%0 Generic %A K., Ito %A H., Ogata %A N., Honma %A K., Shibuya %A T., Mikami %D 2019 %T Supplementary Material for: Expression of mTOR Signaling Pathway Molecules in Triple-Negative Breast Cancer %U https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Expression_of_mTOR_Signaling_Pathway_Molecules_in_Triple-Negative_Breast_Cancer/10271987 %R 10.6084/m9.figshare.10271987.v1 %2 https://karger.figshare.com/ndownloader/files/18567386 %K Triple-negative breast cancer %K mTOR %K Glucose transporter %X Introduction: Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor (ER), progesterone receptor (PgR), and epidermal growth factor receptor 2 (HER2), currently has no effective hormonal or molecular target therapy. Objective and Methods: To elucidate the role of the mammalian target of rapamycin (mTOR) signaling pathway in TNBC, the expression of molecules involved in mTOR signaling including mTOR, phosphorylated (p)-mTOR, p-4EBP1, GLUT1, GLUT3, HIF-1α, and Ki67 was investigated by immunohistochemistry in 35 TNBC and 81 non-TNBC cases. Results: Expression of p-mTOR, the activated form of mTOR, but not unphosphorylated mTOR, was significantly higher in non-TNBC cases than in TNBC cases. Expression of p-4EBP1, GLUT1, and GLUT3 was higher in TNBC cases than in non-TNBC cases. When the localization of p-mTOR was classified as nuclear, perinuclear, or cytoplasmic, nuclear localization of p-mTOR was observed more frequently in TNBC than in non-TNBC cases and was correlated with the expression of GLUT1 and GLUT3, which was related to proliferation activity examined with Ki67. Conclusions: mTOR signaling regulates cell proliferation in some cases of TNBC and may be a potential target of molecular therapy for TNBC. %I Karger Publishers