Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth.

By M. Buzzai, Russell G. Jones, R. Amaravadi, J. Lum, Ralph J. Deberardinis, F. Zhao, B. Viollet, Craig B. Thompson. Cancer Research, 2007

939 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/2edd352cabd4712461a8fab3081e618a9f77ec17

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Citations in the corpus

Targeting Metabolism for Cancer Therapy (2017, background): “The anti-tumorigenic properties of metformin and other biguanides have been modeled in various mouse cancer models (Buzzai et al., 2007; Huang et al., 2008; Shackelford et al., 2013; Wheaton et al., 2014).”
The insulin and insulin-like growth factor receptor family in neoplasia: an update (2012, background): “Experimental tumours that lack LKB1 or p53 seem to be less able to reduce energy consumption to compensate for biguanide-induced energy stress, resulting in severe ATP depletion and necrotic cell deat”
LKB1 and AMPK control of mTOR signalling and growth (2009, methodology): “AMPK activation by metformin or AICAR inhibits the growth of tumour cell in culture as well as in xenograft models (Buzzai et al. 2007).”
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “Treatment with the antidiabetic drug metformin, an inhibitor of complex 1 of the mitochondrial electron transport chain (El-Mir et al., 2000; Owen et al., 2000), is especially toxic to p53-deficient tumor cells (Buzzai et al., 2007).”
G protein-coupled receptors: novel targets for drug discovery in cancer (2010, background): “It is noteworthy that metformin (1,1-dimethylbiguanide hydrochloride), one of the most widely prescribed drugs for the treatment of type 2 diabetes, activates AMP kinase (AMPK), which in turn blocks mTOR complex 1 activity, leading to the inhibition of cancer cell growt”
AMPK is a negative regulator of the Warburg Effect and suppresses tumor growth in vivo (2012, methodology): “Our data provide amechanistic rationale in support of the use of AMPK agonists such as metformin for cancer therapy (Buzzai et al., 2007; Evans et al., 2005), as the efficacy of these agents against tumor growth may lie in their ability to engage AMPK-dependent metabolic checkpoints to restrict…”
Metformin: from mechanisms of action to therapies. (2014, background): “Later, high concentrations of various biguanide derivatives were found to specifically reduce NADH but not succinate oxidation in submitochondrial particles, assigning the inhibitory effect of these compounds on OXPHOS to the 954 Cell Metabolism 20, December 2, 2014 ª2014 Elsevier Inc. complex 1 of ”
Understanding the intersections between metabolism and cancer biology (2017, neutral): “Increased biguanide sensitivity has been attributed to various mutations (Buzzai et al., 2007; Shackelford et al., 2013), but tissue environment also affects response to these drugs (Gui et al., 2016).”