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1. Introduction
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1.1. Exosomes, ncRNAs, and lncRNAs
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Exosomes are a class of small (40–120 nm) extracellular vesicles (EVs) that originate in multivesicular endosomes [1–3] and can be released from a wide range of cells, including cancer cells [4]. Exosomes differ in size from microvesicles (50–1000 nm) and apoptotic bodies (800–5000 nm) and are secreted directly from the cell membrane in a budding form [5–7]. Late endosomes released from multivesicular bodies (MVBs) are integrated with the cell membrane in the extracellular matrix during the release of exosomes. Exosomes released into the extracellular environment can be utilized by tumor cells to alter the tumor microenvironment or to provide a favorable microenvironment for distant metastases by affecting distant organs [8–10]. Therefore, exosomes serve as efficient vehicles for long- and short-distance intercellular communication by signaling molecules in the form of lipids, proteins, DNA, RNAs, and non-coding RNAs (ncRNAs) [11]. Exosomes play an important role in signal transduction between cells.
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In the complicated human genome, approximately 2% of the genomic sequence encodes proteins involved in biological progression [12], of which approximately 90% are ncRNAs. ncRNAs are described as the “noise” of the genome in their primary form, and they can be divided into two subgroups: small ncRNAs (sncRNAs) and long ncRNAs (lncRNAs) [13–16]. If RNA is <200 nt in length, the ncRNAs are defined as sncRNAs, which includes microRNAs (also called miRNAs or miRs). Conversely, long non-coding RNAs (lncRNAs) are >200 nt in length. Previous studies have reported that lncRNAs are involved in numerous physiological and pathological processes.
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In recent years, an increasing number of lncRNAs have been investigated, and play a vital role in various major biological processes associated with promoting proliferation, invasion, and migration metabolism [17–19]. Increasing evidence points to important functional or regulatory roles of lncRNAs in cellular processes, including the cell cycle, proliferation, apoptosis [20–22], RNA processing [23], chromatin modification [24, 25], genomic reprogramming [26, 27], and gene imprinting [28]. They also play a role in cancers resulting from aberrant lncRNA expression. Recent findings indicate that lncRNAs are dysregulated in many kinds of cancer, including pancreatic cancer (PaCa), and they are closely related with tumorigenesis, metastasis, prognosis, and diagnosis.
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2. The physiological function of exosomes
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Exosomes carry a variety of substances from secreted cells, including proteins, lipids, DNA, RNA, and ncRNA [29, 30]. The intercellular communication regulated by exosomes is not only involved in regulating the physiological processes of normal cells but also participates in many pathological processes associated with disease development, including tumors [31–33]. Exosomes regulate biological activity through the rapid reaction of signal molecules on their surface or by the release of extracellular biologically active substances. Exosomal biological activity is mainly determined by its components (i.e., the exosome cell source) [8–10]. Exosomes, which use autocrine, paracrine, and endocrine signaling to exchange biological information, are involved in the transmission of substances and signals between cells.
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In addition, exosomes have immunomodulatory function [34]. Antigen-presenting cell (APC)-derived exosomes can promote the proliferation of T lymphocytes and induce antitumor immune responses in vivo. Exosomes have the features of their original cells because they bring DNA, RNA, and proteins from the original cell and carry a variety of proteins on their surface. Since exosomes are released from endosomes, they carry certain endosomal-specific proteins, including GTPases, flotillin, Alix, Tsg101, CD81 and CD82, heat shock proteins Hsp70 and Hsp90, and epithelial cell adhesion molecules [35–38] that are involved in exosome formation.
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If exosomes are secreted by tumor cells, they can kill the tumor cells by providing information to cytotoxic T lymphocytes by cross-reacting with antigen-presenting cells [39]. However, exosomes from tumor cells have a dual role in that they have antitumor activity and also promote tumor growth. For example, exosomes from colorectal cancer cells contain cell cycle-related mRNAs that promote the proliferation of endothelial cells, which can induce tumor angiogenesis [40]. Exosomes obtained from gastric cancer cells promote tumor progression by activating the NF-kB pathway in macrophages [41]. In ovarian cancer, epithelial ovarian cancer (EOC) cell-derived exosomes promote ovarian cancer metastasis and deterioration by transferring CD44 to peritoneal cells [42].
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3. Exosomes as novel biomarkers of cancer
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The identification of cancer-specific exosomes in bodily fluids, such as serum, plasma, and urine, will be useful for the detection of cancer and will allow for the identification of specific DNA, RNA, and protein content in the absence of contamination from non-cancerous exosomes [43]. The proteoglycan glypican-1 (GPC1) is highly expressed in tumor cell-derived exosomes. GPC1 has been shown to be a specific, sensitive marker in serum from pancreatic patients that are in both the early and late stages but not in benign pancreatic diseases [43]. CD24 and EpCAM are tumor-derived exosome markers isolated by immune-affinity techniques involving anti-CD24 and anti-EpCAM magnetic beads [44]. In serum, CD24 and EpCAM serve as early diagnosis biomarkers [44], while fibronectin can serve as an early diagnosis biomarker in plasma. The ELISA method has been used to detect fibronectin [45]. The levels of exosomal EDIL3 from breast cancer patients can be dramatically reduced with surgery, indicating that EDIL3 can also serve as a diagnostic and prognostic biomarker [46]. Survivin expression has been shown to be significantly increased in patients with prostate cancer, but lower survivin expression has been found in benign prostatic hyperplasia (BPH) and healthy subjects. Additionally, the levels of survivin in BPH and healthy subjects are not significantly different. Thus, survivin can be used as a new diagnostic indicator of prostate cancer [47].
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Separated and purified exosomes not only contain mRNA and miRNA but also tRNA and some lncRNA [11, 48–50]. Six miRNAs (miR-19b-3p, miR-21-5p, miR-221-3p, miR-409-3p, miR-425-5p, and miR-584-5p) were found to be upregulated in lung adenocarcinoma [51]. Eight miRNAs (miR-21, miR-141, miR-200a, miR-200c, miR-200b, miR-203, miR-205, and miR-214) have served as diagnostic biomarkers for ovarian cancer, and these miRNAs have also been identified in exosomes from ovarian cancer patients [52]. miRNAs can also be diagnostic biomarkers for esophageal squamous cell cancer (ESCC), as the serum levels of exosomal miR-21 from patients with ESCC are significantly higher than those of patients with benign diseases without systemic inflammation and are positively correlated with tumor progression and aggressiveness [53].
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4. Exosomes for therapeutic intervention in cancer
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The recent contribution by Zhang et al. reviewed the recent advances in cancer immunotherapy, exosome functions, exosome immunoregulation, and immune cell-derived exosomes [34]. As mentioned in Zhang’s manuscript, exosomes cannot only transfer messages between cells by carrying RNA and proteins but also can modulate the immune response. After reviewing recent findings regarding exosomes and immunity in cancer, we have highlighted the novel insights into the development of efficient exosome-based cancer vaccines for cancer therapeutic intervention. Specifically, exosomes derived from immune cells, such as APCs, dendritic cells (DCs), and NK cells, play a crucial role in the immunomodulation of cancer, and they may be the best cancer vaccine candidates because they can inhibit the malignant activity of cancer cells and leave healthy cells unaffected [54–56]. Recently, researchers have noted that exosomes may lead to key advances in cancer therapy. Exosomes isolated from DCs have been evaluated in clinical trials as treatment for various kinds of cancers [57–59]. In a phase I clinical trial, exosomes derived from autologous DCs loaded with MAGE 3 peptides were applied as cancer therapy for stage III/IV melanoma patients [58]. Several phase I or phase II clinical trials involving exosome-based regimens have occurred in breast cancer, gastric cancer, malignant glioma, and non-small cell lung cancer patients, which demonstrates that exosomes are effective tools for the transportation of anticancer drugs [59]. Exosomes were employed to form a complex with curcumin and delivered to recipient pancreatic cancer cells, which was found to promote cytotoxicity [60]. Moreover, exosomes have been shown to deliver small, molecular anticancer drugs across the blood-brain barrier and significantly inhibit tumor growth in a brain cancer model [61, 62].
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5. Long non-coding RNAs as novel biomarkers in cancer
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lncRNAs modulate gene expression, while lncRNA dysregulation is associated with human cancer. lncRNAs could play a significant role in cancer progression by interacting with proteins. Since they are highly specific and easily detectable in tissue, serum, plasma, and urine, interest in exploring lncRNAs in cancer patients continues to increase. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1, also known as NEAT2), a novel lncRNA, is found on chromosome 11q13 and is well conserved among mammalian species. MALAT-1 is a critical regulator of the metastatic phenotype of lung cancer cells [63] and can enhance proliferation, cell motility, invasion, and metastasis in CNE-1 [64], lung adenocarcinoma [65], thyroid cancer [17], cervical cancer [19], and ovarian cancer cells [18]. MALAT-1 has an important role in regulating the metastasis of bladder cancer and can be a potential application in bladder cancer therapy [66]. The MALAT-1-mediated promotion of renal cell carcinoma (RCC) proliferation and metastasis may be due to the upregulation of Livin expression [67]. MALAT-1 promotes the proliferation of chondrosarcoma cells via activating the Notch-1 signaling pathway [68], indicates poor prognosis in non-small cell lung cancer, and induces migration and tumor growth [69]. Upregulation of MALAT-1 has been associated with survival rate, cell cycle, and migration in patients with esophageal squamous cell carcinoma (ESCC) [70]. However, the loss of MALAT1 is compatible with cell viability and normal development [71]. On the other hand, MALAT-1 is downregulated in preeclampsia and regulates the proliferation, apoptosis, migration, and invasion of JEG-3 trophoblast cells [72]. MALAT-1 is also expected to be a potential therapeutic target in prostate cancer [73]. As another critical oncogenic lncRNA in human cancers [74, 75], the lncRNA HOTTIP promotes tumor growth, inhibits cell apoptosis [76], contributes to the progression of prostate cancer [77] and non-small cell lung cancer [78] by regulating HOXA13, and increases the chemoresistance of osteosarcoma cells by activating the Wnt/β-catenin pathway [79]. HOTTIP is upregulated and associated with poor prognosis in patients with osteosarcoma [80]. Overexpression of HOTTIP can promote tumor invasion and predict poor prognosis in gastric cancer [81]. This accumulating evidence indicates that long non-coding RNAs have immense potential as powerful, non-invasive tumor markers. However, overexpression of HOTTIP inhibits glioma cell growth by brain and reproductive expression [82].
