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Biomedical subjects

Gary M Shaw

Publications and source records attributed to Gary M Shaw.

At least 55 records · Page 3Linked to original sources
PubMed2004

Congenital malformations in births with orofacial clefts among 3.6 million California births, 1983-1997.

Few population-based epidemiologic data are available on malformation phenotypes that co-occur with orofacial clefts. We explored the occurrence of structural congenital malformations in offspring with cleft palate (CP) and in offspring with cleft lip with or without CP (CLP), using data from a population-based active surveillance system. Ascertainment was performed among 3548991 liveborn and 23239 stillborn offspring of California women who delivered in nonmilitary hospitals during the period, 1983-1997. Structural congenital malformations were found in 91888 births. Among them, 2343 had CP and 4072 had CLP. Malformations were grouped according to 3- and 4-digit codes of the British Pediatric Association (BPA). Prevalences of each malformation grouping, defined by these codes, were calculated among: (1). all births with CP; (2). all births with CLP; (3). all births without CP or CLP but with another structural malformation; and (4). all births in the population at risk. These various prevalence measures were the basis of estimating relative risks. Observed relative risks indicated that some phenotypes were more likely and some were less likely to co-occur with either CP or CLP, with relative risks ranging from 0.5 to 2.4. For both CP and CLP, estimated relative risks were highest for malformations involving the respiratory system and lowest for spina bifida. The exclusion of all births (n = 10702) with chromosomal anomalies from comparisons did not materially alter observed relative risk estimates. Computations extended to 4-digit level BPA codes revealed elevated risks for a number of more specific diagnoses seen within the larger (3-digit level) groupings defined as eye, ear, respiratory, upper alimentary tract, and other musculoskeletal anomalies. In this large population-based cohort of infants and fetuses with CLP or CP, we observed several noncleft malformation groupings to be more common and others to be less common in their co-occurrence with orofacial clefts relative to their co-occurrence with any other malformation. These observed patterns tended to be similar for CP and for CLP.

California↗
PubMed2004

Limb deficiency defects, MSX1, and exposure to tobacco smoke.

There is increasing evidence from epidemiologic studies that genetic susceptibilities may modify the teratogenic effects of smoking. A previous study suggested that maternal smoking in the presence of a dinucleotide repeat polymorphism for MSX1 produced an almost fivefold increased risk for limb anomalies, providing evidence for a gene-environment interaction. The current study examined this potential interaction, using case-control data with several methodologic improvements, including a larger sample size and more detailed information on cigarette smoke exposures. Cases (n = 92) were ascertained from pregnancies ending in 1987-1989, and controls (n = 180) were randomly selected from eligible liveborn infants. In telephone interviews, women reported smoking behaviors during the month before pregnancy through the end of the first trimester. Odds ratios (OR) for maternal and paternal smoking ranged from 1.0 to 1.4, risk estimates were imprecise; for example, the OR for maternal smoking >or=20 cigarettes per day, versus none, was 1.3 (95% confidence interval (CI) 0.5-3.4). Relative to the homozygous wildtype, the OR was 1.5 (95% CI 0.7-3.5) for the homozygous variant genotype and 0.8 (95% CI 0.5-1.4) for the heterozygous variant genotype. There was no evidence that maternal smoking or both parents smoking, in combination with a susceptible MSX1 genotype, conferred an additional increase in risk of limb defects. This study did not find a gene-environment interaction between maternal smoking, infant MSX1 CA repeat polymorphism, and risk of limb deficiency defects. This finding contrasts with results of a previous study, which provided initial evidence for such an interaction. Several important methodological differences may have contributed to the differences in findings between the two studies.

Adult↗
PubMed2004

Congenital malformations in offspring of Hispanic and African-American women in California, 1989-1997.

