An Upward Trend in Dna P16ink4a Methylation Pattern and High Risk HPV Infection According to the Severity of the Cervical Lesion

Carestiato, Fernanda Nahoum; Afonso, Larissa Alves; Moysés, Natalia; Filho, Gutemberg L Almeida; Velarde, Luís Guillermo Coca; Cavalcanti, Sílvia M. B.

doi:10.1590/s0036-46652013000500006

Cited by 11 publications

(19 citation statements)

References 22 publications

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“…These results agreed with a previous study, which also showed that higher TIMP3 methylation frequency occurs in HPV 16-positive HNSCC as compared to HPV 16-negative tumors (van Kempen et al, 2014). Several other studies proposed that HPV infection may promote hypermethylation of tumor-related genes, such as DAPK (Flatley et al, 2014), p16 (Carestiato et al, 2013), and CCNA1 (Yanatatsaneejit et al, 2011). Taken together, our data suggest that methylation of TIMP3 may be induced by HPV 16 infection.…”

Section: Discussionsupporting

confidence: 93%

Characterization of gene methylation in human papillomavirus associated-head and neck squamous cell carcinoma

et al. 2016

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ABSTRACT. Head and neck squamous cell carcinoma (HNSCC) has become one of the most common forms of cancer worldwide. Hypermethylation-induced silencing of tumor-associated gene has been proposed as an important cofactor in cancer pathology. This paper aimed to characterize the gene methylation patterns in human papillomavirus (HPV) associated-HNSCC. TIMP3 and APC methylation status in neoplastic (N = 92) and non-neoplastic tissues (N = 92) of HNSCC as well as their association with HPV infection were investigated via methylation-specific PCR assays. Results indicated that methylation level of TIMP3 was markedly higher in HPV-positive tumors as compared with HPV-negative tumors. Both TIMP3 and APC methylation were associated with lymph node metastasis and higher clinical stage of tumors. Patients with methylation at TIMP3 or APC had worse prognoses as compared to those without these alterations. This is the first study that shows a possible linkage between HPV infection and APC methylation. Methylation patterns of tumor-related genes may contribute to different disease prognosis in HNSCC according to the HPV infection status.

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Section: Discussionsupporting

confidence: 93%

Characterization of gene methylation in human papillomavirus associated-head and neck squamous cell carcinoma

et al. 2016

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“…[56,60]. Similarly, cervical cancer studies and penile cancer studies have reported hypermethylation in the CKDN2A locus compared to precancer [85][86][87][88][89]. Some studies have also reported CDKN2A hypermethylation in HPV-driven HNC in subjects with decreased P16 expression [56,64].…”

Section: Alterations In Methylation Patterns In Hpv-driven Hncmentioning

confidence: 99%

DNA Methylation Changes in Human Papillomavirus-Driven Head and Neck Cancers

Weeramange

Tang

Vasani

et al. 2020

Cells

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Disruption of DNA methylation patterns is one of the hallmarks of cancer. Similar to other cancer types, human papillomavirus (HPV)-driven head and neck cancer (HNC) also reveals alterations in its methylation profile. The intrinsic ability of HPV oncoproteins E6 and E7 to interfere with DNA methyltransferase activity contributes to these methylation changes. There are many genes that have been reported to be differentially methylated in HPV-driven HNC. Some of these genes are involved in major cellular pathways, indicating that DNA methylation, at least in certain instances, may contribute to the development and progression of HPV-driven HNC. Furthermore, the HPV genome itself becomes a target of the cellular DNA methylation machinery. Some of these methylation changes appearing in the viral long control region (LCR) may contribute to uncontrolled oncoprotein expression, leading to carcinogenesis. Consistent with these observations, demethylation therapy appears to have significant effects on HPV-driven HNC. This review article comprehensively summarizes DNA methylation changes and their diagnostic and therapeutic indications in HPV-driven HNC.

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“…In addition, transition mutations C→T (or G) in CDKN2A, a gene that codes for p16 and p14arf tumor suppressor proteins are exclusive to HPV+ oropharyngeal and cervical cancers. [89,90] Intriguingly, many soft tissue tumors have an amplicon from host genomic DNA that HPV presumably deleted upon integration into chromosome 12q (12q13-15). [91] In this section of chromosome 12q, many genes related to both cancer and HPV infection are found: AID (12q13), APOBEC1 (12q13.1), [26] the vitamin D receptor (12q13.11), CDK4 (cyclin-dependent kinases), MDM2 (murine double minutes), SAS (sarcoma amplified sequence), [26,92] HMGI-C (high mobility glycoprotein), GLI (Glioblastoma), CHOP(C/EBP Homologue Protein), OS4, and OS9.…”

Section: Discussionmentioning

confidence: 99%

All sites but skin cancer incidences analyzed worldwide by sex, age, and skin type over time (1955-2007), advancing age, and UVB dose reveals important carcinogenic drivers

Godar

Gurov²,

Merrill

2017

JER

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Because we observed increasing incidences over time, advancing age, higher estrogen levels, decreasing UVB (290-315 nm) doses, or lower vitamin D3, and Human Papillomavirus hiding in immune-privileged sites of hair follicles play roles in melanoma, we wondered if the majority of cancers might have similar carcinogenic drivers. To investigate this possibility, we performed worldwide analysis of all sites but skin cancer over time , advancing age, and UVB doses for males and females with all skin types and ages (0-85+) and in five age groups using IARC data. To investigate Human Papillomavirus's role, we analyzed the incidences of breast, prostate, and colon cancers in a developed country with European ancestry (New Zealand) having high amounts of androgenic hair and a developing country with Asian ancestry (India) having low amounts of androgenic hair. To potentially add epidemiology to the already established role of estrogen in cancer, we analyzed males and females in various countries around the world using the incidence of breast cancer (> 70 yr.) as an established indicator of estrogen levels. The analysis reveals cancer incidences are steadily increasing over time in developed but not developing countries regardless of skin type. Only US white, but not black, breast, prostate, and colon cancer incidences in the oldest age group significantly decreased with increasing UVB dose suggesting a role for vitamin D3. The data suggests the carcinogenic drivers in many cancers are estrogen, increasing age (or reactive oxygen species), decreasing vitamin D3 levels, and persistence of Human Papillomavirus infection in immune-privileged sites.

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An Upward Trend in Dna P16ink4a Methylation Pattern and High Risk HPV Infection According to the Severity of the Cervical Lesion

Cited by 11 publications

References 22 publications

Characterization of gene methylation in human papillomavirus associated-head and neck squamous cell carcinoma

Characterization of gene methylation in human papillomavirus associated-head and neck squamous cell carcinoma

DNA Methylation Changes in Human Papillomavirus-Driven Head and Neck Cancers

All sites but skin cancer incidences analyzed worldwide by sex, age, and skin type over time (1955-2007), advancing age, and UVB dose reveals important carcinogenic drivers

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