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Gastrointestinal cancers represent a heterogeneous group of diseases of the gastrointestinal tract. There is an interplay of various non-modifiable and modifiable risk factors that foster the conversion of normal cells to precursor cells, precursor cells to premalignant cells, and premalignant cells to malignant cells. Gastrointestinal cancers are diverse in etiology and clinical management. The chapters of this book explore the clinically relevant aspects of this diversity under three broad categories: epidemiology and pathology, early diagnosis and prognosis, and surgical management. The etiological aspects focus on stomach cancer while the pathological aspects provide an overview of colorectal cancer, how primary colorectal cancer becomes metastatic through epithelial mesenchymal transition, and how macrophage-derived extracellular vesicles drive tumor development and enable the progression of most gastrointestinal cancers. Chapters on early detection and prognosis emphasize on biomarker discovery, both at genetic and proteomic level, and how these can be used to effectively predict the origin, progress, prognosis, and treatment response of gastrointestinal cancers in general and pancreatic cancer in particular. Given that the gastrointestinal tract is solely responsible for the processing of the diet we consume, the impact of diet that we consume cannot be ignored. There is a dedicated chapter that covers the role of diet and lifestyle on colorectal cancer incidence and survival. Despite various treatment modalities, for localized cancers, surgery is still the best form of curative treatment, and the role of surgical management of gastrointestinal stromal tumors and esophageal cancers are elegantly summarized in two chapters. The contents of this book provide the readers with an overview of several important aspects of gastrointestinal cancers and may be of interest to healthcare professionals interested in gastrointestinal cancers.

gastrointestinal cancers --- stomach cancer --- pancreatic cancer --- colorectal cancer --- gastrointestinal stromal tumors --- esophageal cancer

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Pancreatic diseases include intractable ones including acute and chronic pancreatitis, and pancreatic cancer. In recent years, great advances have been made in the field of pancreatology, including the pathogenesis, diagnostic modalities, and development of novel therapeutic interventions. It has been established that pancreatic stellate cells play a pivotal role in the development of pancreatic fibrosis in chronic pancreatitis as well as in pancreatic cancer known as desmoplastic reaction. Although it might be still controversial, accumulating evidence has shown that interaction between pancreatic stellate cells-cancer cells contribute to the progression of pancreatic cancer through the increased proliferation and migration, and production of cytokines and extracellular matrix components. In addition, pancreatic stellate cells lead to the resistance to chemotherapy and radiation therapy. Pancreatic stellate cells attract the researchers as a novel therapeutic target of pancreatic cancer. Genetic studies have shown that mutations in the trypsin-related genes such as cationic trypsinogen (PRSS1) gene and the serine protease inhibitor, Kazal type 1 (SPINK1) gene are associated with pancreatitis. In general, each of these factors appears to limit trypsin activation or enhance inactivation, and is believed to increase intrapancreatic trypsin activity and predispose to pancreatitis when the gene is mutated. These results have supported a concept that pancreatic protease/anti-protease plays pivotal roles in the pathogenesis of pancreatitis. In addition, genetic studies focusing on phenotypic variances would provide us with important information how genetic variants would affect the phenotypic variances. Autophagy is an intracellular bulk degradation system in which cytoplasmic components are directed to the lysosome/vacuole by a membrane-mediated process. Recent studies have highlighted a role of autophagy in acute pancreatitis. Using a conditional knockout mouse that lacks the autophagy-related (Atg) gene Atg5 in the pancreatic acinar cells, autophagy exerts a detrimental effect in pancreatic acinar cells by activation of trypsinogen to trypsin. A theory in which autophagy accelerates trypsinogen activation by lysosomal hydrolases under acidic conditions, thus triggering acute pancreatitis in its early stage. The epithelial-mesenchymal transition is a developmental process that allows a polarized epithelial cell to undergo multiple biochemical changes that enable it to assume a mesenchymal phenotype. The phenotype associated with epithelial-mesenchymal transition includes enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production of extracellular matrix components. In addition to its role in development, tissue regeneration, and fibrosis, epithelial-mesenchymal transition is now considered as a critical process in cancer progression. Induction of epithelial-mesenchymal transition in cancer cells results in the acquisition of invasive and metastatic properties. Epithelial-mesenchymal transition could be an important mechanism in the progression of pancreatic cancer and its poor prognosis. Autoimmune pancreatitis is a unique form of pancreatitis in which autoimmune mechanisms are suspected to be involved in the pathogenesis. There is accumulating study to deal with this new disease concept. In addition to these topics, we have selected several topics in pancreatology, focusing on recent studies increasingly deepening our knowledge in both basic and clinical researches.

Trypsin --- Epithelial-Mesenchymal Transition --- Fibrosis --- Pancreatitis --- autoimmune pancreatitis --- Pancreatic Cancer --- Pancreatic Stellate Cells --- Cystic Fibrosis Transmembrane Conductance Regulator

