Association of Caspase-8 Genotypes With Oral Cancer Risk in Taiwan.
Case–control study
Taiwan
caspase-8
genotype
oral cancer
polymorphism
Journal
In vivo (Athens, Greece)
ISSN: 1791-7549
Titre abrégé: In Vivo
Pays: Greece
ID NLM: 8806809
Informations de publication
Date de publication:
Historique:
received:
27
04
2019
revised:
06
06
2019
accepted:
07
06
2019
entrez:
8
7
2019
pubmed:
8
7
2019
medline:
21
12
2019
Statut:
ppublish
Résumé
Recently, mounting evidence has shown that caspase-8 (CASP8) rs3834129 (-652, 6N insertion/deletion) polymorphism may serve as a genetic biomarker for personal risk of various cancer types. The contribution of CASP8 rs3834129 polymorphism has been investigated in several oral cancer populations, but not in Taiwan. This study investigated the role of CASP8 rs3834129 polymorphism on oral risk in Taiwan. CASP8 rs3834129 polymorphic genotypes were determined and their associations with oral cancer risk were investigated among 788 patients with oral cancer and 956 age- and gender-matched healthy controls via polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP) methodology. In addition, the interaction of CASP8 rs3834129 genotype with personal behavior and clinicopathological features were also examined. The frequencies of II, ID and DD genotypes for CASP8 rs3834129 were 57.5, 36.5 and 6.0% in the patient group and 54.0, 39.0 and 7.0% in the healthy control group, respectively (p for trend=0.3052), genotypes were not significantly differentially distributed between the two groups. The comparisons in allelic frequency distribution also supported the findings that the D variant allele may not serve as a determinant of risk for oral cancer. There was no interaction of CASP8 rs3834129 genotype with age, gender, smoking, alcohol or betel quid consumption in regard to oral cancer risk. Our results indicate that the caspase-8 genotype does not appear to play a direct role in personal susceptibility to oral cancer in Taiwan.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Recently, mounting evidence has shown that caspase-8 (CASP8) rs3834129 (-652, 6N insertion/deletion) polymorphism may serve as a genetic biomarker for personal risk of various cancer types. The contribution of CASP8 rs3834129 polymorphism has been investigated in several oral cancer populations, but not in Taiwan. This study investigated the role of CASP8 rs3834129 polymorphism on oral risk in Taiwan.
MATERIALS AND METHODS
METHODS
CASP8 rs3834129 polymorphic genotypes were determined and their associations with oral cancer risk were investigated among 788 patients with oral cancer and 956 age- and gender-matched healthy controls via polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP) methodology. In addition, the interaction of CASP8 rs3834129 genotype with personal behavior and clinicopathological features were also examined.
RESULTS
RESULTS
The frequencies of II, ID and DD genotypes for CASP8 rs3834129 were 57.5, 36.5 and 6.0% in the patient group and 54.0, 39.0 and 7.0% in the healthy control group, respectively (p for trend=0.3052), genotypes were not significantly differentially distributed between the two groups. The comparisons in allelic frequency distribution also supported the findings that the D variant allele may not serve as a determinant of risk for oral cancer. There was no interaction of CASP8 rs3834129 genotype with age, gender, smoking, alcohol or betel quid consumption in regard to oral cancer risk.
CONCLUSION
CONCLUSIONS
Our results indicate that the caspase-8 genotype does not appear to play a direct role in personal susceptibility to oral cancer in Taiwan.
Identifiants
pubmed: 31280204
pii: 33/4/1151
doi: 10.21873/invivo.11585
pmc: PMC6689357
doi:
Substances chimiques
Caspase 8
EC 3.4.22.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1151-1156Informations de copyright
Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
Références
IUBMB Life. 2000 Aug;50(2):85-90
pubmed: 11185963
Mol Cell. 2001 Mar;7(3):673-82
pubmed: 11463391
Apoptosis. 2002 Aug;7(4):313-9
pubmed: 12101390
Cancer Genet Cytogenet. 2006 Sep;169(2):121-7
pubmed: 16938569
Nat Genet. 2007 May;39(5):605-13
pubmed: 17450141
Hum Mutat. 2008 Dec;29(12):1443-51
pubmed: 18563783
Oncogene. 2008 Oct 20;27(48):6194-206
pubmed: 18931687
J Med Genet. 2009 Aug;46(8):497-510
pubmed: 19505876
J Oral Pathol Med. 2010 Feb;39(2):155-61
pubmed: 20359312
Mol Carcinog. 2010 Jul;49(7):684-92
pubmed: 20564345
Laryngoscope. 2010 Dec;120(12):2417-22
pubmed: 21108427
Ann Surg Oncol. 2011 May;18(5):1431-8
pubmed: 21246406
PLoS One. 2011;6(9):e16374
pubmed: 21915251
Gene. 2012 Aug 15;505(1):176-9
pubmed: 22659694
Anticancer Res. 2012 Sep;32(9):3799-803
pubmed: 22993322
J Urol. 2013 Aug;190(2):717-22
pubmed: 23313206
Med Oncol. 2013;30(3):565
pubmed: 23715747
Anticancer Res. 2014 Jun;34(6):2951-6
pubmed: 24922659
Anticancer Res. 2014 Jul;34(7):3731-7
pubmed: 24982395
Asian Pac J Cancer Prev. 2014;15(18):7713-8
pubmed: 25292051
PLoS One. 2014 Dec 11;9(12):e114696
pubmed: 25502557
J Clin Invest. 2015 Feb;125(2):487-9
pubmed: 25642709
Exp Ther Med. 2015 Dec;10(6):2267-2276
pubmed: 26668627
BMC Cancer. 2016 Jan 12;16:14
pubmed: 26758508
In Vivo. 2016 Jul-Aug;30(4):439-44
pubmed: 27381606
BMC Cancer. 2016 Aug 09;16:618
pubmed: 27507139
Oral Dis. 2017 Jul;23(5):669-673
pubmed: 28181739
J Genet. 2017 Jun;96(2):283-289
pubmed: 28674227
Anticancer Res. 2018 Apr;38(4):2001-2006
pubmed: 29599316
Anticancer Res. 2018 Apr;38(4):2087-2092
pubmed: 29599326
Eur J Cancer Care (Engl). 2019 Jan;28(1):e12891
pubmed: 30015996
J Biomed Res. 2019 Jun 4;33(3):173-180
pubmed: 30057371
CA Cancer J Clin. 2018 Nov;68(6):394-424
pubmed: 30207593
PLoS One. 2018 Oct 18;13(10):e0205731
pubmed: 30335806
Anticancer Res. 2018 Dec;38(12):6821-6826
pubmed: 30504396
J Biol Chem. 1998 Jun 26;273(26):16589-94
pubmed: 9632731