Evaluation of the Caveolin-1 expressions in uterine cervical carcinomas
European Journal of Gynaecological Oncology, cilt.38, sa.5, ss.785-789, 2017 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 38 Sayı: 5
- Basım Tarihi: 2017
- Doi Numarası: 10.12892/ejgo3655.2017
- Dergi Adı: European Journal of Gynaecological Oncology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.785-789
- Anahtar Kelimeler: Uterine cervix, Caveolin-1 (Cav-1), Squamous cell carcinomas (SCC), Adenosquamous carcinoma, Adenocarcinoma
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Aim: Caveolin-1 (Cav-1) is an important regulator of cellular processes and it involves several biological and metabolic functions, including cell growth, apoptosis, angiogenesis, and also carcinogenesis. This retrospective study was designed to evaluate the differences of tissue expressions of Cav-1 in a spectrum of cervical neoplasms. Materials and Methods: Tissue expression of Cav-1 was studied in a total of 107 formalin-fixed, paraffin-embedded uterine cervical tumors specimens and its association with different clinicopathologic parameters was evaluated. Results: In this series, there were 30 low- and 29 high-grade cervical intraepithelial neoplasms, 27 squamous cell carcinomas (SCCs), 15 adenosquamous carcinomas (ASCs), and six adenocarcinomas (ACs). Epithelial Cav-1 expression was determined in most SCCs, while it was negative in all ACs and most ASCs (p < 0.001). Statistically it was determined that the expression of stromal Cav-1 was significantly upregulated in invasive carcinomas when compared with non-invasive squamous cell carcinomas (p < 0.001), and this finding was inconsistent with literature. Conclusions: The present findings demonstrated a link between epithelial Cav-1 expression and the squamous differentiation of uterine neoplasms, as well as the relationship between invasion and stromal Cav-1 expression. Therefore it may be suggested that Cav-1 may play a role in the pathogenesis of cervical SCCs.