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Frequent loss of chromosome arm Ip DNA in parathyroid adenomas
Author(s) -
Cryns Vincent L.,
Yi Su Min,
Tahara Hideki,
Gaz Randall D.,
Arnold Andrew
Publication year - 1995
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/gcc.2870130103
Subject(s) - biology , allele , tumor suppressor gene , genetics , chromosome , chromosome 17 (human) , gene , parathyroid adenoma , cancer research , microbiology and biotechnology , adenoma , carcinogenesis
Two molecular defects have been described in parathyroid adenomas: rearrangement and overexpression of the PRADI /cyclin DI oncogene and allelic loss of chromosome II DNA, often including the multiple endocrine neoplasia type I ( MENI ) putative tumor suppressor gene region. In an effort to identify additional parathyroid tumor suppressor genes, we examined 25 parathyroid adenomas for tumor‐specific allelic loss of polymorphic DNA loci located near known or candidate tumor suppressor genes. Control leukocyte DNA from all 25 patients was heterozygous for I or more of the 9 chromosome I markers examined. Allelic loss at I or more of these informative loci on chromosome I was observed in 10 of 25 (40%) adenomas. Although many tumors lost extensive regions on chromosome I, all but one of these tumors had allelic loss of distal I p (I p32‐pter); four tumors also lost loci on Iq. Allelic loss at IIqI3, the site of the MEN I gene, was detected in 5 of 2I (24%) informative cases, including 3 with Ip loss. In contrast, allelic loss was rarely observed at loci on 99 and Iop and was not observed at loci on 3p, 3q. 4p, 5q, I2q, I4q, I8q, 22q, or Xp. In summary, clonal allelic loss of loci on chromosome arm Ip is a frequent feature of parathyroid adenomas, implying that inactivation of a tumor suppressor gene(s) on Ip commonly contributes to their pathogenesis. © 1995 Wiley‐Liss, Inc.