J
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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Journal ArticleDOI
Extra-virgin olive oil polyphenols inhibit HER2 (erbB-2)-induced malignant transformation in human breast epithelial cells: relationship between the chemical structures of extra-virgin olive oil secoiridoids and lignans and their inhibitory activities on the tyrosine kinase activity of HER2.
Javier A. Menendez,Alejandro Vazquez-Martin,Cristina Oliveras-Ferraros,Rocío García-Villalba,Alegría Carrasco-Pancorbo,Alberto Fernández-Gutiérrez,Antonio Segura-Carretero +6 more
TL;DR: The ability of EVOO polyphenols to modulate HER2 tyrosine kinase receptor-induced in vitro transformed phenotype in human breast epithelial cells is explored and recent epidemiological evidence revealing that EVOO-related anti-breast cancer effects primarily affect the occurrence of breast tumors is supported.
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HER2 (erbB-2)-targeted effects of the omega-3 polyunsaturated fatty acid, alpha-linolenic acid (ALA; 18:3n-3), in breast cancer cells: the "fat features" of the "Mediterranean diet" as an "anti-HER2 cocktail".
Javier A. Menendez,Alejandro Vazquez-Martin,Santiago Ropero,Ramon Colomer,Ruth Lupu,Josep Trueta +5 more
TL;DR: The ω-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab-based immunotherapy.
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Targeting fatty acid synthase-driven lipid rafts: a novel strategy to overcome trastuzumab resistance in breast cancer cells
TL;DR: The specific blockade of a novel molecular linkage between FAS-regulated membrane composition and functioning of transmembrane growth factor receptors EGFR and Her-2/neu may represent a previously unrecognized therapeutic approach circumventing trastuzumab resistance in breast carcinomas.
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Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
Sílvia Cufí,Rosa Bonavia,Alejandro Vazquez-Martin,Cristina Oliveras-Ferraros,Bruna Corominas-Faja,Elisabet Cuyàs,Begoña Martin-Castillo,Enrique Barrajón-Catalán,Joana Visa,Antonio Segura-Carretero,Jorge Joven,Joaquim Bosch-Barrera,Vicente Micol,Javier A. Menendez +13 more
TL;DR: Given that the various mechanisms of resistance to erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following erlot inib treatment.
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AMPK: Evidence for an energy-sensing cytokinetic tumor suppressor
TL;DR: It is suggested that molecular co-evolution of the energy-sensing cytokinetic tumor suppressor AMPK within the chronic biophysical constraints of the tumor microenvironment may inherently promote a continuous generation of structural and numerical changes in chromosomes favoring generation of nascent tumor cells and/or tumor-initiating cells over tumor cell death.