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Your search keyword '"Claudins antagonists & inhibitors"' showing total 2 results
Start Over Descriptor "Claudins antagonists & inhibitors" Topic antineoplastic agents
2 results on '"Claudins antagonists & inhibitors"'

1. Emerging Novel Therapeutic Agents in the Treatment of Patients with Gastroesophageal and Gastric Adenocarcinoma.

Author

Anandappa G and Chau I

Subjects
Claudins antagonists & inhibitors, Claudins genetics, Gelatinases antagonists & inhibitors, Gelatinases genetics, Gelatinases metabolism, Gene Amplification, Humans, Neoplastic Stem Cells metabolism, Neoplastic Stem Cells pathology, Receptor, Fibroblast Growth Factor, Type 2 antagonists & inhibitors, Receptor, Fibroblast Growth Factor, Type 2 genetics, Receptor, Fibroblast Growth Factor, Type 2 metabolism, Adenocarcinoma drug therapy, Adenocarcinoma genetics, Adenocarcinoma metabolism, Adenocarcinoma pathology, Antineoplastic Agents therapeutic use, Esophageal Neoplasms drug therapy, Esophageal Neoplasms genetics, Esophageal Neoplasms metabolism, Esophageal Neoplasms pathology, Neoplasm Proteins antagonists & inhibitors, Neoplasm Proteins genetics, Neoplasm Proteins metabolism, Stomach Neoplasms drug therapy, Stomach Neoplasms genetics, Stomach Neoplasms metabolism, Stomach Neoplasms pathology
Abstract

With further understanding of the biology of gastric and gastroesophageal adenocarcinomas, strides are being made to find effective treatments through novel trial designs. This article focuses on the ongoing trials of drugs targeting specific hallmarks of gastric and gastroesophageal cancers, including oncogene addiction proliferative pathways (fibroblast growth factor receptor 2 amplified tumors), stem cell inhibition, apoptotic induction through claudin inhibitors, and matrix metalloproteinase inhibition. In developing novel therapeutics in treatment of patients with gastroesophageal adenocarcinomas, parallel research efforts to refine target population and biomarkers are crucial, and targeting the tumor genomics and microenvironment may be key in improving overall survival., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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2. Targeting tight junctions during epithelial to mesenchymal transition in human pancreatic cancer.

Author

Kyuno D, Yamaguchi H, Ito T, Kono T, Kimura Y, Imamura M, Konno T, Hirata K, Sawada N, and Kojima T

Subjects
Animals, Claudins antagonists & inhibitors, Claudins metabolism, Humans, Pancreatic Neoplasms metabolism, Pancreatic Neoplasms pathology, Protein Kinase C antagonists & inhibitors, Protein Kinase C metabolism, Protein Kinase Inhibitors therapeutic use, Signal Transduction drug effects, Tight Junction Proteins metabolism, Tight Junctions metabolism, Tight Junctions pathology, Antineoplastic Agents therapeutic use, Drug Design, Epithelial-Mesenchymal Transition drug effects, Molecular Targeted Therapy, Pancreatic Neoplasms drug therapy, Tight Junction Proteins antagonists & inhibitors, Tight Junctions drug effects
Abstract

Pancreatic cancer continues to be a leading cause of cancer-related death worldwide and there is an urgent need to develop novel diagnostic and therapeutic strategies to reduce the mortality of patients with this disease. In pancreatic cancer, some tight junction proteins, including claudins, are abnormally regulated and therefore are promising molecular targets for diagnosis, prognosis and therapy. Claudin-4 and -18 are overexpressed in human pancreatic cancer and its precursor lesions. Claudin-4 is a high affinity receptor of Clostridium perfringens enterotoxin (CPE). The cytotoxic effects of CPE and monoclonal antibodies against claudin-4 are useful as novel therapeutic tools for pancreatic cancer. Claudin-18 could be a putative marker and therapeutic target with prognostic implications for patients with pancreatic cancer. Claudin-1, -7, tricellulin and marvelD3 are involved in epithelial to mesenchymal transition (EMT) of pancreatic cancer cells and thus might be useful as biomarkers during disease. Protein kinase C is closely related to EMT of pancreatic cancer and regulates tight junctions of normal human pancreatic duct epithelial cells and the cancer cells. This review focuses on the regulation of tight junctions via protein kinase C during EMT in human pancreatic cancer for the purpose of developing new diagnostic and therapeutic modalities for pancreatic cancer.

Published
2014
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