Xueren Gao

Institute of Forensic Science under the Ministry of Justice P.R. China, Shanghai, Shanghai Shi, China

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Publications (11)25.07 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Growing evidence has indicated that lysyl oxidase (LOX) G473A polymorphism (rs1800449) is associated with cancer risk among Asians. However, results of single center and small sample study lack enough power. We first investigated the effect of LOX G473A polymorphism on cancer risk among Asians by a meta-analysis, and then further validated this association by a case-control study of colorectal cancer (CRC) with LOX G473A polymorphism in a Chinese population. STATA 12.0 software was used for the meta-analysis. The relationships were evaluated by calculating the pooled odds ratios (ORs) and their 95 % confidence intervals (CIs). In a case-control study comprising 577 CRC patients and 696 controls, LOX G473A polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Logistic regression was used to evaluate genetic associations with the occurrence of CRC. The results of our meta-analysis, including seven case-control studies with a total of 2,377 cancer patients and 2,499 controls, suggested that LOX G473A polymorphism might be associated with an increased risk of cancer among Asians. In addition, results of a case-control study indicated that individuals with the AA or AG genotype had a significantly increased susceptibility to CRC occurrence, compared with individuals who had GG genotype. Overall, this meta-analysis and case-control study of CRC observed convincing association of LOX G473A polymorphism with cancer risk in Asians; our study would contribute to complete elucidation of carcinogenesis.
    Molecular genetics and genomics : MGG. 08/2014;
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    ABSTRACT: Many studies have examined the association between CD28 T > C polymorphism (rs3116496) and cancer risk in various populations. However, results remained controversial. To assess this relationship more precisely, a meta-analysis was performed. A comprehensive literature search was performed using the PubMed database for relevant articles published (updated to January 1, 2014). Odds ratios (ORs) and 95 % confidence intervals (CIs) were used to assess the strength of the association. A total of nine studies were selected for this meta-analysis, including 3,878 cases and 4,424 controls. The results indicated that CD28 T > C polymorphism (rs3116496) was not associated with the risk of cancer in overall population (CC + CT vs. TT, OR = 1.17, 95 %CI = 0.94-1.47, P H = 0.00; CC vs. CT + TT, OR = 1.26, 95 %CI = 0.92-1.73, P H = 0.86; CC vs. TT, OR = 1.27, 95 %CI = 0.92-1.74, P H = 0.85; CT vs. TT, OR = 1.15, 95 %CI = 0.91-1.46, P H = 0.00; and C vs. T, OR = 1.17, 95 %CI = 0.97-1.41, P H = 0.00). In subgroup analysis according to cancer type, no significant association was found in cervical cancer or other cancer. However, in the subgroup analysis by ethnicity, the significant risk was found among Asians (CC + CT vs. TT, OR = 1.51, 95 %CI = 1.24-1.83, P H = 0.05; C vs. T, OR = 1.46, 95 %CI = 1.22-1.74, P H = 0.11), but not among Caucasians. The result of this meta-analysis suggested that CD28 T > C polymorphism (rs3116496) may have an increased risk of cancer in Asians.
    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 06/2014;
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    ABSTRACT: Associations between cytotoxic T lymphocyte antigen-4 (CTLA-4) +49A/G polymorphism and cancer risk are inconclusive. We performed this meta-analysis to derive a more precise estimation of the relationship.
