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  • 1
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    Online Resource
    Genetic variation in the PNPLA3 gene and hepatocellular carcinoma in USA: Risk and prognosis prediction
    Wiley ; 2013
    In:  Molecular Carcinogenesis Vol. 52, No. S1 ( 2013-11), p. 139-147
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 52, No. S1 ( 2013-11), p. 139-147
    Abstract: Nonalcoholic fatty liver disease (NAFLD) is an emerging epidemic with high prevalence in Western countries. Genome‐wide association studies had reported that a variation in the patatin‐like phospholipase domain containing 3 ( PNPLA3 ) gene is associated with high susceptibility to NAFLD. However, the relationship between this variation and hepatocellular carcinoma (HCC) has not been well established. We investigated the impact of PNPLA3 genetic variation (rs738409: C 〉 G) on HCC risk and prognosis in the United States by conducting a case−control study that included 257 newly diagnosed and pathologically confirmed Caucasian patients with HCC (cases) and 494 healthy controls. Multivariate logistics and Cox regression models were used to control for the confounding effects of HCC risk and prognostic factors. We observed higher risk of HCC for subjects with a homozygous GG genotype than for those with CC or CG genotypes, the adjusted odds ratio (OR) was 3.21 (95% confidence interval [CI], 1.68–6.41). We observed risk modification among individuals with diabetes mellitus (OR = 19.11; 95% CI, 5.13–71.20). The PNPLA3 GG genotype was significantly associated with underlying cirrhosis in HCC patients (OR = 2.48; 95% CI, 1.05–5.87). Moreover, GG allele represents an independent risk factor for death. The adjusted hazard ratio of the GG genotype was 2.11 (95% CI, 1.26–3.52) compared with CC and CG genotypes. PNPLA3 genetic variation (rs738409: C 〉 G) may determine individual susceptibility to HCC development and poor prognosis. Further experimental investigations are necessary for thorough assessment of the hepatocarcinogenic role of PNPLA3 . © 2013 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v52.S1
    DOI: 10.1002/mc.22057
    Language: English
    Publisher: Wiley
    Publication Date: 2013
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  • 2
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    Association between hypothyroidism and hepatocellular carcinoma: A case-control study in the United States
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Hepatology Vol. 49, No. 5 ( 2009-05), p. 1563-1570
    Details
    In: Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 49, No. 5 ( 2009-05), p. 1563-1570
    Type of Medium: Online Resource
    ISSN: 0270-9139
    URL: Article
    DOI: 10.1002/hep.22793
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 1472120-X
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  • 3
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    Association Between Hepatitis B Virus and Pancreatic Cancer
    American Society of Clinical Oncology (ASCO) ; 2008
    In:  Journal of Clinical Oncology Vol. 26, No. 28 ( 2008-10-01), p. 4557-4562
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 26, No. 28 ( 2008-10-01), p. 4557-4562
    Abstract: Hepatitis B virus (HBV) and hepatitis C virus (HCV) are considered to be hepatotropic and are a major cause of hepatocellular carcinoma. However, little is known about the role of HBV and HCV infection in other malignancies. This study aimed to determine whether HBV and HCV infections increase the risk for pancreatic cancer development. Patients and Methods At The University of Texas M. D. Anderson Cancer Center, Houston, TX, we recruited 476 patients with pathologically confirmed adenocarcinoma of the pancreas and 879 age-, sex-, and race-matched healthy controls. Blood samples were tested for the presence of HCV antibodies (anti-HCV), HBV surface antigen (HBsAg), antibodies against HBV core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). The positive samples were retested by two confirmatory tests. An unconditional multivariable logistic regression analysis was used to estimate adjusted odds ratios (AORs). Results Anti-HCV was positive in seven cases (1.5%) and nine controls (1%). Anti-HBc was positive in 36 cases (7.6%) and 28 controls (3.2%). The estimated AORs and 95% CIs were as follows: anti-HCV–positive, 0.9 (95% CI, 0.3 to 2.8), anti-HBc–positive, 2.5 (95% CI, 1.5 to 4.2), anti-HBc–positive/anti-HBs–positive, 2.3 (95% CI, 1.2 to 4.2), and anti-HBc–positive/anti-HBs–negative, 4 (95% CI, 1.4 to 11.1). Risk modification by past exposure to HBV was observed among diabetics (AOR, 7.1; 95% CI, 1.7 to 28.7). Conclusion Past exposure to HBV may be associated with pancreatic cancer development. Should such findings be confirmed by other studies, it may offer important insights into the etiology of pancreatic cancer and may suggest the need to consider prevention of HBV reactivation among patients with HBV-related pancreatic cancer during chemotherapy.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2008.17.3526
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2008
    detail.hit.zdb_id: 2005181-5
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  • 4
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    Prognostic effect of angiotensin-converting-enzyme inhibitors (ACEI) and diuretics in patients with pancreatic cancer.
