The Impact of MTHFR 1298 A > C and 677 C > T Gene Polymorphisms as Susceptibility Risk Factors in Cervical Intraepithelial Neoplasia Related to HPV and Sexually Transmitted Infections

Abstract

Background HPV genotypes are the most common etiological factor for genital neoplasia. It would appear that sexually transmitted infections accompanied with HPV genotypes might have synergistic interactions in cancer progression. The genetic polymorphisms are involved in metabolizing carcinogens which may contribute to the susceptibility of developing genital cancers by less efficient or overly down metabolic pathways and cell signaling. MTHFR polymorphisms are related to several metabolic disorders and human cancers. We investigated the contribution of MTHFR 1298 and MTHFR 677 polymorphisms as potential risk factors for outcomes with HPV genotypes and STIs in Iranian population. Materials and Methods As a case-control study, MTHFR A1298C and C677T were assessed for SNPs analysis using a PCR-RFLP assay in 50 cervical intraepithelial neoplasia (CIN) cases, 98 HPV-positive subjects and 47 non-cancerous/ non-HPV patients as healthy controls. Results Finding suggested a significant association between the MTHFR 1298 CC polymorphisms (OR = 3.5, 95% CI = 1.13-10.82, P ≤ 0.05) in women with CIN as compared to non-cancerous/non-HPV subjects. There was not a significant difference of MTHFR 677 between outcomes. Discussion It would seem MTHFR 1298 CC is more likely to be a potential risk factor for HPV-cervical cancer progression. Consequences support further attempts to understand the clinical manifestations of neoplasia related to genital infections and gene mutations.

A Meta-Analysis for Association of XRCC3 rs861539, MTHFR rs1801133, IL-6 rs1800795, IL-12B rs3212227, TNF-α rs1800629, and TLR9 rs352140 Polymorphisms with Susceptibility to Cervical Carcinoma

“…However, Sohrabi et al, in a case-control study evaluated the association of MTHFR A1298C and C677T variants among in 50 cervical intraepithelial neoplasia cases, 98 HPV-positive subjects and 47 non-cancerous/non-HPV patients as healthy controls. Their results showed that MTHFR 1298 CC is more likely to be a potential risk factor for HPV-cervical cancer progression (Sohrabi et al, 2020). Zhou et al, (2020) indicated that the MTHFR rs4846048 enhanced the risk of cervical cancer through association with miR-522.…”

Trends in cocirculation of oncogenic HPV genotypes in single and multiple infections among the unvaccinated community

“…As a result, it can be a health warning for the incidence of cervical carcinoma and genital malignancies. It seems HPV infection is not restricted to a specific age group although the rate of HPV infections is more distinguished in subjects with unsafe sexual activities and multiple partners 8,10,25,30–42 . In the current cross‐sectional descriptive study, the highest prevalence rate of HPV genotypes (56.64%) was observed in the 25–34 years age group of 1, 133 cervical scrapping specimens.…”

“…It seems HPV infection is not restricted to a specific age group although the rate of HPV infections is more distinguished in subjects with unsafe sexual activities and multiple partners. 8,10,25,[30][31][32][33][34][35][36][37][38][39][40][41][42] In the current cross-sectional descriptive study, the highest prevalence rate of HPV genotypes (56.64%) was observed in the 25-34 years age group of 1, 133 cervical scrapping specimens. Our finding revealed that HPV genotypes detected were remarkable in the general population and multiple HPV genotypes were also observed as asymptomatic forms.…”

Genetic Modulation of HPV Infection and Cervical Lesions: Role of Oxidative Stress-Related Genes

“…Meta-analyses, other reviews, and original papers have been describing associations of this MTHFR variant with several types of cancers, such as ovarian cancer, breast cancer, colorectal cancer, bladder cancer, lung cancer, childhood acute lymphoblastic leukemia [71][72][73][74][75][76], and even cervical cancer [77][78][79][80][81]. However, such associations remain contentious [82][83][84][85], potentially due to population differences [81]. Concerning CβS, our bibliographic survey did not reveal any study of this gene in HPV infection, cervical cancer, or precursor lesions.…”