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MTR polymorphic variant A2756G and retinoblastoma risk in Brazilian children
Author(s) -
de Lima Elker Lene Santos,
da Silva Vanessa Cavalcante,
da Silva Hildson Dornelas Angelo,
Bezerra Alexandre Medeiros,
de Morais Vera Lucia Lins,
de Morais Adriana Lins,
Cruz Raquel Vera,
Barros Mário Henrique Magalhães,
Hassan Rocio,
de Freitas Antonio Carlos,
Muniz Maria Tereza Cartaxo
Publication year - 2010
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.22472
Subject(s) - thymidylate synthase , methionine synthase , retinoblastoma , methylenetetrahydrofolate reductase , genetics , genotype , allele , population , methyltransferase , medicine , methylation , oncology , biology , cancer research , microbiology and biotechnology , cancer , gene , methionine , fluorouracil , environmental health , amino acid
Background Polymorphisms in the genes of folate and methionine metabolism enzymes have been associated with some forms of cancer by affecting DNA synthesis, repair, and methylation. Procedure A case–control study of 72 retinoblastoma cases and 98 cancer‐free children controls was performed to investigate whether the polymorphisms of the methylenetetrahydrofolate reductase ( MTHFR C677T and A1298C), methionine synthase ( MTR A2756G), carrier of reduced folate 1 ( RFC ‐1 A80G) and thymidylate synthase ( TYMS 2R > 3R) altered the risk for retinoblastoma. Results MTR A2756G AG plus GG genotype frequencies were higher in patients than in controls (45% vs. 26%, P = 0.03). Individual carriers of the variant allele G had a 2.02 (95% CI: 1.05–3.92)‐fold increased risk for retinoblastoma. In contrast, no association was observed with respect to MTHFR C677T and A1298C, RFC A80G, and TYMS polymorphisms. Conclusions This study presents evidence for an association between the MTR A2756G polymorphism and retinoblastoma susceptibility in a Northeast population from Brazil. Pediatr Blood Cancer 2010;54:904–908 © 2010 Wiley‐Liss, Inc.