BACKGROUND: Little is known about risks of most specific birth defects among infants born to U.S.-born and foreign-born Hispanic or African-American women. METHODS: Using data from a large population-based registry, we explored risks of selected congenital malformation phenotypes in offspring of U.S.-born and foreign-born Hispanic and African-American women, relative to non-Hispanic white women, in California. Approximately 2.2 million live births and stillbirths occurred during the ascertainment period, 1989-1997. Information on maternal racial-ethnic background and other covariates was obtained from birth certificate and fetal death files. RESULTS: Adjusted relative risks (ARRs) for the 20 groupings of malformations designated by three-digit British Pediatric Association (BPA) codes ranged from 0.6 (genital organ malformations, among infants born to foreign-born Hispanics) to 1.7 (anencephaly, also among infants born to foreign-born Hispanics). Grouping by four-digit BPA codes revealed that among infants born to U.S.-born Hispanics, 46 of the ARRs were < or = 0.8 and 12 were > or = 1.3; among infants born to foreign-born Hispanics, 75 of the ARRs were < or = 0.8 and 15 were > or = 1.3; and among infants born to African-American women, 45 ARRs were < or = 0.8 and 25 were > or = 1.3. For each racial-ethnic group of women, the observed variability in risks covered most organ systems. CONCLUSIONS: Although the results suggested that (in comparison with non-Hispanic whites) each racial-ethnic group was more likely to have reduced risk for specific defects (rather than elevated risk), in general, the range of the relative risks was comparatively narrow.

Black or African American↗
PubMed2004

Epidemiologic characteristics of anotia and microtia in California, 1989-1997.

BACKGROUND: There is a paucity of epidemiologic information about the external ear malformations anotia and microtia. METHODS: Using data from a large population-based registry, we explored prevalences and maternal/infant characteristics associated with anotia and microtia. Data were derived from the California Birth Defects Monitoring Program, a population-based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.5 million births (live-born and stillborn) occurred during the ascertainment period, 1989-1997. Information on maternal and infant/fetal characteristics was obtained from California birth certificate and fetal death files. RESULTS: The prevalence of anotia/microtia was 2.50 per 10,000 live births and stillbirths. Isolated cases, i.e., those live births and stillbirths with no other accompanying anomaly diagnoses, revealed a prevalence of 0.63 per 10,000, whereas among nonisolated cases, the prevalence was 1.53 per 10,000 live births and stillbirths. Prevalences of isolated anotia/microtia were substantially higher among U.S.-born Hispanics, foreign-born Hispanics, and Asians compared to non-Hispanic whites, with relative risks ranging from three- to seven-fold. Similar prevalences for maternal race/ethnicity (except for Asians) were observed for live births and stillbirths with nonisolated cases of anotia/microtia, but the magnitude of risks were lower than those observed for isolated cases. Prevalence of nonisolated anotia/microtia was substantially lower among women whose education was 12 years or more. CONCLUSIONS: These data reveal descriptive epidemiologic features of anotia/microtia most notably substantial risks associated with race/ethnic groups and lower maternal education. Additional study for factors associated with these characteristics could reveal clues for the etiology of these ear anomalies.

Adult↗
PubMed2004

Risks of selected congenital malformations among offspring of mixed race-ethnicity.

BACKGROUND: Little is known about the occurrence of specific congenital malformations among offspring of mixed race-ethnicity. METHODS: Using data from a population-based registry, we explored the occurrence of selected malformation phenotypes in offspring to parents who were of different race-ethnicity. Data were derived from the California Birth Defects Monitoring Program, a population-based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.6 million live births and stillbirths occurred during 1989-2000. Information on parental race-ethnicity (non-Hispanic white, Hispanic, black, and Asian) was obtained from birth certificates and fetal death files. Malformation phenotypes studied were spina bifida, anencephaly, cleft lip, cleft palate, tetralogy of Fallot, d-transposition of great arteries, hypospadias, small intestinal atresia, preaxial polydactyly, microtia, and hypertrophic pyloric stenosis. RESULTS: A total of 11.2% of births were to parents of mixed race-ethnicity. Compared to births of parents who were both white, moderately increased risks (risk ratio >/= 1.7) of anencephaly, polydactyly, and microtia, and decreased risks (risk ratio </= 0.6) of hypospadias and hypertrophic pyloric stenosis were observed among births of several mixed race-ethnicity groups. For anencephaly, polydactyly, and microtia, but not other phenotypes, the risks were different depending on whether maternal versus paternal race-ethnicity was considered. Risks observed between births of a nonwhite parent and a white parent and births of parents who were both nonwhite were similar for most malformation phenotypes. CONCLUSIONS: Some malformation phenotypes appear to vary in their risk based on mixed racial-ethnic groupings.

California↗
PubMed2004

Periconceptional multivitamin intake during early pregnancy, genetic variation of acetyl-N-transferase 1 (NAT1), and risk for orofacial clefts.