    American Society of Clinical Oncology (ASCO) ; 2016
    In:  Journal of Clinical Oncology Vol. 34, No. 4_suppl ( 2016-02-01), p. 420-420
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 34, No. 4_suppl ( 2016-02-01), p. 420-420
    Abstract: 420 Background: Prior history of chronic medical conditions and medical treatment exposure has been significantly associated with the development and prognosis of different cancers. Population-based studies reported a reduced cancer-related mortality among patients with pancreatic cancer who were Statin or Metformin users as compared with non-users. We aimed to study the effect of antihypertensive medications on the survival outcome of pancreatic cancer. Methods: Under institutional ethical approval, medical records were reviewed and clinical characteristics at baseline (time of diagnosis) were retrieved. Blood pressure and antihypertensive medications use were documented including Angiotensin Converting Enzyme Inhibitor (ACEI), diuretics, Angiotensin Receptor Blockers (ARBs) and Beta-Blockers (BB). Hazard ratios (HRs) and 95% CIs were calculated by using Cox proportional hazard models with a backward stepwise selection procedure to identify independent prognostic factors for overall survival. Results: A total of 1,204 patients with adenocarcinoma of the pancreas were diagnosed at MD Anderson Cancer center between 1999 and 2009 were identified. The mean age value (± SD) is 61.9± 10 where 58.6% (N=705) were men and 87.5% (N=1,054) were white. The majority of patients were Caucasian (87%). 41.9% had metastatic disease. A total of 639 (53%) patients had chemotherapy with or without radiation. ACEI and diuretics use independently reduced all-cause mortality, ACEI by 24% with HR 0.76 (CI 0.63-0.91), and diuretics by 26% with HR 0.73 (CI 0.60- 0.89). Neither ARBs nor beta blockers use was statistically significant in reducing all-cause mortality (HR.80, CI 0.63 -1.0), BB HR 0.85 (CI 0.7-1.0). Conclusions: Our findings indicate a significant impact of anti-hypertensive medications including ACEI and diuretics on pancreatic cancer outcomes with improved survival in users versus non-users, this effect was independent of the cancer treatment received, tumour histology and site of metastasis. The potential antitumor activities of these agents in pancreatic cancer should be studied further.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2016.34.4_suppl.420
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2016
    detail.hit.zdb_id: 2005181-5
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  • 5
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    Pancreatic injury, genetic variation of PNPLA3 , and risk of pancreatic cancer.
