Document Detail


Programs for cell death: apoptosis is only one way to go.
MedLine Citation:
PMID:  17361099     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cell death programs are major players in tissue homeostasis, development and cellular stress responses. A prominent cause of malignant transformation is the cumulative genetic alterations in pathways that regulate cellular growth and death. The processes that govern cell death following genotoxic stress are a major focus of basic research and are also very relevant to translational research in clinical oncology: understanding cell death following cancer therapy is essential for designing new treatment modalities. Cell death is usually, and sometimes automatically, linked with one of its major programs, apoptosis. Recent advances have led, however, to the emergence of additional, non-apoptotic cell death pathways, each with its triggers and readouts. Genotoxic stress appears to induce several cell death pathways, only part of which fall within the classical definition of apoptosis. Accordingly, solid tumor cells that are refractive to apoptosis were shown to die via non-apoptotic mechanisms. Recently we demonstrated that mitotic cell death induced by DNA damage in cells with defective G2/M checkpoint is mechanistically distinct from apoptosis. This review outlines recent advances in the understanding of molecular networks operative in apoptotic and non-apoptotic cell death mechanisms and their cross-talks.
Authors:
Michael Blank; Yosef Shiloh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2007-03-07
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  6     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-29     Completed Date:  2007-05-10     Revised Date:  2007-06-28    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  686-95     Citation Subset:  IM    
Affiliation:
The David and Inez Myers Laboratory for Genetic Research, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Cell Cycle / physiology*
Humans
Mitosis / physiology
Signal Transduction / physiology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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