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ABSTRACT: P53 is a tumor suppressor gene and plays important role in the etiology of breast cancer. Intron 3 sixteen-bp duplication polymorphism of p53 has been reported to be associated with breast cancer risk. However, the reported results remain conflicting rather than conclusive.
A meta-analysis including 19 case-control studies was performed to address this issue. Odds ratios (ORs) with 95% confidence intervals (CIs) were adopted to evaluate the association.
THE OVERALL RESULTS SUGGESTED THAT THE VARIANT GENOTYPES WERE ASSOCIATED WITH A SIGNIFICANTLY INCREASED BREAST CANCER RISK (DEL/INS VS DEL/DEL: OR = 1.18, 95% CI: 1.00-1.40; Ins/Ins vs Del/Del: OR = 1.42, 95% CI = 1.09-1.84; Ins/Ins+Del/Ins vs Del/Del: OR = 1.21, 95% CI = 1.03-1.41). When stratifying by sample size of studies, a significantly elevated risk was also observed among large sample studies (>500 subjects) but not among small sample studies (≤500 subjects).
These results suggested that the 16-bp duplication polymorphism of p53 may contribute to susceptibility to breast cancer. Additional well-designed large studies were required to validate this association in different populations.
PLoS ONE 01/2013; 8(4):e61662. · 4.09 Impact Factor
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ABSTRACT: Genetic polymorphisms in the promoter regions of FAS, FASL and CASP8 involved in the apoptotic signaling pathway are thought to be associated with susceptibility to cancer. We hypothesized that these functional genetic variants might be associated with the risk of childhood acute lymphoblastic leukemia (ALL). A case-control study in a Chinese population with 361 cases of ALL and 519 controls was performed to evaluate the association between FAS, FASL and CASP8 variants and risk of childhood ALL. Individuals with FAS - 1377AG had an odds ratio (OR) of 0.72 for the risk of ALL compared to - 1377GG and the variant FASL - 844CC was associated with a statistically significantly decreased risk of childhood ALL (OR = 0.38). Furthermore, combined genotypes with 5-8 protective alleles were associated with a significantly decreased risk of childhood ALL compared with those with 0-4 variants, and this decreased risk was more pronounced among the subgroups of age < 6 years, female, parental never-drinking status and never house-painting. Our results provide evidence that FAS-FASL-CASP8 polymorphisms contributed to a reduced risk of childhood ALL in our population. Larger studies are warranted to validate our findings.
Leukemia & lymphoma 01/2012; 53(7):1360-6. · 2.40 Impact Factor
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ABSTRACT: Alcohol dehydrogenase 1C (ADH1C) is the key enzyme catalyze oxidation of alcohol to acetaldehyde, which plays vital roles in the etiology of various cancer. To date, studies investigated the association between a functional polymorphism in ADH1C, Ile350Val (rs698), and risk of cancer have shown inclusive results.
A meta-analysis based on 35 case-control studies was performed to address this issue. Odds ratios (OR) with 95% confidence intervals (CIs) were used to assess the association. The statistical heterogeneity across studies was examined with χ2-based Q-test.
Overall, no significant associations between ADH1C Ile350Val polymorphism and cancer risk were observed in any genetic models (P>0.05). In the stratified analyses, there was a significantly increased cancer risk among African (Val/Val vs. Ile/Ile OR = 2.19, 95% CI = 1.29-3.73, P(heterogeneity) = 0.989; Ile/Val + Val/Val vs. Ile/Ile: OR = 1.79, 95%CI = 1.18-2.71, P(heterogeneity) = 0.761; Val/Val vs. Ile/Val + Ile/Ile: OR = 1.92, 95% CI = 1.16-3.17, P(heterogeneity) = 0.981) and Asian (Ile/Val vs. Ile/Ile: OR = 1.58, 95% CI = 1.32-1.90, P(heterogeneity) = 0.375; Val/Val vs. Ile/Ile: OR = 3.84, 95% CI = 1.74-8.49, P(heterogeneity) = 0.160; Ile/Val + Val/Val vs. Ile/Ile: OR = 1.65, 95% CI = 1.38-1.96, P(heterogeneity) = 0.330; Val/Val vs. Ile/Val + Ile/Ile: OR = 3.54, 95% CI = 1.62-7.75, P(heterogeneity) = 0.154) studies.
The results indicate that ADH1C Ile350Val polymorphism may contribute to cancer risk among Africans and Asians. Additional comprehensive system analyses are required to validate this association combined with other related polymorphisms.
