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Javier A. Menendez

Researcher at NorthShore University HealthSystem

Publications -  336
Citations -  29348

Javier A. Menendez is an academic researcher from NorthShore University HealthSystem. The author has contributed to research in topics: Cancer & Fatty acid synthase. The author has an hindex of 73, co-authored 317 publications receiving 25654 citations. Previous affiliations of Javier A. Menendez include Northwestern University & Boston Biomedical Research Institute.

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Metformin is synthetically lethal with glucose withdrawal in cancer cells

TL;DR: The microenvironment-mediated contextual synthetic lethality of metformin should be expected to enormously potentiate the anti-cancer effect of anti-angiogenesis agents that promote severe oxygen and glucose deprivation in certain areas of the tumor tissues.
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Micro(mi)RNA expression profile of breast cancer epithelial cells treated with the anti-diabetic drug metformin: induction of the tumor suppressor miRNA let-7a and suppression of the TGFβ-induced oncomiR miRNA-181a.

TL;DR: Metformin’s molecular functioning to prevent invasive breast cancer can be explained in terms of its previously unrecognized ability to efficiently up-regulate the tumor-suppressive miRNAs let-7a & mi RNA-96 and inhibit the oncogenic miRNA-181a, thus epigenetically preserving the differentiated phenotype of mammary epithelium while preventing EMT-related cancer-initiating cell self-renewal.
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The angiogenic factor CYR61 in breast cancer: molecular pathology and therapeutic perspectives.

TL;DR: Results delineate a new noteworthy function of a CYR61/alpha(v)beta(3) autocrine-paracrine signaling pathway within both angiogenesis and breast cancer progression, which would allow a dual anti-angiogenic and anti-tumor benefit with a single drug.
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Metabolomic fingerprint reveals that metformin impairs one-carbon metabolism in a manner similar to the antifolate class of chemotherapy drugs

TL;DR: It is suggested for the first time that metformin can function as an antifolate chemotherapeutic agent that induces the ATM/AMPK tumor suppressor axis secondarily following the alteration of the carbon flow through the folate-related one-carbon metabolic pathways.