Cellular senescence as a tumor-protection mechanism: the essential role of counting. Export

@article{citeulike:1263769, abstract = {The term 'cellular senescence' has often been applied indiscriminately to any form of growth arrest of cultured cells that occurs either after some period in culture or following insults such as the overexpression of oncogenes. Recent reports have suggested there may be many mechanisms of cellular senescence. Our increasing understanding of the role of telomere shortening in the replicative aging of cultured fibroblasts now permits a re-examination of what may reasonably be called cellular senescence, and what most likely represents artifacts of the culture environment and/or specific cell-cycle control mechanisms.}, address = {Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9039, USA. Woodring.Wright@UTSouthwestern.edu}, author = {Wright, W. E. and Shay, J. W.}, citeulike-article-id = {1263769}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/11163158}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=11163158}, issn = {0959-437X}, journal = {Curr Opin Genet Dev}, keywords = {cancer, clock, senescence}, month = {February}, number = {1}, pages = {98--103}, posted-at = {2007-04-28 22:26:54}, priority = {2}, title = {Cellular senescence as a tumor-protection mechanism: the essential role of counting.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/11163158}, volume = {11}, year = {2001} }

TY - JOUR ID - citeulike:1263769 L3 - citeulike-article-id:1263769 N2 - The term 'cellular senescence' has often been applied indiscriminately to any form of growth arrest of cultured cells that occurs either after some period in culture or following insults such as the overexpression of oncogenes. Recent reports have suggested there may be many mechanisms of cellular senescence. Our increasing understanding of the role of telomere shortening in the replicative aging of cultured fibroblasts now permits a re-examination of what may reasonably be called cellular senescence, and what most likely represents artifacts of the culture environment and/or specific cell-cycle control mechanisms. IS - 1 JF - Curr Opin Genet Dev SN - 0959-437X AD - Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9039, USA. Woodring.Wright@UTSouthwestern.edu EP - 103 TI - Cellular senescence as a tumor-protection mechanism: the essential role of counting. VL - 11 SP - 98 KW - cancer KW - clock KW - senescence AU - Wright, WE AU - Shay, JW PY - 2001/02// UR - http://view.ncbi.nlm.nih.gov/pubmed/11163158 ER -