Loss of heterozygosity on chromosomes 1, 11, 12, and 14 in hybrid mouse lung adenocarcinomas.

Abstract:

:An allelotype analysis of lung tumors in mouse hybrids was conducted to identify common regions of allelic loss. By using 50 informative genetic markers, the autosomes of 36 (A/J x C3H/HeJ) F1 adenocarcinomas were examined. Additional adenocarcinomas from as many as 72 (C3H/HeJ x A/J) F1 and 15 (BALB/cJ x DBA/2J) F1 hybrids also were analyzed for DNA loss at some of the loci. Loss of heterozygosity (LOH) was observed at multiple loci and occurred with the most regularity at markers on chromosomes 12 (28%), 14 (28%), 11 (21%), and 1 (20%). The frequency of LOH was not greater than 11% on any of the other chromosomes. Chromosomes 11 and 14 often displayed allelic loss at markers located near the p53 and retinoblastoma tumor suppressor loci, respectively. LOH at markers on chromosomes 12 and 14 was associated with tumors having overall frequencies of allelic loss that exceeded the median value. Losses on chromosomes 1, 11, 12, and 14 also showed a significant association with the adenocarcinoma stage of mouse lung tumorigenesis, suggesting that the inactivation of tumor suppressor loci on these chromosomes may participate in the progression of these tumors.

journal_name

Mol Carcinog

journal_title

Molecular carcinogenesis

authors

Herzog CR,Chen B,Wang Y,Schut HA,You M

doi

10.1002/(SICI)1098-2744(199606)16:2<83::AID-MC4>3.

subject

Has Abstract

pub_date

1996-06-01 00:00:00

pages

83-90

issue

2

eissn

0899-1987

issn

1098-2744

pii

10.1002/(SICI)1098-2744(199606)16:2<83::AID-MC4>3.

journal_volume

16

pub_type

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