Genetic and Epigenetic Variations of HPV52 in Cervical Precancer

Bee, Katharine J.; Gradíssimo, Ana; Chen, Zigui; Harari, Ariana; Schiffman, Mark; Raine‐Bennett, Tina; Castle, Philip E.; Clarke, Megan A.; Wentzensen, Nicolas; Burk, Robert D.

doi:10.3390/ijms22126463

Cited by 10 publications

(8 citation statements)

References 73 publications

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“…One thousand bootstrap replicates were used for tree topology evaluation. To construct the phylogenetic branches, HPV52 sequences were downloaded from NCBI ( https://www.ncbi.nlm.nih.gov/ ), including HQ537732 (A1), HQ537739 (A2), HQ537740 (B1), HQ537743 (B2), MZ374448 (B3), HQ537744 (C1), HQ537746 (C2), HQ537748 (D), and MZ374428 (E) [ 12 , 13 ].…”

Section: Methodsmentioning

confidence: 99%

“…When HPV infects cervical epithelial cells and integrates into the host genome, the expression of two major E6 and E7 oncoproteins increases uncontrolled, resulting in host cell immortalization, transformation, and carcinogenesis [ 11 ]. Based on genomic DNA analysis, HPV52 variants are divided into five main phylogenetic lineages (A, B, C, D, and E) and nine sublineages (A1, A2, B1, B2, B3, C1, C2, D, and E) [ 12 , 13 ]. The distribution of HPV variants varies with their geographical location and ethnic group, especially HPV52, which is more likely to infect Chinese women.…”

Section: Introductionmentioning

confidence: 99%

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Genetic variability in the E6 and E7 oncogenes of HPV52 and its prevalence in the Taizhou area, China

Yang

Zhang

et al. 2022

Virol J

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Background Human papillomavirus (HPV) 52 is one of the prevalent oncogenic HPV genotypes in East Asia. Chinese women have the highest susceptibility to the HPV52 type, but research data on HPV52 genetic variability and its carcinogenicity in China is lacking. Methods The present study aimed to investigate the genetic variability of HPV52 currently circulating among Chinese women by PCR sequencing the entire E6 and E7 oncogenes. HPV52 sequence alignment, genetic heterogeneity analyses and maximum-likelihood phylogenetic tree construction were performed by BioEdit software and MEGA X software. Results Between 2016 and 2018, the overall HPV infection rate was 21.3%, of which HPV52 was the most prevalent high-risk type (17.2%) in the Taizhou area, China. A total of 339 single HPV52-positive samples were included in this study. We obtained 27 distinct variation patterns of HPV52 with the accession GenBank numbers ON529577-ON529603. Phylogenetic analysis showed that 96.6% of HPV52 variants belonged to lineage B, which seemed to be uniquely defined by G350T, A379G (K93R) in the E6 gene and C751T, A801G in the E7 gene. Due to the dominance of lineage B in our study population, the results could not be used to assess the association of the HPV52 (sub)lineage with the risk of cervical lesions. In addition, no significant trends were observed between the nucleotide substitutions of HPV52 variants and the risk of cervical carcinogenesis. Conclusion Our data showed that HPV52 variants were strongly biased towards lineage B. These results confirmed that cervical lesions in the Taizhou area are highly attributable to HPV52, which may be due to the high infection rate of lineage B in the population.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genetic variability in the E6 and E7 oncogenes of HPV52 and its prevalence in the Taizhou area, China

Yang

Zhang

et al. 2022

Virol J

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“…Less than 5% of incident HPV infections progress to CIN3, and the methylation of some of the HPV genes is an important biomarker of this subset of clinically relevant transforming HPV infections [ 63 ]. The available literature is consistent with regard to the increased levels of HPV16L1 methylation in cervical cancer compared to low-grade lesions [ 100 , 101 ].…”

Section: Hpv-mediated Dna Methylationmentioning

confidence: 99%

The Role of Methylation of Host and/or Human Papillomavirus (HPV) DNA in Management of Cervical Intraepithelial Neoplasia Grade 2 (CIN2) Lesions

