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Abstract for 95th Annual AACR Meeting Heterocyclic amines (HAs) are potent mutagens formed at elevated levels in well-done cooked meats. HAs induce cancer at multiple sites in bioassays of animals (including rat prostate), and appear to elevate colon and breast cancer risk in humans. To investigate whether relatively greater HA intake by African Americans (AA) vs. whites could explain their ∼2-fold greater risk of prostate cancer (PC), a prospective clinic-based study is comparing PC-screening outcomes with corresponding dietary HA estimates in AA. Preliminary results for 314 participants indicate that average daily intake of PhIP (the major HA in cooked meats) in the AA group studied was 17 ng Kg-1 d-1, which is ∼2 (or ∼3) times greater than previously estimated for AA (or white) men of similar age in the U.S. Estimated PhIP intakes, attributable mostly to cooked chicken (67%), were significantly positively correlated with estimated intakes of saturated fat (SF) (R2 = 0.24, p < 10-10), which has long been hypothesized to be an important environmental PC-risk factor. For a high-risk screening endpoint of PSA ≥ 20 ng/mL, the odds ratio for those in the highest decile of daily PhIP intake (≥44 ng Kg-1 d-1) was estimated to be 37, with 2-tail maximum likelihood 95% confidence limits of (3.4, 850). A p-value for linear trend of <0.0001 (0.001 after adjusting for SF intake) was found for the same endpoint across four PhIP-intake groups (see figure). In contrast, we found neither a significantly elevated OR for PSA ≥ 20 ng/mL in any SF-intake group, nor a significant p-value for linear trend across SF intake groups, regardless of adjustment for PhIP intake. These preliminary results are consistent with the hypothesis that diet and food preparation interventions may help reduce PC risk in AA and perhaps other groups. [Work performed under auspices of the U.S. Department of Energy by the University of California Lawrence Livermore National Laboratory under contract No. W-7405-Eng-48, and by UCSF, with funding by the National Cancer Institute (NIH Grant No. P01 CA55861-01).]

[Proc Amer Assoc Cancer Res, Volume 46, 2005]