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This book contains the art and science in current standards of surgical treatment of pancreatic ductal adenocarcinoma. It explains the clinical role of surgical resection during multimodal treatment in patients with pancreatic ductal adenocarcinoma, novel surgical techniques including extended pancreatectomy and minimally invasive surgery, risk of cancer in IPMN, and the clinical importance of liquid biopsy.

Medicine --- Surgery --- unresectable pancreatic ductal adenocarcinoma --- conversion surgery --- early recurrence --- pancreatic neoplasm/analysis --- pancreatic neoplasm/surgery --- tumor location --- survival --- clinical staging --- branch duct intraductal papillary mucinous neoplasm --- risk factor --- malignancy --- meta-analysis --- laparoscopic --- pancreaticoduodenectomy --- pancreatic cancer --- borderline resectable --- neoadjuvant treatment --- chemoradiotherapy --- prognostic nutritional index --- isolated local recurrence --- pancreatectomy --- pancreatic remnant --- recurrence --- redo surgery --- pancreatic exocrine insufficiency --- adjuvant chemotherapy --- biliary drainage --- prehabilitation --- ERAS --- arterial resection --- total pancreatectomy --- neoadjuvant therapy --- pancreatic ductal adenocarcinoma --- surgical treatment --- technical advances --- pancreatic main duct dilatation --- intraductal papillary mucinous neoplasm --- high grade dysplasia --- invasive carcinoma --- pancreatic cystic neoplasm --- cell-free DNA --- mesopancreas --- superior mesenteric artery --- nerve and fibrous tissues --- lymph node dissection --- R0 resection --- unresectable pancreatic ductal adenocarcinoma --- conversion surgery --- early recurrence --- pancreatic neoplasm/analysis --- pancreatic neoplasm/surgery --- tumor location --- survival --- clinical staging --- branch duct intraductal papillary mucinous neoplasm --- risk factor --- malignancy --- meta-analysis --- laparoscopic --- pancreaticoduodenectomy --- pancreatic cancer --- borderline resectable --- neoadjuvant treatment --- chemoradiotherapy --- prognostic nutritional index --- isolated local recurrence --- pancreatectomy --- pancreatic remnant --- recurrence --- redo surgery --- pancreatic exocrine insufficiency --- adjuvant chemotherapy --- biliary drainage --- prehabilitation --- ERAS --- arterial resection --- total pancreatectomy --- neoadjuvant therapy --- pancreatic ductal adenocarcinoma --- surgical treatment --- technical advances --- pancreatic main duct dilatation --- intraductal papillary mucinous neoplasm --- high grade dysplasia --- invasive carcinoma --- pancreatic cystic neoplasm --- cell-free DNA --- mesopancreas --- superior mesenteric artery --- nerve and fibrous tissues --- lymph node dissection --- R0 resection

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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.

Medicine --- Oncology --- 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

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The extracellular matrix (ECM) scaffold, which surrounds and supports the cells in tissues, consists of fibrillar proteins, proteoglycans, glycosaminoglycans, signaling molecules, and enzymes involved in its remodeling. The stages of cancer progression, e.g., local invasion, intravasation, extravasation, distant invasion and immunosuppression, are obligatorily perpetrated through interactions of these tumor cells with the ECM. Cancer-related ECM changes can be exploited for the evaluation of disease progression, anticancer therapy development, and monitoring of therapy response. Thus, in breast cancer, hyaluronan-mediated wound repair mechanisms are hijacked to promote tumor development. Altered mechanical properties of the pancreatic cancer ECM are immunosuppressive and prevent the penetration of cytotoxic chemotherapy agents. The expression of the proteoglycan syndecan-4 is modulated by anticancer drugs, suggesting its potential druggabilty capacity. Another proteoglycan, lumican, is proposed as a cancer prognosis marker, chemoresistance regulator, and cancer therapy target. Due to their remodeling properties, the MMPs are vital mediators and important therapeutic targets. Treatment of breast cancer cells with sulfated hyaluronan has been shown to attenuate tumor cell growth, migration, and invasion. Extracellular vesicles (EVs), comprising exosomes, microvesicles, and apoptotic bodies, are released by all cells into the ECM and body fluids and can be utilized as diagnostic markers in malignant pleural mesothelioma. These exciting developments encourage tumor biology scientists for further creative research.

