KIT mutations that have been reported in dog MCTs
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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\r\n\tOrganic synthesis has always been one of the central topics of research for the scientific community in the academic laboratories and industrial world. Many striking journal articles and remarkable reviews and books have been published in the past year describing the practicability and applications of the subject demonstrating the importance of organic synthesis. In the present book, we will be putting together the topics in organic synthesis which may include but not limited to, (1) the basic terms and concepts, (2) various organic reactions including reduction, oxidation, addition, elimination, rearrangements, and cycloadditions, (3) Total Synthesis of Natural products, (4) transition metal catalysts, organocatalysts, enzymes and biotransformations, (5) applications in medicinal chemistry and drug design and development, (6) purification methods and characterization techniques, etc. To set a limit and to increase the scope of the book, author(s) are encouraged to send the chapters that include selected examples with practical applications and good yielding reactions reported within the past decade. Older topics with significant findings or their essence to prepare the foundation may be included in the chapter are welcomed as well.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:null,priceUsd:null,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"f3bbbd989d0896f142d317ccb8abcc35",bookSignature:"Dr. Prashant S Deore",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/8807.jpg",keywords:"Natural Product Synthesis, Organic Reaction Mechanism, Stereoselective synthesis, Chirality, C-H Functionalization, Cross-Coupling Reactions, Heterogeneous Catalysis, Homogeneous Catalysis, Green Synthesis, Green Solvents and Reagents, Bioorganic synthesis, Click Chemistry",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 10th 2018",dateEndSecondStepPublish:"January 14th 2019",dateEndThirdStepPublish:"March 15th 2019",dateEndFourthStepPublish:"May 20th 2019",dateEndFifthStepPublish:"July 19th 2019",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"251769",title:"Dr.",name:"Prashant",middleName:"S",surname:"Deore",slug:"prashant-deore",fullName:"Prashant Deore",profilePictureURL:"https://mts.intechopen.com/storage/users/251769/images/system/251769.png",biography:"Dr. Prashant S. Deore was born in India. He received a Master’s degree in organic chemistry from Pune University in 2007. In the same year, he qualified with the SET and CSIR-NET (JRF) and joined in the group of Prof. Narshinha P. Argade for the doctoral studies in National Chemical Laboratory, India. In 2014, he awarded with a Ph. D. in Chemistry and was a recipient of the 2nd prize in “2014 Eli Lilly and Company Asia Outstanding Thesis Awards”. In July 2014 he moved to Canada and joined as a postdoctoral researcher in the group of Prof. Richard Manderville at the University of Guelph, Canada. Presently, Dr. Deore is working on the collaborative project between the University of Guelph and Aterica health Inc., and providing consulting to the company. His research interest includes organic synthesis, fluorescent probes development, nucleic acid synthesis and modifications, and aptasensor development for proteins and food toxins.",institutionString:"University of Guelph",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:null}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"8",title:"Chemistry",slug:"chemistry"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"270935",firstName:"Rozmari",lastName:"Marijan",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/270935/images/7974_n.png",email:"rozmari@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3621",title:"Silver Nanoparticles",subtitle:null,isOpenForSubmission:!1,hash:null,slug:"silver-nanoparticles",bookSignature:"David Pozo Perez",coverURL:"https://cdn.intechopen.com/books/images_new/3621.jpg",editedByType:"Edited by",editors:[{id:"6667",title:"Dr.",name:"David",surname:"Pozo",slug:"david-pozo",fullName:"David Pozo"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"52758",title:"Mast Cell Tumors",doi:"10.5772/65797",slug:"mast-cell-tumors",body:'\nMast cells are originated from hematopoietic stem cells in bone marrow as similar to other granulocytes. However, mast cells are very unique because they are released from bone marrow as undifferentiated progenitor cells to the circulation, and their final maturation is completed in the peripheral tissues. We find mast cells in most of the tissues and organs in our body, particularly in interstitial connective tissues of each organ being close to blood vessels. Mast cells play crucial roles in innate immunity against parasites and microbes that is essential for host defense in humans and animals. In acquired immunity, activation of mast cells is induced by cross‐linkage of IgE that binds to high‐affinity IgE receptors after antigen exposure. Moreover, some chemicals and toxins as well as physical (i.e., scratching and heat) and neurogenic stimuli trigger activation of mast cells. Various chemical mediators and cytokines are released from mast cells after their degranulation, and sometimes initiate allergic inflammation and itch sensation. In canine medicine, serious involvement of mast cells in allergic diseases has been identified, and mast cells are estimated as the most important target in medical treatment of allergy. Although malignancies of mast cell are uncommon disorders in humans, veterinary clinicians frequently encounter mast cell tumors (MCTs) in dogs and cats. The frequency of cutaneous MCTs has been reported to reach 20% of all tumors raised in the skin of dogs. Most of the malignant mast cells existed in a mass have granules in their cytosol, containing pruritogens, inflammatory factors, and various proteases (Figure 1). In this chapter, recent information on both basics in mast cell biology and clinical approaches for canine MCTs is outlined.
Typical histologic features of surgically removed canine MCTs stained with toluidine blue solution. A mass is consisted with numbers of differenced mast cells that show metachromasia. Connective tissues colored in light blue can be identified.
