Cell senescence and cancer
- 1 December 2001
- journal article
- review article
- Published by Springer Nature in Nature Reviews Cancer
- Vol. 1 (3) , 203-213
- https://doi.org/10.1038/35106045
Abstract
Historically, the senescent state has been associated with, and was named after, the cell-cycle arrest that occurs after cells have undergone an intrinsically defined number of divisions in vitro. More recently, however, it has been shown that extrinsic factors, including those encountered in normal tissue-culture environments, can prematurely induce an indistinguishable senescent phenotype. In this review, we discuss the pathways of cell senescence, the mechanisms involved and the role that these pathways have in regulating the initiation and progression of cancer.Keywords
This publication has 102 references indexed in Scilit:
- Modeling chromosomal instability and epithelial carcinogenesis in the telomerase-deficient mouseSeminars in Cancer Biology, 2001
- Lack of Replicative Senescence in Normal Rodent GliaScience, 2001
- The Hallmarks of CancerCell, 2000
- Pharmacological Rescue of Mutant p53 Conformation and FunctionScience, 1999
- Disease states associated with telomerase deficiency appear earlier in mice with short telomeresThe EMBO Journal, 1999
- Short Dysfunctional Telomeres Impair Tumorigenesis in the INK4aΔ2/3 Cancer-Prone MouseCell, 1999
- Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4aCell, 1997
- Specific Association of Human Telomerase Activity with Immortal Cells and CancerScience, 1994
- Cooperative effect of antisense-Rb and antisense-p53 oligomers on the extension of life span in human diploid fibroblasts, TIG-1Biochemical and Biophysical Research Communications, 1991
- Telomeres shorten during ageing of human fibroblastsNature, 1990