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Article

Does telomere shortening drive selection for p53 mutation in human cancer?

Molecular carcinogenesis - 1 Mar 1995

Wynford-Thomas D, Bond J A, Wyllie F S, Jones C J

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 7893364
DOI: 10.1002/mc.2940120302

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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Does telomere shortening drive selection for p53 mutation in human cancer?PMID 7893364Read ↗

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Loss of p53 function accelerates acquisition of telomerase activity in indefinite lifespan human mammary epithelial cell linesSemantic proximity Read ↗

The influence of cell context on the selection pressure for p53 mutation in human cancer.Semantic proximity Read ↗

Evidence for an alternative mechanism for maintaining telomere length in human tumors and tumor-derived cell linesSemantic proximity Read ↗

Telomere Shortening Triggers Senescence of Human Cells through a Pathway Involving ATM, p53, and p21CIP1, but Not p16INK4aSemantic proximity Read ↗

Puma and p21 represent cooperating checkpoints limiting self-renewal and chromosomal instability of somatic stem cells in response to telomere dysfunctionSemantic proximity Read ↗

The shortest telomeres drive karyotype evolution in transformed cellsSemantic proximity Read ↗

Elevated mutagenesis and decreased DNA repair at a transgene are associated with proliferation but not apoptosis in p53-deficient cells.Semantic proximity Read ↗

p53 differentially inhibits cell growth depending on the mechanism of telomere maintenance.Semantic proximity Read ↗

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