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Three Secretory Phospholipase A₂ Genes That Map to Human Chromosome 1P35–36 Are Not Mutated in Individuals with Attenuated Adenomatous Polyposis Colifr1]

Departments of Human Genetics, [L. N. S., M. F. L.], Oncological Sciences [L. N. S., B. P., M. R., E. L., R. W.], and Internal Medicine [R. W. B.] and Program in Human Molecular Biology and Genetics [C. K., S. M. P.], University of Utah, Salt Lake City, Utah 84112, and Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana 46202-5251 [J. A. T.]

Mutation of Pla2g2a, a secretory phospholipase A₂ gene, dramatically increases the number of intestinal polyps that develop in the multiple intestinal neoplasia (Min) mouse, a murine model for adenomatous polyposis coli in humans. We tested the hypothesis that mutation of the human homologue(s) of this gene might be responsible for the more severe phenotype (hundreds of polyps) seen in a subset of individuals with attenuated adenomatous polyposis coli (AAPC). DNA sequence analysis demonstrated that alterations of PLA2G2A, as well as related genes PLA2G2C and PLA2G5, were evenly distributed between three classes of AAPC subjects: those with small, intermediate, and large numbers of adenomatous colonic polyps. Among 67 additional unrelated AAPC subjects, a stop mutation in PLA2G2C did not correlated with an increased burden of adenomatous polyps. Therefore, mutation of the human homologue(s) of murine Pla2g2a does not appear to be responsible for phenotypic variation among subjects with AAPC.

¹ This work was supported by NIH Grants CA40641 (R. W. B.), DK38185 (J. A. T.), and DK38185 (S. M. P.) and by the Huntsman Cancer Institute. L. N. S. is supported by the Department of Energy's Oak Ridge Institute for Science and Education as an Alexander Hollaender Postdoctoral Fellow.

² To whom requests for reprints should be addressed, at Department of Oncological Sciences, University of Utah, Building 533, Room 7410, Salt Lake City, UT 84112.

Received 12/21/95. Accepted 1/17/96.

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