Mast cell progenitors are differentiated from pluripotent hematopoietic stem cells in bone marrow. Being different from other granulocytes, mast cells are transported by blood stream to peripheral tissues as mononuclear immature cells without granules in their cytosol [1]. In peripheral tissues, mast cell precursors complete their differentiation and distribution being ready for the host defense (Figure 2). According to characters of microenvironment of each peripheral tissue, final types of mature mast cells are altered. In the skin, they differenced into connective tissue‐type mast cells that include heparin proteoglycan and abundant granules in cytosol. Various kinds of proteases and chemical mediators are in granules of connective tissue‐type mast cells by which sever inflammation is induced when they are released at the affected sites. Heparin proteoglycan‐positive mast cells can be detected with not only toluidine blue but also berberine sulfate and safranin O. In contrast, mast cells that reach to and invade in mucosal tissues differentiate into mucosal‐type mast cells. Mucosal‐type mast cells include chondroitin sulfate as proteoglycan, and cytosolic granules are very few. Chondroitin sulfate‐positive mast cells are identified with alcian blue staining, but not with toluidine blue, berberine sulfate, or safranin O. Connective tissue‐type mast cells are found in the skin and connective tissues in various organs. On the other hand, mucosal‐type mast cells are differentiated in mucosa of the gastrointestinal tract.
Origin and transportation of mast cell precursors. Immature mast cells without cytosolic granules are released from bone marrow and distributed to peripheral tissues via circulation. Final maturation of mast cells depends on factors and molecules expressed in microenvironment of each tissue. In the skin (the upper panel), connective tissue‐type mast cells with rich cytosolic granules are differentiated. In mucosa of the gastrointestinal tract (the lower panel), mucosal‐type mast cells with few cytosolic granules are differentiated.
Factors that involve in mast cell proliferation are not fully understood. In mice, mast cells proliferate in response to interleukin (IL)‐3, IL‐9, and stem cell factor (SCF). Both IL‐6 and SCF are essential factors for proliferation and survival of human mast cells. Though less is known regarding development of canine mast cells, SCF has been reported to induce proliferation and survival, as well as migration and activation of canine mast cells [2, 3]. The IL dependency varies according to a species from which mast cells are derived. However, SCF is the most important factor for proliferation, differentiation, and survival of mast cells in humans and animals. SCF is the ligand for KIT receptors expressed on cell surface of mast cells. Since mast cells are differentiated from KIT‐positive cell lineage and KIT is retained on the surface of not only immature precursors but also mature mast cells, influence of SCF on mast cells must be crucial for their proliferation and differentiation. In fact, gain‐of‐function mutations in the KIT gene have been identified in mast cells with factor‐independent tumorigenic proliferation in humans, rodents, and dogs. Meanwhile, over 50% of canine MCTs and most of the feline MCTs show KITgen mutation‐independent development. Recent observations have revealed that not only SCF but also other cytokines and growth factors including epidermal growth factor, vascular endothelial growth factor, and nerve growth factor may facilitate proliferation, differentiation, and survival of mast cells. Unfortunately, investigation on development of canine mast cells has been insufficient.
Mast cells play key roles for inflammatory responses through degranulation and cytokine/chemokine production and secretion [4]. However, proteases, chemical mediators, and cytokines included in mast cell granules are different according to types of mast cells. Heterogeneity among mast cells is important to precisely understand the pathophysiological roles of mast cells in each tissue. Connective tissue‐type mast cells include chemical mediators such as histamine that has strong biologic activity on nerve fibers and blood vessels. Histamine is known as a pruritogen that induces itch sensation resulting in scratching behavior in humans and animals. Vasoactive effects of histamine initiate inflammation at the affected sites. Scratching behavior stimulates physical degranulation of mast cells leading to exacerbation of swelling and inflammation. Exact roles of mucosal‐type mast cells are not clearly demonstrated. Since numbers of mucosal‐type mast cells are increased in the gut with parasite infection, roles in host reaction against parasite exclusion have been proposed. However, factors and mechanisms that involve in antiparasite effects of mucosal‐type mast cells are not fully explored.
Most MCTs in dogs are consisted with histamine‐rich connective tissue‐type mast cells. Steps responsible for transformation of mast cells are summarized in Figure 3. Since receptors for histamine are expressed in mucosal cells of the stomach, progression of MCTs has been suggested to induce gastric ulcer and serious damage on gastric function. However, the exact and direct association of MCTs with gastric ulcer remains unclear [5, 6]. Connective tissue‐type mast cells contain tryptase and chymase that possess broad protease activities. Particularly, tryptase has been reported to regulate neovascularization. Connective tissue‐type mast cells can also produce growth factors for vascular endothelial cells; therefore, most of the MCTs must be rich with blood vessels. Moreover, dogs with serious MCTs show deficiency in blood coagulation possibly because connective tissue‐type mast cells have plenty of heparin in their cytosol. Canine mast cells have unique chymase whose name is dog mast cell protease‐3; however, its specific role has not been fully understood [7]. A mass formed with mucosal‐type mast cells rarely develops in the gastrointestinal tract, which induces dysfunction of the gut. Influence of mucosal mast cell tumor on other organs except the gut has not been well documented.
Malignant transformation of mast cells. For tumor formation, mast cell proliferation must be promoted by activation of ligand‐independent activation on growth factor receptors. Also, acquisition of resistance against apoptosis pathways and invasive characters may facilitate malignant expansion of MCTs.
MCTs are characterized by the aberrant proliferation of mast cells, accounting for approximately 20% of cutaneous tumors in dogs [8, 9]. They develop in the subcutaneous tissue and dermis in most cases, and other types of mast cell malignancies such as mast cell leukemia and visceral MCTs are rarely observed. They usually occur in the trunk or limbs and sometimes observed in the head and neck (Figure 4) [9, 10]. Because mast cells release proinflammatory mediators, erythema and wheal called Darier\'s sign are sometimes observed. However, MCT‐specific symptoms that can distinguish MCTs from other tumors are rare.
