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Article: Functional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung cancer

TitleFunctional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung cancer
Authors
Issue Date2005
PublisherB M J Publishing Group. The Journal's web site is located at http://jmg.bmjjournals.com/
Citation
Journal of Medical Genetics, 2005, v. 42 n. 6, p. 479-484 How to Cite?
AbstractBACKGROUND: The FAS and FASL system plays a key role in regulating apoptotic cell death and corruption of this signalling pathway has been shown to participate in immune escape and tumorigenesis. There is reduced expression of FAS but elevated expression of FASL in many types of human cancers including lung cancer. We recently reported an association between functional polymorphisms in FAS (-1377G-->A) and FASL (-844T-->C) and risk of oesophageal cancer. OBJECTIVE: To examine the contribution of these polymorphisms to risk of developing lung cancer. METHODS: Genotypes of 1000 lung cancer patients and 1270 controls were analysed by PCR based restriction fragment length polymorphism. Associations with risk of lung cancer were estimated by logistic regression. RESULTS: Compared with non-carriers, there was a 1.6 fold excess risk of developing lung cancer for carriers of the FAS -1377AA genotype (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.21 to 2.10; p = 0.001), and 1.8 fold excess risk (OR 1.79, 95% CI 1.26 to 2.52; p = 0.001) for carriers of FASL -844CC. Gene-gene interaction of FAS and FASL polymorphisms increased risk of lung cancer in a multiplicative manner (OR for the carriers of both FAS -1377AA and FASL -844CC genotypes 4.18, 95% CI 2.83 to 6.18). Gene-environment interaction of FAS or FASL polymorphism and smoking associated with increased risk of lung cancer was also found. CONCLUSION: These results are consistent with our initial findings in oesophageal cancer and further support the hypothesis that the FAS and FASL triggered apoptosis pathway plays an important role in human carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/42517
ISSN
2015 Impact Factor: 5.65
2015 SCImago Journal Rankings: 3.820
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorMiao, Xen_HK
dc.contributor.authorSun, Ten_HK
dc.contributor.authorTan, Wen_HK
dc.contributor.authorQu, Sen_HK
dc.contributor.authorXiong, Pen_HK
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorLin, Den_HK
dc.date.accessioned2007-01-29T08:51:51Z-
dc.date.available2007-01-29T08:51:51Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal of Medical Genetics, 2005, v. 42 n. 6, p. 479-484en_HK
dc.identifier.issn0022-2593en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42517-
dc.description.abstractBACKGROUND: The FAS and FASL system plays a key role in regulating apoptotic cell death and corruption of this signalling pathway has been shown to participate in immune escape and tumorigenesis. There is reduced expression of FAS but elevated expression of FASL in many types of human cancers including lung cancer. We recently reported an association between functional polymorphisms in FAS (-1377G-->A) and FASL (-844T-->C) and risk of oesophageal cancer. OBJECTIVE: To examine the contribution of these polymorphisms to risk of developing lung cancer. METHODS: Genotypes of 1000 lung cancer patients and 1270 controls were analysed by PCR based restriction fragment length polymorphism. Associations with risk of lung cancer were estimated by logistic regression. RESULTS: Compared with non-carriers, there was a 1.6 fold excess risk of developing lung cancer for carriers of the FAS -1377AA genotype (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.21 to 2.10; p = 0.001), and 1.8 fold excess risk (OR 1.79, 95% CI 1.26 to 2.52; p = 0.001) for carriers of FASL -844CC. Gene-gene interaction of FAS and FASL polymorphisms increased risk of lung cancer in a multiplicative manner (OR for the carriers of both FAS -1377AA and FASL -844CC genotypes 4.18, 95% CI 2.83 to 6.18). Gene-environment interaction of FAS or FASL polymorphism and smoking associated with increased risk of lung cancer was also found. CONCLUSION: These results are consistent with our initial findings in oesophageal cancer and further support the hypothesis that the FAS and FASL triggered apoptosis pathway plays an important role in human carcinogenesis.en_HK
dc.format.extent105548 bytes-
dc.format.extent25088 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jmg.bmjjournals.com/en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Medical Genetics. Copyright © B M J Publishing Group.en_HK
dc.subject.meshAntigens, cd95 - geneticsen_HK
dc.subject.meshCase-control studiesen_HK
dc.subject.meshGenetic predisposition to diseaseen_HK
dc.subject.meshLung neoplasms - geneticsen_HK
dc.subject.meshMembrane glycoproteinsen_HK
dc.titleFunctional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2593&volume=42&issue=6&spage=479&epage=484&date=2005&atitle=Functional+polymorphisms+in+cell+death+pathway+genes+FAS+and+FASL+contribute+to+risk+of+lung+canceren_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/jmg.2004.030106en_HK
dc.identifier.pmid15937082-
dc.identifier.pmcidPMC1736067-
dc.identifier.scopuseid_2-s2.0-20544473024-
dc.identifier.hkuros118963-
dc.identifier.isiWOS:000229579900004-

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