High risk HPV in situ hybridization, p16 INK 4A, and survivin expressions in cervical carcinomas and intraepithelial neoplasms: evaluation of prognostic factors


Demir F. , KIMILOGLU E., IGDEM A. A. , AYANOGLU Y. T. , ERDOGAN N.

EUROPEAN JOURNAL OF GYNAECOLOGICAL ONCOLOGY, cilt.35, ss.708-717, 2014 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 35 Konu: 6
  • Basım Tarihi: 2014
  • Doi Numarası: 10.12892/ejgo25642014
  • Dergi Adı: EUROPEAN JOURNAL OF GYNAECOLOGICAL ONCOLOGY
  • Sayfa Sayıları: ss.708-717

Özet

Background: Cervical carcinoma (CC) is one of the most important health problems of adult women in developing countries. CC is the second most common carcinoma of the women worldwide. Efficient screening and early therapeutic programmes are vital because of the higher burden of the disease. Materials and Methods: The authors included a total of 53 cases in this study. Distribution of diagnoses among cases was as follows: cervical intraepithelial neoplasm (CIN) (n=44), squamous cell carcinoma (SCC) (n=7), adenocarcinoma in situ (n=1), and condyloma accuminatum (n=1). Presence, density, and nuclear identification form of human papilloma virus (HPV) DNA in relation with host cell DNA were evaluated by in situ hybridization (ISH) and p16 and survivin by immunohistochemical methods (IHC). Results: The authors determined that the presence, density, and nuclear identification form of high risk HPV DNA had diagnostic and prognostic importance in CC and CIN (p < 0.05). p16 and survivin also had diagnostic significance. Since p16 and survivin expressions signalled progressive oncogenic events, p16 and survivin were persistent HPV markers (for p16, p < 0.001, for survivin p<0.01). The authors determined that expressions, density, and prevalence of all three markers showed correlation with increasing CIN grade (for p 16, p < 0.001, for survivin, p < 0.01, for HPV, p = 0.002). The episomal pattern which is the independent visit of Hr HPV DNA to host cell DNA, signalled early HPV infection (p = 0.001). When it is integrated into host cell DNA, especially if HPV DNA signal intensity and prevalence increases, then this signal signifies persistent HPV infection (p = 0.001). Conclusion: With the aid of these findings, the authors determined that HPV is infectious in CIN I and proliferative (neoplastic) in CIN II-CIN III lesions.