Tumor necrosis factor A and MHC class I chain related gene A (MIC-A) polymorphisms in Swedish patients with cervical cancer

Ghaderi, Mehran; Zake, Liene Nikitina; Wallin, Keng Ling; Wiklund, Fredrik; Hallmans, Göran; Lenner, Per; Dillner, Joakim; Sanjeevi, Carani B.

doi:10.1016/s0198-8859(01)00306-8

Cited by 39 publications

(21 citation statements)

References 31 publications

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“…Whereas the MHC class I genes have been extensively studied and well documented, the MIC genes have not, despite interesting features such as associations with diseases (37,38). MIC genes are also responsible for an immune system that seems to be, on the whole, more primitive than that controlled by MHC genes (39,40).…”

Section: Origin Of Mica and Micb In Apesmentioning

confidence: 99%

Genomic evolution of MHC class I region in primates

Fukami-Kobayashi

Shiina

Anzai

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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To elucidate the origins of the MHC-B-MHC-C pair and the MHC class I chain-related molecule (MIC)A-MICB pair, we sequenced an MHC class I genomic region of humans, chimpanzees, and rhesus monkeys and analyzed the regions from an evolutionary stand-point, focusing first on LINE sequences that are paralogous within each of the first two species and orthologous between them. Because all the long interspersed nuclear element (LINE) sequences were fragmented and nonfunctional, they were suitable for conducting phylogenetic study and, in particular, for estimating evolutionary time. Our study has revealed that MHC-B and MHC-C duplicated 22.3 million years (Myr) ago, and the ape MICA and MICB duplicated 14.1 Myr ago. We then estimated the divergence time of the rhesus monkey by using other orthologous LINE sequences in the class I regions of the three primate species. The result indicates that rhesus monkeys, and possibly the Old World monkeys in general, diverged from humans 27-30 Myr ago. Interestingly, rhesus monkeys were found to have not the pair of MHC-B and MHC-C but many repeated genes similar to MHC-B. These results support our inference that MHC-B and MHC-C duplicated after the divergence between apes and Old World monkeys

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Section: Origin Of Mica and Micb In Apesmentioning

confidence: 99%

Genomic evolution of MHC class I region in primates

Fukami-Kobayashi

Shiina

Anzai

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…14,15 Numerous studies have evaluated TNF as a candidate gene for cervical cancer susceptibility. [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.…”

Section: Introductionmentioning

confidence: 99%

“…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. 19,20 In an analysis of 11 SNPs in the TNF, two SNPs in the promoter region showed an association in HPV16-infected Hispanic cervical cancer patients, and one SNP showed an association in non-Hispanic whites. 17 In the LTA gene, two polymorphisms, C804A and A252G, which are in complete linkage disequilibrium (LD), have shown a protective effect that is stronger in squamous cell carcinoma than in adenocarcinoma in a Japanese cohort.…”

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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“…Many studies have reported associations between TNF microsatellite alleles and some types of cancer (17,18,35); however, the associations of these markers with cervical cancer and cervical HPV infection have rarely been studied. To address the question of whether the severity of the lesion or the oncogenic HPV type is associated with TNF microsatellites, we analyzed the association of the five TNF microsatellite alleles (a to e) with HPV16 and HPV18 infections.…”

Section: Discussionmentioning

confidence: 99%

“…However, only a few investigations have studied the association between the TNF-␣ microsatellite and HPV infection, two of which were conducted with Swedish women (17,18). In a previous report studying Brazilian patients with HPV infections, we showed a significant association between the TNFa-8 allele and HPV infection ( 2 ϭ 4.79; relative risk ϭ 10.73; 95% confidence interval [CI], 1.28 to 89.9; P ϭ 0.033), irrespective of the HPV type and the severity of the lesion (38).…”

mentioning

confidence: 99%

Association of Tumor Necrosis Factora-2anda-8Microsatellite Alleles with Human Papillomavirus and Squamous Intraepithelial Lesions among Women in Brazil

Simões¹,

Gonçalves²,

Donadi³

et al. 2005

J Clin Microbiol

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Infection with oncogenic human papillomavirus (HPV) is considered to be the major risk factor for cervical cancer. Tumor necrosis factor (TNF) is a pluripotent cytokine that plays an important role in inhibiting the action of microbial agents, and TNF microsatellite polymorphisms have been associated with several diseases, including cancer and viral infections. This study analyzed the associations between TNFa to -e microsatellite polymorphisms and the severity of squamous intraepithelial lesions (SIL), according to the presence of the oncogenic HPV16 and HPV18 types. Samples from 146 HPV-positive women with low-grade SIL (LSIL) and high-grade SIL (HSIL) and samples from 101 healthy women were studied. TNF microsatellite polymorphism typing and HPV detection and typing were performed using PCR-amplified DNA hybridized with sequencespecific primers. Data were analyzed by Fisher's exact test using the GENEPOP software. Significant associations were observed between LSIL and the TNFa-8 allele (4/166; P ‫؍‬ 0.04), as well as between TNFa-2 with HPV18 only (16/44; P ‫؍‬ 0.002) and TNFa-2 with HPV18 coinfection with HPV16 (16/44; P ‫؍‬ 0.001). Patients exhibiting the TNFa-2 allele and harboring HPV18, in the presence or absence of coinfection with HPV16, had an increased risk of HSIL occurrence (13/38; P ‫؍‬ 0.04; 5/10; P ‫؍‬ 0.04) compared to patients with other HPV types. These results suggest that the TNFa-8 allele is associated with increased susceptibility to the occurrence of LSIL and that despite the presence of a high TNF-␣ production allele, the ability of HPV18 to resist the inhibitory effects of TNF-␣ may contribute to the occurrence of infection and consequently to HSIL in women with cervical HPV18 infection.

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Tumor necrosis factor A and MHC class I chain related gene A (MIC-A) polymorphisms in Swedish patients with cervical cancer

Cited by 39 publications

References 31 publications

Genomic evolution of MHC class I region in primates

Genomic evolution of MHC class I region in primates

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

Association of Tumor Necrosis Factora-2anda-8Microsatellite Alleles with Human Papillomavirus and Squamous Intraepithelial Lesions among Women in Brazil

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