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Circulating lncRNAs have shown potential as biomarkers in the diagnosis and prognosis of many cancers, including cervical cancer, colon cancer, hepatocellular carcinoma (HCC), gastric cancer (GC), PaCa, renal cell carcinoma (RCC), ovarian cancer (OC), non-small cell lung cancer (NSCLC), thyroid cancer, and prostate cancer (Table 1). Here, we have identified some interesting circulating lncRNAs (also known as exosomal lncRNAs), including MALAT-1, PVT1, HOTAIR, H19, UCA1, and TUG1, as novel biomarkers in various cancers. MALAT-1 in urine may serve as a potential biomarker for predicting prostate cancer risk. The application of the MALAT-1 model can prevent 30.2–46.5% of unnecessary biopsies in high-grade cancers [83]. PVT1 expression has been shown to be significantly elevated in non-small cell lung cancer (NSCLC), and high PVT1 expression has been associated with poor overall survival and disease-free survival in NSCLC patients; therefore, PVT1 could serve as a promising biomarker for the diagnosis and prognosis of NSCLC. PVT1 knockdown could remarkably inhibit NSCLC cell proliferation [84]. HOTAIR has been shown to be significantly higher in breast cancer patients, and circulating HOTAIR DNA levels were 2.15-fold higher in patients compared with those of healthy controls in one study, which demonstrates a moderate correlation between its expressions in tumor tissues. Plasma HOTAIR levels have been found to be significantly reduced after surgery [85, 86], indicating that plasma HOTAIR might serve as a potential biomarker for diagnosing breast cancer. A multivariate survival analysis also indicated that H19 might serve as a potential biomarker for early detection and prediction of prognosis of breast cancer and gastric cancer. The expression of H19 was remarkably increased in breast cancer and gastric cancer tissues. H19 expression has been shown to be significantly correlated with invasion depth, advanced TNM stage and regional lymph node metastasis in gastric cancer. Additionally, elevated expression levels of H19 have been shown to contribute to the poor overall survival and disease-free survival of gastric cancer patients [87]. This makes H19 closely associated with progressive gastric cancer, and it could be a potential non-invasive diagnostic gastric cancer biomarker for management. Better performance could be achieved using both carcinoembryonic antigen (CEA) and H19 simultaneously [88]. Plasma H19 levels have been shown to be significantly decreased in postoperative breast cancer samples compared to those in preoperative samples [89]. Urothelial cancer-associated 1 (UCA1), originally identified as a lncRNA in bladder cancer, has been proven to play a pivotal role in bladder cancer progression and embryonic development. Upregulation of the lncRNA UCA1 and the lncRNA WRAP53 has been observed in hepatocellular carcinoma (HCC), and CA1 might serve as a novel serum biomarker for HCC. Moreover, the expression levels of UCA1 and WRAP53 in tissue have been shown to be strongly correlated with their levels in sera. Further, the combination of UCA1 and WRAP53 with serum alpha fetoprotein could improve sensitivity to 100% [90]. Further, meta-analysis also found that higher levels of UCA1 were correlated with shorter progression-free survival (PFS) and overall survival (OS) times in cancer [91], indicating that circulating lncRNAs, such as MALAT-1, PVT1, HOTAIR, H19, UCA1, and WRAP53, could serve as novel biomarkers for the early detection and the prediction of prognosis of cancer.
lncRNA
Functions
Detection in cancer
References
MALAT-1
1. Promotes cell proliferation, invasion, and migration
Long non-coding RNAs (lncRNAs) as potential biomarkers for cancer.
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6. Exosomes and lncRNAs in the diagnosis and treatment of pancreatic cancer
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Pancreatic cancer is one of the most lethal tumors, and its main tumor type is that of adenocarcinoma [92–94]. Pancreatic ductal adenocarcinoma (PDAC), the fourth leading cause of cancer-related deaths in both males and females in the USA, is usually asymptomatic [186], and PDAC is one of the most lethal malignant neoplasms worldwide [89, 95, 96]. Statistical analysis indicated that death rates rose from 2001 to 2010 [97]. In America, approximately 53,000 people were diagnosed with pancreatic cancer in 2016, and pancreatic cancer was responsible for 41,750 deaths in the USA [98] in that same year. Additionally, the incidence of pancreatic cancer has shown an increasing trend year-by-year in China, and pancreatic cancer has become one of the top 10 causes of cancer-related deaths [99].
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It is well known that pancreatic cancer has a poor prognosis because it is usually diagnosed after the cancer has already spread, leading to poor patient outcomes. Pancreatic ductal adenocarcinoma patients have a 5-year survival rate of ~5% [100]. Survival can be improved if tumors are detected at an early stage, and the 5-year survival rate is 50% if tumors are <2 cm in size [101]. However, there have been no reliable biomarkers to accurately diagnose, image, or predict the tumor classification and biological behavior of pancreatic cancer until now. Thus, it is urgent to screen potential biomarkers and treatment-related biomarkers, such as exosome-derived proteins, DNA (exoDNA), miRNAs (exosomal miRNAs), and lncRNAs (exosomal lncRNAs), for the early detection of pancreatic cancer. Allenson found that KRAS mutations in the exoDNA of control, localized, locally advanced, and metastatic PDAC patients were 7.4, 66.7, 80, and 85%, respectively, which demonstrates that KRAS in exosomes could be applied to diagnose PDAC [102]. Takikawa also confirmed that pancreatic stellate cell (PSC)-derived exosomes stimulate the proliferation and migration of pancreatic cancer cells and upregulate the mRNA expression of the chemokine (C-X-C motif) ligands 1 and 2 in pancreatic cancer cells [103]. Over the last few years, non-coding RNAs, especially exosomal lncRNAs and exosomal miRNAs, have become a new diagnostic, prognostic, and predictive tool for pancreatic cancer. Exosomal miR-155, miR-196a, miR-17-5p, miR-10b, and miR-21 have good sensitivity and specificity in the serum of PaCa patients and can be useful serum biomarkers for pancreatic cancer [104, 105]. Not only can single exosomes be a diagnosis biomarker, but combined exosomal miRNAs, such as miR-1246, miR-4644, miR-3976, and miR-4306, can also increase sensitivity and specificity for the diagnosis of pancreatic cancer.
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Specifically, exosomal lncRNAs have been identified as potential biomarkers of various cancers in recent years, including gastric cancer, breast cancer, and lung cancer. However, few studies have explored the potential use of exosomal lncRNAs in pancreatic cancer detection and prognosis. MALAT-1, HOTTIP, PVT1, and HOTAIR, which are secreted from PDAC cells to bodily fluids, such as blood, pancreatic juice, cystic fluid, and urine, are some of most widely studied lncRNAs in pancreatic cancer (Figure 1). As a potential oncogenic lncRNA, MALAT-1 involves in proliferation, migration, and invasion and promotes the undifferentiated phenotype of pancreatic tumor cells [106]. MALAT-1 can also promote the tumorigenicity of pancreatic cancer cells, increase the proportion of pancreatic cancer stem cells, maintain a self-renewing capacity, and decrease chemosensitivity to anticancer drugs. Moreover, MALAT-1 has potential effects on the stem cell-like phenotypes of pancreatic cancer cells, which suggests that MALAT-1 has a novel role in tumor stemness [107]. The lncRNA HOTTIP enhances pancreatic cancer cell proliferation, survival, and migration and has been implicated in pancreatic cancer diagnosis and prognosis [108]. The overexpression of HOTAIR has been described as a poor prognostic factor in PDAC and can also be a novel non-invasive salivary biomarker for the early diagnosis of PaCa with PVT1 expression [109]. Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients [110]. PVT1 expression is significantly increased in PDAC and is correlated with tumor progression. Moreover, patients with high PVT1 expression levels have been shown to have shorter overall survival times compared to those with low PVT1 expression levels, which implies that PVT1 could be a potential molecular biomarker for predicting the prognosis of patients with PDAC [110]. H19 has been shown to be overexpressed in PDAC tissues and to be correlated with the histological grade of PDAC. Knockdown of H19 can suppress cell viability, proliferation, and tumor growth, while H19 overexpression can enhance cell viability, proliferation, and tumor growth [111]. UCA1 expression has been shown to be significantly upregulated in PaCa tumor tissues and to be significantly correlated with malignant potential factors, such as tumor size, depth of invasion, CA19-9 levels, and tumor stage. Highly expressed UCA1 has been shown to be an independent prognostic biomarker of PaCa, leading to an obviously shorter 5-year overall survival (OS). Downregulation of UCA1 could effectively inhibit cell proliferative activities, which implies that UCA1 could be a potential prognostic biomarker and therapy target of PaCa [112].
Figure 1.
Exosomal lncRNAs secreted from PDAC cells as potential biomarkers of pancreatic cancer.
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In addition, high expression levels of the lncRNA HOXA13 have been shown to be correlated with lymph node metastasis, poor histological differentiation, and decreased overall survival in PDAC patients. The knockdown of HOXA13 resulted in proliferation arrest and impaired cell invasion in pancreatic cancer [113]. Using microarray analysis, HOTTIP was confirmed to be one of the most significantly upregulated lncRNAs in PDAC [113]. HOTTIP has been shown to be overexpressed in pancreatic cancer, and knockdown of HOTTIP in pancreatic cancer cells decreased proliferation, induced apoptosis, and decreased migration [108]. Using an Arraystar Human lncRNA Microarray, HOTTIP-005, XLOC_006390, and RP11-567G11.1 were found to be the most increased lncRNAs in PaCa. Elevated HOTTIP-005 and RP11-567G11.1 expression could serve as poor prognostic markers for patients with PaCa. Plasma HDRF and RDRF (HOTTIP-005- and RP11-567G11.1-derived RNA fragments in plasma/serum) have also shown to be significantly increased in patients with PaCa, which demonstrates that HDRF and RDRF levels could be promising indicators for distinguishing patients with PC [114]. As an oncogenic lncRNA, uc.345 has been shown to promote tumor progression and to serve as a poor predictor for OS in pancreatic cancer patients. uc.345 was found to be upregulated in tumor tissues, and higher uc.345 expression levels have been associated with cancer invasion and metastasis, which could be an independent risk factor for the OS of pancreatic cancer patients [115]. The lncRNA IRAIN plays an important role in many malignancies, and upregulation of IRAIN has been shown to be significantly correlated with tumor size, the TNM classification of malignant tumors (TNM) stage, and lymph node metastasis in PaCa patients. The knockdown of IRAIN significantly induced cell apoptosis and inhibited cell proliferation in PaCa cells [116]. The lncRNA TUG1 has been shown to be highly expressed in pancreatic tissue compared with its expression in other organ tissues, and downregulation of TUG1 has been shown to affect apoptosis and insulin secretion in pancreatic β cells [117]. CCDC26 might be identified as a novel oncogene in PaCa by regulating proliferating cell nuclear antigen (PCNA) and Bcl2 expression. CCDC26 is significantly upregulated in PaCa, and it is correlated with tumor size, tumor number, and reduced OS [118]. Univariate and multivariate analysis showed that CCDC26 expression can be an independent prognostic factor of OS in patients with PaCa; therefore, CCDC2 could serve as a novel biomarker and therapeutic target of PC for cancer in the future [118]. LINC-ROR has been shown to be upregulated in PaCa tissues, and overexpression of LINC-ROR promoted cell proliferation, migration, invasion, and metastasis both in vitro and in mouse models. LINC-ROR acts as an important regulator of ZEB1 and might represent a novel therapeutic target [119]. The lncRNA LINC-PINT (p53-induced transcript) could also regulate tumor cell viability and proliferation. However, the expression levels of LINC-PINT have been shown to be lower in plasma and tumor tissue samples in PaCa patients. LINC-PINT has been shown to be more sensitive than CA19-9 in detecting PaCa, which suggests that LINC-PINT could be used for distinguishing the cause of malignant obstructive jaundice [120]. The lncRNA HMlincRNA717 has also been shown to be downregulated in pancreatic cancer and associated with overall survival, suggesting that HMlincRNA717 could be a potential prognostic biomarker for pancreatic cancer progression [121]. As a potential tumor suppressor, the long intergenic non-coding RNA (lincRNA) LINC00673 has been associated with pancreatic cancer risk. A G>A mutation at rs11655237 of LINC00673 created a target site for miR-1231 binding, which diminished the effect of LINC00673 in an allele-specific manner and conferred susceptibility to PaCa [122].
