2016
DOI: 10.1007/s12094-016-1521-1
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Proteomic modulation in breast tumors after metformin exposure: results from a “window of opportunity” trial

Abstract: NCT00930579.

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Cited by 10 publications
(8 citation statements)
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“…Our findings require replication with a larger sample of ER– tumors. If confirmed, our findings suggest that targeting the mTOR pathway using pharmacological approaches, such as metformin [ 26 , 27 ] and other mTOR inhibitors, may be able to prevent a subset of ER+ and ER– tumors.…”
Section: Discussionsupporting
confidence: 58%
“…Our findings require replication with a larger sample of ER– tumors. If confirmed, our findings suggest that targeting the mTOR pathway using pharmacological approaches, such as metformin [ 26 , 27 ] and other mTOR inhibitors, may be able to prevent a subset of ER+ and ER– tumors.…”
Section: Discussionsupporting
confidence: 58%
“…As hyperglycemia is a known potential side effect of MK-2206, poorly controlled diabetes (hemoglobin A1C ≥ 8%) was an exclusion criterion. If patients were taking metformin, it was required that the patient had been receiving this medication for > 3 months, given metformin’s potential impact on PI3K/Akt signaling 10 . The study was approved by the CUMC and AECC institutional review boards (clinicaltrials.gov identifier: NCT01319539).…”
Section: Methodsmentioning
confidence: 99%
“…Administration of metformin (1500 mg, daily, NCT00930579, phase II, Table 2) to 35 non-diabetic overweight women (BMI ≥ 25 kg/m 2 ) with breast cancer (stages 0-III) showed no significant difference in the tumor proliferation index (Ki67) when compared to age, BMI, and stage matched historic controls, despite a significant reduction in BMI, cholesterol, and leptin levels in the metformin-treated subjects [158]. Increase in the levels of Raptor, C-Raf, Cyclin B1, Cyclin D1, TRFC, and Syk; while reduction in the levels of pMAPK pT202, Y204 , JNK pT183, pT185 , Bad pS112 , PKCα pS657 , and Src pY416 was observed in the metformin administered (1500 mg, daily, NCT00930579, phase II, Table 2) non-diabetic overweight women with breast cancer when compared to age, BMI, and stage-matched historic controls [159]. This is indicative of the fact that in a clinical setting, metformin administration can influence cancer cell apoptosis, cell cycle, cell signaling, and invasion [159].…”
Section: Clinical Data and Trialsmentioning
confidence: 97%
“…Increase in the levels of Raptor, C-Raf, Cyclin B1, Cyclin D1, TRFC, and Syk; while reduction in the levels of pMAPK pT202, Y204 , JNK pT183, pT185 , Bad pS112 , PKCα pS657 , and Src pY416 was observed in the metformin administered (1500 mg, daily, NCT00930579, phase II, Table 2) non-diabetic overweight women with breast cancer when compared to age, BMI, and stage-matched historic controls [159]. This is indicative of the fact that in a clinical setting, metformin administration can influence cancer cell apoptosis, cell cycle, cell signaling, and invasion [159]. A phase II, single arm, 'window of opportunity' neoadjuvant metformin clinical study (NCT00897884, phase II, Table 2) conducted in non-diabetic early stage breast cancer patients investigated whether taking metformin (500 mg; thrice daily for ≥ 2 weeks after diagnostic biopsy) until surgery could reduce cell proliferation rates in the tumor tissue and reported reduced levels of phosphorylated Akt and ERK1/2, coupled to reduction on the levels of insulin and insulin receptors indicating that the anti-cancer effect of metformin presents insulin-dependent effects in a clinical scenario [136].…”
Section: Clinical Data and Trialsmentioning
confidence: 97%