    Cancer biomarkers: section A of Disease markers 01/2014; 14(4):287-94. · 0.97 Impact Factor
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    ABSTRACT: BRM (Brahma homologue) is well known for its critical role in tumor suppression and cancer development. Genetic variations in the promoter region of BRM have been suggested to be associated with loss of BRM expression and lung cancer risk. To the authors' knowledge, no study on the role of BRM genetic polymorphisms in hepatocellular carcinoma (HCC) risk has been performed. In two independent case-control studies containing 796 HCC cases and 806 cancer-free individuals, we genotyped two putative functional insertion/deletion (indel) polymorphisms [BRM-1321 (rs3832613) and BRM-741 (rs34480940)] within promoter region of BRM in Chinese populations using a PCR-based method. Real-time RT-PCR analysis was used to explore the genotype-phenotype correlation between these polymorphisms and BRM expression in both tissue samples and HCC cell lines. Logistic regression analysis showed that compared to BRM-1321del/del genotype, the ins/del and ins/ins variant genotypes had an increased HCC risk [adjusted odds ratio (OR) = 1.47, 95% confidence interval (CI) = 1.19-1.82; adjusted OR = 2.55, 95% CI = 1.75-3.72, respectively]. No significant association between BRM-741 and HCC incidence was observed. However, stratification analysis revealed a significant association between ins/ins genotype of BRM-741 and increased HCC susceptibility in smokers (adjusted OR = 2.07, 95% CI = 1.33-3.22). Quantitative PCR analyses demonstrated that the genotypes of BRM-1321 and the corresponding haplotypes were significantly correlated with BRM expression in vivo. Compared with ins/ins genotype, subjects carrying ins/del and del/del genotype had 2.30 and 4.99 fold higher BRM expression in HCC tissue samples, respectively. Similar trends were observed in western blot analysis at protein level. Our findings suggest that BRM promoter polymorphism (BRM-1321) could regulate BRM expression and may serve as a potential marker for genetic susceptibility to HCC.
    PLoS ONE 01/2013; 8(1):e55169. · 3.73 Impact Factor
  • Xueren Gao, Haixia Duan, Zhansheng Zhu
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    ABSTRACT: PTEN, a candidate tumor suppressor gene, has been identified within chromosome 10q23 and plays an important role in tumorigenesis. The association between the IVS4 insertion/deletion (I/D) polymorphism of PTEN and cancer risk in several populations has been studied, but results are conflicting. The aim of the present study was to investigate association of PTEN IVS4 polymorphism with cancer risk by conducting a meta-analysis. A literature search was conducted through PubMed, Chinese National Knowledge Infrastructure (CNKI) and WanFang databases (up to October 18, 2013). Six eligible studies with 2,179 cases and 3,132 controls were enrolled in the meta-analysis. The pooled odds ratio (OR) and 95% confidence intervals (CI) were used to assess the strength of association. Our results indicated that the~polymorphism conferred a significantly decreased risk of overall cancer (dominant model: OR=0.87, 95% CI 0.77-0.99; recessive model: OR=0.83, 95% CI: 0.72-0.96; II vs. DD model: OR=0.79, 95% CI: 0.67-0.94; I vs. D model: OR=0.89, 95% CI: 0.82-0.97). Subgroup analysis by cancer type and ethnicity furtherly showed that PTEN gene IVS4 polymorphism was associated with decreased risk of digestive cancers (recessive model: OR=0.77, 95% CI: 0.64-0.92; II vs. DD model: OR=0.72, 95% CI: 0.58-0.91; I vs. D model: OR=0.84, 95% CI: 0.76-0.94), this strong association with reduced risk of cancer was also found in Asian population (recessive model: OR=0.83, 95% CI: 0.71-0.98; II vs. DD model: OR=0.79, 95% CI: 0.65-0.96; I vs. D model: OR=0.89, 95% CI: 0.81-0.98). In conclusion, our meta-analysis suggested that PTEN IVS4 polymorphism might play a protective role in the development of cancer, further independent confirmation of associations observed in PTEN IVS4 polymorphism by more studies was necessary.
