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Mapping of a minimal deleted region in human hepatocellular carcinoma to 1p36.13–p36.23 and mutational analysis of the RIZ ( PRDM2 ) gene localized to the region
Author(s) -
Fang Wei,
Piao Zhe,
Simon Daniela,
Sheu JinChuan,
Huang Shi
Publication year - 2000
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 - 10.1002/1098-2264(200007)28:3<269::aid-gcc4>3.0.co;2-k
Subject(s) - locus (genetics) , loss of heterozygosity , biology , gene , genetics , tumor suppressor gene , hepatocellular carcinoma , homology (biology) , microbiology and biotechnology , cancer research , allele , carcinogenesis
Human chromosome band 1p36 commonly undergoes loss of heterozygosity (LOH) in hepatocellular carcinoma (HCC) but the minimal deleted region remains to be mapped. This chromosomal region contains a candidate HCC suppressor gene, RIZ ( PRDM 2), that is a member of the PR ( P RDI ‐ BF 1‐ R IZ homology)‐domain‐containing zinc finger gene family. One characteristic of this family is the unusual yin‐yang involvement in human cancers. The PR‐domain‐containing RIZ1 product of the RIZ locus, in contrast to the PR‐domain‐minus product RIZ2, is commonly lost or underexpressed in HCC. Furthermore, RIZ1 can induce cell cycle arrest, apoptosis, or both and suppress HCC tumorigenicity in nude mice. To help identify the putative HCC locus on 1p36 and to evaluate a genetic role of RIZ in HCC, we studied 97 HCC cases and mapped a minimal deleted region in HCC to 1p36.13–p36.23 between markers D1S434 and D1S436. Notably, RIZ mapped within this region and was found to undergo LOH in 37% (25/67) of HCC cases. Single‐strand conformation polymorphism (SSCP) analysis, however, did not show mutations in the PR‐domain region of RIZ1 in 49 cases of HCC examined. Our data suggest that the RIZ locus is a target of frequent deletion in HCC, but that the more common way of RIZ inactivation in HCC may not involve mutations that alter peptide sequences. Genes Chromosomes Cancer 28:269–275, 2000. © 2000 Wiley‐Liss, Inc.