TNFα polymorphism frequencies in HPV-associated cervical dysplasia

Kirkpatrick, Alison; Bidwell, J. L.; Brule, Adriaan J. C. van den; Meijer, Chris J.L.M.; Pawade, Joya; Glew, Susan

doi:10.1016/j.ygyno.2003.11.025

Cited by 53 publications

(33 citation statements)

References 18 publications

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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: 66%

“…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. 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.…”

Section: Introductionmentioning

confidence: 95%

“…[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%

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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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Section: Discussioncontrasting

confidence: 66%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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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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“…Interestingly, these cytokines have also been described in relation to their similar modulation by cigarette smoke substituents, along with a noteworthy inhibition of tumor necrosis factor-a in some studies (53,54). Furthermore, association studies of the tumor necrosis factor-a promoter region have implicated the involvement of tumor necrosis factor-a in cervical intraepithelial neoplasia development (55,56). This has been corroborated by the observation that tumor necrosis factor-a and IFN-g act synergistically to destroy ME-180 cervical cancer cells via apoptosis or necrosis (57).…”

Section: Discussionmentioning

confidence: 88%

Synergy between Cigarette Smoking and Human Papillomavirus Type 16 in Cervical Cancer In situ Development

Gunnell

Tran

Torrång

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: A majority of studies have implicated the involvement of cigarette smoking in cervical cancer development, although its mechanism of action remains unclear. We conducted a large population-based case-control study to address the potential interaction between smoking and human papillomavirus type 16 (HPV-16) in development of cervical cancer in situ (CIS). Methods: Information on risk factors for CIS was collected via interview, and archival cervical smears were tested for HPV-16 DNA presence in cases (n = 375) and controls (n = 363). Adjusted odds ratios (OR) for the effects of smoking, HPV-16 presence/absence, and load at first smear (taken, on average, 9 years before diagnosis) were calculated. Results: The risk for CIS among current smokers who were HPV-16 positive at time of first smear was >14-fold [adjusted OR, 14.4; confidence interval (95% CI), 5.6-36.8] compared

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“…Also, it has been shown that TNF stimulates the transcription of the EGFR, which stimulates cell proliferation and tumorgenesis. Many studies show that in women with CIN, the level of TNF in serum is significantly higher than in healthy women, as well as that GA genotype in -308 locus of TNF gene as compared to GG and AA genotypes, has a higher risk for development of cervical tumor in HR HPV positive women [15,16].…”

Section: Cytokine Gene Polymorphisms As Biomarkers Associated With Hrmentioning

confidence: 99%

Cytokine genes polymorphisms of TNF, IFN-y and IL-12 as potential predictors in the onset of cervical disease associated with HR HPV infections

Tasic¹,

Pravica²,

Ćupić³

2015

Med podmladak

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Cervical cancer highly correlates with infection caused by highly oncogenic types of human papillomavirus (high risk HPV, HR HPV), which is one of the most common sexually transmitted pathogens and is a key factor in the development of cervical disease. However, malignant transformation of cells and tumor development are multifactorial and result from the interaction of a large number of factors such as virus genotype and its oncogenic potential, the state of the infected cells, the immune response of the host, as well as many cofactors such as smoking, oral contraceptives, multiparity, early beginning of sexual life, promiscuity, poor socio-economic conditions, poor diet, etc. Recently, an increasing number of studies have focused on examining the role of genetic basis of the pathogenesis and evolution of HR HPV cervical disease. It is known that genes polymorphisms that encode proteins involved in the functioning of Th1 and Th17 cell response may be associated with better or worse prognosis of cervical disease in women with persistent HR HPV infection. Therefore, the single nucleotide polymorphisms (SNP) of the genes encoding TNF, IFN-γ and IL-12 can be considered as putative biomarkers that may have predictive value for the development of the HR HPV cervical carcinoma.Key words: cervical cancer, HR HPV, gene polymorphism, TNF, IFN-γ and IL-12 Sažetak Karcinom grlića materice visoko korelira sa infekcijom uzrokovanom visoko onkogenim tipovima humanog papiloma virusa (engl. high risk HPV, HR HPV), koji je jedan od najčešće seksualno prenosivih patogena i ključni faktor u nastanku cervikalnog tumora. Ipak, maligna transformacija ćelija i nastanak tumora su multifaktorijalni i rezultat su interakcije velikog broja činilaca kao što su: genotip virusa i njegov onkogeni potencijal, stanje inficirane ćelije, imunskog odgovora domaćina, ali i brojnih kofaktora kao što su pušenje, oralni kontraceptivi, multiparitet, rano stupanje u seksualne odnose, promiskuitet, loši socioekonomski uslovi, ishrana i dr. U novije vreme sve veći broj istraživanja usmeren je na ispitivanje uloge genetske osnove u patogenezi i evoluciji HR HPV cervikalne bolesti. Poznato je da polimorfizmi određenih gena koji kodiraju proteine uključene u funkcionisanje Th1 i Th17 ćelijskog odgovora mogu biti povezani sa boljom ili lošijom prognozom cervikalne bolesti kod žena sa perzistentnom HR HPV infekcijom. Stoga se polimorfizmi pojedinačnih nukleotida (SNP) gena za TNF, IFN-γ i IL-12 mogu smatrati biomarkerima koji mogu da imaju prediktivnu ulogu za nastanak HR HPV karcinoma grlića materice.Ključne reči: karcinom grlića materice, genski polimorfizmi, TNF, IFN-γ i IL-12

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TNFα polymorphism frequencies in HPV-associated cervical dysplasia

Cited by 53 publications

References 18 publications

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

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

Synergy between Cigarette Smoking and Human Papillomavirus Type 16 in Cervical Cancer In situ Development

Cytokine genes polymorphisms of TNF, IFN-y and IL-12 as potential predictors in the onset of cervical disease associated with HR HPV infections

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