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Laboratories of Pathology [A. L., L. A. L., P. S. S.], Biochemistry [O. W. M., M. G. W.], Human Carcinogenesis [A. W., C. C. H.], and Tumor Immunology and Biology [C. S. C., R. C.] and Surgery Branch [P. A., W. M. L.], National Cancer Institute, NIH, Bethesda, Maryland 20892; Institute for Cancer Studies, The University of Sheffield Medical School, Sheffield, England S10 2RX [J. R. G., R. C. R.]; and Centre Rene Huguenin, 5 Rue Gaston Latouche, St. Cloud, France 92211 [R. L.]
Tumor progression to the metastatic phenotype is accompanied in certain cell types by reduced expression of the nm23 gene. We have localized human nm23-H1 to chromosome 17 by somatic cell hybrid analysis. Regional localization in the CEPH database and in situ hybridization is reported. Somatic allelic deletion of nm23-H1 was observed in human breast, renal, colorectal, and lung carcinoma DNA samples, as compared to DNA from matched normal tissues. A homozygous deletion of nm23-H1 was observed in a lymph node metastasis of a colorectal carcinoma, indicating that nm23-H1 can be recessively inactivated. The data identify nm23-H1 as a novel, independent locus for allelic deletion in human cancer, a characteristic shared with previously described suppressor genes.
1 To whom requests for reprints should be addressed.
2 Supported in part by the Yorkshire Cancer Research Campaign, England.
Received 2/ 5/91. Accepted 3/18/91.
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