Detection of human papillomavirus type 16 DNA in carcinomas of the palatine tonsil.

Niedobitek, Gerald; Pitteroff, Sibylle; Herbst, Hermann; Shepherd, Phillip; Finn, T; Anagnostopoulos, Ioannis; Stein, H.

doi:10.1136/jcp.43.11.918

Cited by 98 publications

(57 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although the discovery of HPV in patients with OPSCC was reported first as early as 1990, 21 and its prognostic significance is well documented, [8][9][10][11] we observed that only 40.4% of radiation oncology practices (76 of 188 respondents) in our survey across the United States use screening for this prognostic marker. Academic practices screen twice as often as private practices.…”

Section: Discussionmentioning

confidence: 67%

Survey on human papillomavirus/p16 screening use in oropharyngeal carcinoma patients in the United States

Shoushtari

Rahimi

Schlesinger

et al. 2009

Cancer

View full text Add to dashboard Cite

BACKGROUND:Patients with human papillomavirus (HPV)-positive oropharyngeal carcinoma (OC) have better prognosis than patients with HPV-negative OC. The objective of the current study was to assess how different practices across the United States treat patients with OC with respect to screening for HPV DNA or p16. METHODS: Five hundred forty-two randomly selected radiation oncologists were sent an 11-question survey by email regarding the use of HPV/p16 screening in OC. The questionnaire addressed demographics of the practice, intensity-modulated radiotherapy (IMRT) use, screening practices for HPV DNA or p16, which year this began, the use of HPV or p16 data to direct patient care, and future plans for its use if it had not already been instituted. RESULTS: One hundred ninety-two responses (39.6%) were received. Thirty-five percent of respondents (67 of 188) reported screening for HPV DNA routinely, whereas 4.8% of respondents (9 of 188) reported screening for p16. Of the physicians who did not use screening techniques, 37.2% (44 of 118 respondents) reported future plans to institute these screening techniques, 20% (9 of 45 respondents) stated plans to institute these techniques in the next 6 months, 55.5% (25 of 45 respondents) stated plans to institute these techniques within 6 months to 1 year, and 22.2% (10 of 45 respondents) stated plans to institute these techniques within 1 to 2 years. Academic physicians were more likely to use screening techniques (62.7%; P < .001) compared with private practitioners (31.4%). Only 12.4% of respondents reported using HPV or p16 data to direct care. CONCLUSIONS: Approximately 40.4% of radiation oncology practices that responded to a survey in the United States screened for HPV DNA or p16 in OC, whereas only 12.4% used it to further direct care. This number appears to be growing rapidly. Clinical trials to further elucidate how HPV or p16 status should direct care in OC are warranted. Cancer 2010;116:514-9.

show abstract

Section: Discussionmentioning

confidence: 67%

Survey on human papillomavirus/p16 screening use in oropharyngeal carcinoma patients in the United States

Shoushtari

Rahimi

Schlesinger

et al. 2009

Cancer

View full text Add to dashboard Cite

show abstract

“…HPV16, the type associated with the majority of cervical carcinomas, is the HR-HPV linked with the overwhelming majority of HPVpositive HNSCC (95%) (8)(9)(10). Other HR-HPV genotypes have been detected, including HPV18, HPV31, and HPV33.…”

mentioning

confidence: 99%

Identification of biomarkers that distinguish human papillomavirus (HPV)-positive versus HPV-negative head and neck cancers in a mouse model

Strati

Pitot

Lambert

2006

Proc. Natl. Acad. Sci. U.S.A.

131

156

View full text Add to dashboard Cite

Head and neck squamous cell carcinoma (HNSCC) is a leading cause of cancer mortality worldwide. Recent reports have associated a subset of HNSCC with high-risk human papillomaviruses (HPVs), particularly HPV16, the same subset of HPVs responsible for the majority of cervical and anogenital cancers. In this study we describe a mouse model for HPV-associated HNSCC that employs mice transgenic for the HPV16 oncogenes E6 and E7. In these mice, E6 and E7 induce aberrant epithelial proliferation and, in the presence of a chemical carcinogen, they increase dramatically the animal's susceptibility to HNSCC. The cancers arising in the HPV16-transgenic mice mirror the molecular and histopathological characteristics of human HPV-positive HNSCC that distinguish the latter from human HPV-negative HNSCC, including overexpression of p16 protein and formation of more basaloid cancers. This validated model of HPV-associated HNSCC provides the means to define the contributions of individual HPV oncogenes to HNSCC and to understand the molecular basis for the differing clinical properties of HPV-positive and HPV-negative human HNSCC. From this study, we identify minichromosome maintenance protein 7 (MCM7) and p16 as potentially useful biomarkers for HPV-positive head and neck cancer.head and neck squamous cell carcinoma (HNSCC) ͉ human papillomavirus 16 (HPV16) ͉ minichromosome maintenance protein 7 (MCM7) ͉ p16 ͉ transgenic H ead and neck cancers are the sixth most common malignancy in the world (1), and recent advances in treating them are not reflected in improved survival. Head and neck squamous cell carcinoma (HNSCC) is etiologically associated with tobacco use; alcohol consumption; and, in Southeast Asia, chewing of betel nut (2-6). However, more recent studies have implicated high-risk human papillomaviruses (HR-HPVs), the same viruses recognized as the causative agents of cervical and most other anogenital malignancies, in the etiology of a subset of HNSCC (7).HR-HPV DNA has been detected in Ϸ20% of HNSCC, particularly in malignancies of the oropharynx, where Ϸ50% of the cancers have been found to harbor viral DNA. HPV16, the type associated with the majority of cervical carcinomas, is the HR-HPV linked with the overwhelming majority of HPVpositive HNSCC (95%) (8-10). Other HR-HPV genotypes have been detected, including HPV18, HPV31, and HPV33. Viral oncogenes E6 and E7, the papillomaviral genes considered largely responsible for the onset as well as persistence of cervical cancer, have been detected in both integrated and extrachromosomal HPV genomes in HNSCC (11). E6 and E7 are best known for their ability to bind and inactivate the tumor suppressors p53 and pRb (12)(13)(14)(15)(16)(17), and these respective properties have been associated with their oncogenic properties (18,19). Consistent with E6 and E7 contributing to HPV-positive HNSCC is the absence of genetic or epigenetic alterations in the p53 and pRb pathways in HPV-positive HNSCC, in stark contrast to what is observed in HPV-negative HNSCC (11). Furthermore, di...