Representative photograph of MCT‐diagnosed dog. (A) MCT occurred in the left leg in 11‐year‐old female, Shiba. (B) MCT occurred in the left waist in 8‐year‐old female, Pharaoh Hound.
Risk factors for MCTs, age, sex, breed, spay/castration, and tumor grading have been reported [8, 11]. Among these, most factors except sex are deeply related to its incidence [11]. Recently, genetic characteristics have been also investigated, showing the high correlation of KIT mutations with prognosis of dogs with MCTs [12–14]. As Mochizuki et al. [11] presented nice summary on each factor except genetic one, we would like to focus on the genetic characteristics of MCTs in the following sections.
Cytological or histological analyses through a fine needle aspiration or biopsy are required for the diagnosis of MCTs. Typically, round‐shape cells with round nuclei and with rich cytosol are observed. Mast cells have abundant cytosolic granules, and specific staining methods with toluidine blue or safranin O can identify them. However, MCTs with undifferentiated more malignant mast cells possess few granules. Confirmation of the swelling of draining lymph nodes and sometimes fine needle aspiration of the lymph node may help to determine the presence of metastasis. Patnaik grading is mainly used pathological grading in the veterinary field because it is recognized as a good prognostic marker [15]. There are three pathological grades (grades I, II, and III), and higher grade indicates that the tumor is more malignant [15]. Several analyses have been revealed: the correlation between tumor grading and the c‐kit gene mutation, clearly showing that c‐kit mutations are more frequently observed in high‐grade tumor [12–14]. Therefore, analyzing c‐kit sequence can also be a prognostic marker for MCTs. In addition, analyzing c‐kit gene is important in terms of selecting proper treatments because several molecular target inhibitors against KIT protein, a receptor encoded in the c‐kit gene, are currently available for the treatment of MCTs. Polymerase chain reaction that amplifies exon 11 and intron 11 region using tumor genome enables the detection of internal tandem duplications (ITDs) in the juxtamembrane domain, which is the most frequent type of c‐kit mutation. Recently, however, whole sequence of c‐kit mRNA is more common because the proportion of mutations in other region of KIT domain or other type of mutations in the juxtamembrane domain are not negligible. Recent reduction in the cost for sequencing analysis will probably boost this trend (see Section 5).
Mast cell malignancies are observed among species, though the incidence of mast cell malignancies is much lower in human and rodents than in dogs [8, 9]. One of the well‐investigated mechanisms of mast cell tumorigenesis is mutations in the c‐kit gene [9, 10]. We would like to overview the current understandings of the mutant KIT contribution on mast cell tumorigenesis as well as other tumor‐related transformations of mast cells that may correlate with their tumorigenesis in mast cells.
KIT is a type III receptor tyrosine kinase of which ligand is stem cell factor (SCF) (Figure 5). It is consisted of the extracellular domain, transmembrane domain, juxtamembrane domain, and tyrosine kinase domain [16] (Figure 5). In human, aberrant proliferation of mast cell is observed in the patients of systemic/cutaneous mastocytosis, mast cell sarcoma, and mast cell leukemia [17]. Among them, most systemic mastocytosis occurs due to the mutations in the tyrosine kinase domain of KIT, especially a point mutation in Asp816 [12]. In general, SCF binding to KIT triggers the conformational changes in KIT and leads to the dimerization of the protein, allowing the binding of adenosine triphosphate (ATP) and phosphorylation of tyrosine kinase domain [18]. Mutations in the tyrosine kinase domain alter the conformation to the one similar to its active form, thus resulting in the constitutive KIT activation even in the absence of either SCF binding, KIT dimerization, or ATP binding [19]. Neoplastic growth of mast cells is rarely observed in rodents, through currently available rodent‐derived mast cell lines. For example, RBL‐2H3 cells (derived from a Wistar rat) and P815 cells (derived from a DBA/2 mouse) express Asp817Tyr and Asp814Tyr, respectively, which correspond to the Asp816 mutation in human KIT [20]. As far as we know, other mechanisms that trigger rodent mast cell tumorigenesis have not been reported.
Schematic diagram of KIT protein. The numbers of exon correspond to the ones in dog KIT.
In contrast to human and rodents, KIT mutations in dog MCT are frequently observed in the juxtamembrane domain (Table 1). ITDs in the domain are the first discovered and the most frequent mutations in canine MCTs [21] (Table 1). Besides ITDs, other mutations in the juxtamembrane domain or extracellular domain have been also reported [21]. We recently demonstrated that most of these mutations in the extracellular or juxtamembrane domain cause aberrant KIT activation and neoplastic proliferation of mast cells by triggering ligand‐independent dimerization (Ref. [22] and unpublished data). In contrast to the mutations in the tyrosine kinase domain, these mutations require ATP for the phosphorylation of the tyrosine kinase domain, providing a rationale for using ATP‐competitive small molecule inhibitors for suppressing the aberrant KIT activations [18, 23].
