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American Journal of Pathology, Vol 142, 293-305, Copyright © 1993 by American Society for Investigative Pathology
REGULAR ARTICLES |
C Sreekantaiah, JR Davis and AA Sandberg
Memorial Sloan-Kettering Institute, Laboratory of Genetics and Cancer Genetics, New York.
Thirty-eight tumors from 30 patients diagnosed as leiomyosarcoma were cytogenetically assessed after short term culture. The specimens were obtained from the retroperitoneum, gastrointestinal tract, and extremities. Chromosomal abnormalities were present in 18 tumors from 13 patients; 15 tumors had clonal changes, whereas 3 tumors had numerous nonclonal changes. Ten tumors from 10 patients had normal karyotypes and no results were obtained in 10 other tumors from 7 patients. Of the tumors with clonal chromosomal aberrations, 4 had near- diploid (3 hypo- and one hyperdiploid) modes, 8 were polyploid, and 3 were bimodal. No specific karyotypic change appeared to characterize the leiomyosarcomas, although involvement of some chromosomes appeared more frequent than others. A comparison of our findings with those reported in the literature revealed certain consistent structural rearrangements involving chromosomes 1, 7, 10, 13, and 14 at bands 1p36, 1p32, 1p13, 1q32, 7p11.1-p21, 7q32, 10q22, 13q14, and 14p11, respectively. Other bands less frequently rearranged were 3p13-p22, 3q21, 4q13-q23, 6q15-q21, 7q11.2-q22, 12q13-q14, 17q12-q25, 19q13.3- q13.4, and 20q12-q13.1. Numerical changes included recurrent loss of chromosomes 4, 9, 14, 15, 16, 18, 21, and 22. Identification of the abnormalities of these chromosomes is important in that it may predict the existence of oncogenes, tumor suppressor genes, and/or growth factor genes at these sites. Subsequent molecular analysis might then lead to the identification of the genes involved and ultimately to a better understanding of the pathogenesis of leiomyosarcomas.
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