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All the abovementioned exosomal lncRNAs could serve as diagnostic and prognostic factors to complement clinical and pathological parameters in predicting the outcome of patients with pancreatic cancer. Although there are an increasing number of clinical assays for studying exosomes, determining clinical applications for lncRNAs and exosomes is a long ways off. No matter how exosomes have become the most effective cancer vaccines, future research to investigate exosomal lncRNAs as biomarkers for the early detection of pancreatic cancer and to assess the validity and quality of the exosomes as effective vaccines for pancreatic cancer will be valuable. To achieve this long-term goal, further understanding of exosome biology, especially of the molecular mechanisms of tumor- and immune cell-derived exosomes as cancer vaccines, is required.
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Acknowledgments
This research was supported by a grant from the National Natural Science Foundation of China (81672383) and a grant (16PJ1408800) from the Shanghai Pujiang Program in Shanghai, China.
\n',keywords:"exosomes, lncRNA, pancreatic cancer, biomarkers, diagnosis, therapeutic intervention",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/55850.pdf",chapterXML:"https://mts.intechopen.com/source/xml/55850.xml",downloadPdfUrl:"/chapter/pdf-download/55850",previewPdfUrl:"/chapter/pdf-preview/55850",totalDownloads:1523,totalViews:314,totalCrossrefCites:1,totalDimensionsCites:2,totalAltmetricsMentions:0,impactScore:1,impactScorePercentile:60,impactScoreQuartile:3,hasAltmetrics:0,dateSubmitted:"September 28th 2016",dateReviewed:"April 28th 2017",datePrePublished:null,datePublished:"July 12th 2017",dateFinished:"June 5th 2017",readingETA:"0",abstract:"Pancreatic cancer remains a leading cause of cancer-related deaths. Most patients are present with advanced stages of the disease at the time of diagnosis; thus, surgery, which is the best curative option for this malignancy, is no longer an effective treatment modality for affected individuals. As a likely source of “liquid biopsies,” exosomes, which are secreted by fusing intracellular multivesicular bodies with cell membranes, have relative stability and composition, allowing them to cover the entire range of cancer-related biomarkers, including cellular proteins, lipids, DNA, RNA, miRNA, and long non-coding RNAs (lncRNAs). To explore the early detection biomarkers of pancreatic cancer and to develop successful therapeutic intervention for this disease, assessing the implications of exosomes in pancreatic cancer patients is essential. In this chapter, we wish to focus on the possibility of using exosomes and lncRNAs in the clinical management of patients with pancreatic cancer. We will discuss the mechanisms of tumor formation under the exosomal action, demonstrate how circulating exosomes and lncRNAs have come into the research spotlight as likely biomarkers of pancreatic cancer, and discuss the applications of exosomes as transfer vectors in tumor therapeutics.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/55850",risUrl:"/chapter/ris/55850",book:{id:"5793",slug:"novel-implications-of-exosomes-in-diagnosis-and-treatment-of-cancer-and-infectious-diseases"},signatures:"Jin Wang, Xuan Zhang, Chunxia Ji, Lei Zhang, Yang Di, Wenhui Lou,\nXiaoyan Zhang and Jianqing Xu",authors:[{id:"188127",title:"Prof.",name:"Jin",middleName:null,surname:"Wang",fullName:"Jin Wang",slug:"jin-wang",email:"wjincityu@yahoo.com",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188127/images/5841_n.jpg",institution:{name:"Fudan University",institutionURL:null,country:{name:"China"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_1_2",title:"1.1. Exosomes, ncRNAs, and lncRNAs",level:"2"},{id:"sec_3",title:"2. The physiological function of exosomes",level:"1"},{id:"sec_4",title:"3. Exosomes as novel biomarkers of cancer",level:"1"},{id:"sec_5",title:"4. Exosomes for therapeutic intervention in cancer",level:"1"},{id:"sec_6",title:"5. Long non-coding RNAs as novel biomarkers in cancer",level:"1"},{id:"sec_7",title:"6. Exosomes and lncRNAs in the diagnosis and treatment of pancreatic cancer",level:"1"},{id:"sec_8",title:"Acknowledgments",level:"1"},{id:"sec_10",title:"Abbreviations",level:"1"}],chapterReferences:[{id:"B1",body:'Tkach M, Thery C. Communication by extracellular vesicles: Where we are and where we need to go. Cell. 2016;164:1226-1232\ufeff\ufeff'},{id:"B2",body:'Thery C, Zitvogel L, Amigorena S. Exosomes: Composition, biogenesis and function. Nature Reviews Immunology. 2002;2:569-579\ufeff\ufeff'},{id:"B3",body:'Keller S, Sanderson MP, Stoeck A, Altevogt P. 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Integrative functional genetic-epigenetic approach for selecting genes as urine biomarkers for bladder cancer diagnosis. Tumour Biology. 2015;36(12):9545-9552\ufeff\ufeff'},{id:"B215",body:'Srivastava AK, Singh PK, Rath SK, Dalela D, Goel MM, Bhatt ML. Appraisal of diagnostic ability of UCA1 as a biomarker of carcinoma of the urinary bladder. Tumour Biology. 2014;35(11):11435-11442\ufeff\ufeff'},{id:"B216",body:'Zhang Z, Hao H, Zhang CJ, Yang XY, He Q, Lin J. Evaluation of novel gene UCA1 as a tumor biomarker for the detection of bladder cancer. [Article in Chinese] Zhonghua Yi Xue Za Zhi. 2012;92(6):384-387\ufeff\ufeff'},{id:"B217",body:'Wang XS, Zhang Z, Wang HC, Cai JL, Xu QW, Li MQ, et al. Rapid identification of UCA1 as a very sensitive and specific unique marker for human bladder carcinoma. Clinical Cancer Research. 2006;12(16):4851-4858\ufeff\ufeff'},{id:"B218",body:'Zhao XB, Ren GS. WITHDRAWN: LncRNA TUG1 promotes breast cancer cell proliferation via inhibiting miR-9. 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The long non-coding RNA TUG1 indicates a poor prognosis for colorectal cancer and promotes metastasis by affecting epithelial-mesenchymal transition. Journal of Translational Medicine. 2016;14:42'},{id:"B227",body:'Jiang L, Wang W, Li G, Sun C, Ren Z, Sheng H, et al. High TUG1 expression is associated with chemotherapy resistance and poor prognosis in esophageal squamous cell carcinoma. Cancer Chemotherapy and Pharmacology. 2016;78(2):333-339\ufeff\ufeff'},{id:"B228",body:'Li J, Zhang M, An G, Ma Q. LncRNA TUG1 acts as a tumor suppressor in human glioma by promoting cell apoptosis. Experimental Biology and Medicine (Maywood, N.J.). 2016;241(6):644-649\ufeff\ufeff'},{id:"B229",body:'Ma B, Li M, Zhang L, Huang M, Lei JB, Fu GH, et al. Upregulation of long non-coding RNA TUG1 correlates with poor Tumour Biology. 2016;37(4):4445-4455\ufeff\ufeff'},{id:"B230",body:'Isin M, Ozgur E, Cetin G, Erten N, Aktan M, Gezer U, et al. Investigation of circulating lncRNAs in B-cell neoplasms. Clinica Chimica Acta. 2014;431:255-259\ufeff\ufeff\ufeff\ufeff'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Jin Wang",address:"wangjin@shaphc.org",affiliation:'
Scientific Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
Scientific Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
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1. Introduction
Proprietary or “paywall” publishing mode dominated the scholarly world throughout the late 20th and early 21st centuries. This is for-profit commercial publishing where publishers make their returns by the collection of research of scholars, application of peer-review, offering of editorial and formatting services, the collation of this research into subject-specific journals, and then selling subscription-based access of these works to academic libraries, scholarly societies and individual researchers. Access to individual articles on a short-term basis (typically 24 hours) is also supplied on a pay-for-use model. Commercial publishers also provide publishing facilities for books and monographs, although these have been on the decline [1]. The advent and wide use of the internet have strongly affected the process of scholarly publishing worldwide. A new mode of publication has emerged and widely employed by scholars and researchers. This new mode is Open Access (OA) publishing of scholarly work. This chapter will discuss OA focusing on its benefits to all the stakeholders and presenting other aspects of this new way of scholarly communication including its definition, types, development, its pros and cons and the myths and misconceptions surrounding it.
2. Definition and types of open access
2.1 Definition
Open access refers to free, unrestricted online access to research outputs such as journal articles and books. OA content is open to all, with no access fees. Open access is more than free access. When people think about open access (OA), they immediately relate it with free access. Providing reuse rights is another important asset of open access. Open access in its purest form is “digital, online, free of charge, and free of most copyright and licensing restrictions”. Open access entails a new model of publishing wherein the author, supported by an institution or funding agency, pays the publishing costs and owns the copyright. The publisher manages the peer review process and publishes directly to the Internet, where content is accessible free of charge to the public. Open access publishers take full advantage of available computing technology to streamline the publishing process [2]. Open Access aims to provide users with information that is unconstrained by the motive of financial gain or profits [3]. Furthermore, Open access implies that “users must be able to copy, use, distribute, transmit and display the work publicly and to make and distribute derivative works, in any digital medium for any responsible purpose, subject to proper attribution of authorship” [4, 5].
