Document Detail


Telomerase, checkpoints and cancer.
MedLine Citation:
PMID:  9338104     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Telomere dynamics and changes in telomerase activity are consistent elements of cellular alterations associated with changes in proliferative state. In particular, the highly specific correlations and early causal relationships between telomere loss in the absence of telomerase activity and replicative senescence or crisis, on the one hand, and telomerase reactivation and cell immortality, on the other, point to a new and important paradigm in the complementary fields of ageing and cancer. Although the signalling pathways between telomeres and transcriptional and cell cycle machinery remain undefined, recently described homologies between telomeric proteins and lipid/protein kinase activities important in chromosome stability provide evidence for the existence of pathways transducing signals originating in chromosome structure to cell cycle regulatory processes. Similarities between cell cycle arrest at senescence and the response of mortal cells to DNA/oxidative damage suggest overlap in the signal transduction mechanisms culminating in irreversible and stable cell cycle arrest. The feasibility of targeting telomeres/telomerase as a strategy for antiproliferative therapeutics has been shown in studies in yeast, in which mutations in specific telomere associated genes result in delayed cell death. Similarly, antisense oligonucleotide inhibition of telomerase activity in human tumour cells (HeLa) results in delayed cell death. The mechanism of cell death and possible escape from this fate require further study. In human cells, however, it would seem reasonable to predict that in these circumstances, apoptosis is induced in the vast majority of cells either directly in response to a DNA damage signal arising from critically shortened telomeres or as a secondary consequence of genetic instability.
Authors:
C B Harley; S W Sherwood
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Cancer surveys     Volume:  29     ISSN:  0261-2429     ISO Abbreviation:  Cancer Surv.     Publication Date:  1997  
Date Detail:
Created Date:  1997-11-14     Completed Date:  1997-11-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8218015     Medline TA:  Cancer Surv     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  263-84     Citation Subset:  IM    
Affiliation:
Geron Corporation, Menlo Park, CA 94025, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging / genetics*,  physiology
Apoptosis
Cell Aging / genetics*,  physiology
Cell Cycle / physiology
Cyclin-Dependent Kinases / metabolism
DNA Damage / genetics
Genes, p53
Humans
Neoplasms / etiology,  genetics*,  physiopathology
Signal Transduction
Telomerase / metabolism*
Telomere / genetics*,  physiology
Chemical
Reg. No./Substance:
EC 2.7.11.22/Cyclin-Dependent Kinases; EC 2.7.7.49/Telomerase

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


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