Genetic susceptibility in pancreatic ductal adenocarcinoma

Lochan, Rajiv; Daly, Ann K.; Reeves, Helen L.; Charnley, Richard

doi:10.1002/bjs.6049

Cited by 18 publications

(7 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…No association between the risk of AP and family history was detected in this study (Table 1). It is indicated that smoking status, duration and intensity were risk factors for AP by the researchers [25–27]. We found that there was a weak association between cigarette smoking and development of AP in the study population (OR = 1.59; 95% CI: 0.89−2.84; P = .075) (Table 1).…”

Section: Discussionmentioning

confidence: 69%

Polymorphisms in Tumour Necrosis Factor Alpha (TNFα) Gene in Patients with Acute Pancreatitis

Özhan

Yanar

Ertekın

et al. 2010

Mediators of Inflammation

View full text Add to dashboard Cite

Proinflammatory cytokines, such as tumour necrosis factor α (TNFα), play fundamental roles in the pathogenesis of acute pancreatitis (AP). The aim of this study was to determine if polymorphisms in the TNFα gene are associated with AP. Two polymorphisms located in the promoter region (positions −308 and −238) in TNFα gene were determined using polymerase chain reaction- (PCR-) restriction fragment length polymorphism (RFLP) methods in 103 patients with AP and 92 healthy controls. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using logistic regression analysis adjusted for age, sex, BMI and smoking. The frequencies of TNFα polymorphisms were both similar in patients with mild or severe pancreatitis, so were in pancreatitis patients and in controls. We suggest that both SNPs of TNFα are not genetic risk factor for AP susceptibility (OR = 1.63; 95% CI: 1.13−4.01 for TNFα −308 and OR = 0.86; 95% CI: 0.75−1.77 for TNFα −238).

show abstract

Section: Discussionmentioning

confidence: 69%

Polymorphisms in Tumour Necrosis Factor Alpha (TNFα) Gene in Patients with Acute Pancreatitis

Özhan

Yanar

Ertekın

et al. 2010

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…This interindividual genetic variation modulates risk for malignancy [15] and identification of these genetic differences forms the basis of risk stratification thereby enabling targeted prevention or earlier diagnosis [16, 17]. This is especially pertinent to pancreatic cancer, as it has a particularly poor prognosis and palliation of symptoms is the most common therapy patients receive—mainly because of late diagnosis although there are other biological factors that play a role.…”

Section: Introductionmentioning

confidence: 99%

Family History of Cancer and Tobacco Exposure in Index Cases of Pancreatic Ductal Adenocarcinoma

Lochan

Daly

Reeves

et al. 2011

Journal of Oncology

View full text Add to dashboard Cite

Aim. To examine interaction between history of cancer in first-degree relatives and tobacco smoking in index patients of pancreatic adenocarcinoma. Methods. We carried out a case-control involving 113 patients with pancreatic adenocarcinoma and 110 controls over a 12-month period at the Freeman Hospital, Newcastle upon Tyne, UK. They were all administered a detailed tobacco exposure questionnaire and a family history questionnaire. We calculated cumulative tobacco exposure and risk for pancreas cancer. Results. Both smokers (OR 3.01 (95% CI: 1.73 to 5.24)) and those with a family history of malignancy (OR 1.98 (95% CI: 1.15–3.38)) were more likely to develop pancreatic cancer. Having more than one first-degree relative with cancer did not significantly further increase the risk of pancreatic cancer. Amongst pancreatic cancer cases, cumulative tobacco exposure was significantly decreased (P = .032) in the group of smokers (current and ex-smokers) who had a family history of malignancy [mean (SD): 30.00 (24.77) pack-years versus 44.69 (28.47) pack-years with no such history]. Conclusions. Individuals with a family history of malignancy are at an increased risk of pancreatic cancer. Furthermore, individuals with a family history of malignancy and who smoke appear to require a lesser degree of tobacco exposure for the development of pancreatic cancer.

show abstract

“…For the nonfamilial (sporadic) pancreatic cancer, a few low penetrance genes have been identified by genome-wide association studies (GWAS). Pancreatic cancer candidate genes have also been reported from studies that examined the biological pathways known to be important in the development of pancreatic cancer, for example, tobacco metabolism, DNA repair, inflammation, and folate metabolism [19, 20]. …”

Section: Discussionmentioning

confidence: 99%

ATP-Binding Cassette Genes Genotype and Expression: A Potential Association with Pancreatic Cancer Development and Chemoresistance?

Pang

Word

et al. 2014

Gastroenterology Research and Practice

View full text Add to dashboard Cite

Genetic polymorphisms in ABC (ATP-binding cassette) transporter genes are associated with differential responses to chemotherapy in various cancers including pancreatic cancer. In this study, four SNPs in the ABCB1, ABCC1, and ABCG2 genes were investigated in normal and pancreatic cancerous specimens. The expression of the three transporters was also analyzed. The TT genotypes of G2677T and C3435T in ABCB1 gene were associated with lower risk of developing pancreatic cancer (P = 0.013, OR = 0.35 and P = 0.015, OR = 0.29, resp.). To our knowledge, this is the first report of the common polymorphisms in the ABCB1 gene affecting the genetic risk of developing pancreatic cancer. Moreover, the expression of ABCB1 in 2677TT and 3435TT carriers was lower compared to the wild-type homozygotes and heterozygotes. A cell viability assay, using standard pancreatic cancer cell lines, revealed that the ABCB1 2677TT-3455TT haplotype was more sensitive than the other haplotypes to gemcitabine. Conclusion. Polymorphisms in ABCB1 G2677T and G3435T were associated with differential susceptibility to pancreatic cancer and may predict responses to chemotherapy.

show abstract

Genetic susceptibility in pancreatic ductal adenocarcinoma

Abstract: There is great scope for further investigation of critical pathways and unidentified genetic influences may be revealed. This may eventually allow the identification of individuals at high risk who might be targeted for screening.

Cited by 18 publications

References 78 publications

Polymorphisms in Tumour Necrosis Factor Alpha (TNFα) Gene in Patients with Acute Pancreatitis

Polymorphisms in Tumour Necrosis Factor Alpha (TNFα) Gene in Patients with Acute Pancreatitis

Family History of Cancer and Tobacco Exposure in Index Cases of Pancreatic Ductal Adenocarcinoma

ATP-Binding Cassette Genes Genotype and Expression: A Potential Association with Pancreatic Cancer Development and Chemoresistance?

Contact Info

Product

Resources

About