Alos Llucia, Moyano Susana, Nadal Alfons, Alobid Isam, Blanch Jose L, Ayala Edgar, Lloveras Belén, Quint Wim, Cardesa Antonio, Ordi Jaume
Department of Pathology, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain.
Cancer. 2009 Jun 15;115(12):2701-9. doi: 10.1002/cncr.24309.
The role of human papillomavirus (HPV) in the pathogenesis of squamous cell carcinomas (SCCs) of the sinonasal tract and its clinicopathological implications were evaluated.
All SCCs of the sinonasal tract diagnosed in the Hospital Clinic of Barcelona from 1981 to 2006 were retrospectively evaluated (N = 60). Clinical and pathological data were reviewed. HPV infection was determined and typed by amplification of HPV DNA by polymerase chain reaction using the SPF-10 primers. p16(INK4a) expression was determined by immunohistochemistry. Overall and progression-free survival for HPV-positive and -negative patients was estimated by Kaplan-Meier analysis and by the use of a multivariate Cox proportional hazards model.
HPV DNA was detected in tumor tissue of 12 of 60 (20%) patients. HPV16 was identified in 11 tumors and HPV35 in 1. Immunohistochemistry for p16(INK4a) stained all HPV-positive and no HPV-negative tumors (P < .001). No differences were observed in terms of site and histological grade or stage at presentation between HPV-positive and -negative tumors. However, HPV-positive patients had a significantly better 5-year progression-free survival (62%; 95% confidence interval [CI], 23%-86% vs 20%; 95% CI, 9%-34%; P = .0043, log-rank test) and overall survival (80%; 95% CI, 20%-96% vs 31%; 95% CI, 15%-47%; P = .036, log-rank test) than patients with HPV-negative tumors. In multivariate analysis, HPV-positive tumors were associated with improved progression-free survival (hazard ratio, 0.21; 95% CI, 0.17-0.98; P = .012).
A subgroup of sinonasal SCCs is associated with HPV infection. These tumors have a significantly better prognosis.
评估人乳头瘤病毒(HPV)在鼻窦鳞状细胞癌(SCC)发病机制中的作用及其临床病理意义。
回顾性评估1981年至2006年在巴塞罗那医院诊所诊断的所有鼻窦SCC(N = 60)。复查临床和病理数据。使用SPF-10引物通过聚合酶链反应扩增HPV DNA来确定HPV感染并进行分型。通过免疫组织化学确定p16(INK4a)表达。通过Kaplan-Meier分析和使用多变量Cox比例风险模型估计HPV阳性和阴性患者的总生存率和无进展生存率。
60例患者中有12例(20%)的肿瘤组织中检测到HPV DNA。11例肿瘤中鉴定出HPV16,1例中鉴定出HPV35。p16(INK4a)免疫组织化学染色显示所有HPV阳性肿瘤,而HPV阴性肿瘤均未染色(P <.001)。HPV阳性和阴性肿瘤在发病部位、组织学分级或分期方面未观察到差异。然而,HPV阳性患者的5年无进展生存率(62%;95%置信区间[CI],23%-86% vs 20%;95%CI,9%-34%;P =.0043,对数秩检验)和总生存率(80%;95%CI,20%-96% vs 31%;95%CI,15%-47%;P =.036,对数秩检验)明显优于HPV阴性肿瘤患者。在多变量分析中,HPV阳性肿瘤与无进展生存率提高相关(风险比,0.21;95%CI,0.17-0.98;P =.012)。
一部分鼻窦SCC与HPV感染有关。这些肿瘤的预后明显更好。