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Pancreatic diseases include intractable ones including acute and chronic pancreatitis, and pancreatic cancer. In recent years, great advances have been made in the field of pancreatology, including the pathogenesis, diagnostic modalities, and development of novel therapeutic interventions. It has been established that pancreatic stellate cells play a pivotal role in the development of pancreatic fibrosis in chronic pancreatitis as well as in pancreatic cancer known as desmoplastic reaction. Although it might be still controversial, accumulating evidence has shown that interaction between pancreatic stellate cells-cancer cells contribute to the progression of pancreatic cancer through the increased proliferation and migration, and production of cytokines and extracellular matrix components. In addition, pancreatic stellate cells lead to the resistance to chemotherapy and radiation therapy. Pancreatic stellate cells attract the researchers as a novel therapeutic target of pancreatic cancer. Genetic studies have shown that mutations in the trypsin-related genes such as cationic trypsinogen (PRSS1) gene and the serine protease inhibitor, Kazal type 1 (SPINK1) gene are associated with pancreatitis. In general, each of these factors appears to limit trypsin activation or enhance inactivation, and is believed to increase intrapancreatic trypsin activity and predispose to pancreatitis when the gene is mutated. These results have supported a concept that pancreatic protease/anti-protease plays pivotal roles in the pathogenesis of pancreatitis. In addition, genetic studies focusing on phenotypic variances would provide us with important information how genetic variants would affect the phenotypic variances. Autophagy is an intracellular bulk degradation system in which cytoplasmic components are directed to the lysosome/vacuole by a membrane-mediated process. Recent studies have highlighted a role of autophagy in acute pancreatitis. Using a conditional knockout mouse that lacks the autophagy-related (Atg) gene Atg5 in the pancreatic acinar cells, autophagy exerts a detrimental effect in pancreatic acinar cells by activation of trypsinogen to trypsin. A theory in which autophagy accelerates trypsinogen activation by lysosomal hydrolases under acidic conditions, thus triggering acute pancreatitis in its early stage. The epithelial-mesenchymal transition is a developmental process that allows a polarized epithelial cell to undergo multiple biochemical changes that enable it to assume a mesenchymal phenotype. The phenotype associated with epithelial-mesenchymal transition includes enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production of extracellular matrix components. In addition to its role in development, tissue regeneration, and fibrosis, epithelial-mesenchymal transition is now considered as a critical process in cancer progression. Induction of epithelial-mesenchymal transition in cancer cells results in the acquisition of invasive and metastatic properties. Epithelial-mesenchymal transition could be an important mechanism in the progression of pancreatic cancer and its poor prognosis. Autoimmune pancreatitis is a unique form of pancreatitis in which autoimmune mechanisms are suspected to be involved in the pathogenesis. There is accumulating study to deal with this new disease concept. In addition to these topics, we have selected several topics in pancreatology, focusing on recent studies increasingly deepening our knowledge in both basic and clinical researches.

Trypsin --- Epithelial-Mesenchymal Transition --- Fibrosis --- Pancreatitis --- autoimmune pancreatitis --- Pancreatic Cancer --- Pancreatic Stellate Cells --- Cystic Fibrosis Transmembrane Conductance Regulator

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Pancreas --- Cancer. --- Pancreatic Neoplasms --- Cancer of the Pancreas --- Neoplasms, Pancreatic --- Pancreas Cancer --- Pancreas Neoplasms --- Cancer of Pancreas --- Pancreatic Cancer --- Cancer, Pancreas --- Cancer, Pancreatic --- Cancers, Pancreas --- Cancers, Pancreatic --- Neoplasm, Pancreas --- Neoplasm, Pancreatic --- Neoplasms, Pancreas --- Pancreas Cancers --- Pancreas Neoplasm --- Pancreatic Cancers --- Pancreatic Neoplasm --- Pancreatic Neoplasms. --- Cancer --- pancreas --- pancreatic cancer --- peripancreatic region --- oncology --- Oncology. Neoplasms --- Digestive organs --- Endocrine glands --- Exocrine glands --- Oncology --- Càncer de pàncrees. --- Càncer

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Pancreatic neoplasms include different pathological entities with variable biological behavior and different treatment modalities. Surgery and adjuvant therapy are the cornerstones of the therapeutic approach; however, even after radical resection, the majority of patients experience disease recurrence and the prognosis of pancreatic cancer remains dismal. A multimodal therapeutic approach, based on a combination of neoadjuvant therapy, chemotherapy, radiotherapy, immunotherapy and surgery, appears fundamental to improving the outcomes. This Special Issue of the Journal of Clinical Medicine, entitled “Recent Advances in Pancreatic Neoplasms”, focuses on possible new strategies to treat pancreatic neoplasms.

PIWI proteins --- PIWIL3 --- PIWIL4 --- pancreatic cancer --- EMT --- chemoresistance --- motility --- HNF4A --- survival --- pancreatic neuroendocrine neoplasm --- primary pancreatic carcinoid --- serotonin-secreting pancreatic tumour --- serotonin-producing pancreatic tumour --- neoadjuvant chemotherapy --- response --- carbohydrate antigen 19-9 --- fluorodeoxyglucose --- pancreatectomy --- positron emission tomography --- prognosis --- standardized uptake value --- Pancreatic ductal adenocarcinoma --- microRNAs --- pancreatic fistula --- pancreatic neoplasm --- renal cell carcinoma --- pancreatic neoplasms --- PET-CT scan --- pancreatic ductal adenocarcinoma --- pancreatic cancer prognosis --- completion total pancreatectomy --- pooled analysis --- recurrent pancreatic cancer --- repeated pancreatectomy --- pancreas --- neuropathy --- taxanes --- biomarker --- C-reactive protein to albumin ratio --- inflammation --- intraductal papillary mucinous neoplasm --- modified Glasgow prognostic score --- neutrophyl lymphocite ratio --- platelet-to-lymphocyte ratio --- robotic pancreatic surgery --- pancreato-gastrostomy --- low muscle mass --- sarcopenia --- pancreatic adenocarcinoma --- pancreatic surgery --- body composition --- n/a