作者: Stephen J. Hankinson , Mina Fam , Nitin N. Patel
DOI: 10.1016/J.UROLONC.2016.10.009
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摘要: Abstract Objectives Metformin has numerous antineoplastic effects including an AMP-activated protein kinase–dependent mechanism, kinase–independent mechanisms, alteration of insulin and insulin-like growth factor signaling pathways, suppression androgen pathways that trigger prostate cancer proliferation. In contrast to other malignancies are associated with increased incidence among patients obesity type II diabetes mellitus (T2DM), epidemiological studies suggest T2DM may impart a protective effect on by creating set metabolic conditions lower levels. Methods materials The PubMed Web Science databases were searched using the terms “prostate cancer,” “metformin,” “antineoplastic,” “antitumorigenic,” “diabetes” up first week August 2016. Articles regarding metformin’s properties reviewed. Results Treating metformin reverse suppress levels, thereby enabling higher levels androgens stimulate growth, proliferation, tumorigenesis. Thus, not be appreciable in early stages development because corrects for cancer. These findings, although inconclusive, do support use as preventive agent However, future appears bright either monotherapy or adjunct deprivation therapy, external-beam radiation prostatectomy, chemotherapy. Support this includes meta-analyses mortality benefit metformin, clinical trial demonstrates leads significant improvement syndrome parameters shows modest activity treatment some asymptomatic minimally symptomatic metastatic castration–resistant Conclusions This review summarizes literature implications, trajectory research