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Article

Inactivation of the INK4A/ARF locus frequently coexists with TP53 mutations in non-small cell lung cancer.

Oncogene - 21 Oct 1999

Sanchez-Cespedes M, Reed A L, Buta M, Wu L, Westra W H, Herman J G, Yang S C, Jen J, Sidransky D

Abstract excerpt

Inactivation of the P16 (INK4A)/retinoblastoma (RB) or TP53 biochemical pathway is frequent event in most human cancers. Recent evidence has shown that P14ARF binds to MDM2 leading to an increased availability of wild type TP53 protein. Functional studies also support a putative tumor suppressor gene function for p14ARF suggesting that p14ARF or p53 inactivation may be functionally equivalent in tumorigenesis. To...

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Share to Carcinoma, Non-Small-Cell Lung
Share to Cyclin-Dependent Kinase Inhibitor p16

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 10557071
DOI: 10.1038/sj.onc.1203003

Genes

TP53
MDM2

Provenance

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

Source receipt: pubmed, retrieved 7 Sept 2026.

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Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

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