In subscription-based publishing, authors are required to transfer the copyright of their works to the publisher who makes profits via the dissemination and reproduction of the works. Contrary to this, with OA publishing, authors can retain copyright to their work and license its reproduction to the publisher. The most commons licenses used in open access publishing are the Creative Commons (CC) licenses. The widely used Creative Commons By Attribution (CC BY) license is one of the most permissive, only requiring attribution to be allowed to use the material (and allowing derivations and commercial use). A range of more restrictive creative commons licenses are also used. More rarely, some of the smaller academic journals use custom open access licenses. Some publishers (e.g. Elsevier) use “author nominal copyright” for OA articles, where the author retains copyright in name only and all rights are transferred to the publisher [6].
2.2 Brief background of the development of the OA movement
The OA movement can be said to have started in the year 1971 with Project Gutenburg Founded by Michael Hart [7]. This project is now providing free public domain text files with more than 60,000 eBooks. However, the modern open access movement began in the 1990s with the wide availability and access to the World Wide Web and online publishing became the norm. Starting in the early years of the 21st century there was a significant momentum towards making access to published research free of charge to scholars and universities through the Open Access movement. Three pioneering initiatives laid the foundation for the ideas and principles of OA movement. These are The Budapest Open Access Initiative on Feb. 14, 2002, The Bethesda Statement on Open Access Publishing on Apr. 11, 2003, and The Berlin Declaration on Open Access on Oct. 22, 2002 [8]. The Budapest Open Access Initiative was worked out during the human rights proponents gathering for the Open Society Institute meeting in December 2001. During the meetings a number of participants suggested that a global support is needed to create open information access within the scientific community. A draft was created during that meeting, and formalized two months later, in February 2002 as the Budapest Initiative. In April 2003, the United States and the United Kingdom based biomedical community convened and drafted a set of publishing principles guiding scientific dissemination. These principles were finalized and published in June 2003 as the Bethesda Statement. In October 2003, the European scientific community called for support by European researchers to engage in Open Access, with the Berlin Declaration [9].
Many stakeholders contributed to building institutions and resources for shaping up the global OA movements. Some of the institutions emerged during the first two decades of the third millennium are namely, Public Library of Science (PLOS), BioMed Central (BMC) – publishers of peer-reviewed OA journals, the Scholarly Publishing and Academic Resources Coalition (SPARC), and Open Access Scholarly Publishers Association (OASPA) [10]. In addition to the previously mentioned (BBB); the Budapest, Berlin and Bethesda OA declarations or statements got signed by the scholarly communities, particularly by the funding agencies, research councils, learned societies, institutions, universities, and scientists for the OA dissemination of public funded research.
The latest strong support for the OA movement is represented by what is known as PLAN S where the s could stand for “science, or shock” but “speed” is the most relevant where it refers to speed with the transition to direct and open access [11]. Plan S is an initiative for Open Access publishing that was launched in September 2018. The plan is supported by cOAlition S, an international consortium of research funders. Plan S requires that, from 2021, scientific publications that result from research funded by public grants must be published in compliance with Open Access journals or platforms.
2.3 Types of open access
There are three basic types of open access publishing. These are Green Open Access, Gold Open Access, and Hybrid Open Access [12].
2.3.1 Green open access
Green Open access publishing refers to the self-archiving of published or pre-publication works for free public use. Authors provide access to preprints or post-prints of their works with publisher permission in an institutional or disciplinary digital repository. Thus, Green open access refers to the practice of republishing a publication in an open access institutional or disciplinary repository. In this case the publication is first published in a traditional, closed-access journal. These materials are then made available to all via the internet, without restrictions or pay walls. In the “Green Route” of open access, institutions create repositories for their own research which is made open after an appropriate embargo period agreed upon with commercial publishers. As such Green Open Access generally refers to the post-print of an article [1]. In this context, there are three basic version types that can be self-archived in repositories: These are:
Pre-Prints – The author’s copy of article before it has been reviewed by the publisher, or pre-reviewed.
Post-Prints – The author’s copy of article after it has been reviewed and corrected, but before the publisher has formatted it for publication, or post-reviewed.
Publisher’s Version – The version that is formatted and appears in print or online.
2.3.2 Gold open access
Gold open access publishing refers to works published in an open access journal and accessed via the journal or publisher’s website. The Gold Route involves publishing in an open access journal, which then provides the dissemination and curation services in the same way as current proprietary publishers. This form of publishing is funded through government, society or institutional grants, and sometimes through charging authors a fee for deposit, known as an article processing charge (APC). However, the latter practice is implemented by a minority of open access journals and most journals do not charge any fees at all [13].
2.3.3 Hybrid open access
Hybrid open access publishing is mostly associated with gold open access. It takes place in journals that offer authors the option of making their articles open access, for a fee. Hybrid journals are subscription-based journals that make individual articles openly available in return for a fee. The hybrid route has been suggested as a means for traditional publishers to make a transition to open access publishing without significantly decreasing revenue, by charging fees for open access articles equal to the average subscription revenue per article. In the Hybrid Open Access publishing type, sometimes called Paid Open Access, the fee is paid to the publisher or journal by the author, the author’s organization, or the research funder [14, 15].
There are a number of other variations of these major types of open access publishing types. These include the Diamond Open access and the Platinum Open Access. The Diamond Open access journals provide scholarly publishing free of fees and access charges. They have direct or indirect subsidies from institutions like universities, research centres, government agencies etc. Whereas the Platinum model of open access publishing refers to the situation in which journals are published directly by the research or funding institutions themselves.
In Gold and Hybrid OA models, publishers usually publish articles with Creative Commons (CC) licenses. Open Access does not imply there is no copyright attached to the open document; rather, in most cases the Creative Commons Attribution License (CCAL) model is used. Founded in 2001, the CCAL states that users are free to share, adapt, or use the work as long as they give attribution in the manner specified by the author or licensor [16]. The Attribution License is one of six codes under the Creative Commons License. Thus Open Access journals do not charge subscription or pay-per-view fees compared to traditional journals. The authors, their institutions, or the research funders pay the “open access” fee to make it free to readers; authors retain copyright for the article and most permission barriers are removed [17, 18].
There is a controversial type of open access called the Bronze Open Access. In the Bronze model no open access Fee is paid but the publisher chooses to make a publication freely available to read. Many Open Access advocates and research funders would not regard Bronze as truly Open Access because the publisher can stop the publications being freely available at any time, whereas genuinely Open Access publications have a specific licence that means the publication is irrevocably open access and the terms of use and reuse are clearly stated [19].
Although bronze OA lacks a license, it is temporarily free to read only on the publisher’s website, and Publishers can deny access to the majority of open-access articles at their discretion [20].
2.3.4 Gratis vs. libre open access
These two terms are interlinked to the basic three types of open access. But in contrast to Gold, Green and Hybrid OA, they do not describe forms of publication, but define the attributes of an article published in OA. Therefore an article might be described jointly as Gratis Open Access, or Gratis Gold or Green Open Access, etc. [21]. Gratis Open Access means free of charge Open Access. This means that price barriers alone are removed from access to the publication. It allows no uses beyond what is considered legitimate under copyright and fair use. Libre Open Access, on the other hand, means free of charge and free of at least some permission barriers. This means that the article is free for some kinds of further use and reuse, and presupposes some kind of open licence that allows types of uses that are not permitted by default [22].
3. Advantages and disadvantages of open access publishing
3.1 Advantages and benefits
Open access publishing has a plethora of advantages for authors, institutions and readers across all sections of society. These advantages can be summarised as follows [8, 23]:
Increased accessibility of research work by users and other researchers. This leads to the enhancement and acceleration of the research cycle when results are available on an Open Access basis, where work is published, read, cited and then built upon by other researchers.
Increased visibility for authors and institutions, resulting in a higher impact of the research. There are no financial or copyright barriers so the readership continues to increase, enhancing the visibility and impact of the author’s Work. There is a greater chance of research results being seen when scientific journals are free to read and use, thus influencing the thinking of others. This state of affairs results in the increase of the academic’s impact factor.
Immediacy and Shorter publication times compared to non-open access publishing. Open access publishing takes shorter period of time from the date of submission of an article to a journal to its publication date.
Increased citations. A number of studies revealed that open access publishing leads to a greater number of citations. There is accumulating evidence showing that open access research articles are cited more often than those closed access articles. The studies reveal that across most subject areas there is at least a twofold increase in citation rate and that in some subject areas it is even higher [24].
Removing of price barriers. Open access removes price barriers and that openly accessible works are often full-text indexed, helping potential readers easily locate a work using a search engine, and access the work without being turned away by pay walls.
Contribution to author royalties. Some authors found that widespread dissemination of their openly accessible works stimulates demand for print copies of their works, contributing to royalties for these authors [23].
Those seeking wider visibility of their research work, higher impact for their research, less publication cost, and a shorter period of time from the date of submission to the publication date, should opt for publication in an OA journal [25].
3.2 Disadvantages
The most prominent and prevalent disadvantage of OA publishing is the emergence of predatory publishers and predatory journals. A predatory journal will not maintain the academic standards that are expected of a reputable scientific journal. The objective of the predatory journal is to make money for the owners without concern for the quality of the research published. A predatory journal will pretend to follow the essential editorial processes required for authentic academic publishing, but will not so do. Thus the quality of the research published in a predatory journal is likely to be low. Predatory journals can be identified by a number of characteristics, the most important of which may be the fact that they tend to market themselves through intensive e-mailing to invite selective victims who might otherwise have difficulty in having their research published in reputable journals. This lead to the development of what has become known as the predatory journal, which for a fee paid by the author delivers an un-scrutinised and unedited piece of writing purporting to be a high quality report on a piece of rigorously conducted scientific research. These journals are then presented to the public as Open Access journals [8, 26, 27].
Another claimed disadvantage of Open Access publishing is that some OA journals do not have high impact factors and this is considered detrimental to a researcher, though this is questionable as many OA journals are new and have not yet received their first impact factor (IF). However, high-IF OA journals are available in a variety of fields [25].
4. Myths and misconceptions about OA
There are a number of myths and misconceptions surrounding open access publishing mode. Some of the most common myths include the following:
Myth 1: “open access journals are not peer reviewed”.
Myth 2: “all open journals charge publication fees”.
Myth 3: “authors must choose between prestigious publication and Open Access publication”.
Below is a discussion of these myth and misconceptions about open access publishing with points that help dispel them.