\nAnalyzed exons | \nDomain | \nExon | \nMutation | \nFrequency (%) | \nReferences | \n
---|---|---|---|---|---|
All | \nExtracellular | \n8 | \n417‐421ITD | \n8/202 (4.2%) | \n[24] | \n
\n | \n | 8 | \nGln430Arg | \n1/202 (0.5%) | \n\n |
\n | \n | 9 | \nSer479Ile | \n5/202 (2.5%) | \n\n |
\n | \n | 9 | \nAsn508Ile | \n3/202 (1.5%) | \n\n |
\n | Juxtamembrane | \n11 | \n555–557 mutation | \n7/202 (3.5%) | \n\n |
\n | \n | 11 | \nITD | \n25/202 (12.4%) | \n\n |
\n | Tyrosine kinase | \n17 | \ndel826–828 | \n1/202 (0.5%) | \n\n |
All | \nExtracellular | \n6, 7, 8 | \ndel102AA, Thr414Ala | \n1/47 (2.1%) | \n[25] | \n
\n | \n | 8 | \n417‐420ITD | \n3/47 (6.4%) | \n\n |
\n | Extracellular, transmembrane | \n9,10 | \nins4AA | \n1/47 (2.1%) | \n\n |
\n | Juxtamembrane | \n11 | \ndel558 | \n1/47 (2.1%) | \n\n |
\n | \n | 11 | \nLeu575Pro | \n1/47 (2.1%) | \n\n |
\n | \n | 11 | \nITD | \n8/47 (17.0%) | \n\n |
\n | Tyrosine kinase | \n15 | \ndel714 | \n1/47 (2.1%) | \n\n |
11 | \nJuxtamembrane | \n11 | \nITD | \n8/88 (9.1%) | \n[12] | \n
\n | \n | 11 | \ndel | \n4/88 (4.5%) | \n\n |
11 | \nJuxtamembrane | \n11 | \nITD | \n8/60 (13.3%) | \n[13] | \n
11 | \nJuxtamembrane | \n11 | \nITD | \n7/68 (10.3%) | \n[14] | \n
11 | \nJuxtamembrane | \n11 | \nITD | \n24/118 (20.3%) | \n[26] | \n
8, 9, 11 | \nExtracellular | \n8 | \n421‐429del, ins3AA | \n1/21 (4.8%) | \n[27] | \n
KIT mutations that have been reported in dog MCTs
AA, amino acid.
Few mechanisms of mast cell tumorigenesis except KIT mutations have been identified, but we recently demonstrated that MCT cells produce SCF and support their growth in a paracrine/autocrine manner [28]. In the analyses, high SCF production was confirmed in multiple clinical MCT samples [29]. It may explain the high response of clinical MCTs to KIT‐specific molecular inhibitors even when the tumor cells express wild‐type KIT. This will be further discussed in the following section.
\nRecent approaches such as next‐generation sequencing will reveal even minor mutations or single nucleotide polymorphisms in neoplastic mast cells. In fact, Spector et al. [30] and Youk et al. [31] discovered a human mast cell leukemia‐specific mutation in several genes. As the cost of these approaches decreases, they will be introduced in the veterinary field, probably leading to the deep understanding of mast cell tumorigenesis among species. Another approach aiming at the control of tumor growth is modifying epigenetic status in tumor genome [32]. Regarding an epigenetic alteration in MCTs, Morimoto et al. [33] showed that DNA hypomethylation widely occurred in malignant, higher‐grade MCTs. Moreover, antitumor effects of AR‐42, a histone deacetylase inhibitor, on several MCT cell lines as well as primary tumor cells have been demonstrated [34]. Thus, the characterization of epigenetic alteration is likely to be an effective approach to reveal MCT transformation.
Complete surgical removal with wide margin is the best way for solitary cutaneous MCTs. However, for dogs with multiple masses, metastasis, or sever invasive MCTs, surgical removal is sometimes incompetent. Chemotherapies have failed to overcome MCTs. However, to reduce tumor size, some combination chemotherapies have applied. Glucocorticoid is one of the most important drugs for treatment of MCTs. More than 70% of cutaneous MCTs in dogs respond well to oral administration of glucocorticoid [35–37]. Expression levels of glucocorticoid receptors in MCT cells have been reported to associate with glucocorticoid sensitivity [37]. Glucocorticoid shows strong antitumor effects on MCT cells with high expression of glucocorticoid receptors. Oral administration of glucocorticoid must be an easy and effective chemotherapy for canine MCTs. Since side effects induced by glucocorticoid administration will sometimes be concerned, clinicians must pay attention on blood chemistry data and general conditions of dog patients. Glucocorticoid is usually applied as a part of multidrug chemotherapies for MCTs. Anticancer drugs, such as vincristine, vinblastine, cyclophosphamide, and CCNU, have been tested for combination chemotherapies for MCTs with or without glucocorticoid [38–42]. However, very little information on the chemotherapeutic response of MCTs can be obtained. Since recent studies have been based on small numbers of cases and have often included MCTs of different pathologic grades and clinical stages, data must be carefully evaluated [43]. Recently, adjuvant chemotherapies have been proposed in treatment of various cancers and sarcomas. Since neo‐adjuvant administration with glucocorticoid usually reduces mass size of MCTs, wide surgical margins will be obtained [37]. On the other hand, postoperative adjuvant chemotherapy is suggested to kill MCT cells that remain at the affected site after incomplete excision. Several trials on adjunctive chemotherapy have been reported. However, most of the adjunctive chemotherapy does not appear to increase survival times. Although surgical removal with radiation has been tested for MCTs, remarkable improvement is not provided. No difference in overall survival rate has been observed between dogs with MCTs receiving and not receiving prophylactic irradiation of the regional lymph node [44].
Because aberrant activation of mutant KIT is one of the causes in mast cell tumorigenesis, anticancer effects of KIT inhibitors have been investigated. In fact, clinical trials that enrolled MCT‐diagnosed dogs have been undertaken to evaluate the efficacy of molecular targeting agents against KIT. We would like to overview the history of the research on KIT inhibitors and discuss therapeutic perspective for MCTs.
