Lack of evidence of human papillomavirus-induced squamous cell carcinomas of the oral cavity in southern Germany

• Verfasst von: Reuschenbach, Miriam [VerfasserIn]
• Verfasst von: Kansy, Julia Katharina [VerfasserIn]
• Verfasst von: Garbe, Kira [VerfasserIn]
• Verfasst von: Vinokurova, Svetlana [VerfasserIn]
• Verfasst von: Flechtenmacher, Christa [VerfasserIn]
• Verfasst von: Tóth, Csaba [VerfasserIn]
• Verfasst von: Prigge, Elena-Sophie [VerfasserIn]
• Verfasst von: Thiele, Oliver C. [VerfasserIn]
• Verfasst von: Reinert, Siegmar [VerfasserIn]
• Verfasst von: Hoffmann, Jürgen [VerfasserIn]
• Verfasst von: Knebel Doeberitz, Magnus von [VerfasserIn]
• Verfasst von: Freier, Kolja [VerfasserIn]
• Titel: Lack of evidence of human papillomavirus-induced squamous cell carcinomas of the oral cavity in southern Germany
• Verf.angabe: Miriam Reuschenbach, Katinka Kansy, Kira Garbe, Svetlana Vinokurova, Christa Flechtenmacher, Csaba Toth, Elena-Sophie Prigge, Oliver C. Thiele, Siegmar Reinert, Jürgen Hoffmann, Magnus von Knebel Doeberitz, Kolja Freier
• E-Jahr: 2013
• Jahr: 19 April 2013
• Umfang: 6 S.
• Fussnoten: Gesehen am 03.01.2022
• Titel Quelle: Enthalten in: Oral oncology
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1997
• Jahr Quelle: 2013
• Band/Heft Quelle: 49(2013), 9 vom: Sept., Seite 937-942
• ISSN Quelle: 1879-0593
• DOI: doi:10.1016/j.oraloncology.2013.03.451
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Human papillomavirus
• Sach-SW: Ki-67
• Sach-SW: Oral cavity
• Sach-SW: p16
• Sach-SW: Squamous cell cancer
• K10plus-PPN: 1784468797

Abstract

Objectives - The aim of the present study was to identify HPV-attributable SCC of the oral cavity (OSCC) in a cohort of patients from southern Germany. - Materials and methods - A sensitive PCR-enzyme immunoassay (EIA) was followed by a more specific in situ hybridization (ISH) to detect high risk human papillomavirus (HPV). An immunohistochemical dual-staining for p16INK4a and the proliferation marker Ki-67 was used to assess whether co-expression of p16INK4a/Ki-67 is a better surrogate marker for HPV in OSCC than p16INK4a alone, based on the hypothesis that combined p16INK4a and Ki-67 expression might specifically discriminate oncogene-induced p16INK4a expression from cell-cycle arrest-inducing senescence-associated p16INK4a expression. - Results - HPV-DNA by PCR-EIA could be detected in 25.1% (69/275) of the tumors, but ISH was negative in all of them. Diffuse p16INK4a overexpression was detected in 11 HPV PCR-positive tumors, but also in 6 HPV PCR-negative tumors. p16INK4a-expressing cells in diffusely positive tumors co-expressed Ki-67, irrespective of the HPV status. Neither the sole HPV status nor combined HPV/p16INK4a status nor the sole p16INK4a status was significantly associated with disease free or overall survival, however a trend towards better overall survival of patients whose tumor expressed p16INK4a in a focal pattern (=p16INK4a-positive/Ki-67-negative cells) compared to no p16INK4a expression (p=0.09) was observed. - Conclusion - Viral DNA can be detected in some tumors by a sensitive PCR, but absence of ISH signals indicates that the HPV-attributable fraction is smaller than estimated from PCR positivity. p16INK4a/Ki-67 co-expression is detectable in a fraction of OSCC irrespective of the HPV status.