PLoS ONE 01/2012; 7(5):e37227. · 4.09 Impact Factor
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Lizhen Huang,
Jie Huang,
Peng Wu,
Qian Li,
Liucheng Rong, Yao Xue,
Qin Lu,
Jie Li,
Na Tong,
Meilin Wang,
Zhengdong Zhang,
Yongjun Fang
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ABSTRACT: The mammalian target of rapamycin (mTOR) is an important protein kinase regulating cell survival and apoptosis. To determine whether genetic variations in mTOR are associated with risk of acute lymphoblastic leukemia (ALL) in Chinese children, we genotyped two tag single nucleotide poymorphisms (SNPs) in mTOR (rs2536 and rs2295080) in a case-control study. We observed that the variant genotype TC of mTOR rs2536 was associated with a significantly decreased risk of childhood ALL (adjusted odds ratio [OR] = 0.67, 95% confidence interval [CI] = 0.46-0.96), and the association was more pronounced in high-risk ALL and T-phenotype ALL groups. Additionally, we found that the combined genotypes TC/CC decreased the risk of ALL only in the high-risk ALL group (adjusted OR = 0.54, 95% CI = 0.32-0.91) and T-phenotype ALL group (adjusted OR = 0.29, 95% CI = 0.10-0.84). These results suggest that the mTOR rs2536 polymorphism is involved in the susceptibility to childhood ALL in a Chinese population.
Leukemia & lymphoma 12/2011; 53(5):947-51. · 2.40 Impact Factor
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Qian Li,
Lizhen Huang,
Liucheng Rong, Yao Xue,
Qin Lu,
Yaoyao Rui,
Jie Li,
Na Tong,
Meilin Wang,
Zhengdong Zhang,
Yongjun Fang
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ABSTRACT: Oxidative DNA damage caused by reactive oxygen species can produce 8-oxoguanine (8-oxoG) in DNA, which is misread and leads to G:C→T:A transversions. This can be carcinogenic. Repair of 8-oxoG by the base excision repair pathway involves the activity of human 8-oxoG DNA glycosylase 1 (hOGG1). Accumulating evidence suggests that the hOGG1 Ser326Cys polymorphism affects the activity of hOGG1 and might serve as a genetic marker for susceptibility to several cancers. To determine whether this polymorphism is associated with risk of childhood acute lymphoblastic leukemia (ALL) in Chinese children, we genotyped the hOGG1 Ser326Cys polymorphism (rs1052133) in a case-control study including 415 cases and 511 controls. We found that there was a significant difference in the genotype distributions of the hOGG1 Ser326Cys polymorphism between cases and controls (P = 0.046), and the combined genotypes Ser/Ser and Ser/Cys were associated with a statistically significantly decreased risk of ALL (adjusted odds ratio [OR] = 0.66, 95% confidence interval [CI] = 0.49-0.88, P = 0.005). Furthermore, we found a decreased risk for high risk ALL (adjusted OR = 0.60, 95% CI = 0.40-0.88, P = 0.005), low risk ALL (adjusted OR = 0.68, 95% CI = 0.47-0.99, P = 0.042), and B-phenotype ALL (adjusted OR = 0.63, 95% CI = 0.46-0.86, P = 0.003) among children with the Ser/Ser and Ser/Cys genotypes. Our results suggest that the hOGG1 Ser326Cys polymorphism is associated with susceptibility to childhood ALL in a Chinese population.
Cancer Science 03/2011; 102(6):1123-7. · 3.33 Impact Factor
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ABSTRACT: Migration inhibitory factor (MIF) has recently been defined as a novel pro-tumorigenic factor that promotes cell proliferation, migration, and invasion. The MIF -173C allele results in increased MIF promoter activity and is associated with a higher serum MIF level. We hypothesized that this polymorphism may contribute to childhood acute lymphoblastic leukemia (ALL) susceptibility. We genotyped the MIF -173G/C polymorphism (rs755622) in 346 ALL cases and 516 cancer-free controls in a Chinese population and found that the variant genotype GC and the combined genotypes GC/CC were associated with a significantly higher risk of childhood ALL [adjusted odds ratio (OR)=1.39, 95% confidence interval (CI)=1.01-1.93 for GC and adjusted OR=1.38, 95% CI=1.01-1.89 for GC/CC]. In addition, we found that the increased risk was more pronounced among high-risk ALL and B-phenotype ALL patients. Our results suggest that the MIF -173G/C polymorphism is involved in the etiology of childhood ALL and is a potential candidate gene for determining cancer susceptibility. Further validations in other populations are warranted.
Leukemia research 05/2010; 34(10):1282-6. · 2.36 Impact Factor