\nThe first molecular inhibitor applied to human was the imatinib mesylate, which repress activations of KIT, platelet‐derived growth factor receptor (PDGFR), and Bcr‐Abl [45]. It was first administered to the patient of gastrointestinal stromal tumor with a mutation in the juxtamembrane domain of KIT [46]. At around the same time, KIT mutations in canine MCT were first discovered [21], suggesting the possibility that KIT inhibitors can be applied to dog MCTs. Actually, there have been several reports that show the inhibitory effects of imatinib mesylate on MCTs, especially for the tumor cells with KIT mutations in either the extracellular domain or juxtamembrane domain [22, 47]. Based on these results from basic researches, some clinicians administered imatinib mesylate to MCT‐diagnosed dogs and obtained partial response at least in some of them [47]. However, there was no rationale for the administration of imatinib mesylate to MCT‐diagnosed dogs through the clinical trials. In contrast to that, both masitinib mesylate and toceranib phosphate are approved by either the Food and Drug Administration (FDA) in the United States or European Medicines Agency based on the results from the clinical trials enrolling MCT‐diagnosed dogs [26, 48,49]. Basically, imatinib mesylate, masitinib mesylate, and toceranib phosphate are all ATP‐competitive inhibitors, and they suppress the activation of mutant KITs that require ATP binding for their activation.
\nResults of clinical trials for toceranib phosphate, which is a random double‐blind trials, are summarized in Table 2 [26]. In this trial, more than 150 MCT patients were enrolled. After the six‐week treatment, either complete response (CR) or partial response (PR) was obtained 32 in 86 (37.2%) patients in the treatment group, while the proportion of CR/PR was only 7.9% (5 in 63 patients) in the placebo group. In addition, a group treated with toceranib phosphate following placebo‐escape, which administered toceranib phosphate after the placebo treatment, responded the agent, resulting in the CR/PR in 24 cases out of 58 (41.4%). At least in this trial, significant increase in severe adverse effects (grade III or IV) was not detected. In case of mastinib mesylate, a phase III trial was carried out in France, enrolling more than 130 MCT patients. One‐year survival and two‐year survival were 62.1 and 39.8%, respectively, in the treatment group, though the ones were 36.0 and 15.0%, respectively, in the placebo group [49].
\n\n | All MCTs | \nMCTs with mutant KIT | \nMCTs without mutant KIT | \n|||
---|---|---|---|---|---|---|
Cases | \nCR + PR | \nCases | \nCR + PR | \nCases | \nCR + PR | \n|
Toceranib | \n86 | \n32 (37.2%) | \n20 | \n12(60.0%) | \n66 | \n20(30.3%) | \n
Placebo | \n63 | \n5(7.9%) | \n9 | \n1(11.1%) | \n54 | \n4(7.4%) | \n
Placebo>toceranib | \n58 | \n24 (41.4%) | \n9 | \n7(77.8%) | \n49 | \n17(34.7%) | \n
Summary of a clinical trial of toceranib phosphate [26]
The number of the enrolled patients and the proportion of CR/PR cases are indicated.
Interestingly, both agents showed antitumor effects even on MCTs expressing wild‐type KIT (Tables 2 and 3). Though the agents suppress the activation of other receptor tyrosine kinases such as platelet‐derived growth factor receptor or vascular endothelial growth factor receptor 2 [50, 51], aberrant activations of principal targets except KIT were not observed in our study using more than 30 clinical MCT tissue samples (unpublished data). Thus, it is likely that the data in Table 2 indicate that tumor growth in no more than 30% of MCT was dependent on KIT signaling even though they express wild‐type KIT. We consider that these can be at least partly explained by SCF autoproduction from tumor cells as described above [28, 29]. Though further investigations are necessary, analyses to determine the KIT activation status will probably be a direct diagnostic agent to accurately predict the therapeutic efficacy of KIT targeting inhibitors.
\n\n | All MCTs | \nMCTs with mutant KIT | \nMCTs without mutant KIT | \n|||
---|---|---|---|---|---|---|
1 year | \n2 years | \n1 year | \n2 years | \n1 year | \n2 years | \n|
Toceranib | \n59/95(62.1%) | \n33/83(39.8%) | \n17/27 (63.0%) | \n7/23 (30.4%) | \n38/62 (61.3%) | \n23/54 (42.6%) | \n
Placebo | \n9/25(36.0%) | \n3/20(15.0%) | \n1/7 (14.3%) | \n0/6(0%) | \n7/16 (43.8%) | \n2/12 (16.7%) | \n
Summary of a clinical trial of masitinib phosphate [49]
The number and proportion of the patients that survived more than 1 or 2 years are indicated.
As described, molecular biological approaches to MCTs have started, and new findings are accumulating. However, some clinical researches present very limited information obtained from few cases. Therefore, clinicians should carefully collect information and evaluate data before clinical application of anticancer drugs and molecular targeting drugs to dogs with MCTs. It is dangerous to trust all data reported in few research reports or on few clinical cases. Knowledge on basic biology of mast cells will help clinicians to understand the recent molecular approaches to MCTs.
While studying any physical phenomena be it of practical or academic importance, it is not always possible to mimic the exact system. For an example, if we want to study the flow of air past a moving train engine, we might have to build a wind tunnel along with a provision for a railway track for the engine to move in and out. We should have sensitive measuring instruments fixed at different places to measure various parameters. Again, finding the right locations for fixing these instruments can only be determined by carefully performing large number of iterations because the margin for errors in real-life problems are miniscule. For example, if the paint on the car is not done correctly even in some parts, it may contribute hugely to skin-friction drag and thereby reducing the mileage of the car.
