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Article

Gene Amplification in a p53-Deficient Cell Line Requires Cell Cycle Progression under Conditions That Generate DNA Breakage

1 May 1998

Abstract excerpt

Amplification of genes involved in signal transduction and cell cycle control occurs in a significant fraction of human cancers. Loss of p53 function has been proposed to enable cells with gene amplification to arise spontaneously during growth in vitro. However, this conclusion derives from studies employing the UMP synthesis inhibitor N-phosphonacetyl-L-aspartate (PALA), which, in addition to selecting for...

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PMID: 9566927
DOI: 10.1128/mcb.18.5.3089

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Gene Amplification in a p53-Deficient Cell Line Requires Cell Cycle Progression under Conditions That Generate DNA BreakagePMID 9566927Read ↗

Induction of gene amplification as a gain-of-function phenotype of mutant p53 proteins.Semantic proximity Read ↗

Normal diploid human and rodent cells lack a detectable frequency of gene amplification.Semantic proximity Read ↗

Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53.Semantic proximity Read ↗

p53-dependent growth arrest of REF52 cells containing newly amplified DNA.Semantic proximity Read ↗

A p53-dependent S-phase checkpoint helps to protect cells from DNA damage in response to starvation for pyrimidine nucleotidesSemantic proximity Read ↗

Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles.Semantic proximity Read ↗

Gene amplification in fibroblasts from ataxia telangiectasia (AT) patients and in X-ray hypersensitive AT-like Chinese hamster mutants.Semantic proximity Read ↗

Late onset of CAD gene amplification in unamplified PALA resistant Chinese hamster mutants.Semantic proximity Read ↗

Amplification of the dihydrofolate reductase gene is a mechanism of acquired resistance to methotrexate in patients with acute lymphoblastic leukemia and is correlated with p53 gene mutationsSemantic proximity Read ↗

Chromosomal destabilization during gene amplification.Semantic proximity Read ↗

Dihydrofolate reductase amplification and sensitization to methotrexate of methotrexate-resistant colon cancer cellsSemantic proximity Read ↗

Antifolates targeting purine synthesis allow entry of tumor cells into S phase regardless of p53 function.Semantic proximity Read ↗

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