Tumor markers and rectal cancer: Support for an inflammation-related pathway

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Inflammation may be a key element in the etiology of colorectal cancer. In our study, we examine associations between factors related to inflammation and specific rectal cancer mutations. A population-based study of 750 rectal cancer cases with interview and tumor DNA were compared to 1,205 population-based controls. Study participants were from Utah and the Northern California Kaiser Permanente Medical Care Program. Tumor DNA was analyzed forTP53andKRAS2mutations and CpG Island methylator phenotype. We assessed how these tumor markers were associated with use of anti-inflammatory drugs, polymorphisms in theIL6genes (rs1800795 and rs1800796) and dietary antioxidants. Ibuprofen-type drugs,IL6polymorphisms (rs1800796) and dietary alpha-tocopherol and lycopene significantly altered likelihood of having aTP53mutation. This was especially true forTP53transversion mutations and dietary antioxidants (OR for beta-carotene 0.51 95% CI 0.27, 0.97,ptrend 0.03; alpha-tocopherol 0.41 95% CI 0.20, 0.84,ptrend 0.02) Beta-carotene and ibuprofen significantly altered risk ofKRAS2tumors. The associations between lutein and tocopherol andTP53andKRAS2mutations were modified byIL6genotype. These results suggest that inflammation-related factors may have unique associations with various rectal tumor markers. Many factors involved in an inflammation-related pathway were associated withTP53mutations and some dietary factors appeared to be modified byIL6genotype. © 2009 UICC

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