show abstract

“…[2][3][4] As already suggested in 1983, these OPSCC are characterized by human papilloma virus (HPV) infection. 5 Viral DNA of high risk HPV 16 can be detected in nuclei of tonsillar cancer cells, 6 and is responsible for the vast majority of HPV positive tumors. 7 These tumors arise mainly in the lingual and palatal tonsils and are characterized as being a type of HNSCC with different distinct epidemiological, molecular, and clinical characteristics.…”

mentioning

confidence: 99%

Is the improved prognosis of p16 positive oropharyngeal squamous cell carcinoma dependent of the treatment modality?

Fischer

Zlobec

Green

et al. 2009

Intl Journal of Cancer

167

132

View full text Add to dashboard Cite

The incidence of human papilloma virus (HPV) induced oropharyngeal squamous cell carcinoma (OPSCC) increases in the western countries. These OPSCC show distinct molecular characteristics and are characterized by an overexpression of p16, considered a surrogate marker for HPV infection. When compared to patients with p16 negative OPSCC, patients with HPV induced p16 positive OPSCC show a significantly better prognosis, which is reported to be caused by increased radiosensitivity. The objective of the present study was to analyze the impact of p16 expression status on the prognosis of OPSCC treated by either radiotherapy (RT) or primary surgery. Results are based upon a tissue microarray (TMA) of 365 head neck squamous cell carcinomas (HNSCC) including 85 OPSCC with clinico-pathological and follow-up data. p16 positivity correlated significantly with oropharyngeal tumor localization (p < 0.001). Patients with p16 positive OPSCC exhibited a significantly better overall survival than those with p16 negative tumors (p 5 0.007). In a multivariate analysis, survival benefit of patients with p16 positive OPSCC was independent of clinico-pathological parameters such as cT and cN classification and treatment modality. The improved prognosis of p16 positive OPSCC is found after RT as well as after surgery.Although incidence of head and neck squamous cell carcinoma (HNSCC) in general has decreased progressively during the last two decades, 1 an increased incidence of oral and oropharyngeal squamous cell carcinoma (OPSCC) was reported in the United States as well as in Europe. [2][3][4] As already suggested in 1983, these OPSCC are characterized by human papilloma virus (HPV) infection. 5 Viral DNA of high risk HPV 16 can be detected in nuclei of tonsillar cancer cells, 6 and is responsible for the vast majority of HPV positive tumors. 7 These tumors arise mainly in the lingual and palatal tonsils and are characterized as being a type of HNSCC with different distinct epidemiological, molecular, and clinical characteristics. 8 The main risk factor for these HPV positive OPSCC is sexual behavior with a high number of vaginal or oral sex partners. 8,9 HPV-induced OPSCC show distinct molecular characteristics suggesting a different pathway in carcinogenesis compared to HPV negative HNSCC. 10 One particular molecular difference among others concerns p16 expression. p16 functions as a cell-cycle checkpoint regulator, a tumor suppressor gene located on chromosome 9p21.In HPV negative HNSCC p16 is frequently inactivated by deletions, mutations or promoter methylation. 11 In HPV positive OPSCC, overexpressed viral oncoprotein E7 degrades pRb, 12 which otherwise inhibits p16 transcription. 13 The resulting nuclear and cytoplasmic p16 overexpression correlates precisely to HPV positivity and is suggested to be specific for HPV positive OPSCC. 14,15 As p16 overexpression is very rarely seen in HPV negative HNSCC it is considered a surrogate marker for HPV positive OPSCC. Direct diagnosis of HPV in HNSCC is only reliably possible by in s...

show abstract

Detection of human papillomavirus type 16 DNA in carcinomas of the palatine tonsil.

Cited by 98 publications

References 18 publications

Survey on human papillomavirus/p16 screening use in oropharyngeal carcinoma patients in the United States

Survey on human papillomavirus/p16 screening use in oropharyngeal carcinoma patients in the United States

Identification of biomarkers that distinguish human papillomavirus (HPV)-positive versus HPV-negative head and neck cancers in a mouse model

Is the improved prognosis of p16 positive oropharyngeal squamous cell carcinoma dependent of the treatment modality?

Contact Info

Product

Resources

About