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• W2149447714 abstract "BackgroundInsulin/insulin-like growth factor-I (IGF-I) signaling is a mechanism mediating the promoting effect of type 2 diabetes (DM2) on cancer. Human epidermal growth factor receptor (HER2), insulin receptor and IGF-I receptor involve the same PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer.MethodsWe reviewed 1983 consecutive patients with HER2+ breast cancer treated between 1 January 1998 and 30 September 2010. The overall survival, breast cancer-specific death rate, age, race, nuclear grade, stage, menopausal status, estrogen and progesterone receptor status, body mass index and classes of antidiabetic pharmacotherapy were analyzed.ResultsA Cox regression analysis showed that DM2 [P = 0.026, hazard ratio (HR) = 1.42, 95 % confidence interval (95 % CI) 1.04–1.94] predicted poor survival of stage ≥2 HER2+ breast cancer. In Kaplan–Meier analysis, metformin predicted lengthened survival and so did thiazolidinediones. Analyzing only the diabetics, Cox regression showed that metformin (P = 0.041, HR = 0.52, 95 % CI 0.28–0.97) and thiazolidinediones (P = 0.036; HR = 0.41, 95 % CI 0.18–0.93) predicted lengthened survival, and competing risk analysis showed that metformin and thiazolidinediones were associated with decreased breast cancer-specific mortality (P = 0.023, HR = 0.47, 95 % CI 0.24–0.90 and P = 0.044, HR = 0.42, 95 % CI 0.18–0.98, respectively).ConclusionsThiazolidinediones and metformin users are associated with better clinical outcomes than nonusers in diabetics with stage ≥2 HER2+ breast cancer. The choice of antidiabetic pharmacotherapy may influence prognosis of this group." @default.
• W2149447714 created "2016-06-24" @default.
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• W2149447714 date "2012-07-01" @default.
• W2149447714 modified "2023-10-16" @default.
• W2149447714 title "Metformin and thiazolidinediones are associated with improved breast cancer-specific survival of diabetic women with HER2+ breast cancer" @default.
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• W2149447714 doi "https://doi.org/10.1093/annonc/mdr534" @default.
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