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Control of Replicative Life Span in Human Cells: Barriers to Clonal Expansion Intermediate Between M1 Senescence and M2 Crisis
ABSTRACT The accumulation of genetic abnormalities in a developing tumor is driven, at least in part, by the need to overcome inherent restraints on the replicative life span of human cells, two ofExpand
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Posttranslational Modifications of p53 in Replicative Senescence Overlapping but Distinct from Those Induced by DNA Damage
ABSTRACT Replicative senescence in human fibroblasts is absolutely dependent on the function of the phosphoprotein p53 and correlates with activation of p53-dependent transcription. However, noExpand
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Escape from senescence in human diploid fibroblasts induced directly by mutant p53.
Cellular senescence is thought to be a key restraint on the progression of human tumours, escape from which involves loss of function of tumour suppressor genes. The number and nature of the genesExpand
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Activated ras and ret oncogenes induce over-expression of c-met (hepatocyte growth factor receptor) in human thyroid epithelial cells
Hepatocyte Growth Factor (HGF) receptor, encoded by the protooncogene c-met, is overexpressed in many human tumours, including those of thyroid epithelium. The absence in most cases of any primaryExpand
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Evidence that transcriptional activation by p53 plays a direct role in the induction of cellular senescence.
Wild-type p53 is necessary for the growth arrest of human diploid fibroblasts (HDF) (and many other cell types) at the end of their proliferative lifespan. Although p53 may actively mediateExpand
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Papillary thyroid carcinoma oncogene (RET/PTC) alters the nuclear envelope and chromatin structure.
Current evidence suggests the papillary thyroid carcinoma oncogene (RET/PTC) generates papillary thyroid carcinomas in one genetic step. We tested a resulting prediction that RET/PTC expression inExpand
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Evidence for a Telomere-Independent “Clock” Limiting RAS Oncogene-Driven Proliferation of Human Thyroid Epithelial Cells
ABSTRACT An initiating role for RAS oncogene mutation in several epithelial cancers is supported by its high incidence in early-stage tumors and its ability to induce proliferation in theExpand
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Does telomere shortening drive selection for p53 mutation in human cancer?
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Mutation of the p53 gene in a differentiated human thyroid carcinoma cell line, but not in primary thyroid tumours.
The p53 gene has been implicated as a tumour suppressor, with mutations occurring in many carcinomas, such as colon, breast and lung. We have sequenced exons 5, 7 and 8 containing conserved geneExpand
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Stepwise transformation of primary thyroid epithelial cells by a mutant Ha-ras oncogene: an in vitro model of tumor progression.
Activating mutations of the ras oncogene family occur at high frequency in all stages of thyroid tumorigenesis, both human and experimental. To test the causal nature of this association, and toExpand
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