RGD Reference Report - Combined effects of polymorphisms of DNA-repair protein genes and metabolic enzyme genes on the risk of cholangiocarcinoma. - Rat Genome Database

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Combined effects of polymorphisms of DNA-repair protein genes and metabolic enzyme genes on the risk of cholangiocarcinoma.

Authors: Zeng, Lu  You, Gyokukou  Tanaka, Hideaki  Srivatanakul, Petcharin  Ohta, Emi  Viwatthanasittiphong, Chutiwan  Matharit, Mantana  Chenvidhya, Dhiraphol  Jedpiyawongse, Adisorn  Tanaka, Masakazu  Fujii, Takahiro  Sripa, Banchob  Ohshima, Kazuhiko  Miwa, Masanao  Honjo, Satoshi 
Citation: Zeng L, etal., Jpn J Clin Oncol. 2013 Dec;43(12):1190-4. doi: 10.1093/jjco/hyt138. Epub 2013 Sep 18.
RGD ID: 14700980
Pubmed: PMID:24049014   (View Abstract at PubMed)
DOI: DOI:10.1093/jjco/hyt138   (Journal Full-text)


OBJECTIVE: Although Opisthorchis viverrini is a risk factor for cholangiocarcinoma, not all the infected individuals develop cholangiocarcinoma. We investigated whether the base excision repair enzyme gene polymorphisms with differentiated repair capacities of inflammation-related deoxyribonucleic acid damage may play a key role and such possible effects from those genes may be increased or diminished in co-existence of polymorphisms of metabolic enzymes, including glutathione-S-transferases mu 1 and glutathione-S-transferases θ1.
METHODS: We genotyped five non-synonymous single-nucleotide polymorphisms of three genes, including the human homolog of the 8-oxoguanine glycosylase 1 Ser326Cys, X-ray repair cross-complementing protein 1 Arg194Trp, Arg280His and Arg399Gln and poly (adenosine diphosphate ribose) polymerase 1 Val762Ala in 87-94 matched case-control pairs, and examined relations between those polymorphisms and the risk of cholangiocarcinoma.
RESULTS: Any single polymorphism did not have a measurable association with the risk of cholangiocarcinoma. However, when considering glutathione-S-transferases mu 1 polymorphism together, the human homolog of the 8-oxoguanine glycosylase 1 codon 326 polymorphism was related to the decreased risk; odds ratios were 1.00 (reference), 0.06 (95% confidence interval 0.01-0.53), 0.06 (0.01-0.54) and 0.14 (0.02-1.08) for persons with human homolog of the 8-oxoguanine glycosylase 1 Ser/Ser and glutathione-S-transferases mu 1 wild, ones with Ser/Ser and glutathione-S-transferases mu 1 null, ones with Ser/Cys or Cys/Cys and glutathione-S-transferases mu 1 wild and ones with Ser/Cys or Cys/Cys and glutathione-S-transferases mu 1 null, respectively (P for interaction <0.01). Further adjustment for the presence of anti-Opisthorchis viverrini antibody, smoking and alcohol drinking did not change the decreased risk. Other combinations of deoxyribonucleic acid-repair gene polymorphism and glutathione-S-transferases were not associated with the risk of cholangiocarcinoma.
CONCLUSIONS: The present findings suggested that decreased capacity of deoxyribonucleic acid-repair gene, human homolog of the 8-oxoguanine glycosylase 1, may be related to decreased risk if much damaged cells die before malignant transformation.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cholangiocarcinoma  IAGP 14700980 RGD 
cholangiocarcinoma  ISOGSTM1 (Homo sapiens)14700980; 14700980 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gstm1  (glutathione S-transferase mu 1)

Genes (Mus musculus)
Gstm1  (glutathione S-transferase, mu 1)

Genes (Homo sapiens)
GSTM1  (glutathione S-transferase mu 1)


Additional Information