ABSTRACT
Differences in incidence and outcome of cancer among ethnic groups may be explained by biological and/or socio-economic factors. Genetic variations that affect chronic inflammation, a potentially important risk factor for carcinogenesis, may differ across ethnic groups. Such differences may help explain cancer disparities among these groups. Single nucleotide polymorphisms (SNPs) within cytokine genes can affect cytokine levels and the degree of inflammation. Associations between cancer and some cytokine SNPs have been suggested. However, these have not been consistently replicated among populations, suggesting that SNP function may differ according to ethnicity, or that SNPs alone do not completely account for regulation of inflammation. We examined seven polymorphisms in African-American (n = 294) and Caucasian (n = 299) newborns in Louisiana: IL1B-511C > T, IL1B-31T > C, IL1B + 3954C > T, IL1RN*2, IL10-1082G > A, IL10-592C > A, and TNF-308G > A. African-American newborns had significantly higher frequencies of IL1B-511T, IL1B-31C, IL10-1082A and IL10-592A alleles and complete linkage equilibrium between IL1B + 3954 and IL1B-31. In contrast, IL1B + 3954T, IL1RN*2, and TNF-308A were more frequent in Caucasian newborns and exhibited strong linkage disequilibrium between IL1B + 3954 and IL1B-31. All allelic frequencies were significantly different between groups. We hypothesize that these dissimilarities may contribute to differences in the inflammatory response and cancer incidence and mortality between African-Americans and Caucasians in Louisiana.
Subject(s)
Black or African American/genetics , Cytokines/genetics , Genetic Predisposition to Disease , Neoplasms/ethnology , Neoplasms/genetics , White People/genetics , Black or African American/ethnology , Female , Gene Frequency , Humans , Infant, Newborn , Inflammation/ethnology , Inflammation/genetics , Male , Polymorphism, Single Nucleotide , White People/ethnologyABSTRACT
Tyrosinemia resulting from administration of protein-dense infant diets was detected by newborn screening in two infants. Change of formula resulted in rapid resolution of the hypertyrosinemia. These cases identify nonstandard infant diets as a benign and reversible cause of tyrosinemia and a potential cause of positive newborn phenylketonuria screening.
