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Article Abstract
Background: Cholangiocarcinoma (CCA) is an intractable cancer, and its incidence in northeastern Thailand is the highest worldwide. Infection with the liver fluke (OV) has been associated with CCA risk. However, animal experiments have suggested that OV alone does not induce CCA, but its combination with a chemical carcinogen like nitrosamine can cause experimentally induced CCA in hamsters. Therefore, in humans, other environmental and genetic factors may also be involved.
Aim: To examine relations between risk for CCA and genetic polymorphisms in carcinogen-metabolizing and inflammation-related genes.
Methods: This hospital-based case-control study enrolled 95 case-control pairs matched by age (± 5 years) and sex. We examined relations between risk for CCA and genetic polymorphisms in carcinogen-metabolizing and inflammation-related genes, serum anti-OV, alcohol consumption, and smoking. Polymorphisms of , (-174 and -634), (-819), and (-94) and their co-occurrence with polymorphisms in the drug-metabolizing enzyme gene or were also analyzed.
Results: Although CCA risk was not significantly associated with any single polymorphism, persons with the wild-type and c1/c2 + c2/c2 genotype had an increased risk (OR = 3.33, 95%CI: 1.23-9.00) as compared with persons having the wild-type and c1/c1 wild genotype. The presence of anti-OV in serum was associated with a 7- to 11-fold increased risk, and smoking level was related to an OR of 1.5-1.8 in multivariable analyses adjusted for each of the seven genetic polymorphisms.
Conclusion: In addition to infection with OV, gene-gene interactions may be considered as one of the risk factors for CCA development.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10074948 | PMC |
| http://dx.doi.org/10.4291/wjgp.v14.i2.21 | DOI Listing |
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