Supplementary Material for: Expression of mTOR Signaling Pathway Molecules in Triple-Negative Breast Cancer Ito K. Ogata H. Honma N. Shibuya K. Mikami T. 10.6084/m9.figshare.10271987.v1 https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Expression_of_mTOR_Signaling_Pathway_Molecules_in_Triple-Negative_Breast_Cancer/10271987 <b><i>Introduction:</i></b> 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. <b><i>Objective and Methods:</i></b> 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. <b><i>Results:</i></b> 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. <b><i>Conclusions:</i></b> mTOR signaling regulates cell proliferation in some cases of TNBC and may be a potential target of molecular therapy for TNBC. 2019-11-08 10:32:51 Triple-negative breast cancer mTOR Glucose transporter