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Substantial reduction of the gastric carcinoma critical region at 6q16.3–q23.1
Author(s) -
Carvalho Beatriz,
Seruca Raquel,
Carneiro Fátima,
Buys Charles H.C.M.,
Kok Klaas
Publication year - 1999
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199909)26:1<29::aid-gcc4>3.0.co;2-d
Subject(s) - loss of heterozygosity , locus (genetics) , biology , carcinogenesis , gastric carcinoma , cancer , allele , genetics , gene , cancer research
Deletions of the long arm of chromosome 6 are a common event in gastric carcinomas. In a previous study, deletion mapping of 6q identified two smallest regions of overlap (SROs) of heterozygous deletions: one interstitial, spanning 12–16 cM, bordered by D6S268 (6q16.3–q21) and ARG1 (6q22.3–q23.1), and one distal to IFNGR1 (6q23–q24), spanning more than 30 cM. Loss of heterozygosity (LOH) of the interstitial SRO was detected in 50% of informative tumors. We analyzed 60 primary gastric tumors with 19 highly polymorphic markers from 6q16.3–q23.3 to delimit the interstitial SRO further. Of the 50 tumors that were informative for at least one locus, 18 (36%) showed allelic imbalance (AI). The overlap of these cases allowed us to define an SRO of approximately 3 Mb flanked by D6S278 and D6S404 . AI or LOH of this region occurs in all histologic types of gastric carcinoma and in early stages of development, indicating that loss of a gene from this region of 6q is a crucial step in a main route of gastric carcinogenesis. For cases with retention of 6q, alternative routes of gastric carcinogenesis may exist. Genes Chromosomes Cancer 26:29–34, 1999. © 1999 Wiley‐Liss, Inc.