4.1 Myth 1: “open access journals are not peer reviewed”
Studies show that the majority of OA journals are peer-reviewed with the same or higher standards as traditional scholarly journals. However, it takes time for a new OA journal to build a high impact factor [18, 28]. Indexing of a journal in a major citation database is also considered a reflection of a journal’s quality. Indexing newly established OA journals in major citation databases is complex and time-consuming, furthering existing misconceptions of quality [8]. This myth entails that Open access journals are intrinsically low in quality. But as early as 2004, it was found that in every field of the sciences there was at least one open access title that ranked at or near the top of its field in citation impact. It’s quite normal that open access journals can be of high quality and first-rate: the quality of a scholarly journal depends on its authors, editors, and referees, not its business model or access policy [29, 30].
4.2 Myth 2: “all open journals charge publication fees”
There are a number of OA journal business models and a number of OA book business models available. The models include the following options and variations:
Author-Pays model, author pays publishing fee.
Research funder subsidies, funding organisations pay author fees.
Institutional membership, author fees are paid as a lump sum.
Publishing support funds, institutions reserve funds for author fees.
Hybrid business model, journals mix subscription based and author pays content.
Community-fee model, societies fund journals by both subscriptions and membership fees.
Institutional subsidies, institutions support their own university presses.
Charging publication fees in the form of author fees or article processing charges is the best-known business model for open access journals, but it is not the most common. Most peer-reviewed open access journals nowadays charge no fees at all. The Directory of Open Access Journals (DOAJ) [31] provides information about open access journals that do and do not charge fees. It is also well known that most conventional or non-open access journals do charge author-side fees, on top of reader-side subscription fees.
4.3 Myth 3: “Authors must choose between prestigious publication and Open Access publication”
OA is compatible with prestige for two reasons: First, a growing number of OA journals have already earned high levels of prestige, and others are earning it. The second reason is that most pay wall (Toll Access) journals allow OA archiving. When authors retain the right to self-archive, all journals willing to publish their work also allow self-archiving. The current misunderstanding has some negative effects. When scholars know about OA and don’t choose it, they are generally not opposed to it; many support it strongly. They are simply giving higher priority to prestige. But because OA is compatible with prestige, authors rarely have to choose. But they have to choose only when a prestigious journal doesn’t already permit post print archiving and when it rejects the authors’ individualized request for permission. Authors rarely have to choose between them, but to have both at once they will often have to choose to self-archive [32].
Most publishers allow their authors to self-archive their articles in institutional repositories or on their own personal websites. However, conditions and restrictions are frequently imposed. For example, authors are often obliged to observe an embargo period between the publication date and the date on which the document is made openly accessible online. The SHERPA/Romeo Listings provide information on the self-archiving policies of individual publishers. They used to classify publishers in different colours depending on their archiving policies; green publishers let authors archive preprint and post print or publisher’s version/PDF, blue publishers let authors archive post print or publisher’s version/PDF, yellow publishers let authors archive preprint, and white publishers do not formally support archiving. But they recently stated that they have now retired the Romeo colours, as open access policies have become more complicated and the colours no longer gave a clear overview [33]. Many of those authors, whose publishers do not allow self-archiving, supplement their standard publishing agreements with contract addenda which enable them to provide open access to their work in parallel with publication [34].
4.5 Myth 5: “OA invites plagiarism”
In the early days of the OA movement some authors worried that OA would increase the incentive to plagiarize their work. On the contrary, OA might make plagiarism easier to commit, for people trolling for text to cut and paste. But for the same reason, OA makes plagiarism more risky to commit. Plagiarism from OA sources is the easiest kind to detect. Some of the misunderstanding here may arise from confusing plagiarism and copyright infringement. Plagiarism and infringement are two separate things although they are overlapping offenses. “Someone can commit plagiarism without infringing copyright (by copying a fair-use excerpt and claiming it as one’s own) and infringe copyright without committing plagiarism (by copying a larger excerpt but with attribution). One can also commit both together (by copying a large excerpt and claiming it as one’s own)” [32].
4.6 Myth 6: “OA helps readers but not authors”
OA articles are accessible to everyone with an internet connection, a vastly larger audience than any scholarly journal can claim. Not all internet users will care to read your research, of course. But making your work universally accessible to the connected guarantees that it will be accessible to the subset which does care. If there’s an exception for the digital divide, there’s a larger exception for the non-digital or print divide. Moreover, there’s abundant evidence that OA articles are cited more often than non-OA articles, even more than non-OA articles from the same issues of the same journals [35, 36]. Many different studies have tackled this phenomenon, taking on different bodies of literature, using different methods, controlling different variables. They disagree on whether the OA impact advantage is large or small, and whether OA causes the increase in citations or is merely correlated with it. But they agree that OA articles are cited more often than non-OA articles. Authors may hope to earn royalties from their books, but they write journal articles for impact, not for money [37].
4.7 Myth 7: “All OA is gratis OA”
Gratis OA removes price barriers but not permission barriers. It makes content free of charge but not free of copyright or licensing restrictions. It gives users no more reuse rights than they already have through fair use or the local equivalent. Libre OA removes price barriers and at least some permission barriers. It loosens copyright and licensing restrictions and permits at least some uses beyond fair use [38]. There is some excuse for the opposite view, that all OA is libre OA. The Budapest, Bethesda, and Berlin definitions of OA all describe forms of libre OA. The current misunderstanding accepts that gratis OA is a kind of OA, but goes one step too far and assumes that gratis OA is the only kind of OA. The misunderstanding is that there is no libre OA, that libre OA adds nothing to gratis OA, or that what libre OA adds isn’t necessary or desirable. In general, OA repositories have good reasons to stick to gratis OA but OA journals don’t. Repositories can’t generate the needed permissions on their own, but journals can [37].
5. Future of open access
5.1 Prevalence of open access
A large-scale study that investigates the prevalence and impact of OA publishing found that almost half of the scholarly papers that people attempt to access online are now freely and legally available [39]. The study tracked 100,000 online requests for journal papers in 2017. It examined reader data from a web-browser extension called Unpaywall which finds free-to-read versions of pay-walled papers in the Internet. The study authors analysed server logs of 100,000 papers that Unpaywall users tried to access during one week, and found that 47% of accessed studies were legally available to read for free somewhere on the web, and that around half the content being accessed was published in the previous two years. Their study also revealed that more than 20% of scholarly articles searched for through Unpaywall were available directly from journals, with clear licences describing whether the papers were free not just to read, but also to download or redistribute. Another 9% of the papers were still published behind a pay-wall, but authors later uploaded their paper to an online repository. The most intriguing category of papers was the 15% that were posted on a publisher’s site as free to read, but without any explicit open licence. The authors say this type of open-access — which they call ‘bronze’, in contrast to the widely used ‘gold’ and ‘green’ definitions — has been scarcely discussed. Of papers published in the most recent year examined −2015- 45% were freely available, which suggests that newer articles are more likely to be open. The authors of the study concluded that the percentage of literature that is OA continues to grow steadily, and that “In the next few decades, we’re going to be seeing nearly all the literature available freely.” [39].
5.2 Plan S and the future of open access
Plan S is the latest initiative to promote and support open access publishing. Below is an excerpt from the Coalition website [40] which is the body responsible for the Plan S, revealing the target of this open access plan:
With effect from 2021, all scholarly publications on the results from research funded by public or private grants provided by national, regional and international research councils and funding bodies, must be published in Open Access Journals, on Open Access Platforms, or made immediately available through Open Access Repositories without embargo [41].
6. Conclusion
This chapter presented an overview of the basic principles and common practices of open access publishing as an emerging and expanding mode of scholarly publishing. The chapter started with an introduction to the concept of open access publishing with a brief background of the development of the open access movement. The different types of open access publishing are then highlighted and defined. These types include Gold Open Access, Green Open Access, and Hybrid Open Access, in addition to other variations of these basic types namely, the Diamond Open Access and the Platinum Open Access. The concepts of Gratis vs. Libre Open Access are also defined and explained. The chapter then discussed the advantages and disadvantages of open access focusing on the various advantages of this mode of scholarly publishing to authors and readers as well. The chapter then proceeded to discuss and refute the most common myths and misconceptions about open access publishing. The chapter is concluded with some views on the prevalence and future of open access publishing.
