A novel high mobility group protein gene is a candidate for Xp22 abnormalities in uterine leiomyomas and other benign tumors

Because genes of the high mobility group protein family HMGI(Y) are known t o take part in the development of a variety of benign solid tumors, the aim of the present study It as to search for further members of that family in the human genome. Analysis for HMGI(Y)-related sequences by the polymerase chain reaction (PCR) with the use of cDNA-specific primers offered evidenc e for HMGIY-like sequences, whereas HMGIC-related sequences were apparently absent. By chromosomal assignment of somatic cell hybrids PCR, HMGIY cDNA- related sequences Mere detected on seven chromosomes. Positive clones were obtained by screening of a PI-derived artificial chromosome library and map ped by fluorescence in situ hybridization. One of these clones assigned to Xp22.1 was chosen for further analysis because Xp22 is a target region for clonal aberrations in benign solid tumors. Sequence analysis of a DNA fragm ent of this clone, designated as HMGIYL1, revealed a 94.4% homology to the coding region of HMGIY. Within the HMGIYL1 sequence, no nucleotide sequence divergences leading to a frame shift or a new termination codon compared t o HMGIY were found, and a TATA-box-like motif 5' of if was detected. By rev erse transcriptase PCR experiments with the use of HeLa cells and human fet al tissue, HMGIYL1 expression was not detectable. Nevertheless, if not acti ve by itself, it is possible that HMGIYL1 may become activated by chromosom al rearrangements of Xp22 observed in benign solid tumors. (C) 2000 Elsevie r Science Inc. All rights reserved.