The role of senescence and immortalization in carcinogenesis - PubMed (original) (raw)
Review
The role of senescence and immortalization in carcinogenesis
R R Reddel. Carcinogenesis. 2000 Mar.
Abstract
Normal somatic cells are able to divide only a limited number of times before they become senescent. The occurrence of intratumoral cell death and the need for clonal evolution mean that many more cell divisions are required for tumorigenesis than is possible unless cells breach the senescence proliferation barrier and become immortalized. Senescence may therefore be a major tumor suppressor mechanism. During the past decade the study of senescence and immortalization has entered the mainstream of cancer research. A major reason for the current interest in this subject is the observation that most cancers have an activated telomere maintenance mechanism, a marker of immortalization. It has also been found that some of the most common genetic changes known to occur in cancer have a key role in the immortalization process.
Similar articles
- The significance of telomerase activation and cellular immortalization in human cancer.
Newbold RF. Newbold RF. Mutagenesis. 2002 Nov;17(6):539-50. doi: 10.1093/mutage/17.6.539. Mutagenesis. 2002. PMID: 12435851 Review. - Human epithelial cell immortalization as a step in carcinogenesis.
Stampfer MR, Yaswen P. Stampfer MR, et al. Cancer Lett. 2003 May 15;194(2):199-208. doi: 10.1016/s0304-3835(02)00707-3. Cancer Lett. 2003. PMID: 12757978 Review. - Critical pathways in cellular senescence and immortalization revealed by gene expression profiling.
Fridman AL, Tainsky MA. Fridman AL, et al. Oncogene. 2008 Oct 9;27(46):5975-87. doi: 10.1038/onc.2008.213. Epub 2008 Aug 18. Oncogene. 2008. PMID: 18711403 Free PMC article. Review. - [The role of telomere-binding proteins in carcinogenesis].
Aragona M, Pontoriero A, Panetta S, La Torre I, La Torre F. Aragona M, et al. Minerva Med. 2000 Nov-Dec;91(11-12):299-304. Minerva Med. 2000. PMID: 11253711 Review. Italian. - Cancer, aging and cellular senescence.
Campisi J. Campisi J. In Vivo. 2000 Jan-Feb;14(1):183-8. In Vivo. 2000. PMID: 10757076 Review.
Cited by
- An alternative lifestyle for immortalized oral keratinocytes.
Reddel RR. Reddel RR. J Clin Invest. 2001 Sep;108(5):665-7. doi: 10.1172/JCI13818. J Clin Invest. 2001. PMID: 11544271 Free PMC article. No abstract available. - Cyclin D1 overexpression and p53 inactivation immortalize primary oral keratinocytes by a telomerase-independent mechanism.
Opitz OG, Suliman Y, Hahn WC, Harada H, Blum HE, Rustgi AK. Opitz OG, et al. J Clin Invest. 2001 Sep;108(5):725-32. doi: 10.1172/JCI11909. J Clin Invest. 2001. PMID: 11544278 Free PMC article. - Inhibitor of differentiation 1 (ID1) promotes cell survival and proliferation of prostate epithelial cells.
Schmidt M, Asirvatham AJ, Chaudhary J. Schmidt M, et al. Cell Mol Biol Lett. 2010 Jun;15(2):272-95. doi: 10.2478/s11658-010-0007-3. Epub 2010 Feb 25. Cell Mol Biol Lett. 2010. PMID: 20186495 Free PMC article. - MicroRNA-296 is enriched in cancer cells and downregulates p21WAF1 mRNA expression via interaction with its 3' untranslated region.
Yoon AR, Gao R, Kaul Z, Choi IK, Ryu J, Noble JR, Kato Y, Saito S, Hirano T, Ishii T, Reddel RR, Yun CO, Kaul SC, Wadhwa R. Yoon AR, et al. Nucleic Acids Res. 2011 Oct;39(18):8078-91. doi: 10.1093/nar/gkr492. Epub 2011 Jun 30. Nucleic Acids Res. 2011. PMID: 21724611 Free PMC article. - Caenorhabditis elegans POT-2 telomere protein represses a mode of alternative lengthening of telomeres with normal telomere lengths.
Cheng C, Shtessel L, Brady MM, Ahmed S. Cheng C, et al. Proc Natl Acad Sci U S A. 2012 May 15;109(20):7805-10. doi: 10.1073/pnas.1119191109. Epub 2012 Apr 30. Proc Natl Acad Sci U S A. 2012. PMID: 22547822 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous