233 South 10th Street
Room 1050
Philadelphia, PA 19107
(215) 503-5692
(215) 503-9334 fax
Room 1050
Philadelphia, PA 19107
(215) 503-5692
(215) 503-9334 fax
Most Recent Peer-reviewed Publications
- Nutrient restriction and radiation therapy for cancer treatment: When less is more
- Novel oncogene-induced metastatic prostate cancer cell lines define human prostate cancer progression signatures
- Double homozygous missense mutations in DACH1 and BMP4 in a patient with bilateral cystic renal dysplasia
- Bioinformatics analysis reveals transcriptome and microRNA signatures and drug repositioning targets for IBD and other autoimmune diseases
- Cancer stem cells
- Expression of cyclin D1a and D1b as predictive factors for treatment response in colorectal cancer
- 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
- Metabolic remodeling of the tumor microenvironment: Migration stimulating factor (MSF) reprograms myofibroblasts toward lactate production, fueling anabolic tumor growth
- Metabolic reprogramming and two-compartment tumor metabolism: Opposing role(s) of HIF1α and HIF2α in tumor-associated fibroblasts and human breast cancer cells
- 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
- Mitochondrial fission induces glycolytic reprogramming in cancer-associated myofibroblasts, driving stromal lactate production, and early tumor growth
- CCR5 antagonist blocks metastasis of basal breast cancer cells
- Caveolin-1 and accelerated host aging in the breast tumor microenvironment: Chemoprevention with rapamycin, an mTOR inhibitor and anti-aging drug
- Two-compartment tumor metabolism: Autophagy in the tumor microenvironment, and oxidative mitochondrial metabolism (OXPHOS) in cancer cells
- CTGF drives autophagy, glycolysis and senescence in cancer-associated fibroblasts via HIF1 activation, metabolically promoting tumor growth
- Autophagy and senescence in cancer-associated fibroblasts metabolically supports tumor growth and metastasis, via glycolysis and ketone production
- Warburg meets autophagy: Cancer-Associated fibroblasts accelerate tumor growth and metastasis via oxidative stress, mitophagy, and aerobic glycolysis
- Genetic ablation of Cav1 differentially affects melanoma tumor growth and metastasis in mi Role of Cav1 in Shh heterotypic signaling and transendothelial migration
- Breast cancer stem cells
- Mitochondrial metabolism in cancer metastasis: Visualizing tumor cell mitochondria and the "reverse Warburg effect" in positive lymph node tissue