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Novel gene fusion of COX6C at 8q22–23 to HMGIC at 12q15 in a uterine leiomyoma
Author(s) -
Kurose Keisuke,
Mine Nobuya,
Doi Daisuke,
Ota Yujiro,
Yoneyama Koichi,
Konishi Hideki,
Araki Tsutomu,
Emi Mitsuru
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/(sici)1098-2264(200003)27:3<303::aid-gcc11>3.0.co;2-3
Subject(s) - biology , fusion gene , complementary dna , exon , gene , carcinogenesis , microbiology and biotechnology , leiomyoma , uterine leiomyoma , genetics , pathology , uterus , medicine
Cytogenetic analyses have shown that aberrations involving 12q13–15 are frequent chromosomal changes in a variety of human benign mesenchymal tumors, e.g., pleomorphic adenomas of the parotid gland, pulmonary chondroid hamartomas, lipomas, and uterine leiomyomas. Recently, the high‐mobility group protein gene HMGIC was identified as the target gene affected by the 12q13–15 aberrations. Using 3′ rapid amplification of cDNA ends experiments, we isolated novel ectopic sequences fused to HMGIC in a uterine leiomyoma. Cloning of the fusion cDNA identified the human cytochrome c oxidase subunit VIc ( COX6C ) gene on 8q22–23 as the fusion partner of HMGIC . Nucleotide sequences of the fusion transcript revealed that the first 3 exons of the HMGIC gene, encoding the 3 DNA binding domains, was fused to the exon 2 of the COX6C gene. The identification of a gene rearrangement suggests a role for HMGIC in tumorigenesis of uterine leiomyoma and suggests a possible involvement of HMGIC in mesenchymal differentiation. Genes Chromosomes Cancer 27:303–307, 2000. © 2000 Wiley‐Liss, Inc.