{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,14]],"date-time":"2023-10-14T12:10:11Z","timestamp":1697285411392},"reference-count":30,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,6,7]],"date-time":"2004-06-07T00:00:00Z","timestamp":1086566400000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Birth Defects Research"],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>There is compelling evidence that the risk of spina bifida, a malformation of the caudal neural tube, is associated with maternal and\/or embryonic disturbances in folate\/homocysteine metabolism. Hence, functional variants of genes that influence folate\/homocysteine metabolism constitute a biologically plausible group of candidate risk factors for spina bifida and other neural tube defects. One such candidate is <jats:italic>ABCC2<\/jats:italic>, the gene encoding ABCC2, (a.k.a. canalicular multispecific organic anion transporter [cMOAT], multidrug resistance related protein 2 [MRP2]), a member of the ABC transporter family that effluxes natural folates and anti\u2010folate drugs such as methotrexate.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>The association between the risk of spina bifida and both the maternal and embryonic <jats:italic>ABCC2<\/jats:italic> C(\u201324)T genotype was evaluated by using the transmission disequilibrium test and log\u2010linear modeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>These analyses provided no evidence that the risk of spina bifida was significantly related to either the maternal or embryonic <jats:italic>ABCC2<\/jats:italic> C(\u201324)T genotype.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>The results of the present analyses suggest that the C(\u201324)T variant of the <jats:italic>ABCC2<\/jats:italic> gene is not a major determinant of spina bifida risk. Birth Defects Research (Part A), 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bdra.20023","type":"journal-article","created":{"date-parts":[[2004,6,7]],"date-time":"2004-06-07T15:21:56Z","timestamp":1086621716000},"page":"396-399","source":"Crossref","is-referenced-by-count":8,"title":["A common <i>ABCC2<\/i> promoter polymorphism is not a determinant of the risk of spina bifida"],"prefix":"10.1002","volume":"70","author":[{"given":"Liselotte E.","family":"Jensen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amelia M.","family":"Wall","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michelle","family":"Cook","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katy","family":"Hoess","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Caroline F.","family":"Thorn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander S.","family":"Whitehead","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laura E.","family":"Mitchell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,6,7]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199911113412001"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/00001648-200201000-00021"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.aje.a010290"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1086\/344213"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/bdra.20002"},{"key":"e_1_2_6_7_1","first-page":"811","article-title":"A note on the application of the transmission disequilibrium test when a parent is missing","volume":"56","author":"Curtis D","year":"1995","journal-title":"Am J Hum Genet"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199212243272602"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1086\/344209"},{"key":"e_1_2_6_10_1","first-page":"2532","article-title":"Antifolate resistance mediated by the multidrug resistance proteins MRP1 and MRP2","volume":"59","author":"Hooijberg JH","year":"1999","journal-title":"Cancer Res"},{"key":"e_1_2_6_11_1","first-page":"703","article-title":"Maternal plasma folate and vitamin B12 are independent risk factors for neural tube defects","volume":"86","author":"Kirke PN","year":"1993","journal-title":"QJM"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1006\/mgme.1998.2738"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(95)90165-5"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(91)90133-A"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1067\/mpp.2000.112052"},{"key":"e_1_2_6_16_1","unstructured":"Online Medelian Inheritance in Man (OMIM). 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