Ubaldo Martinez-Outshoorn, MD

Contact Dr. Martinez-Outshoorn

925 Chestnut Street
Suite 220A
Philadelphia, PA 19107

(215) 955-8874
(215) 955-2340 fax

Research and Clinical Interests
Medical Oncology, Bone Marrow Transplant, Hematologic Malignancies, Leukemia, Lymphoma

Publications

Most recent Peer-reviewed Publications

1. Compartment-specific activation of PPARγ governs breast cancer tumor growth, via metabolic reprogramming and symbiosis
2. Cancer metabolism, stemness and tumor recurrence : MCT1 and MCT4 are functional biomarkers of metabolic symbiosis in head and neck cancer
3. Cigarette smoke metabolically promotes cancer, via autophagy and premature aging in the host stromal microenvironment
4. Ethanol exposure induces the cancer-associated fibroblast phenotype and lethal tumor metabolism Implications for breast cancer prevention
5. Creating a tumor-resistant microenvironment Cell-mediated delivery of TNFα completely prevents breast cancer tumor formation in vivo
6. Mitochondrial dysfunction in breast cancer cells prevents tumor growth: Understanding chemoprevention with metformin
7. Mitochondria "fuel" breast cancer metabolism: Fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cells
8. Genetic induction of the Warburg effect inhibits tumor growth
9. BRCA1 mutations drive oxidative stress and glycolysis in the tumor microenvironment: Implications for breast cancer prevention with antioxidant therapies
10. Hereditary ovarian cancer and two-compartment tumor metabolism: Epithelial loss of BRCA1 induces hydrogen peroxide production, driving oxidative stress and NFκB activation in the tumor stroma
11. Ketone body utilization drives tumor growth and metastasis
12. The milk protein α-casein functions as a tumor suppressor via activation of STAT1 signaling, effectively preventing breast cancer tumor growth and metastasis
13. Ketone bodies and two-compartment tumor metabolism: Stromal ketone production fuels mitochondrial biogenesis in epithelial cancer cells
14. CDK inhibitors (p16/p19/p21) induce senescence and autophagy in cancer-associated fibroblasts, "fueling" tumor growth via paracrine interactions, without an increase in neo-angiogenesis
15. Metabolic remodeling of the tumor microenvironment: Migration stimulating factor (MSF) reprograms myofibroblasts toward lactate production, fueling anabolic tumor growth
16. Metabolic reprogramming and two-compartment tumor metabolism: Opposing role(s) of HIF1α and HIF2α in tumor-associated fibroblasts and human breast cancer cells
17. Metabolic reprogramming of cancer-associated fibroblasts by TGF-β drives tumor growth: Connecting TGF-β signaling with "Warburg- like" cancer metabolism and L-lactate production
18. Mitochondrial fission induces glycolytic reprogramming in cancer-associated myofibroblasts, driving stromal lactate production, and early tumor growth
19. Two-compartment tumor metabolism: Autophagy in the tumor microenvironment, and oxidative mitochondrial metabolism (OXPHOS) in cancer cells
20. CTGF drives autophagy, glycolysis and senescence in cancer-associated fibroblasts via HIF1 activation, metabolically promoting tumor growth

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