LOSS OF HETEROZYGOSITY ON CHROMOSOME-1, CHROMOSOME-11, CHROMOSOME-12,AND CHROMOSOME-14 IN HYBRID MOUSE LUNG ADENOCARCINOMAS

Citation
Cr. Herzog et al., LOSS OF HETEROZYGOSITY ON CHROMOSOME-1, CHROMOSOME-11, CHROMOSOME-12,AND CHROMOSOME-14 IN HYBRID MOUSE LUNG ADENOCARCINOMAS, Molecular carcinogenesis, 16(2), 1996, pp. 83-90
Citations number
34
Categorie Soggetti
Oncology,Biology
Journal title
ISSN journal
08991987
Volume
16
Issue
2
Year of publication
1996
Pages
83 - 90
Database
ISI
SICI code
0899-1987(1996)16:2<83:LOHOCC>2.0.ZU;2-5
Abstract
An allelotype analysis of lung tumors in mouse hybrids was conducted t o identify common regions of allelic loss. By using 50 informative gen etic 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 fo r DNA loss at some of the loci. Loss of heterozygosity (LOH) was obser ved at multiple loci and occurred with the most regularity at markers on chromosomes 12 (28%), 14 (28%), 11 (21%), and 1 (20%). The frequenc y of LOH was not greater than 11% on any of the other chromosomes. Chr omosomes 11 and 14 often displayed allelic loss at markers located nea r 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. Lo sses on chromosomes 1, 11, 12, and 14 also showed a significant associ ation with the adenocarcinoma stage of mouse lung tumorigenesis, sugge sting that the inactivation of tumor suppressor loci on these chromoso mes may participate in the progression of these tumors. (C) 1996 Wiley -Liss, Inc.