Research & information: general --- elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases --- elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases

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The extracellular matrix (ECM) scaffold, which surrounds and supports the cells in tissues, consists of fibrillar proteins, proteoglycans, glycosaminoglycans, signaling molecules, and enzymes involved in its remodeling. The stages of cancer progression, e.g., local invasion, intravasation, extravasation, distant invasion and immunosuppression, are obligatorily perpetrated through interactions of these tumor cells with the ECM. Cancer-related ECM changes can be exploited for the evaluation of disease progression, anticancer therapy development, and monitoring of therapy response. Thus, in breast cancer, hyaluronan-mediated wound repair mechanisms are hijacked to promote tumor development. Altered mechanical properties of the pancreatic cancer ECM are immunosuppressive and prevent the penetration of cytotoxic chemotherapy agents. The expression of the proteoglycan syndecan-4 is modulated by anticancer drugs, suggesting its potential druggabilty capacity. Another proteoglycan, lumican, is proposed as a cancer prognosis marker, chemoresistance regulator, and cancer therapy target. Due to their remodeling properties, the MMPs are vital mediators and important therapeutic targets. Treatment of breast cancer cells with sulfated hyaluronan has been shown to attenuate tumor cell growth, migration, and invasion. Extracellular vesicles (EVs), comprising exosomes, microvesicles, and apoptotic bodies, are released by all cells into the ECM and body fluids and can be utilized as diagnostic markers in malignant pleural mesothelioma. These exciting developments encourage tumor biology scientists for further creative research.

elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases --- n/a

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Dear Readers, Oncolytic Viruses (OV) are self-propagating agents that can selectively induce the lysis of cancer cells while sparing normal tissues. OV-mediated cancer cell death is often immunogenic and triggers robust anticancer immune responses and immunoconversion of tumor microenvironments. This makes oncolytic virotherapy a promising new form of immunotherapy and OVs ideal candidates for combination therapy with other anticancer agents, including other immunotherapeutics. There are more than 40 OVs from nine different families in clinical development and many more at the preclinical stage. Each OV has its own unique characteristics, its pros and cons. Although herpes simplex virus is currently the lead clinical agent, a real champion among the OVs has not yet emerged, justifying the continuous development and optimization of these agents. This book, “Oncolytic Virus Immunotherapy”, summarizes the state-of-the-art and gives a comprehensive overview of the OV arena with a particular focus on new trends, directions, challenges, and opportunities.

Medicine --- Clinical & internal medicine --- oncolytic viruses --- melanoma --- immunotherapy --- checkpoint inhibitors --- combinatory therapy --- reovirus --- oncolytic virus --- adenovirus --- oncolytic --- virotherapy --- targeting --- immunogenic cell death --- αvβ6 integrin --- oncolytic adenovirus --- cancer immunotherapy --- multi-stage --- immunostimulatory --- arming --- HSV-1 --- clinical trials --- newcastle disease virus --- NDV --- cancer --- immune checkpoint inhibitor --- PD-1 --- PD-L1 --- CTLA-4 --- type I interferon --- herpes simplex virus --- retargeted virus --- tropism retargeting --- tumor --- checkpoint inhibitor --- vaccination --- antigen-agnostic vaccination --- HER2 --- parvovirus --- tumor microenvironment --- combination therapy --- glioblastoma --- pancreatic cancer --- colorectal cancer --- measles virus --- vector engineering --- immune checkpoint blockade --- antitumor immune response --- delivery --- genetic modification --- biomarkers --- personalized oncolyticvirotherapy --- class I HLA --- immunosurveillance --- immunoediting --- oncogenic signaling --- RAS --- DNA methyltransferase inhibitor (DNMTi) --- viral mimicry --- epigenetic silencing --- adoptive T cell therapy --- CAR T cell --- pancreatic ductal adenocarcinoma --- vesicular stomatitis virus --- small molecule --- cancer immune therapy --- cancer therapy --- oncolytic viruses --- melanoma --- immunotherapy --- checkpoint inhibitors --- combinatory therapy --- reovirus --- oncolytic virus --- adenovirus --- oncolytic --- virotherapy --- targeting --- immunogenic cell death --- αvβ6 integrin --- oncolytic adenovirus --- cancer immunotherapy --- multi-stage --- immunostimulatory --- arming --- HSV-1 --- clinical trials --- newcastle disease virus --- NDV --- cancer --- immune checkpoint inhibitor --- PD-1 --- PD-L1 --- CTLA-4 --- type I interferon --- herpes simplex virus --- retargeted virus --- tropism retargeting --- tumor --- checkpoint inhibitor --- vaccination --- antigen-agnostic vaccination --- HER2 --- parvovirus --- tumor microenvironment --- combination therapy --- glioblastoma --- pancreatic cancer --- colorectal cancer --- measles virus --- vector engineering --- immune checkpoint blockade --- antitumor immune response --- delivery --- genetic modification --- biomarkers --- personalized oncolyticvirotherapy --- class I HLA --- immunosurveillance --- immunoediting --- oncogenic signaling --- RAS --- DNA methyltransferase inhibitor (DNMTi) --- viral mimicry --- epigenetic silencing --- adoptive T cell therapy --- CAR T cell --- pancreatic ductal adenocarcinoma --- vesicular stomatitis virus --- small molecule --- cancer immune therapy --- cancer therapy