Depletion of the cdk Inhibitor p16
            <sup>INK4a</sup>
            Differentially Affects Proliferation of Established Cervical Carcinoma Cells

Pauck, Alexander; Lener, Barbara; Hoell, Monika; Kaiser, Andreas M.; Kaufmann, Andreas M.; Zwerschke, Werner; Jansen‐Dürr, Pidder

doi:10.1128/jvi.03817-13

Cited by 23 publications

(24 citation statements)

References 26 publications

(23 reference statements)

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“…These data suggest that the E7 protein levels in cervical cancer cells are variable and that cervical cancer cells might have the ability to temporary regulate their E7 protein levels. These data are in keeping with our recent finding that the E7 level can be regulated by p16 INK4A in different cervical cancer cells [36]. We showed in IF-CLSM and Western blot experiments also that the HPV E7 protein levels differ strongly between the two HPV-16 positive cervical cancer cell lines CaSki and SiHa.…”

Section: Resultssupporting

confidence: 92%

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

et al. 2014

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High-risk human papillomaviruses (HPV) are the main etiologic factor for the development of cervical cancer. Infections by these viruses have been detected in virtually all cervical cancers. C-33A is one of the rare cervical cancer derived cell lines considered as HPV-negative. Employing monoclonal antibodies raised against a conformational epitope of the HPV-16 E7 oncoprotein, we present evidence suggesting that E7-positive cells can be sporadically and transiently detected in C-33A cell cultures. Immunoblotting with affinity-purified rabbit polyclonal anti-HPV 16 E7 antisera and q-RT-PCR analysis suggest that these cells do probably not express HPV-16 E7. Moreover, we show that the HPV E7 protein level differs considerably between individual cells in cultures of several established cervical cancer cell lines. Our data suggest that expression of the E7 protein is variable in established cervical cancer cell lines including C-33A cells.

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Section: Resultssupporting

confidence: 92%

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

et al. 2014

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“…Moreover, p16 has been identified to have a distinct function in cellular transformation and is not just a surrogate marker. Knock out of p16 in HPV E7 expressing cells can lead to induction of apoptosis showing a physiological role in transformation despite its original role in the process of senescence [41,49].…”

Section: Discussionmentioning

confidence: 99%

Meta-analysis of survival in patients with HNSCC discriminates risk depending on combined HPV and p16 status

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et al. 2015

Eur Arch Otorhinolaryngol

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Data indicate a better prognosis for human papillomavirus (HPV)-associated head and neck squamous cell carcinoma (HNSCC). HPV and p16 detection are established markers for HPV-related HNSCC. Both are accepted as survival-independent predictors. Previous studies investigating the survival in HNSCC patients depending on HPV(+/-) and p16(+/-) status consistently found discordant results with p16(-)/HPV(+) and p16(+)/HPV(-). However, no meta-analysis regarding the survival according to combined HPV/p16 status has been performed yet. The objective of this study was to discriminate the impact of combined HPV(+/-) and p16(+/-) status on survival. Data sources were identification and review of publications assessing survival of the distinct subgroups with both p16 and HPV investigated in HNSCC until February, 2015. A meta-analysis was performed to classify survival and clinical outcomes. 18 out of 397 articles (4424 patients) were eligible for the meta-analysis. The percent proportion of the subgroups was 25 % for HPV(+)/p16(+), 61.2 % for HPV(-)/p16(-), 7.1 % for HPV(-)/p16(+) and 6.8 % for HPV(+)/P16(-). The meta-analysis showed a significantly improved 5-year overall survival (OS), 5-year disease-free survival and their corresponding hazard ratio for HPV(+)/p16(+) HNSCC in comparison to HPV(-)/p16(-), HPV(+)/p16(-) and HPV(-)/p16(+). The 5-year OS of the HPV(-)/p16(+) subgroup was intermediate while HPV(+)/p16(-) and HPV(-)/p16(-) HNSCC had the shortest survival. With current therapeutic strategies, survival of patients with HNSCC is better if associated with HPV(+)/p16(+) or HPV(-)/p16(+). Clinical trials are needed to confirm the distinct survival pattern and to investigate possible differences in survival for HPV(+)/p16(-) and HPV(-)/p16(+) HNSCC. To further differentiate p16(+) HNSCC, HPV testing may be advisable.

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“…The p16 accumulation can be explained as a possible attempt of the hr‐HPV‐infected cells to counteract the impact of the viral oncoproteins in the regulation of the cell cycle. However, recent studies also provided lines of evidence that p16 accumulation in hr‐HPV‐infected cells is necessary for cell viability, highlighting a pro‐proliferation function of p16 in a specific context …”

Section: Rationale and Pitfalls Of P16 Ihc For The Diagnosis Of Hr‐hpmentioning

confidence: 99%

HPV as a marker for molecular characterization in head and neck oncology: Looking for a standardization of clinical use and of detection method(s) in clinical practice

et al. 2019

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Background A consensus about the most appropriate diagnostic method(s) for head and neck human papillomavirus (HPV)‐induced carcinogenesis is still lacking because most of the commercially available assays have been designed for the cervix. Methods This article summarizes current data and trends concerning HPV diagnostic strategies in oropharyngeal squamous cell carcinoma (OPSCC). Six main approaches are described. Results The diagnostic gold standard for HPV‐related OPSCC, focusing on E6/E7 mRNA detection, requires fresh samples. Because most frequently available samples are formalin‐fixed paraffin‐embedded (FFPE), the pros and cons of the different approaches were analyzed. Conclusions In the FFPE samples, the immunohistochemistry of p16, which is considered appropriate to assess HPV‐driven carcinogenesis in OPSCC according to the 8th American Joint Committee on Cancer TNM classification, may not be specific enough to become the diagnostic standard in the perspective of treatment deintensification. p16 may play a safer role in combination with another highly sensible assay. Other promising approaches are based on DNA detection through real‐time polymerase chain reaction and RNAscope.

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Depletion of the cdk Inhibitor p16 ^INK4a Differentially Affects Proliferation of Established Cervical Carcinoma Cells

Abstract: Infections with high-risk human papillomaviruses (hrHPV

Cited by 23 publications

References 26 publications

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

Meta-analysis of survival in patients with HNSCC discriminates risk depending on combined HPV and p16 status

HPV as a marker for molecular characterization in head and neck oncology: Looking for a standardization of clinical use and of detection method(s) in clinical practice

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Depletion of the cdk Inhibitor p16 INK4a Differentially Affects Proliferation of Established Cervical Carcinoma Cells

Abstract: Infections with high-risk human papillomaviruses (hrHPV

Cited by 23 publications

References 26 publications

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

Analysis of human papillomavirus E7 protein status in C-33A cervical cancer cells

Meta-analysis of survival in patients with HNSCC discriminates risk depending on combined HPV and p16 status

HPV as a marker for molecular characterization in head and neck oncology: Looking for a standardization of clinical use and of detection method(s) in clinical practice

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Depletion of the cdk Inhibitor p16 ^INK4a Differentially Affects Proliferation of Established Cervical Carcinoma Cells