Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties

Autor:	James A. McCubrey, Akshaya K. Meher, Shaw M. Akula, Stephen L. Abrams, Linda S. Steelman, Michelle M. LaHair, Richard A. Franklin, Alberto M. Martelli, Stefano Ratti, Lucio Cocco, Fulvio Barbaro, Przemysław Duda, Agnieszka Gizak
Rok vydání:	2022
Předmět:	Mitogen-Activated Protein Kinase Kinases Aging Cell Biology Mechanistic Target of Rapamycin Complex 1 ErbB Receptors Pancreatic Neoplasms Proto-Oncogene Proteins p21(ras) Glycogen Synthase Kinase 3 Phosphatidylinositol 3-Kinases Cell Line Tumor Gain of Function Mutation Dietary Supplements Mutation Humans Tumor Suppressor Protein p53 Carcinoma Pancreatic Ductal Cell Proliferation Phosphoinositide-3 Kinase Inhibitors
Zdroj:	Aging. 14:3365-3386
ISSN:	1945-4589
Popis:	TP53 is a master regulator of many signaling and apoptotic pathways involved in: aging, cell cycle progression, gene regulation, growth, apoptosis, cellular senescence, DNA repair, drug resistance, malignant transformation, metastasis, and metabolism. Most pancreatic cancers are classified as pancreatic ductal adenocarcinomas (PDAC). The tumor suppressor gene
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7edd25c24fbd50ad712ed6ca3b0705ab https://doi.org/10.18632/aging.204038 Zobrazit plný text záznamu