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Costs and Benefits of Open Access: A Guide for Managers in Southern African Higher Education [Internet]. 2014. Available from: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.899.9086&rep=rep1&type=pdf [Accessed: 2020-07-08]'},{id:"B2",body:'Gale Oren. The Crisis in Scholarly Publishing: Open Access to the Rescue? Journal of Neuro-Ophthalmology. 2008;1:1-4. DOI: 10.1097/WNO.0b013e3181678618'},{id:"B3",body:'Devika P Madalli. Concepts of Openness and Open Access [Internet]. 2015. Available from: https://unesdoc.unesco.org/ark:/48223/pf0000232207 [Accessed: 2020-07-09]'},{id:"B4",body:'Bethesda Statement on Open Access Publishing [Internet]. 2003. Available from: https://dash.harvard.edu/bitstream/handle/1/4725199/suber_bethesda.htm?sequence=1&isAllowed=y [Accessed: 2020-07-08]'},{id:"B5",body:'Berlin Declaration on Open Access to Knowledge in the Sciences and Humanities [Internet]. 2003. Available from: https://openaccess.mpg.de/Berlin-Declaration [Accessed: 2020-07-08]'},{id:"B6",body:'Wikipedia. Open Access [Internet]. 2020. Available from: https://en.wikipedia.org/wiki/Open_access [Accessed: 2020-08-05]'},{id:"B7",body:'Paul Royster. A Brief History of Open Access [Internet]. (2016). Available from: https://digitalcommons.unl.edu/library_talks/123 [Accessed: 2020-07-12]'},{id:"B8",body:'S Singh and D Remenyi. Researchers Beware of Predatory and Counterfeit Journals: Are Academics Gullible? The Electronic Journal of Business Research Methods. 2016;1:50-59'},{id:"B9",body:'Meenu Kumari. Open access to scholarly communication: Issues and challenges. International Journal of Advanced Educational Research. 2017;6:117-122'},{id:"B10",body:'UNESCO. Introduction to Open Access [book on the Internet].Paris: UNESCO. Available from: https://wiki.lib.sun.ac.za/images/e/ed/L1.pdf [Accessed: 2020-08-14]'},{id:"B11",body:'Jacqui Thornton. Transition to immediate open access publishing under Plan S will be smooth, promise backers. BMJ. 2018;363. Doi: https://doi.org/10.1136/bmj.k5019'},{id:"B12",body:'Laura Burtle. Open Access: Types of OA [Internet]. 2018. Available from: https://research.library.gsu.edu/c.php?g=115588&p=754380 [Accessed: 2020-08-14]'},{id:"B13",body:'Witold Kieńć. Green OA vs. Gold OA: Which one to choose? [Internet]. 2015. Available from: https://openscience.com/green-oa-vs-gold-oa-which-one-to-choose/ [Accessed: 2020-09-03]'},{id:"B14",body:'Thomas J. Walker. Electronic reprints -- segueing into electronic publication of biological journals. BioScience. 1996;46;3:171. DOI: https://doi.org/10.1093/bioscience/46.3.171'},{id:"B15",body:'Bo-Christer Bjork. The hybrid model for open access publication of scholarly articles: A failed experiment? Journal of the American Society for Information Science and Technology. 2012;63:1496-1504. DOI: 10.1002/asi.22709'},{id:"B16",body:'Creative Commons Attribution License. About the licenses [Internet]. 2020. Available from: https://creativecommons.org/licenses/ [Accessed: 2020-09-03]'},{id:"B17",body:'Jan M. Nick . Open Access Part I: The Movement, The Issues, and The Benefits. OJIN [journal on the internet]. 2012; 17;1. DOI: 10.3912/OJIN.Vol17No01PPT02'},{id:"B18",body:'Darshana T. Shah. Open Access Publishing: Pros, Cons, and Current Threats. Marshall Journal of Medicine. 2017;3. DOI: http://dx.doi.org/10.18590/mjm.2017.vol3.iss3.1'},{id:"B19",body:'Brookes O.A. The different models of Open Access [Internet]. 2020. Available from: https://brookesoa.blog/open-access/the-different-models-of-open-access/ [Accessed: 2020-08-20]'},{id:"B20",body:'Jon Brock. ‘Bronze’ open access supersedes green and gold [Internet]. 2018. Available from: https://www.natureindex.com/news-blog/bronze-open-access-supersedes-green-and-gold [Accessed: 2020-08-12]'},{id:"B21",body:'Kamil Mizera. Green, Gold, Gratis and Libre Open Access: brief overview for beginners [Internet]. 2013. Available from: https://openscience.com/green-gold-gratis-and-libre-open-access-brief-overview-for-beginners/#:~:text=“Libre”%20access%20is%20free%20of,(or%20the%20local%20equivalent) [Accessed: 2020-09-04]'},{id:"B22",body:'Meg Hunt and Alma Swan. Briefing paper: Open Access [Internet]. 2012. Available from: http://www.pasteur4oa.eu/sites/pasteur4oa/files/resource/Open%20Access%20-%20basic%20briefing%20.pdf [Accessed: 2020-12-01]'},{id:"B23",body:'Lexi Rubow, Rachael Shen and Brianna Schofield. Understanding Open Access: When, Why, & How to Make Your Work Openly Accessible [Internet]. 2015. Available from: https://authorsalliance.org/wp-content/uploads/Documents/Guides/Authors%20Alliance%20-%20Understanding%20Open%20Access.pdf [Accessed: 2020-09-03]'},{id:"B24",body:'Alma Swan. JISC Open Access Briefing Paper [Internet]. 2005. Available from: http://eprints.soton.ac.uk/id/eprint/261005 [Accessed: 2020-12-01]'},{id:"B25",body:'Sarah Conte. Making the Choice: Open Access vs. Traditional Journals [Internet]. 2018. Available from: https://www.aje.com/en/arc/making-the-choice-open-access-vs-traditional-journals/ [Accessed: 2020-09-01]'},{id:"B26",body:'Jeffrey Beall. Predatory Publishers Are Corrupting Open Access [Internet]. 2012. available from: https://www.nature.com/news/predatory-publishers-are-corrupting-open-access-1.11385 [Accessed: 2020-08-25]'},{id:"B27",body:'Rosanna Tamburri. Publishers with questionable practices prey on academics: Canadian researchers are being inundated with offers to publish their work by dubious online publishers [Internet] 2013. Available from: https://www.universityaffairs.ca/news/news-article/publishers-with-questionable-practices-prey-on-academics/ [Accessed: 2020-08-25]'},{id:"B28",body:'B C Björk and D Solomon. Open access versus subscription journals: a comparison of scientific impact. BMC Med.2012;10;73. DOI: https://doi.org/10.1186/1741-7015-10-73'},{id:"B29",body:'Open Access: Benefits of Open Access [Internet]. 2020. Available from: https://subjectguides.library.westernsydney.edu.au/c.php?g=165246&p=667613 [Accessed: 2020-08-05]'},{id:"B30",body:'Marie E. McVeigh. Open Access Journals in the ISI Citation Databases: Analysis of Impact Factors and Citation Patterns a citation study from Thomson Scientific [Internet]. 2004. Available from: https://d1wqtxts1xzle7.cloudfront.net/39476484/openaccesscitations2.pdf?1445994076=&response-content-disposition=inline%3B+filename%3DOpen_Access_Journals_in_the_ISI_Citation.pdf&Expires=1598855598&Signature=C2UTE7x78ziI~KTDnK4C8VSxstoSrcu3DlDp--rn7UyEV~8ccETnwiaK60b-eH9xJALq~5FserNllyqMrcy8uB3Ipa5BcXabehVigz1YHobs76WNhYtezVZzg5e-7vjxrsjioZ2kqJSa~kB~x-L4A~TJTsMfBzKy9NIMKmiFehIGH687siXNlnGo5EPQVmlz2~9S~~t2F4bwxnaU17by4xCtXy5ThG7IQ5TeJvrvq66S~fRpfqFscNSIZAbwc1jhGq6mYfA0tsB218y9pX2uoI1F3RtrgSt1bU~ePGjmihEHHLp17LuOBWt0iTTxlpGqf8lHoAlvtqf5Knc1EpBHw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA [Accessed: 2020-12--2]'},{id:"B31",body:'Directory of Open Access Journals (DOAJ) [Internet]. 2020. Available from: https://doaj.org [Accessed: 2020-07-25]'},{id:"B32",body:'Peter Suber. A field guide to misunderstandings about open access [Internet] 2009. Available from: http://legacy.earlham.edu/~peters/fos/newsletter/04-02-09.htm#fieldguide [Accessed: 2020-07-18]'},{id:"B33",body:'Sherpa Romeo 2020 [Internet] 2020. Available from: https://v2.sherpa.ac.uk/romeo/ [Accessed: 2020-12-02]'},{id:"B34",body:'Elizabeth Gadd, Jenny Fry and Claire Creaser. The influence of journal publisher characteristics on open access policy trends [Internet]. 2018. Available from: https://link.springer.com/article/10.1007/s11192-018-2716-8 [Accessed: 2020-09-25]'},{id:"B35",body:'Peter Suber. Gratis and libre open access [Internet]. 2008. Available from: http://www.earlham.edu/~peters/fos/newsletter/08-02-08.htm#gratis-libre [Accessed: 2020-07-10]'},{id:"B36",body:'Stevan Harnad and Tim Brody. Comparing the Impact of Open Access (OA) vs. Non-OA Articles in the Same Journals. D-Lib Magazine. June 2004;10:6'},{id:"B37",body:'Peter Suber. Open access policy options for funding agencies and universities [Internet]. 2009. Available from: http://www.earlham.edu/~peters/fos/newsletter/02-02-09.htm#4 [Accessed: 2020-08-25]'},{id:"B38",body:'Heather Piwowar, Jason Priem, Vincent Larivière, Juan Pablo Alperin, Lisa Matthias, Bree Norlander, Ashley Farley, Jevin West and Stefanie Haustein. The State of OA: A large-scale analysis of the prevalence and impact of Open Access articles [Internet]. 2017. Available from: https://peerj.com/preprints/3119/ [Accessed: 2020-08-25]'},{id:"B39",body:'Dalmeet Singh Chawla. Half of papers searched for online are free to read: Large study of open research analysed reader data from Unpaywall tool, which finds freely available versions of articles [Internet]. 2017. Available from: https://www.nature.com/news/half-of-papers-searched-for-online-are-free-to-read-1.22418 [Accessed: 2020-09-01]'},{id:"B40",body:'Plan S: Making Full and Immediate Open Access a Reality [Internet]. 2020. Available from: https://www.coalition-s.org [Accessed: 2020-08-25]'},{id:"B41",body:'Plan S: Principles and Implementation [Internet] 2020. Available from: https://www.coalition-s.org/addendum-to-the-coalition-s-guidance-on-the-implementation-of-plan-s/principles-and-implementation/ [Accessed: 2020-08-25]'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Omer Hassan Abdelrahman",address:"omhass@hotmail.com",affiliation:'
Department of Library and Information Science, University of Khartoum, Khartoum, Sudan
