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Loss of Heterozygosity at the Human RAP1A/Krev-1 Locus Is a Rare Event in Colorectal Tumors¹

Queensland Cancer Fund Research Unit, Joint Oncology Program, Queensland Institute of Medical Research and Department of Pathology, University of Queensland [J. Y., G. C-T.], and Department of Pathology [J. S.] and Department of Gastroenterology [R. S., A. C., M. W.], Royal Brisbane Hospital, Brisbane Q 4006, Australia

Kirsten-ras-revertant-1 (Krev-1/Rap1A) is a recently identified tumor suppressor gene which induces flat revertants when introduced into a variety of ras-transformed cell lines in vitro. Since 47% of colorectal carcinomas have transforming mutations in ras protooncogenes, and since Krev-1 is expressed at high levels in normal colonic mucosa, we hypothesized that inactivation at the Krev-1 locus may be necessary for transformation of colonic cells. Loss of heterozygosity is a common method of inactivation of tumor suppressor genes in colorectal tumors. Therefore, we analyzed loss of heterozygosity in 52 patients with sporadic colorectal cancer. Because Krev-1 had no previously described polymorphisms, we first identified a BclI restriction fragment length polymorphism which showed 40% heterozygosity in 50 unrelated individuals. However, only one tumor from 18 informative patients showed allelic loss at the Krev-1 locus. This suggests that loss of heterozygosity is not a common mechanism of inactivation at the Krev-1 locus in colorectal cancer. However, the results do not exclude a role for Krev-1 in the etiology of this neoplasm because inactivation may occur by other mechanisms.

¹ This work was supported by a grant from the Queensland Cancer Fund.

² To whom requests for reprints should be addressed, at Joint Oncology Program, Queensland Institute of Medical Research, Bramston Terrace, Herston, Q 4006, Australia.

Received 7/11/91. Accepted 10/31/91.

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