BACKGROUND: Periconceptional supplementation of multivitamins that include folic acid have been shown to prevent several birth defects, including neural tube defects and orofacial clefts. We investigated whether polymorphic variants of fetal acetyl-N-transferase 1 (NAT1), an enzyme involved in the catabolism of folates, differentially interacted with maternal multivitamin use during early pregnancy to alter the risk of delivering an infant with an orofacial cleft malformation. METHODS: Using a large population-based case-control study, we genotyped 421 California infants born with an isolated cleft and 299 controls for two NAT1 polymorphisms. RESULTS: Compared to the homozygous wild-type genotypes, odds ratios for isolated cleft lip with/without cleft palate were slightly increased among infants who were homozygous for the variant alleles of NAT1 1088 and 1095. For isolated cleft palate, no similar associations with these two NAT1 variants were observed. For NAT1 1088 genotypes, we did not observe any differential risks for clefts related to maternal multivitamin intake. For NAT1 1095 genotypes, however, we found a two-fold higher risk for isolated cleft lip with/without cleft palate among infants who were homozygous for the variant allele and whose mothers did not take multivitamins during early pregnancy. CONCLUSIONS: We found evidence suggestive of an interaction between the NAT1 1095 polymorphism and lack of maternal multivitamin use that increased risks of isolated cleft lip with/without cleft palate.

Adult↗
PubMed2004

Promoter haplotype combinations for the human PDGFRA gene are associated with risk of neural tube defects.

Recent animal studies suggested that deregulated expression of the platelet-derived growth factor receptor alpha (PDGFRalpha) may contribute to the failure of normal neural tube closure (NTC). There is also suggestive evidence that the promoter haplotype of the PDGFRA is associated with genetic susceptibility in human neural tube defects (NTDs). The purpose of our study was to investigate the association between promoter haplotype combinations of the human PDGFRA gene and risk for NTDs in a Hispanic population from the Texas-Mexico border region. This population has a considerably higher prevalence of NTDs (16/10,000 live births) than that generally reported in the United States (8-10/10,000 live births). In the present study, NTDs were defined as spina bifida or anencephaly. The haplotype of PDGFRA gene promoter was determined by direct DNA sequence analysis. Two novel haplotypes, H2epsilon and H1beta, were found. We observed significant differences among variable haplotype groups from in vitro transient transfection studies in U2-OS osteosarcoma cell and two other cell lines (HeLa cell and MCF7 cell). Result from our case-control study demonstrated that the frequencies of haplotypes with low transcription activity were significantly higher in NTD mothers than that observed in control mothers (odds ratio=2.2, 95% CI=1.0-4.6). Infants with at least one low activity allele showed slightly higher risk (odds ratio=1.5, 95%=0.8-3.1). Our study suggests that the reduced transcriptional activity of PDGFRA gene could increase the risk of having an NTD-affected pregnancy.

Adult↗
PubMed2004

Maternal smoking and the risk of orofacial clefts: Susceptibility with NAT1 and NAT2 polymorphisms.

BACKGROUND: Orofacial clefts are etiologically heterogeneous malformations. One probable cause is maternal smoking during pregnancy. The effect of maternal smoking may be modified by genes involved in biotransformation of toxic compounds derived from tobacco. We investigated whether polymorphic variants of fetal acetyl-N-transferases 1 (NAT1) and 2 (NAT2) interact with maternal cigarette smoking during early pregnancy to increase the risk of delivering an infant with an orofacial cleft. METHODS: In a California population-based case-control study, we genotyped 421 infants born with an isolated cleft and 299 nonmal-formed controls for 2 NAT1 and 3 NAT2 single nucleotide polymorphisms RESULTS: Although smoking was independently associated with increased risks for both isolated cleft lip +/- cleft palate and isolated cleft palate, no independent associations were found for NAT1 1088 or 1095 genotypes or for NAT2 acetylator status. However, the infant NAT1 1088 and 1095 polymorphisms were strongly associated with the risk of clefts among smoking mothers; infants with NAT1 1088 genotype AA versus TT (odds ratio [OR] = 3.9; 95% confidence interval = 1.1-17.2) and with NAT1 1095 genotype AA versus CC (OR = 4.2; 1.2-18.0). Infant NAT2 acetylator status did not appreciably affect susceptibility of the fetus to the teratogenic effects of maternal smoking. CONCLUSIONS: Our results suggest that maternal smoking during pregnancy may increase risk for orofacial clefts particularly among smokers whose fetuses have polymorphic variants of NAT1, an enzyme involved in phase II detoxification of tobacco smoke constituents.

