Paweł Golusiński1,2, Jakub Pazdrowski1, Mateusz Szewczyk1, Maciej Misiołek3, Wioletta Pietruszewska4, Janusz Klatka5, Sławomir Okła6, Henryk Kaźmierczak7, Andrzej Marszałek8,9, Violetta Filas8,9, Augusto Schneider10,11, Michał M Masternak11, Katarzyna Stęplewska12, Katarzyna Miśkiewicz-Orczyk3, Wojciech Golusiński1. 1. Department of Head and Neck Surgery, Poznan University of Medical Sciences, Greater Poland Cancer Centre, Poznan, Poland. 2. Department of Biology and Environmental Studies, Poznan University of Medical Sciences, Poznan, Poland. 3. Department of Otolaryngology and Laryngological Oncology in Zabrze, Medical University of Silesia in Katowice, Poland. 4. Department of Otolaryngology and Laryngological Oncology, Medical University of Lodz, Poland. 5. Department of Otolaryngology and Laryngological Oncology, Medical University of Lublin, Poland. 6. Department of Otolaryngology and Head and Neck Surgery, Regional Cancer Center, Kielce, Poland. 7. Department of Otolaryngology, Ludwik Rydgier Medical College in Bydgoszcz, Nicolaus Copernicus University in Toruń, Poland. 8. Department of Oncologic Pathology and Prophylactics, Poznan University of Medical Sciences, Greater Poland Cancer Centre, Poznan, Poland. 9. Department of Oncologic Pathology, Greater Poland Cancer Centre, Poznan, Poland. 10. Department of Nutrition, Federal University of Pelotas, Pelotas, RS, Brazil. 11. University of Central Florida, Burnett School of Biomedical Sciences, College of Medicine, Orlando, FL, USA. 12. Department of Patomorphology, Medical University of Silesia in Katowice, Poland.
Abstract
AIM: Our goal was to determine the expression levels of p16 in the cohort of the OPSCC patients and evaluation of the pathological and clinical differences between these two groups including patients' survival. BACKGROUND: HPV infection is the main causative factor of oropharyngeal cancer (OPSCC). Identification of HPV status in OPSCC requires positive evaluation of viral DNA integration into host cell however, p16 accumulation in the proliferating cell layers has been accepted as an alternative marker for HPV infection. MATERIAL AND METHODS: The IHC staining for p16 has been performed in tumor tissue from 382 OPSCC patients. The sample was considered positive based on more than 70% of carcinoma tissue showing strong and diffused nuclear and cytoplasmic immunostaining. The clinicopathological characteristics of the patients including site, age, gender, tumor grade, tumor stage, the nodal status, smoking and survival have been analyzed when comparing p16 positive and p16 negative tumors. RESULTS: Out of our cohort in 38.2% cases positive staining for p16 has been recorded. Our analysis did not indicate significant differences in the distribution of the p16 positive patients and age of the patients, stage of the disease. Among the patients who have presented with the N+ neck, there were significantly more p16 positive tumors than in the group with N0 neck (p = 0.0062). There was highly significant correlation between the expression of p16 and smoking (p < 0.0001). The significant difference in survival (p < 0.0001) with more favorable prognosis in the p16 positive group has been observed. CONCLUSIONS: Overexpression of p16 is accepted as a surrogate diagnostic marker for detecting HPV infection in oropharyngeal cancer. However, one should remember about existence of the small subgroups of p16 positive but HPV negative tumors, with relatively worse prognosis. Immunostaining for p16, however useful on everyday basis, should be complemented with other techniques in terms of reliable identification of the HPV infection.
AIM: Our goal was to determine the expression levels of p16 in the cohort of the OPSCC patients and evaluation of the pathological and clinical differences between these two groups including patients' survival. BACKGROUND:HPV infection is the main causative factor of oropharyngeal cancer (OPSCC). Identification of HPV status in OPSCC requires positive evaluation of viral DNA integration into host cell however, p16 accumulation in the proliferating cell layers has been accepted as an alternative marker for HPV infection. MATERIAL AND METHODS: The IHC staining for p16 has been performed in tumor tissue from 382 OPSCC patients. The sample was considered positive based on more than 70% of carcinoma tissue showing strong and diffused nuclear and cytoplasmic immunostaining. The clinicopathological characteristics of the patients including site, age, gender, tumor grade, tumor stage, the nodal status, smoking and survival have been analyzed when comparing p16 positive and p16 negative tumors. RESULTS: Out of our cohort in 38.2% cases positive staining for p16 has been recorded. Our analysis did not indicate significant differences in the distribution of the p16 positive patients and age of the patients, stage of the disease. Among the patients who have presented with the N+ neck, there were significantly more p16 positive tumors than in the group with N0 neck (p = 0.0062). There was highly significant correlation between the expression of p16 and smoking (p < 0.0001). The significant difference in survival (p < 0.0001) with more favorable prognosis in the p16 positive group has been observed. CONCLUSIONS: Overexpression of p16 is accepted as a surrogate diagnostic marker for detecting HPV infection in oropharyngeal cancer. However, one should remember about existence of the small subgroups of p16 positive but HPV negative tumors, with relatively worse prognosis. Immunostaining for p16, however useful on everyday basis, should be complemented with other techniques in terms of reliable identification of the HPV infection.
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