    Cancer biomarkers: section A of Disease markers 01/2013; 13(6):465-70. · 0.97 Impact Factor
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    ABSTRACT: The Prolyl hydroxylase 1 (EGLN2) is known to affect tumorigenesis by regulating the degradation of hypoxia-inducible factor (HIF). Polymorphisms in EGLN2 may facilitate cancer cell survival under hypoxic conditions and directly associate with cancer susceptibility. Here, we examined the contribution of a 4-bp insertion/deletion polymorphism (rs10680577) within the distal promoter of EGLN2 to the risk of hepatocelluar carcinoma (HCC) in Chinese populations. The contribution of rs10680577 to HCC risk was investigated in 623 HCC cases and 1242 controls and replicated in an independent case-control study consisting of 444 HCC cases and 450 controls. Logistic regression analysis showed that the deletion allele of rs10680577 was significantly associated with increased risk for HCC occurrence in both case-control studies (OR=1.40; 95%C.I.=1.18-1.66, P<0.0001; OR=1.49; 95%C.I.=1.18-1.88, P=0.0007). Such positive association was more pronounced in current smokers (OR=3.49, 95%C.I.=2.24-5.45) than non-smokers (OR=1.24, 95%C.I.=1.03-1.50) (heterogeneity P=0.0002). Genotype-phenotype correlation studies demonstrated that the deletion allele was significantly correlated with higher expression of both EGLN2 and RERT-lncRNA (a long non-coding RNA whose sequence overlaps with Ras-related GTP-binding protein 4b (RAB4B) and EGLN2) in vivo and in vitro. Furthermore, RERT-lncRNA expression was also significantly correlated with EGLN2 expression in vivo, consistent with in vitro gain-of-function study that showed overexpressing RERT-lncRNA up-regulated EGLN2. Finally, in-silico prediction suggested that the insertion allele could disrupt the structure of RERT-lncRNA. Taken together, our findings provided strong evidence for the hypothesis that rs10680577 contributes to hepatocarcinogenesis, possibly by affecting RERT-lncRNA structure and subsequently EGLN2 expression, making it a promising biomarker for early diagnosis of HCC.
    Cancer Research 10/2012; · 9.28 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) represents the most common primary malignancy of the liver with a worldwide increasing incidence. Although the risk factors for HCC are well characterized, the molecular mechanisms responsible for malignant transformation of hepatocytes are not well understood. In this study, a case-control study including 291 HCC patients and 294 healthy controls was conducted to investigate the association between HCC susceptibility and with a 4-bp insertion/deletion polymorphism (rs66465034) in the proximal promoter of CD3G. Logistic regression analysis showed that the heterozygote and the homozygote 4-bp ins/ins confer a significantly increased risk of HCC after controlling for other covariates (adjusted odds ratio [OR]=1.51, 95% confidence interval [C.I.] 1.01-2.27, p=0.040; OR=1.71, 95% C.I. 1.07-2.89, p=0.025, respectively). Carriage of the 4-bp insertion allele was associated with a greatly increased risk of developing the disease (OR=1.30, 95% C.I. 1.02-1.64, p=0.027). Moreover, hepatitis B virus (HBV) stratification analysis showed that the differences between cases and controls were more obvious in HBV-positive than in the HBV-negative population, suggesting a possible role of this polymorphism in the immune regulation during HBV infection. Further, luciferase-based transient transfection assays revealed that rs66465034 can affect promoter activity of CD3G, indicating its possible functional significance. Our data suggested that common genetic polymorphisms in CD3G may influence HCC risk in Chinese population. Considering the relative small sample size, replication in other populations with larger sample size and further functional analysis are required for fully understanding the roles of CD3G polymorphisms in predisposition for HCC.
    DNA and cell biology 06/2012; 31(9):1480-5. · 2.28 Impact Factor
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    ABSTRACT: The pathogenesis of HCC is a multistage process with the involvement of genetic factors. The aim of the present study is to investigate the possible association between a 40-bp insertion/deletion polymorphism (indel) at constitutive promoter of MDM2 and risk of hepatocellular carcinoma (HCC) in a Chinese population. Using 420 HCC patients and 423 control subjects, we genotyped the indel polymorphism (rs3730485) using polymerase chain reaction method. Logistic regression was used to analyze the association between the polymorphism and HCC susceptibility. Under co-dominant model, we found that the ins/del and del/del genotype of indel was associated with a significantly increased risk of HCC compared with its homozygote ins/ins (OR=1.39, 95%C.I.=1.03-1.87; OR=1.68, 95%C.I.=1.03-2.73, respectively). Presence of 40-bp deletion allele of MDM2 seemed to confer higher risk for HCC when compared with non-carriers (OR=1.30, 95%C.I.=1.06-1.60, P=0.011). Further stratification analysis showed that this association was more pronounced in patients with a family history of HCC, early tumor stage and higher serum alpha-fetoprotein (AFP). These findings indicated that the MDM2 indel polymorphism may be a genetic modifier for developing HCC in Chinese population.