Dovnik

Poljak

2023

IJMS

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Cervical intraepithelial neoplasia grade 2 (CIN2) is an intermediate stage between CIN 1, which is a low-grade lesion, and CIN3, which is the immediate precursor of cervical cancer (CC). Traditionally, CIN2 was regarded as a high-grade lesion and was treated with conization or ablative methods. In recent years, there has been a shift in the management of younger patients, who are now more often being managed conservatively due to frequent spontaneous CIN2 regression and possible adverse effects of treatment on future pregnancies. Because the risk of progression to CC still exists with conservative management, a personalized approach is needed to identify patients with a higher probability of progression. In this regard, research has focused on the role of host and human papillomavirus (HPV) gene methylation. This systematic review summarizes the current knowledge regarding conservative CIN2 management focusing on the main methylation markers and its implementation in conservative CIN2 management, and it describes major ongoing longitudinal studies on the subject. The review showed that DNA methylation is an accurate predictor of disease progression and a valid triage tool for HPV-positive women, with CIN2 performing better than triage cytology. Because virtually all CCs are methylation-positive, methylation-negative women at baseline have an extremely low risk of CC.

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“…Several authors have reported increased methylation in the L1 region associated with CIN3 or CC. Recently Bee et al identified that methylation of the CpG 5615 site of L1 of HPV52 is most frequently associated with NIC3, and SNPs associated with the C clade ( Bee et al, 2021 ). Additionally, increased DNA methylation has been observed in the L1, L2, E2, and E5 regions in high-grade lesions.…”

Section: Changes In the Human Papillomavirus Epigenomementioning

confidence: 99%

Epigenetic and Transcriptomic Regulation Landscape in HPV+ Cancers: Biological and Clinical Implications

Castro-Oropeza

Piña‐Sánchez²

2022

Front. Genet.

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Human Papillomavirus (HPV) is an oncogenic virus that causes the highest number of viral-associated cancer cases and deaths worldwide, with more than 690,000 new cases per year and 342,000 deaths only for cervical cancer (CC). Although the incidence and mortality rates for CC are declining in countries where screening and vaccination programs have been implemented, other types of cancer in which HPV is involved, such as oropharyngeal cancer, are increasing, particularly in men. Mutational and transcriptional profiles of various HPV-associated neoplasms have been described, and accumulated evidence has shown the oncogenic capacity of E6, E7, and E5 genes of high-risk HPV. Interestingly, transcriptomic analysis has revealed that although a vast majority of the human genome is transcribed into RNAs, only 2% of transcripts are translated into proteins. The remaining transcripts lacking protein-coding potential are called non-coding RNAs. In addition to the transfer and ribosomal RNAs, there are regulatory non-coding RNAs classified according to size and structure in long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and small RNAs; such as microRNAs (miRNAs), piwi-associated RNAs (piRNAs), small nucleolar RNAs (snoRNAs) and endogenous short-interfering RNAs. Recent evidence has shown that lncRNAs, miRNAs, and circRNAs are aberrantly expressed under pathological conditions such as cancer. In addition, those transcripts are dysregulated in HPV-related neoplasms, and their expression correlates with tumor progression, metastasis, poor prognosis, and recurrence. Nuclear lncRNAs are epigenetic regulators involved in controlling gene expression at the transcriptional level through chromatin modification and remodeling. Moreover, disruption of the expression profiles of those lncRNAs affects multiple biological processes such as cell proliferation, apoptosis, and migration. This review highlights the epigenetic alterations induced by HPV, from infection to neoplastic transformation. We condense the epigenetic role of non-coding RNA alterations and their potential as biomarkers in transformation’s early stages and clinical applications. We also summarize the molecular mechanisms of action of nuclear lncRNAs to understand better their role in the epigenetic control of gene expression and how they can drive the malignant phenotype of HPV-related neoplasia. Finally, we review several chemical and epigenetic therapy options to prevent and treat HPV-associated neoplasms.

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Genetic and Epigenetic Variations of HPV52 in Cervical Precancer

Cited by 10 publications

References 73 publications

Genetic variability in the E6 and E7 oncogenes of HPV52 and its prevalence in the Taizhou area, China

Genetic variability in the E6 and E7 oncogenes of HPV52 and its prevalence in the Taizhou area, China

The Role of Methylation of Host and/or Human Papillomavirus (HPV) DNA in Management of Cervical Intraepithelial Neoplasia Grade 2 (CIN2) Lesions

Epigenetic and Transcriptomic Regulation Landscape in HPV+ Cancers: Biological and Clinical Implications

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