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To establish new topical PDT, protocols are necessary first to conduct studies in vivo using animal skin models. The goal of this study is to evaluate the robust correlation between porcine and human skin models in vivo by optical methods to confirm the suitability of porcine skin models to predict drug behavior in the human skin on topical PDT protocols. Methods: The study was performed in vivo using porcine and human skin models. In human skin, ALA and MAL cream mixture samples were applied to the inner arm in a circular area of 1 cm2. In porcine skin, the cream was applied on the back in an area of 4 cm2, over which an occlusive dressing was placed. PPIX production was monitored for up to 5 h using widefield fluorescence imaging and fluorescence spectroscopy techniques. Results: Human skin models showed similar behavior to porcine skin models, which indicates high similarity between both models and confirms that porcine skin is an adequate model to establish new clinical PDT protocols in human volunteers.",signatures:"Alessandra Keiko Lima Fujita, Rozana Wendler da Rocha, André\nEscobar, Andrigo Barboza de Nardi, Vanderlei Salvador Bagnato\nand Priscila Fernanda Campos de Menezes",authors:[{id:"36412",title:"Dr.",name:"Priscila",surname:"Menezes",fullName:"Priscila Menezes",slug:"priscila-menezes",email:"priscilamene2015@gmail.com"},{id:"72297",title:"Prof.",name:"Vanderlei Salvador",surname:"Bagnato",fullName:"Vanderlei Salvador Bagnato",slug:"vanderlei-salvador-bagnato",email:"vander@ifsc.usp.br"},{id:"220461",title:"Dr.",name:"Alessandra",surname:"Fujita",fullName:"Alessandra Fujita",slug:"alessandra-fujita",email:"alessandra.keiko@gmail.com"},{id:"227389",title:"MSc.",name:"Rozana",surname:"Da Rocha",fullName:"Rozana Da Rocha",slug:"rozana-da-rocha",email:"rozana_wendler@hotmail.com"},{id:"227390",title:"Dr.",name:"André",surname:"Escobar",fullName:"André Escobar",slug:"andre-escobar",email:"aescobarvet@yahoo.com.br"},{id:"227391",title:"Prof.",name:"Andrigo",surname:"De Nardi",fullName:"Andrigo De Nardi",slug:"andrigo-de-nardi",email:"andrigobarboza@yahoo.com.br"}],book:{id:"6078",title:"Human Skin Cancers",slug:"human-skin-cancers-pathways-mechanisms-targets-and-treatments",productType:{id:"1",title:"Edited Volume"}}},{id:"73612",title:"Anatomically Adjustable Device for Large-Area Photodynamic Therapy",slug:"anatomically-adjustable-device-for-large-area-photodynamic-therapy",abstract:"The illumination system composed of LEDs is an anatomically adjustable device of high intensity that can be applied in different areas of the body. It can be applied in health care, as in the dermatological and esthetic treatments. The device improved the treatment of pathological diseases (e.g. actinic keratosis) since disseminated lesions were reached in a single application, thus reducing the time of the procedure and ensuring homogeneous light distribution. It was compared with a smaller and non-adjustable illumination device and evaluated in the treatment of actinic keratosis. The results showed its versatile application and a uniform adjustment to body curvatures.",signatures:"Alessandra Keiko Lima Fujita, Daniel José Chianfrome, Vinicius Sigari Moreira, Anderson Luiz Zanchin, Priscila Fernanda Campos de Menezes and Vanderlei Salvador Bagnato",authors:[{id:"36412",title:"Dr.",name:"Priscila",surname:"Menezes",fullName:"Priscila Menezes",slug:"priscila-menezes",email:"priscilamene2015@gmail.com"},{id:"72297",title:"Prof.",name:"Vanderlei Salvador",surname:"Bagnato",fullName:"Vanderlei Salvador Bagnato",slug:"vanderlei-salvador-bagnato",email:"vander@ifsc.usp.br"},{id:"220461",title:"Dr.",name:"Alessandra",surname:"Fujita",fullName:"Alessandra Fujita",slug:"alessandra-fujita",email:"alessandra.keiko@gmail.com"},{id:"326980",title:"BSc.",name:"Daniel",surname:"Chianfrone",fullName:"Daniel Chianfrone",slug:"daniel-chianfrone",email:"danielljc@hotmail.com"},{id:"326982",title:"Mr.",name:"Vinicius",surname:"Moreira",fullName:"Vinicius Moreira",slug:"vinicius-moreira",email:"vinicius_sigari@hotmail.com"},{id:"326985",title:"BSc.",name:"Anderson",surname:"Zanchin",fullName:"Anderson Zanchin",slug:"anderson-zanchin",email:"anderson.zanchin@mmo.com.br"}],book:{id:"7886",title:"Photodynamic Therapy",slug:"photodynamic-therapy-from-basic-science-to-clinical-research",productType:{id:"1",title:"Edited Volume"}}}],collaborators:[{id:"46010",title:"Prof.",name:"Gabriela",surname:"Negroiu",slug:"gabriela-negroiu",fullName:"Gabriela Negroiu",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"206108",title:"Dr.",name:"Marcela",surname:"Valko-Rokytovská",slug:"marcela-valko-rokytovska",fullName:"Marcela Valko-Rokytovská",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Veterinary Medicine in Košice",institutionURL:null,country:{name:"Slovakia"}}},{id:"209093",title:"B.A.",name:"Yixuan James",surname:"Zheng",slug:"yixuan-james-zheng",fullName:"Yixuan James Zheng",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"209094",title:"Dr.",name:"Suzana",surname:"Ortiz",slug:"suzana-ortiz",fullName:"Suzana Ortiz",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"214089",title:"B.A.",name:"Adriana",surname:"Lopez",slug:"adriana-lopez",fullName:"Adriana Lopez",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Columbia University",institutionURL:null,country:{name:"United States of America"}}},{id:"216042",title:"Dr.",name:"Jana",surname:"Šimková",slug:"jana-simkova",fullName:"Jana Šimková",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"216043",title:"Dr.",name:"Mária",surname:"Milkovičová",slug:"maria-milkovicova",fullName:"Mária Milkovičová",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"216044",title:"Prof.",name:"Zuzana",surname:"Kostecká",slug:"zuzana-kostecka",fullName:"Zuzana Kostecká",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"217160",title:"Dr.",name:"Adina",surname:"Milac",slug:"adina-milac",fullName:"Adina Milac",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Institute of Biochemistry",institutionURL:null,country:{name:"Romania"}}},{id:"217602",title:"Dr.",name:"Ricardo",surname:"Traspas",slug:"ricardo-traspas",fullName:"Ricardo Traspas",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null}]},generic:{page:{slug:"attribution-policy",title:"Attribution Policy",intro:"
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Therefore, the dog has become an important spontaneous animal model for the study of human oral clefts. In order to provide an overview of CL/P in dogs to people with an interest in this area, we present in this chapter the main medical aspects, ranging from the etiology to the prevention, and also the main genetic aspects, including inheritance mechanisms and highlighting the homology between the two species, and the most recent molecular findings.",book:{id:"5428",slug:"designing-strategies-for-cleft-lip-and-palate-care",title:"Designing Strategies for Cleft Lip and Palate Care",fullTitle:"Designing Strategies for Cleft Lip and Palate Care"},signatures:"Enio Moura and Cláudia Turra Pimpão",authors:[{id:"91097",title:"Prof.",name:"Enio",middleName:null,surname:"Moura",slug:"enio-moura",fullName:"Enio Moura"},{id:"194711",title:"Dr.",name:"Cláudia",middleName:null,surname:"Pimpão",slug:"claudia-pimpao",fullName:"Cláudia Pimpão"}]},{id:"67059",title:"Oncoplastic Surgery in Breast Cancer",slug:"oncoplastic-surgery-in-breast-cancer",totalDownloads:1060,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Oncoplastic surgery is an emerging approach which combines breast-conserving surgery and plastic surgery techniques. It aims to provide wider volume resection with oncologically clear margins and at the same time to maintain the breast shape and optimize cosmetic outcomes. Inspired from esthetic breast surgery techniques, oncoplasty consists of breast volume displacement to fill the defect of large resections and optimize the cosmetic outcomes without interfering with the oncoplastic safety. In this chapter, the concept, indications, and principles of oncoplastic techniques used in conservative breast surgeries will be exposed. A photo-based atlas for oncoplastic incisions will concern seven cases starting with the preoperative planning and marking and ending up with the long-term postoperative outcomes.",book:{id:"8853",slug:"breast-cancer-and-breast-reconstruction",title:"Breast Cancer and Breast Reconstruction",fullTitle:"Breast Cancer and Breast Reconstruction"},signatures:"Atallah David, Moubarak Malak and Abdallah Abdallah",authors:[{id:"219535",title:"Associate Prof.",name:"David",middleName:null,surname:"Atallah",slug:"david-atallah",fullName:"David Atallah"},{id:"221488",title:"Dr.",name:"Malak",middleName:null,surname:"Moubarak",slug:"malak-moubarak",fullName:"Malak Moubarak"},{id:"299454",title:"Dr.",name:"Abdallah",middleName:null,surname:"Abdallah",slug:"abdallah-abdallah",fullName:"Abdallah Abdallah"}]},{id:"53788",title:"Surgical Techniques for Treatment of Unilateral Cleft Lip",slug:"surgical-techniques-for-treatment-of-unilateral-cleft-lip",totalDownloads:4043,totalCrossrefCites:1,totalDimensionsCites:2,abstract:"A surgeon intending habilitation of a child with cleft lip should be familiar with the normal anatomy of the lip and nose, the distortions introduced by the cleft deformity, and the many techniques available to employ those best suited to correction of that child’s deformity.",book:{id:"5428",slug:"designing-strategies-for-cleft-lip-and-palate-care",title:"Designing Strategies for Cleft Lip and Palate Care",fullTitle:"Designing Strategies for Cleft Lip and Palate Care"},signatures:"Mustafa Chopan, Lohrasb Sayadi and Donald R. Laub",authors:[{id:"67264",title:"Dr.",name:"Donald",middleName:"R",surname:"Laub Jr.",slug:"donald-laub-jr.",fullName:"Donald Laub Jr."},{id:"189368",title:"Mr.",name:"Mustafa",middleName:null,surname:"Chopan",slug:"mustafa-chopan",fullName:"Mustafa Chopan"},{id:"189370",title:"Mr.",name:"Lorasb",middleName:null,surname:"Sayadi",slug:"lorasb-sayadi",fullName:"Lorasb Sayadi"}]},{id:"53918",title:"Epidemiology of Cleft Lip and Palate",slug:"epidemiology-of-cleft-lip-and-palate",totalDownloads:2836,totalCrossrefCites:5,totalDimensionsCites:8,abstract:"Orofacial cleft (OFC) anomalies are amongst the most common congenital anomalies and the most common craniofacial anomalies. Despite their poorly characterized etiologies, cases of OFC are usually grouped by epidemiological studies as cleft lip, with or without cleft palate (CL/P), and cleft palate alone (CPO). Incidence of CL/P and CPO differs according to gender and ancestry and may vary widely across studies. Cases of OFC are characterized as either “syndromic” or “nonsyndromic,” with further classification of nonsyndromic cases into isolated cases and cases that present with additional malformations. The genetic bases for many syndromic cases of OFC have been previously elucidated. Genetic associations have been described for nonsyndromic OFC as well. Importantly, etiology of OFC is known to involve interaction between genetic and environmental factors, including maternal nutrition and exposure to teratogenic agents. Furthermore, evidence points toward epigenetic as well as genetic factors influencing OFC etiology. Recent studies have begun to explore the association between CL/P and cancer. These studies report higher incidence of cancer among patients with CL/P and their family members as well as identification of common genetic markers mediating this increased risk, although much remains unknown about this link.",book:{id:"5428",slug:"designing-strategies-for-cleft-lip-and-palate-care",title:"Designing Strategies for Cleft Lip and Palate Care",fullTitle:"Designing Strategies for Cleft Lip and Palate Care"},signatures:"Mairaj K. Ahmed, Anthony H. Bui and Emanuela Taioli",authors:[{id:"188212",title:"Dr.",name:"Mairaj K.",middleName:null,surname:"Ahmed",slug:"mairaj-k.