Jae Hong No, Yong-Tark Jeon, In-Ae Park, Daehee Kang, Jae Weon Kim, Noh-Hyun Park, Soon-Beom Kang, Yong-Sang Song
Med Sci Monit 2009; 15(10): BR301-305
Available online: 2009-09-30
Mammalian target of rapamycin (mTOR) plays a crucial role in carcinogenesis by regulating protein synthesis, and mTOR inhibitors have been identified as potential anticancer agents in various cancers. Since the most common genetic change in endometrial cancer is the mutation of phosphatase and tensin homologue (PTEN), a negative regulator of mTOR, we evaluated mTOR expression in endometrial cancer and its relationship with other clinicopathological characteristics and expression patterns of cyclooxygenase-2 (COX-2) and p53.
Material and Method: Immunohistochemical analysis of mTOR was performed on paraffin-embedded tissue specimens obtained from 141 patients with endometrial carcinoma. Results were correlated with the clinicopathological characteristics and expression pattern of COX-2 and p53.
Results: mTOR overexpression was detected in 7.1% (10/141) of patients. mTOR expression was highly correlated with old age, menopausal status and COX-2 expression (P<0.05). Multivariate analysis revealed that COX-2 was the only independent factor related to expression of mTOR. However, there was no correlation of mTOR expression with prognostic factors such as histologic type, grade, invasion of myometrium, lymph node metastasis, stage, and survival.
Conclusions: Our findings suggest that the expression of mTOR is infrequent and is associated with COX-2 overexpression. Careful selection of patients might be necessary in the use of mTOR inhibitor as a molecular targeted therapy for patients with endometrial cancer.
Keywords: TOR Serine-Threonine Kinases, Protein Kinases - metabolism, Endometrial Neoplasms - pathology, Cyclooxygenase 2 - metabolism, Tumor Suppressor Protein p53 - metabolism