2): Project \\"Histological evidence of reproductive activity in lizards of the Manso region, Chapada dos Guimarães, Mato Grosso, Brazil\\". Master\\\'s degree in Ecology and Biodiversity Conservation at Federal University of Mato Grosso with a scholarship by CAPES/REUNI program: Project \\"Reproductive biology of Melanorivulus punctatus\\". PhD\\\'s degree in Science (Cell and Tissue Biology Area) \n at University of Sao Paulo with scholarship granted by FAPESP; Project \\"Development of morphofunctional changes in ovary of Astyanax altiparanae Garutti & Britski, 2000 (Teleostei, Characidae)\\". She has experience in Reproduction of vertebrates and Morphology, with emphasis in Cellular Biology and Histology. She is currently a teacher in the medium / technical level courses at IFMT-Alta Floresta, as well as in the Bachelor\\\'s degree in Animal Science and in the Bachelor\\\'s degree in Business.',institutionString:null,institution:null},{id:"442807",title:"Dr.",name:"Busani",middleName:null,surname:"Moyo",slug:"busani-moyo",fullName:"Busani Moyo",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Gwanda State University",country:{name:"Zimbabwe"}}},{id:"423023",title:"Dr.",name:"Yosra",middleName:null,surname:"Soltan",slug:"yosra-soltan",fullName:"Yosra Soltan",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Alexandria University",country:{name:"Egypt"}}},{id:"349788",title:"Dr.",name:"Florencia Nery",middleName:null,surname:"Sompie",slug:"florencia-nery-sompie",fullName:"Florencia Nery Sompie",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Sam Ratulangi University",country:{name:"Indonesia"}}},{id:"208123",title:"Dr.",name:"Mari-Carmen",middleName:null,surname:"Uribe",slug:"mari-carmen-uribe",fullName:"Mari-Carmen Uribe",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"National Autonomous University of Mexico",country:{name:"Mexico"}}},{id:"345713",title:"Dr.",name:"Csaba",middleName:null,surname:"Szabó",slug:"csaba-szabo",fullName:"Csaba Szabó",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Debrecen",country:{name:"Hungary"}}},{id:"345719",title:"Mrs.",name:"Márta",middleName:null,surname:"Horváth",slug:"marta-horvath",fullName:"Márta Horváth",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Debrecen",country:{name:"Hungary"}}},{id:"420151",title:"Prof.",name:"Novirman",middleName:null,surname:"Jamarun",slug:"novirman-jamarun",fullName:"Novirman Jamarun",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Andalas University",country:{name:"Indonesia"}}}]}},subseries:{item:{id:"15",type:"subseries",title:"Chemical Biology",keywords:"Phenolic Compounds, Essential Oils, Modification of Biomolecules, Glycobiology, Combinatorial Chemistry, Therapeutic peptides, Enzyme Inhibitors",scope:"Chemical biology spans the fields of chemistry and biology involving the application of biological and chemical molecules and techniques. In recent years, the application of chemistry to biological molecules has gained significant interest in medicinal and pharmacological studies. This topic will be devoted to understanding the interplay between biomolecules and chemical compounds, their structure and function, and their potential applications in related fields. Being a part of the biochemistry discipline, the ideas and concepts that have emerged from Chemical Biology have affected other related areas. 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