Identification of human papillomavirus type 16 integration sites in high-grade precancerous cervical lesions

Matovina, Mihaela; Sabol, Ivan; Grubišić, Goran; Gašperov, Nina Milutin; Grce, Magdalena

doi:10.1016/j.ygyno.2008.12.004

Cited by 60 publications

(54 citation statements)

References 41 publications

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“…We also showed that deletions and complex rearrangements frequently occurred in the cellular sequences targeted by the integrations, and the integrations clustered in FRA13C (13q22), FRA3B (3p14.2), and FRA17B (17q23) . Studies from other groups also suggested that chromosome bands that contain CFS regions are the preferred sites for HPV integrations in both cervix carcinoma-derived cell lines and clinical samples [Hidalgo et al, 2003;Dall et al, 2008;Matovina et al, 2009]. Furthermore, we also found a hot spot of HPV18 integrations within one of the CFSs in chromosomal band 8q24 near the c-Myc proto-oncogene [Ferber et al, 2003].…”

Section: Cfss and Large Cfs Genes In Cervical Cancersupporting

confidence: 80%

Role of the Common Fragile Sites in Cancers with a Human Papillomavirus Etiology

Gao

Smith²

2016

Cytogenet Genome Res

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High-risk human papillomaviruses (HPVs) are known to be associated with different anogenital cancers including cervical, anal, penile, and vaginal cancers. They are also found to be responsible for the dramatic increases in oropharyngeal squamous cell carcinoma (OPSCC) observed in the United States and Europe. The model for how high-risk HPVs induce cancer formation comes from studies of cervical cancer which usually involves integration of the HPV into the human genome and subsequent changes due to induced chromosomal instability. Recent work, discussed here, however suggests that this model may not be completely correct. In addition, we summarize studies now done in OPSCC which demonstrate that the role of HPV in these cancers may be different from that in cervical cancer. Finally, we propose new models for how HPV may be involved in the formation of these 2 cancers.

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Section: Cfss and Large Cfs Genes In Cervical Cancersupporting

confidence: 80%

Role of the Common Fragile Sites in Cancers with a Human Papillomavirus Etiology

Gao

Smith²

2016

Cytogenet Genome Res

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“…Other groups also reported that chromosome bands that contain CFS regions are the preferred sites for HPV integrations in both cervix carcinoma-derived cell lines and clinical samples [Hidalgo et al, 2003;Dall et al, 2008;Matovina et al, 2009]. In addition, we also found a hotspot of HPV18 integration located within one of the CFSs at chromosomal band 8q24 near the c-MYC proto-oncogene [Ferber et al, 2003].…”

Section: Hpv and Cervical Cancersupporting

confidence: 79%

Human Papillomavirus and the Development of Different Cancers

Gao¹,

Smith²

2016

Cytogenet Genome Res

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Human papillomaviruses (HPV) are responsible for the development of almost all cervical cancers. HPV is also found in 85% of anal cancer and in 50% of penile, vulvar, and vaginal cancers, and they are increasingly found in a subset of head and neck cancers, i.e., oropharyngeal squamous cell carcinomas (OPSCC). The model for how HPV causes cancer is derived from several decades of study on cervical cancer, and it is just presumed that this model is not only completely valid for cervical cancer but for all other HPV-driven cancers as well. Next-generation sequencing (NGS) has now provided the necessary tools to characterize genomic alterations in cancer cells and can precisely determine the physical status of HPV in those cells as well. We discuss recent discoveries from different applications of NGS in both cervical cancer and OPSCCs, including whole-genome sequencing and mate-pair NGS. We also discuss what NGS studies have revealed about the different ways that HPV can be involved in cancer formation, specifically comparing cervical cancer and OPSCC.

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“…Of particular interest was the finding that all of the samples harboring integration in 17q23 were advanced lesions of CINII-III or SCC. The affected gene, TMEM49, also known as the VMP1 (vacuole membrane protein-1), encodes a stress-induced autophagy-associated protein and has been repeatedly reported to be affected by HPV16 integration in high-grade cervical lesions and squamous carcinomas [20,29], making it of particular interest for its role in tumor formation. Another frequently targeted gene is TP63, which acts as a tumor suppressor and has been found to be overexpressed in human cervical cancers cells [30,31].…”

Section: Discussionmentioning

confidence: 99%

Physical Status and Variant Analysis of Human Papillomavirus 16 in Women from Shanghai

Guo

Zhu

et al. 2015

Gynecol Obstet Invest

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Background/Aims: Human papillomavirus type 16 (HPV16) is the cause of more than half of all cases of cervical cancer. Genetic mutations in HPV16 and the integration of HPV16 DNA in the human genome are considered important genetic changes in cervical lesion progression. However, limited data concerning HPV16 lineages and physical integration status have been reported for Shanghai, China. The current study analyzed the genetic mutations in complete HPV16 genomes and the physical integration status of HPV16 DNA. Methods: A total of 30 samples of cervical exfoliated cells from patients with HPV16 infection were collected. The entire HPV16 genome was isolated, amplified by PCR and directly sequenced. The physical integration status was determined by 3′RACE nested PCR. Results: A total of 13 integration sites were identified, including 9 in common fragile sites and 1 not close to any fragile sites. Phylogenetic analysis identified two HPV lineages: the European (E) lineage and the East Asian (EA) lineage. Amino acid changes of D25E and N29S were the most common variations across the genome. The HPV16 early genes E1 and E7 and the late gene L1 tended to be highly conserved, whereas the early genes E2, E4 and E6 were more variable. Furthermore, 10 novel variations were identified in this study, which led to the 3 amino acid changes of S23I in E2 and E244K and T269I in E2/E4. Conclusion: Integrated HPV16 viruses were detected in all stages of cervical samples. Many variants in E2, E4, E7, and the long control region co-varied with E6 variations and helped to define the HPV16 lineages.

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Identification of human papillomavirus type 16 integration sites in high-grade precancerous cervical lesions

Cited by 60 publications

References 41 publications

Role of the Common Fragile Sites in Cancers with a Human Papillomavirus Etiology

Role of the Common Fragile Sites in Cancers with a Human Papillomavirus Etiology

Human Papillomavirus and the Development of Different Cancers

Physical Status and Variant Analysis of Human Papillomavirus 16 in Women from Shanghai

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