\nOne might argue that we can use scaled models keeping the physics of the problems same. These models induce errors during extrapolation to the actual situation besides being very costly in terms of infrastructure, resources and time. If we try to write a mathematical function and solve it, we should know all the pertinent parameters and laws that govern the flow. Then we might use various techniques like dimensional analysis and arrive at an equation. The validation of this mathematical equation again, can only be done by experiments. Once we get an equation, solving it for various cases is in itself a major challenge because we almost always end up with differential, integral or Integro-Differential equations. Till date, exact solutions to some of these equations are still open problems. So, approximate solutions are desired as against exact solutions. The advent of advanced computers brought along the solution for this in the form of Computational Fluid Dynamics (CFD). We can now analyze various types of fluid flows with numerical simulations and also develop suitable simulation algorithms. In most practical problems, the state variables of the fluids can be treated as continuous functions of space for which we already have conservation laws for mass, momentum, and energy. For many fluids that are used in engineering applications, there are well-accepted constitutive relations.
\nThe fundamental fluid mechanics is put in the form of Navier Stokes equations way back in 1800s and thereupon many attempts were made to find the general solutions for the equations but even today it is an open millennium problem [1, 2, 3]. Based on the physics of interest, we make certain approximations to Navier–Stokes equations and therefore obtain the governing partial differential equations to be solved [4]. When tried to solve such governing equations using a numerical methods a suitable discretization procedure will be adopted and the problem will be attacked to solve using a better solver. Here we convert the mathematical model into a discrete system of algebraic equations. We even call it to be a difference equation in some gut words while the chosen method to solve the equations is Finite difference method (FDM). Many of this kind of solving methods have been evolved and to mention a few the finite element method (FEM), the finite volume method (FVM), boundary element method (BEM) are a few popular methods among so many numerical techniques. Out of many factors that influence selection, some are very crucial like problem defined on the geometry, the analyst’s preference, and the predominant trend of solution may be in a selected and particular area of the problem space. Nonetheless it will be decided later about which numerical algorithm to be adopted and solve these equations and develop a computer programs [5, 6, 7]. After the advent of enormous speed in graphics processing units the computer graphics and animations formed from large output of numerical values make the visualization of the simulation results easier to human comprehension and draw the conclusions henceforth.
\nThe nature of fluid flow is such a complicated phenomenon no matter what governing equations we formulate and try even more numerical solutions for the same, it can well be understood with a single classic statement of legendary Nobel Laureate R. P. Feynman in his popular scientific texts, in a quote “The efforts of a child trying to dam a small stream flowing in the street and his surprise at the strange way the water works its way out has its analog in our attempts over the years to understand the flow of fluids. We have tried to dam the water up—in our understanding—by getting the laws and the equations that describe the flow” depicts how novice the formulations are. The statement given by Feynman has already been proved more than quite often times in the applications of Fluid Dynamics in modern engineering and science, and more profoundly to the computational fluid dynamists.
\nNonetheless an additional unique feature relates to the mathematical nature of Navier-Stokes equations. Steady-state Navier-stokes equations are elliptic in nature, whereas unsteady Navier-Stokes equations are parabolic in nature. As numerous problems associated with the methods of solution of the completely defined elliptic Partial differential equations the Navier-Stokes equations generally solved as an unsteady problem even in the case if the flow is steady, using a time marching schemes [8, 9, 10]. The transient solution of Navier-Stokes problem yields the solution but not be any easy compared to the steady state flow problem in more general geometric case.
\nTurbulent flows involve randomly fluctuating flow variables such as velocity, pressure, and temperature.
\nWithin the defined flow decomposition in accordance with Reynolds, a flow variable at a given spatial point at a given instant can be represented as the sum of a mean value and a random fluctuation about this mean value, and the process of obtaining the average or a mean value is represented as the technique of Reynolds averaging. Therefore, for any flow variable\n
Where \n
\n\n
Where T represents the averaging time interval, which must be large compared to the typical time scales of fluctuations throughout the flow length.
\nFor unsteady flows, \n
where N is the number of identical experiments.
\nThe Reynolds averaging applied to the continuity and momentum equations of an incompressible fluid flow would be obtained in the following set of equations.
\nWhere \n
The Reynolds averaged transport equation for a scalar \n
Where \n
The higher order correlations appear in Reynold’s stress equation is due to non-linearity of Navier–Stokes equation, despite the fact that we try an attempt to derive the governing equation for higher-order terms, they would always result in equations with even higher order correlations.
\nThe Eddy viscosity models are evolved basing on the Boussinesq proposition, which defines the Reynolds stresses which would be proportional to mean velocity gradients, as that of Deviatoric Reynolds stress. This stress is proportional to the mean rate of strain. Numerical computation of eddy viscosity possibly would be required for the solution of the set of transport equations.
\nThus, the Reynolds averaged NS model turbulence models are going to be categorized on some of the several additional partial differential equations that are to be solved to enforce closure and find the final flow behavior in any of the defined topology. The zero-equation model is actually the one that computes the eddy viscosity solely from the Reynolds-averaged velocity field. The transport equation that is solved simultaneously with the Reynolds-averaged Navier–Stokes equations to determine the eddy viscosity is in other words known as one-equation model that refers to the family of turbulence models [11, 12, 13].