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 4_suppl ( 2013-02-01), p. 141-141
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 4_suppl ( 2013-02-01), p. 141-141
    Abstract: 141 Background: Similar to primary liver cancer, obesity, diabetes mellitus and hepatitis B virus infection have been associated with increased risk of pancreatic cancer (PC) development. A genome-wide association study has reported that a polymorphic variant of the patatin-like phospholipase domain containing 3 (PNPLA3) gene was associated with a higher susceptibility to fatty liver and liver cancer. The relationship between this variation and PC has not been previously examined. We investigated the correlation in the degree of organ damage between the liver and the pancreas in patients with PC. In addition, we examined the effect of PNPLA3genetic variation (rs738409: C 〉 G) on PC development. Methods: Using resources of our case-control study in MD Anderson Cancer Center, we analyzed 544 pathologically confirmed PC patients and 498 healthy controls. Cases and controls were frequency matched by age, gender, and race. Multivariate logistic regression analysis was performed to adjust for the confounding factors. Medical records of PC patients were reviewed for pancreatic and liver fatty changes. Results: We found that 18.8% of PC patients had evidence of pancreatic steatosis, fibrosis, or pancreatitis. Fatty liver was observed in 14.5% of PC patients which was frequently detected in patients with pancreatitis (p=0.002). A significant correlation between pancreatitis and cirrhosis was observed in PC patients with a prior history of obesity but not in patients without a history of obesity (p=0.001). On the other hand, we observed no significant association between PNPLA3 genotype and risk of PC. The adjusted odds ratio (OR) was 1.4 (95% confidence interval [CI], 0.7-2.7) for the homozygous variant GG genotype compared with the CC/CG genotypes. Conclusions: We concluded that despite the similarities between the liver and the pancreas, genetic susceptibility to fatty infiltration and its effect on cancer development may differ between the two organs. Evaluation and assessment of nonalcoholic fatty pancreatic disease (NAFPD) in PC patients and genetic susceptibility of NAFPD may be warranted in future research.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2013.31.4_suppl.141
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
    detail.hit.zdb_id: 2005181-5
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  • 6
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    Obesity Early in Adulthood Increases Risk but Does Not Affect Outcomes of Hepatocellular Carcinoma
    Elsevier BV ; 2015
    In:  Gastroenterology Vol. 149, No. 1 ( 2015-07), p. 119-129
    Details
    In: Gastroenterology, Elsevier BV, Vol. 149, No. 1 ( 2015-07), p. 119-129
    Type of Medium: Online Resource
    ISSN: 0016-5085
    URL: Article
    DOI: 10.1053/j.gastro.2015.03.044
    RVK:
    XA 44500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
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  • 7
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    Reply to passive smoking and the use of noncigarette tobacco products in association with risk for pancreatic cancer : A case-control study
    Wiley ; 2008
    In:  Cancer Vol. 112, No. 3 ( 2008-02-01), p. 672-673
    Details
    In: Cancer, Wiley, Vol. 112, No. 3 ( 2008-02-01), p. 672-673
    Type of Medium: Online Resource
    ISSN: 0008-543X , 1097-0142
    URL: Issue
    URL: Journal
    URL: Article
    DOI: 10.1002/cncr.v112:3
    DOI: 10.1002/(ISSN)1097-0142
    DOI: 10.1002/cncr.23198
    Language: English
    Publisher: Wiley
    Publication Date: 2008
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    detail.hit.zdb_id: 2599218-1
    detail.hit.zdb_id: 2594979-2
    detail.hit.zdb_id: 1429-1
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  • 8
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    Significant Effect of Homologous Recombination DNA Repair Gene Polymorphisms on Pancreatic Cancer Survival
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Research Vol. 66, No. 6 ( 2006-03-15), p. 3323-3330
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 6 ( 2006-03-15), p. 3323-3330
    Abstract: Genetic variation in DNA repair may affect the clinical response to cytotoxic therapies. We investigated the effect of six single nucleotide polymorphisms of the RecQ1, RAD54L, XRCC2, and XRCC3 genes on overall survival of 378 patients with pancreatic adenocarcinoma who were treated at University of Texas M.D. Anderson Cancer Center during February 1999 to October 2004 and were followed up to October 2005. Genotypes were determined using the MassCode method. Survival was determined from pathologic diagnosis to death. Patients who were alive at the last follow-up evaluation were censored at that time. Kaplan-Meier plot, log-rank test, and Cox regression were used to compare overall survival by genotypes. A significant effect on survival of all patients was observed for RecQ1 and RAD54L genes. The median survival time was 19.2, 14.7, and 13.2 months for the RecQ1 159 AA, AC, and CC genotypes, and 16.4, 13.3, and 10.3 months for RAD54L 157 CC, CT, and TT genotypes, respectively. A significantly reduced survival was associated with the variant alleles of XRCC2 R188H and XRCC3 A17893G in subgroup analysis. When the four genes were analyzed in combination, an increasing number of adverse alleles were associated with a significantly decreased survival. Subgroup analyses have shown that the genotype effect on survival was present among patients without metastatic disease or among patients who receive radiotherapy. These observations suggest that polymorphisms of genes involved in the repair of DNA double-strand breaks significantly affect the clinical outcome of patients with pancreatic cancer. (Cancer Res 2006; 66(6): 3323-30)
