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Endocannabinoid system expression in ovarian epithelial tumors according to the dualistic model of ovarian carcinogenesis.
- Source :
- European Review for Medical & Pharmacological Sciences; 7/15/2021, Vol. 25 Issue 14, p4678-4686, 9p
- Publication Year :
- 2021
-
Abstract
- OBJECTIVE: Our study aimed to confirm the expression of the endocannabinoid system in the human epithelial ovarian tumors, assessing the immunohistochemical expression of Cannabinoid Receptor Type 1 and Fatty Acid Amide Hydrolase in benign, borderline and malignant tumors. MATERIALS AND METHODS: Cannabinoid Receptor Type 1 and Fatty Acid Amide Hydrolase immunohistochemical expression was determined in 118 epithelial ovarian tumors sequentially treated during the last decade in our department: 36 benign, 34 borderline and 48 malignant neoplasms. Cannabinoid Receptor type 1 and Fatty Acid Amide Hydrolase expression resulted predominantly weak-moderate in the benign and borderline forms. RESULTS: concerning malignant tumors, Cannabinoid Receptor Type 1 expression resulted predominantly moderate-strong in Type I tumors and negative-weak in Type II tumors. Fatty Acid Amide Hydrolase expression resulted, instead, independent by the tumor types. Furthermore, there was no significant difference in the Cannabinoid Receptor Type 1 and Fatty Acid Amide Hydrolase expression relatively to the tumoral stages. CONCLUSIONS: The present study confirmed a variable expression of the endocannabinoid system in human ovarian tumors. Cannabinoid Receptor Type 1 expression was significantly different in malignant epithelial ovarian tumors according to dualistic model of ovarian carcinogenesis. Thus, in the most aggressive types II ovarian tumors, Cannabinoid Receptor Type 1 expression resulted predominantly negative or weak. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11283602
- Volume :
- 25
- Issue :
- 14
- Database :
- Supplemental Index
- Journal :
- European Review for Medical & Pharmacological Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 151691382