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Loss of Heterozygosity Analysis Defines a Critical Region in Chromosome 1p22 Commonly Deleted in Human Malignant Mesothelioma¹

Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 [W-C. L., B. B., Z. L., J. R. T.], and Department of Human Genetics, Memorial Sloan-Ketering Cancer Center, New York, New York 10021 [S. C. J.]

Previous cytogenetic analysis has revealed frequent losses of chromosome 1p21–22 in human malignant mesothelioma, suggesting that the loss or inactivation of a tumor suppressor gene(s) residing at this site may contribute to the tumorigenic conversion of mesothelial cells. To more precisely define the location of the target gene, primary tumor specimens and cell lines from 50 malignant mesotheliomas were examined for loss of heterozygosity using short tandem repeat polymorphism (STRP) markers. Nineteen STRP markers established by the Cooperative Human Linkage Center were selected for the initial screening of the entire short arm of chromosome 1. Thirty-seven cases (74%) showed allelic losses at least at one locus in 1p. Thirty-six of these cases showed losses of 1p21–22, including 23 with partial deletions involving this region. To obtain a higher resolution map of this region, another 13 STRP markers from the Genethon map were used to define the shortest region of overiapping deletions to a 4-cM segment flanked by the loci D1S435 and D1S236. The chromosomal location of the critically deleted region was confirmed to be within 1p22 by karyotypic and fluorescence in situ hybridization analyses.

¹ Supported by National Cancer Institute Grants CA-45745 and CA-06927, by a gift from the International Association of Heat and Frost Insulators & Asbestos Workers Local #14, and by an appropriation from the Commonwealth of Pennsylvania. W-C. L. is a Fellow of the Leukemia Society of America.

² To whom requests for reprints should be addressed, at Department of Medical Oncology, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111.

Received 7/ 2/96. Accepted 8/14/96.

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