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-05-3032
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Analysis of Heritability and Genetic Architecture of Pancreatic Cancer: A PanC4 Study
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 28, No. 7 ( 2019-07-01), p. 1238-1245
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 28, No. 7 ( 2019-07-01), p. 1238-1245
    Abstract: Pancreatic cancer is the fourth-leading cause of cancer death in both men and women in the United States. The currently identified common susceptibility loci account for a small fraction of estimated heritability. We sought to estimate overall heritability of pancreatic cancer and partition the heritability by variant frequencies and functional annotations. Methods: Analysis using the genome-based restricted maximum likelihood method (GREML) was conducted on Pancreatic Cancer Case-Control Consortium (PanC4) genome-wide association study (GWAS) data from 3,568 pancreatic cancer cases and 3,363 controls of European Ancestry. Results: Applying linkage disequilibrium- and minor allele frequency-stratified GREML (GREML-LDMS) method to imputed GWAS data, we estimated the overall heritability of pancreatic cancer to be 21.2% (SE = 4.8%). Across the functional groups (intronic, intergenic, coding, and regulatory variants), intronic variants account for most of the estimated heritability (12.4%). Previously identified GWAS loci explained 4.1% of the total phenotypic variation of pancreatic cancer. Mutations in hereditary pancreatic cancer susceptibility genes are present in 4% to 10% of patients with pancreatic cancer, yet our GREML-LDMS results suggested these regions explain only 0.4% of total phenotypic variance for pancreatic cancer. Conclusions: Although higher than previous studies, our estimated 21.2% overall heritability may still be downwardly biased due to the inherent limitation that the contribution of rare variants in genes with a substantive overall impact on disease are not captured when applying these commonly used methods to imputed GWAS data. Impact: Our work demonstrated the importance of rare and common variants in pancreatic cancer risk.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-18-1235
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 10
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    5,10-Methylenetetrahydrofolate Reductase Polymorphisms and the Risk of Pancreatic Cancer
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 14, No. 6 ( 2005-06-01), p. 1470-1476
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 14, No. 6 ( 2005-06-01), p. 1470-1476
    Abstract: To test the hypothesis that 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphisms modify the risk of pancreatic cancer, we conducted a hospital-based, case-control study involving 347 patients with newly diagnosed pancreatic adenocarcinoma and 348 healthy controls, frequency matched by age, sex, and race. MTHFR polymorphisms were determined using the PCR-RFLP method. Association of these polymorphisms with the risk of pancreatic cancer was estimated by unconditional logistic regression analysis. We found that the C667T (but not the A1298C) polymorphism had a significant main effect on the risk of pancreatic cancer. The frequencies of the MTHFR 667CC, 667CT, and 667TT genotypes were 49.5%, 38.6%, and 11.9%, respectively, among cases compared with 48.5%, 45.0%, and 6.5%, respectively, among controls. Individuals with the 667TT genotype displayed a 2-fold increased risk for pancreatic cancer compared with those with the CC/CT genotypes [adjusted odds ratio (OR), 2.14; 95% confidence interval (95% CI), 1.14-4.01]. Multivariate analyses found that the effect of the 677TT genotype on the risk of pancreatic cancer was present among ever smokers (OR, 5.53; 95% CI, 2.0-15.3) and ever alcohol drinkers (OR, 3.16; 95% CI, 1.30-7.69) but not in never smokers (OR, 0.82; 95% CI, 0.33-2.06) and never drinkers (OR, 1.42; 95% CI, 0.56-3.62). Furthermore, a positive interaction between the MTHFR TT genotype and heavy smoking or heavy alcohol consumption was detected. The OR (95% CI) of pancreatic cancer was 6.83 (1.91-24.38) for heavy smokers among the TT carriers compared with never smokers with the CC/CT genotypes and 4.23 (0.88-20.3) for heavy drinkers with the TT genotype compared with nondrinkers with the CC/CT genotypes. These observations support a role for folate metabolism in pancreatic cancer, especially among smokers and heavy drinkers.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-04-0894
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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