Acetyltransferases↗
PubMed2003

Dieting behaviors and risk of neural tube defects.

The authors examined whether maternal dieting behaviors were associated with increased neural tube defect (NTD) risk among offspring, using population-based, case-control data. The analysis included 538 cases and 539 nonmalformed controls delivered from 1989 to 1991 in selected California counties, and exposures were assessed by in-person maternal interview. Among four reported dieting behaviors involving restricted food intake, diets to lose weight (odds ratio=2.1, 95% confidence interval: 1.1, 4.1), fasting diets (odds ratio=5.8, 95% confidence interval: 1.7, 20.0), and eating disorders (odds ratio=1.7, 95% confidence interval: 0.8, 3.6) were associated with increased NTD risk during the first trimester of pregnancy. Risk estimates for these behaviors during the 3 months before conception tended to be closer to 1. The fourth behavior, "other special diets," was not associated with increased NTD risk during either period. Women also reported whether they took diet pills, laxatives, or diuretics, engaged in binge eating, induced vomiting, or exercised excessively from the first 3 months before conception through the end of pregnancy. Only the intake of diuretics was associated with substantially increased NTD risk (odds ratio=2.7, 95% confidence interval: 0.7, 10.2). This study suggests that maternal dieting behaviors involving restricted food intake during the first trimester may be associated with increased NTD risk.

California↗
PubMed2003

Genetic variation of infant reduced folate carrier (A80G) and risk of orofacial and conotruncal heart defects.

How folate reduces the risks of congenital anomalies is unknown. The authors focused on a gene involved in folate transport-reduced folate carrier-1 gene (RFC1). Using data from a California case-control study (1987-1989 births), the authors investigated whether the risks of orofacial clefts or conotruncal heart defects were influenced by a polymorphism of infant RFC1 or by an interaction between the RFC1 gene and maternal periconceptional use of vitamins containing folic acid. A total of 305 liveborn infants with cleft lip with or without cleft palate, 123 with cleft palate, 163 with conotruncal heart defects, and 364 nonmalformed controls were genotyped. Odds ratios of 1.6 (95% confidence interval: 0.9, 2.8) for the G80/G80 genotype and of 2.3 (95% confidence interval: 1.3, 3.9) for the G80/A80 genotype were observed relative to the A80/A80 genotype for conotruncal defects. Among mothers who did not use vitamins, the risk of conotruncal defects was 2.1 (95% confidence interval: 0.7, 5.9) for infants with genotype G80/G80 compared with those with the A80/A80 genotype. Among mothers who did use vitamins, the risk was 1.3 (95% confidence interval: 0.7, 2.7). Substantially elevated risks for either cleft group were not observed irrespective of genotype and use/nonuse of vitamins. Thus, this study found modest evidence for a gene-nutrient interaction between infant RFC1 genotype and periconceptional intake of vitamins on the risk of conotruncal defects.

California↗
PubMed2003

Food fortification with folic acid and twinning among California infants.

This study sought to determine whether a change in twinning prevalence was associated with mandatory folic acid fortification. As of January 1998, it became mandatory in the United States that grain products be fortified with folic acid. The effectiveness of this fortification for neural tube defects has been explored, but other possible implications of fortification has not. We computed the prevalence of twinning among more than 2.5 million California births occurring from 1990 to 1999. The prevalence of twin births in California increased over the last decade with increases observed among most maternal race/ethnic, age, and parity groupings. Unadjusted prevalence measures did not reveal substantial increases in twinning prevalence among these groupings after the fortification period relative to the period immediately preceding it. Analyses that simultaneously adjusted for age, parity, race/ethnicity, sexes of twin pair (as a measure of zygosity), year of birth, and fortification period also did not reveal an association between fortification and twinning. Our results do not suggest a change in twinning prevalence associated with folic acid fortification of the US food supply among women delivering in California.

California↗
PubMed2003

Maternal occupational chemical exposures and biotransformation genotypes as risk factors for selected congenital anomalies.

