The -238 tumor necrosis factor-α promoter polymorphism is associated with decreased susceptibility to cancers

Jang, Won Hee; Yang, Young‐Il; Yea, Sung Su; Lee, Youn Jae; Chun, Jin Ho; Kim, Hyeong-In; Kim, Mi Seong; Paik, Kye-Hyung

doi:10.1016/s0304-3835(01)00438-4

Cited by 160 publications

(128 citation statements)

References 28 publications

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“…Our result shows that TNF-α-308*A/G gene polymorphism is not related to hepatocellular carcinoma. This finding parallels other research, which could prove no association between the TNF-α-308 polymorphism and gastric cancer, uterine cervical cancer, colorectal cancer, or renal cell carcinoma (Jang et al, 2001).…”

Section: Discussionsupporting

confidence: 91%

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

Shi

Ren²,

Lu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 91%

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

Shi

Ren²,

Lu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Many previous studies have investigated the TNF À238 and À308 SNPs. [16][17][18][21][22][23][24][25] The number of cases genotyped in the current investigation exceeds all previous studies taken together and we could not detect any association for these polymorphisms.…”

Section: Discussioncontrasting

confidence: 65%

“…[16][17][18][19][20][21][22][23][24][25] Most studies of TNF as a risk factor for cervical cancer have focused on the -238 and -308 promoter single nucleotide polymorphisms (SNPs). For -238, three of five studies show a protective effect of the A allele 16,21,23 and two studies report no association, 17,24 whereas for -308, six of eight studies showed no association, 16,17,[21][22][23]25 and one study reports an association of the A allele with risk 18 and another study associates the G allele with risk. 24 The TNFa microsatellite, located in the TNF region of MHC class III, showed no association to disease, but the TNFa-11 allele was associated with cervical intraepithelial neoplasia and invasive cervical cancer in Swedish carriers of DQB1*0602.…”

Section: Introductionmentioning

confidence: 99%

MHC loci affecting cervical cancer risk: distinguishing the effects of HLA-DQB1 and non-HLA genes TNF, LTA, TAP1 and TAP2

Ivansson

Magnusson

et al. 2008

Genes Immun

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Cervical cancer has been associated with specific human leukocyte antigen (HLA) haplotypes/alleles and with polymorphisms at the nearby non-HLA loci TNF, LTA, TAP1 and TAP2. Distinguishing effects of individual loci in the major histocompatibility complex (MHC) region are difficult due to the complex linkage disequilibrium (LD) pattern characterized by high LD, punctuated by recombination hot spots. We have evaluated the association of polymorphism at HLA class II DQB1 and the TNF, LTA, TAP1 and TAP2 genes with cervical cancer risk, using 1306 familial cases and 288 controls. DQB1 was strongly associated; alleles *0301, *0402 and *0602 increased cancer susceptibility, whereas *0501 and *0603 decreased susceptibility. Among the non-HLA loci, association was only detected for the TAP2 665 polymorphism, and interallelic disequilibrium analysis indicated that this could be due to LD with DQB1. As the TAP2 665 association was seen predominantly in non-carriers of DQB1 susceptibility alleles, we hypothesized that TAP2 665 may have an effect not attributable to LD with DQB1. However, a logistic regression analysis suggested that TAP2 665 was strongly influenced by LD with DQB1. Our results emphasize the importance of large sample sizes and underscore the necessity of examining both HLA and non-HLA loci in the MHC to assign association to the correct locus.

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“…However, this polymorphism does not influence colorectal cancer risk or severity (Park et al, 1998). The -238 A allele has been reported to be protective against cancers in general (Jang et al, 2001b), but this needs to be confirmed in larger studies. We have recently studied both the -308 and -238 polymorphisms in 711 breast cancer patients and 498 age and sex-matched controls, but were unable to demonstrate any association (unpublished data).…”

Section: Tumour Necrosis Factormentioning

confidence: 95%

Role of genetic polymorphisms in tumour angiogenesis

2002

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Angiogenesis plays a crucial role in the development, growth and spread of solid tumours. Pro-and anti-angiogenic factors are abnormally expressed in tumours, influencing tumour angiogenesis, growth and progression. Polymorphisms in genes encoding angiogenic factors or their receptors may alter protein expression and/or activity. This article reviews the literature to determine the possible role of angiogenesis-related polymorphisms in cancer. Further research studies in this potentially crucial area of tumour biology are proposed.

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The -238 tumor necrosis factor-α promoter polymorphism is associated with decreased susceptibility to cancers

Cited by 160 publications

References 28 publications

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

MHC loci affecting cervical cancer risk: distinguishing the effects of HLA-DQB1 and non-HLA genes TNF, LTA, TAP1 and TAP2

Role of genetic polymorphisms in tumour angiogenesis

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