\nThe highly established standard k -ε model which has been developed and contributed by Launder and Spalding makes use of two model equations, one for the turbulent kinetic energy k and the dissipation rate of turbulent kinetic energy per unit mass ε. The transport equations are solved using the Reynolds averaged Navier–Stokes equations. The k-€ turbulence model is well established and the most widely validated and uses the eddy Viscosity turbulence model [14]. Diverse modifications of the standard model have been recommended to account for the near-wall flow region and low Reynolds number turbulent flows. Nevertheless the Eddy viscosity models have significant deficiencies, which are due to some eddy viscosity assumptions. The experimental measurements and numerical simulations have indicated that in the cases of three dimensional turbulent flow the eddy viscosity turns out to be a tensor quantity [15]. Therefore, the use of a scalar eddy viscosity for computation of Reynolds stresses is might not be appropriate. It would as an alternative be recommendable to compute Reynolds stresses directly using its dynamic transport equations. This idea has been the basis of the Reynolds stress model though it the most expensive methods of the turbulence models in use in the present day CFD solutions and particularly for RANS simulations. It is relatively expensive computationally in comparison to eddy diffusivity models since it requires solving seven additional PDEs for every grid solution in this case. Hence these models are not used as widely as expected from the analysis’s the eddy diffusivity models in practical analyses.
\nIn the later days one of the most adoptable and practically sensible methods that have surfaced is Large Eddy simulation (LES). The method in which the Large scales of motion or large eddies of fluids which possess more energy than a smaller one have been taken to be most critical in the solving for turbulent flow cases and has been proved to be more effective in most of the cases both in the experimental and industrial applications [16]. The most effective transporters of conserved quantities viz. mass, momentum, and energy remain to be only large eddies compared to the smaller eddies. The momentum, and energy exchange is so minimal in such cases that they can be neglected. Moreover the behavior of these smaller scales of motion is universal in turbulent flows irrespective of the flow’s context and geometry.
\nIt is moderately undemanding to capture the effect of smaller eddies through a model. The underlying principle of LES is to treat the large eddies of the flow precisely and model the more universal small scale eddies, however this method is inherently time-dependent and are highly suitable for three-dimensional simulations. Such approach is less costly than DNS but a lot more expensive than RANS model for the same flow. Large Eddy Simulation (LES) is mostly preferred method for obtaining accurate time history for high Reynolds number and complex geometry flows. It separates the larger and smaller eddies through spatial filtering operation [17].
\nThe conceptual steps are somewhat like this, it begins with the spatial filter to decompose velocity field \n
On the other hand due to the rapid growth in the computational resource Direct Numerical Simulation (DNS) of turbulent flows has become one of the crucial tools in turbulence research. Though DNS has gained its importance and has been universally recognized about its technique and methodology the kind of resources it consumes to figure out turbulence in some of the fundamental geometries is in itself a complicated affair.
\nIt is also able to provide statistical information difficult to obtain by experimental measurements. Among effects to be observed in the DNS prior to laboratory experiments about flow velocity and vorticity vectors such effects are not present in if the modeling is done gaussian fields. However the attainment of high Reynolds number flow analysis necessitates the use of subgrid scale model to represent the effects of the unresolved small-scale turbulence on the explicitly designed and simulated large-scale flow. The leading length scales are considered to be of the order of higher dimension of flow region in the fluid flows or of the size of largest Eddie leading to turbulence in the fluid flow. The nominal scale of size of eddies in the inertia forces and viscous forces are of comparable magnitude so that the energy is cascaded to the Eddie, it is directly dissipated. Consecutively to simulate whole scales in turbulent flows, the computational domain must be sufficiently larger than the largest characteristic length scale of the flow L and the grid size must be smaller than the finest turbulence scale η.
\nThe turbulent flows are essentially three-dimensional in nature and to satisfactorily model it needs at least require \n
In the present work, turbulent flows have been selected to investigate using large eddy simulation (LES) principles and also to understand the direct numerical simulation methodology to model and study the turbulence in fluid flow in nano channels of an electronic device. The nano channel is designed to transit the fluid and therefore removes the heat from the plate. The fluid considered to be multiphase as there would be a base fluid in which the nanoparticles will be suspended and hence an Eulerian multiphase as well as VoF techniques is being implemented. The same conditions are been attempted to solve directly using the techniques of DNS code of Geris flow solver for a simple 2D model and an unified flow field has been created as an initial flow conditions to capture the turbulent flow along the length scale and adaptive mesh refinement has been adopted while selecting the flow solvers in the three dimensional flow generation in such nano channel. The problem uses a finite volume method (FVM), in which the conservation equations in their weak formulation are solved in a discrete number of cells, determining one value for the flow parameters in each cell. The visualization has been taken in paraview and the exported combined file is processed as a data file in commercial code to make a comparative study about the two well developed turbulence modeling techniques. The nano channel considered as a rectangular pipe flow shown in Figure 1. The turbulent channel flow is often referred to as a canonical flow of Poiseuille flow case, since it is one of the simplest flows one can think of to attack using the direct numerical simulation. Therefore, this test case is suitable to verify if a numerical solver is able to accurately predict the turbulent vortices near the wall of the tube particularly at the bottom of the channel as the fluid is incompressible.
\nGeometry of pipe.
Simulations between all the Reynolds numbers in the range of 100 ≥ Re ≥ 320 the grids have been selected in the stream wise, the wall-normal, and the pipe length of the computational domain are \n
In the Figures 2,3 and 4 it has been shown about the convergence of the statistical data in the cases of turbulent intensity along the pipe length as the flow becomes steadily turbulent.
\nMean axial velocity.
RMS value along the pipe length.
Turbulent KE distribution record.
