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Tumor Cells Utilize Multiple Pathways to Down‐modulate Apoptosis: Lessons from a Mouse Model of Islet Cell Carcinogenesis
Author(s) -
HAGER JEFFREY H.,
HANAHAN DOUGLAS
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07929.x
Subject(s) - apoptosis , carcinogenesis , biology , mitosis , programmed cell death , genetically modified mouse , pathological , cancer research , disease , microbiology and biotechnology , immune system , cancer , neuroscience , immunology , transgene , pathology , medicine , genetics , gene
Apoptosis, the process of programmed cell death, plays a critical role in many normal and pathological (disease) processes. 1 In normal tissues, apoptosis functions in the homeostatic maintenance of proper tissue and organ size by eliminating aged cells to offset the birth of new cells that arise by mitosis. In disease, apoptosis can affect the pathological process is two disparate ways. There are diseases that have too much apoptosis such as autoimmune diabetes and Alzheimer's, or those that have too little apoptosis, such as cancer. This review will focus on the latter and, more specifically, detail and summarize some important lessons learned about apoptosis and cancer from studying a transgenic mouse model of islet cell carcinoma, RIP‐Tag, as outlined below.