Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Thanks to their rich chemodiversity, marine natural products represent a unique source of new bioactive metabolites. As the new leading compounds in drug discovery and development, these molecules may represent challenges for the treatment of a number of human diseases, attracting the attention of many researchers during their chemical and biological studies. This Special Issue covers all fields of drugs research in which marine natural products are involved, including their isolation and characterization, biological activities, and medicinal applications as well as synthetic approaches and their related analogues. The cover picture shows “The Nudibranch mollusk Godiva quadricolor on a sponge, reflected under the surface during the low tide. Fusaro Lagoon, Bacoli (Naples)”.

Research & information: general --- Biology, life sciences --- Biochemistry --- alginate --- Sargassum duplicatum --- okra --- antioxidant --- diabetic --- wound healing --- sulfavant --- sulfoquinovosyldiacylglycerols --- sulfoglycolipids --- mass spectrometry --- UHPLC-MS --- lipids --- cancer therapy --- gold nanoparticles --- marine products --- natural products --- photosensitizer --- purpurin 18 --- reactive oxygen species --- seaweed --- biosilica --- diatom frustule --- sustainable production --- drug delivery --- Sargassum ilicifolium --- mangosteen rind --- diabetic mice --- Aquimarina sp. --- diketopiperazine --- N-phenethylacetamide --- epithelial-mesenchymal transition (EMT) --- A549 cells --- n/a

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Despite the efficiency of current cancer treatments, cancer is still a deadly disease for too many. In 2008, 7.6 million people died of cancer; with the current development, it is estimated that the annual cancer death number will grow to 13 million by 2030. There is clearly a need for not only more research but also more innovative and out of the mainstream scientific ideas to discover and develop even better cancer treatments. This book presents the collective works published in the recent Special Issue entitled “Killing Cancer: Discovery and Selection of New Target Molecules”. These articles comprise a selection of studies, ideas, and opinions that aim to facilitate knowledge, thoughts, and discussion about which biological and molecular mechanisms in cancer we should target and how we should target them.

ferlin --- myoferlin --- dysferlin --- otoferlin --- C2 domain --- plasma membrane --- sulconazole --- NF-κB --- IL-8 --- mammosphere --- breast cancer stem cells --- AF1Q --- MLLT11 --- WNT --- STAT --- esophageal cancer --- prognosis --- mTORC1 --- mTORC2 --- metabolism --- rapalogs --- mTOR inhibitors --- cancer metabolism --- mTOR in immunotherapy --- nutrient metabolism --- kinase inhibitors --- mTOR signaling --- MAPK kinase --- ERK1 --- ERK2 --- CD domain --- Rolled --- SCH772984 --- VRT-11E --- sevenmaker --- cancer therapy --- EMT --- lysosome --- lysosome-mediated invasion --- MZF1 --- phosphorylation --- PAK4 --- SUMOylation --- transcription factor --- zinc finger --- glucocorticoids --- 3D growth --- nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) --- epithelial–mesenchymal transition --- anoikis --- proliferation --- targeted cancer therapy --- disulfiram --- NPL4 --- replication stress --- DNA damage --- BRCA1 --- BRCA2 --- ATR pathway --- PDAC --- TCIRG1 --- ATP6V0a3 --- invasion --- migration --- matrix degradation --- pH-regulation --- autophagy --- multidrug resistance in cancer --- drug efflux pumps --- ATP-binding cassette transporter --- breast cancer resistance protein (BCRP) --- ABCG2 --- pyrazolo-pyrimidine derivative --- SCO-201 --- colorectal cancer --- immunotherapy --- inflammation --- microsatellite instability --- oncofetal chondroitin sulfate --- chondroitin sulfate --- cancer --- solid tumors --- target --- pediatric cancer --- VAR2 --- dexamethasone --- thyroid cancer --- microgravity --- space environment --- n/a --- epithelial-mesenchymal transition

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The Special Issue "In Vitro and In Vivo Models of Colorectal Cancer for Clinical Application", edited by Marta Baiocchi and Ann Zeuner for Cancers, collects original research papers and reviews, depicting the current state and the perspectives of CRC models for preclinical and translational research. Original research papers published in this issue focus on some of the hottest topics in CRC research, such as circulating tumor cells, epigenetic regulation of stemness states, new therapeutic targets, molecular CRC classification and experimental CRC models such as organoids and PDXs. Additionally, four reviews on CRC stem cells, immunotherapy and drug discovery provide an updated viewpoint on key topics linking benchtop to bedside research in CRC.

colorectal cancer --- organoids --- 3D bioprinting --- patient-derived xenograft --- cancer-on-chip --- drug combination --- cancer stem cells --- drug resistance --- clinical trials --- tumor-initiating cells --- tumor heterogeneity --- patient-derived cancer models --- single-cell RNA-sequencing --- tumor metabolism --- transcriptional programs --- tumor cell differentiation --- immunotherapy --- methods --- chromosomal instability --- DNA damage --- targeted therapy --- decitabine --- colon cancer --- DNA methylation --- clinical translation study --- machine learning --- patient-derived tumor organoid --- precision medicine --- radiation response --- rectal cancer --- PDX model --- CRC --- mutation analysis --- histological examination --- animal models --- in vitro culture --- cancer stem cell methods --- SATB2 --- colorectal carcinoma --- prognosis --- CDX2 --- circulating tumor cells --- CTC cluster --- size-based method --- ScreenCell® --- epithelial mesenchymal transition --- hypoxia --- HIF-1α --- immunofluorescence analysis --- sequential filtration