{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T19:25:10Z","timestamp":1761765910618,"version":"build-2065373602"},"reference-count":41,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2015,3,10]],"date-time":"2015-03-10T00:00:00Z","timestamp":1425945600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Harvard School of Public Health Gene"},{"name":"Environment Initiative and the National Institute of Environmental Health Sciences","award":["R01 ES016454","K01 ES017800","P30 ES00002"],"award-info":[{"award-number":["R01 ES016454","K01 ES017800","P30 ES00002"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>Single\u2010nucleotide polymorphisms (SNPs) in inflammation, one\u2010carbon metabolism, and skin cancer genes might influence susceptibility to arsenic\u2010induced skin lesions.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>A case\u2010control study was conducted in Pabna, Bangladesh (2001\u20102003), and the drinking\u2010water arsenic concentration was measured for each participant. A panel of 25 candidate SNPs was analyzed in 540 cases and 400 controls. Logistic regression was used to estimate the association between each SNP and the potential for gene\u2010environment interactions in the skin lesion risk, with adjustments for relevant covariates. Replication testing was conducted in an independent Bangladesh population with 488 cases and 2,794 controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>In the discovery population, genetic variants in the one\u2010carbon metabolism genes phosphatidylethanolamine <jats:italic>N<\/jats:italic>\u2010methyltransferase (rs2278952, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.004; rs897453, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.05) and dihydrofolate reductase (rs1650697, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.02), the inflammation gene interleukin 10 (rs3024496, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.04), and the skin cancer genes inositol polyphosphate\u20105\u2010phosphatase (<jats:italic>INPP5A<\/jats:italic>; rs1133400, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.03) and xeroderma pigmentosum complementation group C (rs2228000, <jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.01) significantly modified the association between arsenic and skin lesions after adjustments for multiple comparisons. The significant gene\u2010environment interaction between a SNP in the <jats:italic>INPP5A<\/jats:italic> gene (rs1133400) and water arsenic with respect to the skin lesion risk was successfully replicated in an independent population (<jats:italic>P<\/jats:italic> for interaction\u2009=\u2009.03).<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>Minor allele carriers of the skin cancer gene <jats:italic>INPP5A<\/jats:italic> modified the odds of arsenic\u2010induced skin lesions in both main and replicative populations. Genetic variation in <jats:italic>INPP5A<\/jats:italic> appears to have a role in susceptibility to arsenic toxicity. <jats:bold><jats:italic>Cancer<\/jats:italic> 2015;121:2222\u20132229.<\/jats:bold> \u00a9 <jats:italic>2015 American Cancer Society<\/jats:italic>.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cncr.29291","type":"journal-article","created":{"date-parts":[[2015,3,10]],"date-time":"2015-03-10T17:27:57Z","timestamp":1426008477000},"page":"2222-2229","source":"Crossref","is-referenced-by-count":8,"title":["A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate\u20105\u2010phosphatase modifies the susceptibility of arsenic\u2010associated skin lesions in Bangladesh"],"prefix":"10.1002","volume":"121","author":[{"given":"Wei Jie","family":"Seow","sequence":"first","affiliation":[{"name":"Department of Environmental Health Harvard School of Public Health Boston Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wen\u2010Chi","family":"Pan","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Harvard School of Public Health Boston Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Molly L.","family":"Kile","sequence":"additional","affiliation":[{"name":"College of Public Health and Human Sciences Oregon State University Corvallis Oregon"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Tong","sequence":"additional","affiliation":[{"name":"Department of Health Studies University of Chicago Chicago Illinois"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea A.","family":"Baccarelli","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Harvard School of Public Health Boston 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