In a case-control study using an assessment of occupational tasks by an industrial hygienist, the authors investigated whether women's occupational exposures increased risks of delivering infants with cleft palate (CP), cleft lip with or without cleft palate (CLP), conotruncal defects, or limb deficiencies. For CP and CLP, exposures were further considered in the presence/absence of infant genetic variants for glutathione-S-transferase M1, glutathione-S-transferase T1, and N-acetyltransferases 1 and 2. The study included 1987-1989 California stillbirths and livebirths. Telephone interviews were conducted with mothers of 662 CLP and CP cases, 207 conotruncal defect cases, 165 limb deficiency cases, and 734 nonmalformed controls. Occupational tasks were assigned to a priori-defined exposure categories: 74 chemical groups and nine "end-use" chemical groups. Odds ratios of 1.5 or greater were observed for a small number of exposure-defect comparisons. Risks associated with end-use groups revealed odds ratios of 1.5 or greater for exposures to dyes and pigments (conotruncal and CP), propellants (CP), and insecticides (conotruncal and CP). Numerous odds ratios of 2.5 or greater were observed for combined effects of exposures and homozygous mutant genotypes, particularly for CP. Although potential associations were observed, most results suggested that maternal occupational chemical exposures did not contribute substantially to the occurrence of these anomalies in this California population.

Abnormalities, Drug-Induced↗
PubMed2003

Risk of mental retardation among children born with birth defects.

BACKGROUND: A paucity of epidemiologic research exists concerning the co-occurrence of birth defects and mental retardation (MR). Study of this co-occurrence may yield important clues about the causes of both. OBJECTIVE: To examine the co-occurrence of birth defects and MR, taking into consideration the type of birth defect, level of MR, co-occurrence of MR with other developmental disabilities, and individual and maternal factors. DESIGN: A retrospective cohort study of infants born in the California Central Valley with and without a structural birth defect by 1 year of age, and with or without MR by 7 to 9 years of age. SETTING AND PARTICIPANTS: One-year survivors (N = 119 556) born in nonmilitary hospitals in 8 California counties between January 1, 1992, and December 31, 1993, for whom information about birth defects was recorded within the first year of life. MAIN OUTCOME MEASURE: Diagnosis of MR by age 7 years considered as being mild or severe and as occurring without other developmental disabilities (isolated MR) or as occurring with other developmental disabilities, including cerebral palsy, epilepsy, or a pervasive developmental disorder. RESULTS: Children with birth defects were nearly 27 times more likely to have MR by 7 years of age compared with children without a diagnosed birth defect regardless of type of defect (prevalence ratio, 26.8; 95% confidence interval, 22.7-31.7). Among those with birth defects, children with Down syndrome (prevalence ratio, 211.7; 95% confidence interval, 171.3-261.5) and children with sex chromosomal defects (prevalence ratio, 57.4; 95% confidence interval, 23.7-138.6) were at the highest risk for MR. Children with nonchromosomal defects, including central nervous system defects and all types of organ and system defects, were at substantially increased risk for all levels of MR. Risks of MR among children with Down syndrome and nonchromosomal defects were not substantially altered when adjusted for individual and maternal factors. CONCLUSIONS: Children with chromosomal and other structural birth defects are at a substantially increased risk for having MR by 7 years of age compared with children born without a birth defect. Children with birth defects are at an especially increased risk for having severe MR and MR occurring independently of other developmental disabilities.

California↗
PubMed2003

Evaluation of infant methylenetetrahydrofolate reductase genotype, maternal vitamin use, and risk of high versus low level spina bifida defects.

