Lifang Cui1, Congling Qu2, Honggang Liu1. 1. Department of Pathology, Beijing Key Laboratory of Head and Neck Molecular Diagnostic Pathology, Beijing Tongren Hospital, Capital Medical University, Beijing, China. 2. The Department of Pathology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Abstract
OBJECTIVE: To investigate the role of human papillomavirus (HPV) in laryngeal squamous cell carcinoma (LSCC) and analyse the relationship between HPV and the expression of cell cycle-related proteins. DESIGN: The study consisted of LSCC between 2005 and 2011 in Tongren Hospital. Clinical data such as age, sex, smoking/alcohol consumption, and TNM stage were collected. HPV DNA and cell cycle-related proteins were assessed in terms of clinical features. SETTING: Single-centre study. PARTICIPANTS: A total of 332 LSCC patients were included in the study. MAIN OUTCOME MEASURES: The presence of genotype-specific HPV DNA was evaluated using PCR-RDB in formalin-fixed paraffin-embedded tissues. All samples were also evaluated for p16INK4A , p21WAF1/CIP1 , P53, Cyclin D1, and Ki67 immunohistochemical staining by tissue microarray. RESULTS: HPV DNA was detected in 45 of 332 (13.55%) patients with LSCC, with HPV-16 being the predominant genotype. The presence of HPV-16 DNA was significantly associated with basaloid squamous cell carcinoma and cystic lymph node metastasis (P < 0.05). Of the 332 patients, 36 (10.84%) were scored as p16INK4A positivity and they were more likely to be female (P < 0.05). Cyclin D1-positivity and p21WAF1/CIP1 -positivity were observed in 60.24% (200/332) and 40.66% (135/332), respectively. In 114 cases (34.33%), LSCCs had moderate- to -strong p53 accumulation, which was correlated with TNM stage (P < 0.05). HPV-16 DNA was correlated with p16INK4A and manifested a higher Ki-67 labelling index and p21WAF1/CIP1 expression than HPV-16-negative tumours (P < 0.05). No relationship was observed between Cyclin D1or P53 expression and HPV-16 infection (P > 0.05). CONCLUSION: HPV DNA was detected in 13.55% patients with LSCC, with HPV-16 being the predominant genotype and it was correlated with p16INK4A and manifested a higher Ki-67 labelling index and p21WAF1/CIP1 expression than HPV-16-negative tumours.
OBJECTIVE: To investigate the role of human papillomavirus (HPV) in laryngeal squamous cell carcinoma (LSCC) and analyse the relationship between HPV and the expression of cell cycle-related proteins. DESIGN: The study consisted of LSCC between 2005 and 2011 in Tongren Hospital. Clinical data such as age, sex, smoking/alcohol consumption, and TNM stage were collected. HPV DNA and cell cycle-related proteins were assessed in terms of clinical features. SETTING: Single-centre study. PARTICIPANTS: A total of 332 LSCC patients were included in the study. MAIN OUTCOME MEASURES: The presence of genotype-specific HPV DNA was evaluated using PCR-RDB in formalin-fixed paraffin-embedded tissues. All samples were also evaluated for p16INK4A , p21WAF1/CIP1 , P53, Cyclin D1, and Ki67 immunohistochemical staining by tissue microarray. RESULTS:HPV DNA was detected in 45 of 332 (13.55%) patients with LSCC, with HPV-16 being the predominant genotype. The presence of HPV-16 DNA was significantly associated with basaloid squamous cell carcinoma and cystic lymph node metastasis (P < 0.05). Of the 332 patients, 36 (10.84%) were scored as p16INK4A positivity and they were more likely to be female (P < 0.05). Cyclin D1-positivity and p21WAF1/CIP1 -positivity were observed in 60.24% (200/332) and 40.66% (135/332), respectively. In 114 cases (34.33%), LSCCs had moderate- to -strong p53 accumulation, which was correlated with TNM stage (P < 0.05). HPV-16 DNA was correlated with p16INK4A and manifested a higher Ki-67 labelling index and p21WAF1/CIP1 expression than HPV-16-negative tumours (P < 0.05). No relationship was observed between Cyclin D1or P53 expression and HPV-16 infection (P > 0.05). CONCLUSION:HPV DNA was detected in 13.55% patients with LSCC, with HPV-16 being the predominant genotype and it was correlated with p16INK4A and manifested a higher Ki-67 labelling index and p21WAF1/CIP1 expression than HPV-16-negative tumours.