-ahmed",fullName:"Mairaj K. Ahmed"},{id:"194367",title:"Dr.",name:"Emanuela",middleName:null,surname:"Taioli",slug:"emanuela-taioli",fullName:"Emanuela Taioli"},{id:"203416",title:"Dr.",name:"Anthony",middleName:null,surname:"Bui",slug:"anthony-bui",fullName:"Anthony Bui"}]},{id:"54055",title:"Cleft Lip and Palate Patients: Diagnosis and Treatment",slug:"cleft-lip-and-palate-patients-diagnosis-and-treatment",totalDownloads:2493,totalCrossrefCites:2,totalDimensionsCites:2,abstract:"Cleft lip or palate is one of the most common types of craniomaxillofacial birth anomalies. Midface deficiency is a common feature of cleft lip and palate patients due to scar tissue of the lip and palate closure. Cleft lip and palate patients should be carefully evaluated by the craniofacial team in order to detect potentially serious deformities. Craniofacial team is involved with diagnosis of facial morphology, feeding problems, guidance of the growth and development of the face, occlusion, dentition, hearing and speech problems, and psychosocial issues and jaw discrepancy of the patients with cleft lip and palate or craniofacial syndromes. Treatment for cleft children requires a multidisciplinary approach including facial surgery in the first months of life, preventive and interceptive treatment in primary dentition, speech therapy, orthodontics in the mixed dentition phase, oromaxillofacial surgery, and implant and prosthetics in adults. Treatment plan from orthodontic perspective can be divided into the following stages based on the dentition stages: (1) presurgical orthopedics, (2) primary dentition, (3) mixed dentition, and (4) permanent dentition. The aim of this chapter is to assess a rational team work approach in the management of the patient with cleft lip and/or palate from birth to adulthood.",book:{id:"5428",slug:"designing-strategies-for-cleft-lip-and-palate-care",title:"Designing Strategies for Cleft Lip and Palate Care",fullTitle:"Designing Strategies for Cleft Lip and Palate Care"},signatures:"Letizia Perillo, Fabrizia d’Apuzzo, Sara Eslami and Abdolreza\nJamilian",authors:[{id:"171777",title:"Prof.",name:"Abdolreza",middleName:null,surname:"Jamilian",slug:"abdolreza-jamilian",fullName:"Abdolreza Jamilian"},{id:"173044",title:"Prof.",name:"Letizia",middleName:null,surname:"Perillo",slug:"letizia-perillo",fullName:"Letizia Perillo"},{id:"197679",title:"Dr.",name:"Sara",middleName:null,surname:"Eslami",slug:"sara-eslami",fullName:"Sara Eslami"},{id:"198961",title:"MSc.",name:"Fabrizia",middleName:null,surname:"D'Apuzzo",slug:"fabrizia-d'apuzzo",fullName:"Fabrizia D'Apuzzo"}]}],onlineFirstChaptersFilter:{topicId:"1152",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[],lsSeriesList:[],hsSeriesList:[],sshSeriesList:[],testimonialsList:[]},series:{item:{},subseries:{},overviewPageOFChapters:[],overviewPagePublishedBooks:[],openForSubmissionBooks:{},onlineFirstChapters:{},subseriesFiltersForOFChapters:[],publishedBooks:{},subseriesFiltersForPublishedBooks:[],publicationYearFilters:[],authors:{}},subseries:{item:{id:"18",type:"subseries",title:"Proteomics",keywords:"Mono- and Two-Dimensional Gel Electrophoresis (1-and 2-DE), Liquid Chromatography (LC), Mass Spectrometry/Tandem Mass Spectrometry (MS; MS/MS), Proteins",scope:"With the recognition that the human genome cannot provide answers to the etiology of a disorder, changes in the proteins expressed by a genome became a focus in research. Thus proteomics, an area of research that detects all protein forms expressed in an organism, including splice isoforms and post-translational modifications, is more suitable than genomics for a comprehensive understanding of the biochemical processes that govern life. The most common proteomics applications are currently in the clinical field for the identification, in a variety of biological matrices, of biomarkers for diagnosis and therapeutic intervention of disorders. From the comparison of proteomic profiles of control and disease or different physiological states, which may emerge, changes in protein expression can provide new insights into the roles played by some proteins in human pathologies. Understanding how proteins function and interact with each other is another goal of proteomics that makes this approach even more intriguing. Specialized technology and expertise are required to assess the proteome of any biological sample. Currently, proteomics relies mainly on mass spectrometry (MS) combined with electrophoretic (1 or 2-DE-MS) and/or chromatographic techniques (LC-MS/MS). MS is an excellent tool that has gained popularity in proteomics because of its ability to gather a complex body of information such as cataloging protein expression, identifying protein modification sites, and defining protein interactions. The Proteomics topic aims to attract contributions on all aspects of MS-based proteomics that, by pushing the boundaries of MS capabilities, may address biological problems that have not been resolved yet.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/18.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11414,editor:{id:"200689",title:"Prof.",name:"Paolo",middleName:null,surname:"Iadarola",slug:"paolo-iadarola",fullName:"Paolo Iadarola",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSCl8QAG/Profile_Picture_1623568118342",biography:"Paolo Iadarola graduated with a degree in Chemistry from the University of Pavia (Italy) in July 1972. He then worked as an Assistant Professor at the Faculty of Science of the same University until 1984. In 1985, Prof. Iadarola became Associate Professor at the Department of Biology and Biotechnologies of the University of Pavia and retired in October 2017. Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. In this context, he has developed and validated new methodologies (e.g., Capillary Electrophoresis coupled to Laser-Induced Fluorescence, CE-LIF) whose application enabled him to determine both the amounts of biochemical markers (Desmosines) in urine/serum of patients affected by Chronic Obstructive Pulmonary Disease (COPD) and the activity of proteolytic enzymes (Human Neutrophil Elastase, Cathepsin G, Pseudomonas aeruginosa elastase) in sputa of these patients. More recently, Prof. Iadarola was involved in developing techniques such as two-dimensional electrophoresis coupled to liquid chromatography/mass spectrometry (2DE-LC/MS) for the proteomic analysis of biological fluids aimed at the identification of potential biomarkers of different lung diseases. He is the author of about 150 publications (According to Scopus: H-Index: 23; Total citations: 1568- According to WOS: H-Index: 20; Total Citations: 1296) of peer-reviewed international journals. He is a Consultant Reviewer for several journals, including the Journal of Chromatography A, Journal of Chromatography B, Plos ONE, Proteomes, International Journal of Molecular Science, Biotech, Electrophoresis, and others. He is also Associate Editor of Biotech.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorTwo:{id:"201414",title:"Dr.",name:"Simona",middleName:null,surname:"Viglio",slug:"simona-viglio",fullName:"Simona Viglio",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRKDHQA4/Profile_Picture_1630402531487",biography:"Simona Viglio is an Associate Professor of Biochemistry at the Department of Molecular Medicine at the University of Pavia. She has been working since 1995 on the determination of proteolytic enzymes involved in the degradation process of connective tissue matrix and on the identification of biological markers of lung diseases. She gained considerable experience in developing and validating new methodologies whose applications allowed her to determine both the amount of biomarkers (Desmosine and Isodesmosine) in the urine of patients affected by COPD, and the activity of proteolytic enzymes (HNE, Cathepsin G, Pseudomonas aeruginosa elastase) in the sputa of these patients. Simona Viglio was also involved in research dealing with the supplementation of amino acids in patients with brain injury and chronic heart failure. She is presently engaged in the development of 2-DE and LC-MS techniques for the study of proteomics in biological fluids. The aim of this research is the identification of potential biomarkers of lung diseases. She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null,series:{id:"11",title:"Biochemistry",doi:"10.5772/intechopen.72877",issn:"2632-0983"},editorialBoard:[{id:"72288",title:"Dr.",name:"Arli Aditya",middleName:null,surname:"Parikesit",slug:"arli-aditya-parikesit",fullName:"Arli Aditya Parikesit",profilePictureURL:"https://mts.intechopen.com/storage/users/72288/images/system/72288.jpg",institutionString:null,institution:{name:"Indonesia International Institute for Life Sciences",institutionURL:null,country:{name:"Indonesia"}}},{id:"40928",title:"Dr.",name:"Cesar",middleName:null,surname:"Lopez-Camarillo",slug:"cesar-lopez-camarillo",fullName:"Cesar Lopez-Camarillo",profilePictureURL:"https://mts.intechopen.com/storage/users/40928/images/3884_n.png",institutionString:null,institution:{name:"Universidad Autónoma de la Ciudad de México",institutionURL:null,country:{name:"Mexico"}}},{id:"81926",title:"Dr.",name:"Shymaa",middleName:null,surname:"Enany",slug:"shymaa-enany",fullName:"Shymaa Enany",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRqB9QAK/Profile_Picture_1626163237970",institutionString:null,institution:{name:"Suez Canal University",institutionURL:null,country:{name:"Egypt"}}}]},onlineFirstChapters:{},publishedBooks:{},testimonialsList:[{id:"8",text:"I work with IntechOpen for a number of reasons: their professionalism, their mission in support of Open Access publishing, and the quality of their peer-reviewed publications, but also because they believe in equality.",author:{id:"202192",name:"Catrin",surname:"Rutland",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/202192/images/system/202192.png",slug:"catrin-rutland",institution:{id:"134",name:"University of Nottingham",country:{id:null,name:"United Kingdom"}}}},{id:"27",text:"The opportunity to work with a prestigious publisher allows for the possibility to collaborate with more research groups interested in animal nutrition, leading to the development of new feeding strategies and food valuation while being more sustainable with the environment, allowing more readers to learn about the subject.",author:{id:"175967",name:"Manuel",surname:"Gonzalez Ronquillo",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/175967/images/system/175967.png",slug:"manuel-gonzalez-ronquillo",institution:{id:"6221",name:"Universidad Autónoma del Estado de México",country:{id:null,name:"Mexico"}}}},{id:"18",text:"It was great publishing with IntechOpen, the process was straightforward and I had support all along.",author:{id:"71579",name:"Berend",surname:"Olivier",institutionString:"Utrecht University",profilePictureURL:"https://mts.intechopen.com/storage/users/71579/images/system/71579.png",slug:"berend-olivier",institution:{id:"253",name:"Utrecht University",country:{id:null,name:"Netherlands"}}}}]},submityourwork:{pteSeriesList:[],lsSeriesList:[],hsSeriesList:[],sshSeriesList:[],subseriesList:[],annualVolumeBook:{},thematicCollection:[],selectedSeries:null,selectedSubseries:null},seriesLanding:{item:null},libraryRecommendation:{success:null,errors:{},institutions:[]},route:{name:"chapter.detail",path:"/chapters/55850",hash:"",query:{},params:{id:"55850"},fullPath:"/chapters/55850",meta:{},from:{name:null,path:"/",hash:"",query:{},params:{},fullPath:"/",meta:{}}}},function(){var e;(e=document.currentScript||document.scripts[document.scripts.length-1]).parentNode.removeChild(e)}()