BACKGROUND: Several studies have suggested that homozygosity for the C677T 5,10-methylenetetrahydrofolate reductase (MTHFR) variant is a potential risk factor for neural tube defects (NTDs), as individuals homozygous for the C677T allele have slightly elevated homocysteine concentrations under conditions of low folic acid intake. It has been hypothesized that maternal folic acid supplementation prevents NTDs by partially correcting reduced MTHFR activity associated with the variant form of the enzyme. METHODS: Genomic DNA was extracted from newborn screening blood spots obtained from 145 infants with spina bifida (SB) and 260 nonmalformed control infants. The MTHFR C677T genotype was determined by restriction enzyme digestion of PCR amplification products with Hinf1. We investigated whether infant MTHFR genotype influenced the risk for the anatomic level of the SB lesion (high vs. low); we also explored whether maternal vitamin use influenced this risk. RESULTS: Compared to controls, the frequency of SB infants with the homozygous 677 TT genotype was greatest in those infants with high level SB defects (26%; odds ratio [OR] = 2.9; 95% confidence interval [CI] = 0.9-10.1) than for those with low level SB defects (22%; OR = 1.8; 95% CI = 0.9-3.2). Furthermore, homozygous 677TT infants whose mothers did not use vitamins containing folic acid had a modestly increased risk of SB (OR = 1.8; 95% CI = 0.8-3.9), with this risk increasing more than three-fold (OR = 5.5; 95% CI = 0.8-28.1) for those infants with high level SB defects whose mothers did not use vitamins. CONCLUSIONS: Based upon our observations, it is suggested that the association between the infant MTHFR homozygous variant genotype and spina bifida risk may be conditional upon both lesion level and maternal vitamin use.

California↗
PubMed2003

Risk factors for neural tube defects: associations between uncoupling protein 2 polymorphisms and spina bifida.

BACKGROUND: Polymorphisms in the mitochondrial membrane transporter gene UCP2 are capable of affecting energy metabolism, body weight regulation, and possibly preventing the buildup of reactive oxygen species, all factors that could contribute to neural tube defect risk through maternal obesity and diabetes. METHODS: Genomic DNA was extracted from newborn screening blood spots obtained from infants with spina bifida and nonmalformed control infants. Genotype frequencies of two genetic variants in the UCP2 gene, an amino acid substitution of valine for alanine at codon 55 in exon 4, and a 45-base pair insertion/deletion in the 3' untranslated region of exon 8,were determined by restriction enzyme digestion of PCR amplification products. RESULTS: We found the frequency of the 3' untranslated region deletion homozygous genotype (256/256) as well as the A55V homozygous (Val/Val) genotype to be higher in SB infants than in controls (odds ratio [OR], 3.1; 95% confidence interval [CI], 0.9-10.4 and OR = 2.0; 95% CI = 0.3-11.1, respectively). Additionally, the frequency of the combined homozygous 256/256,+ / + genotype was higher in cases and resulted in more than a threefold higher spina bifida risk (OR = 3.6; 95% CI = 1.0-13.1). CONCLUSIONS: These data are the first to suggest that polymorphisms in the UCP2 gene may be genetic risk factors of spina bifida.

California↗
PubMed2003

Associations between polymorphisms within the thymidylate synthase gene and spina bifida.

BACKGROUND: Polymorphisms within the thymidylate synthase (TS) gene that influence enzyme activity may affect plasma folate levels and, indirectly, plasma homocysteine concentrations. We investigated whether TS polymorphisms contribute to spina bifida (SB) risk, given that a reduction in the risk of SB has been linked to folate metabolism. METHODS: Genomic DNA was extracted from newborn-screening blood spots obtained from case infants with SB, and randomly selected, nonmalformed control infants. Genotype frequencies of two polymorphisms in the TS gene-a 28-bp tandem repeat in the promoter enhancer region (TSER) and a 6-bp deletion in the 3'UTR-were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. Additionally, all seven exons of the TS gene were sequenced to identify variations within the coding region of the gene. RESULTS: We found that the TSER 2/2 homozygous genotype was associated with a slightly increased risk for SB infants (odds ratio [OR] = 1.4 [0.8-2.4], p = 0.1). When the cohort was divided into separate ethnic groups, this risk increased by 4-fold with the TSER 2/2 homozygous genotype (OR = 4.0 [1.8-8.8], p = 0.001), and by 3-fold with the 3'UTR +/+ homozygous genotype (OR = 3.6 [1.3-10.1], p = 0.02) in non-Hispanic white cases. The combined TSER,3'UTR (2/2,+/+) genotype showed a more than 4-fold increased risk for SB within this specific ethnic group (OR = 4.7 [1.1-19.8], p = 0.04). CONCLUSIONS: This study is the first to evaluate how TS polymorphisms contribute to the risk of SB. The current findings indicate that polymorphisms in the untranslated regions of the TS gene are associated with 4-fold or more increased risks of SB in non-Hispanic whites, but not in Hispanic whites, African-Americans, or Asian-Americans.

3' Untranslated Regions↗