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Loss of heterozygosity on chromosomes 1, 11, 12, and 14 in hybrid mouse lung adenocarcinomas
Author(s) -
Herzog Christopher R.,
Chen Bin,
Wang Yian,
Schut Herman A. J.,
You Ming
Publication year - 1996
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(199606)16:2<83::aid-mc4>3.0.co;2-o
Subject(s) - biology , loss of heterozygosity , lung , genetics , adenocarcinoma , cancer research , evolutionary biology , gene , medicine , cancer , allele
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) F 1 adenocarcinomas were examined. Additional adenocarcinomas from as many as 72 (C3H/HeJ x A/J) F 1 and 15 (BALB/cJ x DBA/2J) F 1 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. © 1996 Wiley‐Liss, Inc.