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
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.