Selective loss of resistant alleles at p15INK4B and p16INK4A genes in chemically-induced rat tongue cancers

Oral Oncology
Kotaro OgawaMotoo Kitano

Abstract

We previously reported that susceptibility to 4-nitroquinoline 1-oxide (4NQO)-induced tongue cancer in Dark-Agouti (DA) and Wistar/Furth (WF) rats was determined by a number of quantitative trait loci. In this article, we further scrutinized one of the quantitative trait loci at a suggestive level on rat chromosome 5. Analyzing a DNA panel of 130 (DAxWF) F2 rats treated with 4NQO showed a quantitative trait loci, containing p15INK4B and p16INK4A. To study the possible relevance of these genes in the development of tongue cancer, we examined 45 4NQO-induced tongue cancers in 100 (DAxWF) F1 rats for loss of heterozygosity. The incidence of loss of heterozygosity at p15INK4B and p16INK4A genes in large advanced tongue cancers was 37.8% and 40.0%, respectively, and the WF allele was selectively lost. Accumulation of loss of heterozygosity and methylation of the promoter regions in the tumour suppressor genes in advanced tumours suggests that they may play a role in tongue cancer progression.

References

Aug 1, 1992·Japanese Journal of Cancer Research : Gann·M KitanoH Shisa
Jan 8, 1991·Biochemistry·T J McBrideL A Loeb
Sep 1, 1973·Transplantation·F Listing
Jan 1, 1995·Nature Genetics·H J JacobA Lernmark
Mar 9, 1995·Nature·D O Morgan
Dec 16, 1994·Science·L H Hartwell, M B Kastan
Mar 1, 1997·Molecular and Cellular Biology·D S SwaffordS A Belinsky
Jun 17, 1999·International Journal of Cancer. Journal International Du Cancer·M PartridgeJ Langdon
Jun 29, 2001·Japanese Journal of Cancer Research : Gann·J I TanumaM Kitano
Nov 26, 2002·International Journal of Cancer. Journal International Du Cancer·Jun-ichi TanumaMotoo Kitano

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Citations

Mar 4, 2009·Journal of Molecular Histology·Eliana Maria MinicucciDaisy Maria Favero Salvadori
Nov 21, 2013·Oncology Reports·Hirohiko SuwaJun-Ichi Tanuma
Apr 14, 2010·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·E M MinicucciD M F Salvadori
Apr 13, 2007·Experimental and Molecular Pathology·Daniel Araki RibeiroDaisy Maria Favero Salvadori
Feb 6, 2007·Oral Oncology·Crispian Scully, Jose V Bagan
Jan 14, 2011·Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology·Ana C C FracalossiDaniel A Ribeiro

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