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Article

Epigenetic inactivation of 14-3-3 sigma in oral carcinoma: association with p16(INK4a) silencing and human papillomavirus negativity.

Cancer research - 1 Apr 2002

Gasco Milena, Bell Alexandra K, Heath Victoria, Sullivan Alex, Smith Paul, Hiller Louise, Yulug Isik, Numico Gianmauro, Merlano Marco, Farrell Paul J, Tavassoli Mahvash, Gusterson Barry, Crook Tim

Abstract excerpt

In vitro studies have identified 14-3-3sigma as a regulator of senescence in human keratinocytes. To assess its contribution to squamous neoplasia, we have analyzed genetic and epigenetic changes in this gene in squamous cell carcinomas (SCCs) and dysplastic lesions of the oral cavity. No mutations were detected in the coding sequence of 14-3-3sigma in 20 oral carcinomas, and there was loss of heterozygosity in...

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PMID: 11929827

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Epigenetic inactivation of 14-3-3 sigma in oral carcinoma: association with p16(INK4a) silencing and human papillomavirus negativity.PMID 11929827Read ↗

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Downregulation of 14-3-3sigma prevents clonal evolution and leads to immortalization of primary human keratinocytes.Semantic proximity Read ↗

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14-3-3sigma, a p53 regulator, suppresses tumor growth of nasopharyngeal carcinoma.Semantic proximity Read ↗

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IKKalpha shields 14-3-3sigma, a G(2)/M cell cycle checkpoint gene, from hypermethylation, preventing its silencing.Semantic proximity Read ↗

14-3-3σ Positively Regulates p53 and Suppresses Tumor GrowthSemantic proximity Read ↗

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