The gradual development from uniform turbulence to a pattern at Reynolds number180 has been accounted and presented in the Figure 4. The energy distribution plays a key role in the flow transition and henceforth is to be tracked quantitatively and with the probability distribution. The velocity gradients near the pipe walls after the flow is fully developed would exhibit the axial flow velocity as shown in Figure 2 and consecutively the root mean square velocity computed is presented in Figure 3. These plots are developed on the basis of non dimensional number along the length of the pipe. At the maximum fluid velocity along the channel it has been recorded that there is no significant raise or dip in the Reynolds number in all the runs.
\nThe propagation velocity of the pattern is approximately that of the mean flux and is a decreasing function of Reynolds number. Examination of the time-averaged flow shows that a turbulent band is associated with two counter-rotating cells stacked in the cross-channel direction and that the turbulence is highly concentrated near the walls. Near the wall, the Reynolds stress force accelerates the fluid through a turbulent band while viscosity decelerates it; advection by the laminar profile acts in both directions. In the center, the Reynolds stress force decelerates the fluid through a turbulent band while advection by the laminar profile accelerates it. These characteristics are compared with those of turbulent-laminar banded patterns in plane Couette flow.
\nThe average Reynolds number varies in the different cases, from 120 in the bare flow case to 512 in the fully developed convective flow conditions as a working nanofluid cooling device. Though the primary aspect of heat transfer is not considered until the turbulent flow did not notice during the flow through the channel, the swirling velocity component is completely ignored. The pressure drop is exactly getting equated to the experimentally verified case in the case of LES calculated value in almost all the cases as shown in Figure 5. Once the LES model could capture the significant turbulence properties, the problem is attempted on geris flow solver code for DNS solution for one such case to be verified with the already obtained results. Some of the results obtained are presented in Figure 6.
\nLES based simulation.
DNS on LES based simulation.
A direct numerical simulations (DNS) has been performed over a nano channel considering as that of a nono pipe used for electronics cooling purpose with various set of Reynolds numbers and the effects of Reynolds number on the turbulence properties have been investigated. Since DNS of experimental-scale setups are beyond the author’s computational resources, DNSs on a reduced computational domain were performed. The unified flow solver will be taking the job of adaptive mesh refinement (AMR) with automatic selection of fluid solver that has been implemented in whole range of computational domain. In contrast to the microchannel flow the nano channel flow case has been much qualitatively trivial once the LES solution is available and further solving for a DNS solution of the problem at any particular Reynolds number. It has been shown that Kolmogrov length and velocity scales are more appropriate compared to the other such approximations while modeling DNS at significantly low Reynolds numbers including any other energy diffusion during the course of fluid flow through rectangular channels.
\nIntechOpen implements a robust policy to minimize and deal with instances of fraud or misconduct. As part of our general commitment to transparency and openness, and in order to maintain high scientific standards, we have a well-defined editorial policy regarding Retractions and Corrections.
",metaTitle:"Retraction and Correction Policy",metaDescription:"Retraction and Correction Policy",metaKeywords:null,canonicalURL:"/page/retraction-and-correction-policy",contentRaw:'[{"type":"htmlEditorComponent","content":"IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
\\n\\n1. RETRACTIONS
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\\n\\n4. FINAL REMARKS
\\n\\nIntechOpen wishes to emphasize that the final decision on whether a Retraction, Statement of Concern, or a Correction will be issued rests with the Academic Editor. The publisher is obliged to act upon any reports of scientific misconduct in its publications and to make a reasonable effort to facilitate any subsequent investigation of such claims.
\\n\\nIn the case of Retraction or removal of the Work, the publisher will be under no obligation to refund the APC.
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
\n\n1. RETRACTIONS
\n\nA Retraction of a Chapter will be issued by the Academic Editor, either following an Author’s request to do so or when there is a 3rd party report of scientific misconduct. Upon receipt of a report by a 3rd party, the Academic Editor will investigate any allegations of scientific misconduct, working in cooperation with the Author(s) and their institution(s).
\n\nA formal Retraction will be issued when there is clear and conclusive evidence of any of the following:
\n\nPublishing of a Retraction Notice will adhere to the following guidelines:
\n\n1.2. REMOVALS AND CANCELLATIONS
\n\n2. STATEMENTS OF CONCERN
\n\nA Statement of Concern detailing alleged misconduct will be issued by the Academic Editor or publisher following a 3rd party report of scientific misconduct when:
\n\nIntechOpen believes that the number of occasions on which a Statement of Concern is issued will be very few in number. In all cases when such a decision has been taken by the Academic Editor the decision will be reviewed by another editor to whom the author can make representations.
\n\n3. CORRECTIONS
\n\nA Correction will be issued by the Academic Editor when:
\n\n3.1. ERRATUM
\n\nAn Erratum will be issued by the Academic Editor when it is determined that a mistake in a Chapter originates from the production process handled by the publisher.
\n\nA published Erratum will adhere to the Retraction Notice publishing guidelines outlined above.
\n\n3.2. CORRIGENDUM
\n\nA Corrigendum will be issued by the Academic Editor when it is determined that a mistake in a Chapter is a result of an Author’s miscalculation or oversight. A published Corrigendum will adhere to the Retraction Notice publishing guidelines outlined above.
\n\n4. FINAL REMARKS
\n\nIntechOpen wishes to emphasize that the final decision on whether a Retraction, Statement of Concern, or a Correction will be issued rests with the Academic Editor. The publisher is obliged to act upon any reports of scientific misconduct in its publications and to make a reasonable effort to facilitate any subsequent investigation of such claims.
\n\nIn the case of Retraction or removal of the Work, the publisher will be under no obligation to refund the APC.
\n\nThe general principles set out above apply to Retractions and Corrections issued in all IntechOpen publications.
\n\nAny suggestions or comments on this Policy are welcome and may be sent to permissions@intechopen.com.
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