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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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Managing hypertension by polyphenols.

TL;DR: Whether and how limitations of scientific knowledge, data derived from large randomized clinical trials, and an accurate assessment of the bioactive components provided by common foodstuff may complicate the extensive use of plant-derived products in the management of hypertension are discussed.
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Rejuvenating regeneration: metformin activates endogenous adult stem cells.

TL;DR: This work presents a novel probabilistic approach that allows us to assess the immune response to ‘cell reprograming’ and assess the importance of immune ‘ ‘clinically checkpoints’ during cell reprogramming.
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The metastasis inducer CCN1 (CYR61) activates the fatty acid synthase (FASN)-driven lipogenic phenotype in breast cancer cells.

TL;DR: FASNdependent endogenous lipogenesis as a new mechanism controlling the metastatic phenotype promoted by CCN1 is uncovered, which represents a novel metabolic target to clinically manage metastatic disease progression.
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The Activation of the Sox2 RR2 Pluripotency Transcriptional Reporter in Human Breast Cancer Cell Lines is Dynamic and Labels Cells with Higher Tumorigenic Potential.

TL;DR: The S4+ pluripotency transcriptional reporter allows the isolation of cells with enhanced tumorigenic potential and its activation was switched on and off in the cell lines studied, reflecting a plastic cellular process.
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Metformin inhibits RANKL and sensitizes cancer stem cells to denosumab.

TL;DR: It is reported that the biguanide metformin prevents BRCA1 haploinsufficiency-driven RANKL gene overexpression, thereby disrupting an auto-regulatory feedback control of RankL-addicted cancer stem cell-like states within B RCA1mut/− cell populations.