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Oncogene Division, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104 [K. Y., M. I., H. I., T. S.], and Department of Internal Medicine, School of Medicine, The University of Tokushima, 3-18-15, Kuramoto-cho, Tokushima 770 [R. Y., H. S., S. S.], Japan
The DNAs from two independent pancreatic cancers (tumors 1 and 2) in a patient with multiple endocrine neoplasia type 1 were analyzed. No amplification or gross rearrangement of 19 protooncogenes was observed. However, Southern blot analysis using polymorphic DNA probes revealed loss of heterozygosity at loci on chromosome 11p in both tumors. In tumor 1, an extensive region including the HRAS1, PTH, CALCA, and D11S151 loci was deleted, while in tumor 2 loss of heterozygosity was limited at the HRAS1 and D11S151 loci. Because loss of heterozygosity at other chromosomal loci in the two tumors was quite rare, loss of genes on 11p might be nonrandom. It is noteworthy that the same allele at the HRAS1 locus and also the same allele at the D11S151 locus were lost in the two independent tumors. These results suggest that loss of genes at the HRAS1 and/or D11S151 loci plays an important role unmasking the remaining sequences probably having a recessive mutation.
1 Supported by a Grant-in-Aid from the Ministry of Health and Welfare for a Comprehensive 10-Year Strategy for Cancer Control, Japan, and a grant from the Special Coordination Fund of the Science and Technology Agency of Japan. Katsuhiko Yoshimoto and Hiroyuki Iwahana were recipients of Research Resident Fellowships from the Foundation for Promotion of Cancer Research.
2 To whom requests for reprints should be addressed.
Received 4/ 4/88. Revised 1/ 6/89. Accepted 2/15/89.
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