Whole Genome Analysis of Human Papillomavirus Type 16 Multiple Infection in Cervical Cancer Patients

Chansaenroj, Jira; Theamboonlers, Apiradee; Junyangdikul, Pairoj; Swangvaree, Sukumarn; Karalak, Anant; Poovorawan, Yong

doi:10.7314/apjcp.2012.13.2.599

Cited by 18 publications

(11 citation statements)

References 53 publications

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“…However, consensus sequences in LCR, including some associated with hormonal response, have several mutated sites in lineage D variants. One of them (A7729T), located in a putative glucocorticoid response element (GRE) binding site [47, 48, 49], is detected mostly in the LCR of D2. Whether this change could be involved in hormonal response and with the shorter development of CC is not known.…”

Section: Discussionmentioning

confidence: 99%

Different Association of Human Papillomavirus 16 Variants with Early and Late Presentation of Cervical Cancer

et al. 2016

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The median age of cervical cancer (CC) presentation coincides with the mean age of menopause presentation (49 years) in Mexico. Here, we investigated the association between different HPV16 variants and early (≤ 49 years) or delayed (≥ 50 years) CC presentation. We conducted a case-case study that included 462 CCs, 386 squamous cell carcinomas (SCC), 63 adenocarcinomas (ACC), and 13 additional cell types. Variants were identified by PCR and DNA sequencing. The risk conferred by each variant for developing CC earlier than 50 years was analyzed using a univariate logistic regression model considering old-aged patients (≥ 50 years) and non-HPV16 cases as the reference variables. Overall, the frequency of HPV16 was 50.9%, and the only identified variants were the European A1/2 (31.2%) and the Asian-American D2 (10.8%), and D3 (8.9%). D2 was mainly associated with ≤ 49-year-old patients (15.9%); A1/2 was uniformly distributed between the two age groups (~31%), whereas D3 increased with age to a frequency of 11.8% in the older group. Only the D2 variant conferred a 3.3-fold increase in the risk of developing CC before 50 years of age (OR = 3.3, 95% CI = 1.7–6.6, p < 0.001) in relation with non-HPV16 cases. Remarkably, this risk was higher for ACC (OR = 6.0, 95% CI = 1.1–33, p < 0.05) than for SCC (OR = 2.8, 95% CI = 1.3–5.9, p < 0.01). Interestingly, when analyzing only the HPV16-positive CC, D2 increases (OR = 2.5, 95% CI = 1.2–5, p < 0.05) and D3 decreases (OR = 0.45, 95% CI 0.2–0.9, p < 0.05) the risk to develop CC before 50 years old in relation with A1/2 variant. These results indicated that D2 variant is associated with early and D3 with delayed CC presentation, whereas A1/2 variant was uniformly distributed between the two age groups.

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Section: Discussionmentioning

confidence: 99%

Different Association of Human Papillomavirus 16 Variants with Early and Late Presentation of Cervical Cancer

et al. 2016

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“…The standard organic method (phenol-chloroform) and alcohol precipitation of the specimens as described by Chansaenroj et al (2012) was applied for DNA extraction. The purified substance was re-suspended in a final volume of 30 µl of deionized water.…”

Section: Laboratory Methodsmentioning

confidence: 99%

Polymorphisms in TP53 (rs1042522), p16 (rs11515 and rs3088440) and NQO1 (rs1800566) Genes in Thai Cervical Cancer Patients with HPV 16 Infection

Chansaenroj

Theamboonlers²,

Junyangdikul³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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The risk of cervical cancer development in women infected with HPV varies in relation to the individual host's genetic makeup. Many studies on polymorphisms as genetic factors have been aimed at analyzing associations with cervical cancer. In this study, single nucleotide polymorphisms (SNPs) in 3 genes were investigated in relation to cervical cancer progression in HPV16 infected women with lesions. Two thousand cervical specimens were typed by PCR sequencing methods for TP53 (rs1042522), p16 (rs11515 and rs3088440) and NQO1 (rs1800566). Ninety two HPV16 positive cases and thirty two normal cases were randomly selected. Analysis of TP53 (rs1042522

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“…Secondly, potential cervical cases were possible because some studies may have included the control groups selected mainly from nonsymptom populations. Thirdly, our results were based on unadjusted estimates, while a more precise analysis should be conducted if all individual data were available, which would allow for the adjustment by other co-variants including smoking status, environmental factors, and HPV infection status (Chansaenroj et al, 2012). Thus, further large sample size studies with gene-gene and geneenvironment interactions need performing to identify this association more comprehensive.…”

Section: Discussionmentioning

confidence: 99%

Methylenetetrahydrofolate Reductase C677T Polymorphism and Cervical Cancer Risk: a Meta-Analysis

Guo

2012

Asian Pacific Journal of Cancer Prevention

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Whole Genome Analysis of Human Papillomavirus Type 16 Multiple Infection in Cervical Cancer Patients

Cited by 18 publications

References 53 publications

Different Association of Human Papillomavirus 16 Variants with Early and Late Presentation of Cervical Cancer

Different Association of Human Papillomavirus 16 Variants with Early and Late Presentation of Cervical Cancer

Polymorphisms in TP53 (rs1042522), p16 (rs11515 and rs3088440) and NQO1 (rs1800566) Genes in Thai Cervical Cancer Patients with HPV 16 Infection

Methylenetetrahydrofolate Reductase C677T Polymorphism and Cervical Cancer Risk: a Meta-Analysis

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