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Novel gene fusion ofCOX6C at 8q22-23 toHMGIC at 12q15 in a uterine leiomyoma

2000; Wiley; Volume: 27; Issue: 3 Linguagem: Inglês

10.1002/(sici)1098-2264(200003)27

1098-2264

Keisuke Kurose, Nobuya Mine, Daisuke Doi, Yujiro Ota, Koichi Yoneyama, Hideki Konishi, Tsutomu Araki, Mitsuru Emi,

Cardiac tumors and thrombi

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.