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Spina bifida (SB) is one of the most prevalent congenital anomalies known as neural tube defects (NTD) in Yucatan, at Southeast Mexico. NTD results from failures of normal neural tube closure between the third and fourth week of embryonic development (Chen, 2008; Ramirez-Espitia et al., 2003). The majority of NTD cases can be categorized as either anencephaly with a lack of closure in the region of the head; or spina bifida with a lack of closure below the head (Au et al., 2010). SB refers to defects in the vertebral arches that obligatorily accompany open lesions. When the neural folds remain open, the sclerotome is unable to cover the neuroepithelium and skeletogenesis occurs abnormally, leaving the midline exposed (Greene & Copp, 2009). SB encompasses several subgroups of defects including the protrusion of the nervous tissue and its covering through a defect in the vertebrae named myelomeningocele, meningocele, and lipomeningocele. Myelomeningocele is by far the most common, accounting for greater than 90% of SB cases (Au et al., 2010). Wide variations in SB prevalence based on geography, race/ethnicity, and socioeconomic level suggest that genetic and environmental factors contribute to its etiology (Chen, 2008). Maternal folate status is critical for proper neural tube closure during embryogenesis. However epidemiological studies suggest that factors other than maternal deficiency of folic acid are involved in the etiology of SB. Numerous environmental and genetic influences

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Association of A80G Polymorphism in the RFC1 Gene with the Risk for Having Spina Bifida-Affected Offspring in Southeast Mexico and Interaction with C677T-MTHFR