    Gene 04/2012; 497(1):66-70. · 2.20 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. Although molecular biology of carcinogenesis and tumor progression of HCC has been increasingly understood with intense research in recent years, the molecular and cellular mechanisms of HCC pathogenesis are still poorly understood. In the present study, a case-control study including 390 HCC patients and 431 healthy controls was conducted to investigate the association of HCC susceptibility with the mitochondrial DNA (mtDNA) 9-bp deletion polymorphism in Chinese population. Chi-square testing showed that frequencies of 9-bp one repeat or two repeats were significantly different between HCC and control groups. Carriage of 9-bp one repeat fragment was associated with a significantly increased risk of developing HCC (odds ratio=1.48, 95% confidence interval: 1.03-2.14, p=0.027). Stratification analysis further showed that the differences between cases and controls were more obvious in drinkers than nondrinkers. Computational modeling of the 9-bp deletion polymorphism suggests that the mtDNA sequence without the 9-bp deletion polymorphism lies within a predicted binding site (seed region) for hsa-miR-519c-5p and hsa-miR-526a. Our data suggested that the 9-bp deletion polymorphism in mitochondria may influence HCC risk, likely through specific microRNA-mediated regulation, which was possibly involved in the pathogenesis of HCC. The replication of our studies in other populations with larger sample size is warranted.
    Genetic Testing and Molecular Biomarkers 01/2012; 16(5):330-4. · 1.44 Impact Factor
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    ABSTRACT: The 14-bp insertion/deletion (indel) polymorphism located in the 3' UTR of the human leukocyte antigen-G (HLA-G) gene plays a role in several autoimmune and chronic inflammatory diseases. HLA-G expression is associated with hepatocellular carcinoma (HCC) prognosis, especially in early stage, with high expression independently associated with shortened overall survival and increased tumor recurrence. In the present study, we carried out a case-control study in a Chinese population (318 cases and 599 controls) to estimate the susceptibility to HCC associated with the 14-bp indel polymorphism. Logistic regression analysis showed that the heterozygote and the homozygote 14-bp ins/ins confer a lower risk of HCC (adjusted OR = 0.75, 95% CI: 0.57-1.01, p = 0.061; OR = 0.54, 95% CI: 0.30-0.98, p = 0.031, respectively). Hepatitis B virus (HBV) stratification analysis showed that the associations were stronger in the HBV-positive population. Immunohistochemical analysis further showed that HLA-G expression in HCC tissues with 14-bp del/del genotype was more prominent than for heterozygous and 14-bp ins/ins genotype (p < 0.01). Taken together, our results suggested that the HLA-G 14-bp indel polymorphism may be a marker for genetic susceptibility to HCC in Chinese populations. Further studies from different populations with larger sample size are warranted to validate our findings.
    DNA and cell biology 05/2011; 30(12):1027-32. · 2.28 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most common and severe diseases in the world. Besides the influence of environmental factors, such as viral infection, an increasing number of novel genetic components identified by genome-wide association studies have been associated with predisposition to HCC. Thus, studies focusing on functional variants in these findings are indispensable. In the present study, based on in-silico analysis, we carried out a case-control study in a Chinese population (207 cases and 245 controls) to investigate the association between HCC susceptibility with a 7 base pair (bp) insertion/deletion polymorphism (rs3917) in the 3'UTR of COL1A2. Our results showed that the ins/del + del/del genotype had an odds ratio of 1.76 (95% C.I.=1.03-3.01; P=0.028) for developing HCC compared to the ins/ins genotype. Carriers for the "del" allele of rs3917 were associated with a 1.73-fold increased risk for HCC (95% C.I.=1.06-2.84; P(trend)=0.02). Computational modeling suggests that this polymorphism is located in the hsa-let-7 g potential target sequence in the COL1A2 3' untranslated region. Our data suggest that most likely, common genetic changes in COL1A2 may influence HCC risk, at least in part by let-7 g-mediated regulation, which is possibly involved in the pathogenesis of HCC. The replication of our studies in other populations will further strengthen our understanding of this association.
    Cancer Genetics 05/2011; 204(5):265-9. · 1.92 Impact Factor

Publication Stats

35 Citations
25.07 Total Impact Points

Institutions

  • 2011
    • Institute of Forensic Science under the Ministry of Justice P.R. China
      Shanghai, Shanghai Shi, China
    • Soochow University (PRC)
      • Department of Chinese Medicine
      Wu-hsien, Jiangsu Sheng, China