A5011348783- Pancreatic and Hepatic Oncology Research
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Cancer Genomics and Diagnostics
- Pancreatic function and diabetes
- Genetic factors in colorectal cancer
- Cancer Research and Treatments
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Amino Acid Enzymes and Metabolism
- Cancer Cells and Metastasis
- Colorectal Cancer Treatments and Studies
- PI3K/AKT/mTOR signaling in cancer
- Radiomics and Machine Learning in Medical Imaging
- Protein Degradation and Inhibitors
- RNA modifications and cancer
- Ferroptosis and cancer prognosis
- Multiple Myeloma Research and Treatments
- Phagocytosis and Immune Regulation
- Metabolism, Diabetes, and Cancer
- Mitochondrial Function and Pathology
- Cancer-related Molecular Pathways
- Caveolin-1 and cellular processes
- Endoplasmic Reticulum Stress and Disease
- Ubiquitin and proteasome pathways
New York University
2017-2025
NYU Langone Health
2001-2024
NYU Langone’s Laura and Isaac Perlmutter Cancer Center
2017-2023
Columbia University Irving Medical Center
2022
Dana-Farber Cancer Institute
2011-2020
Harvard University
2011-2020
Brigham and Women's Hospital
2007-2020
Dana-Farber Brigham Cancer Center
2011-2020
University Medical Center
2020
National Institutes of Health
1997-2016
Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer complex may differ depending on tumor type or context. Here we show that pancreatic cancers have distinct dependence autophagy. Pancreatic primary tumors cell lines elevated under basal conditions. Genetic pharmacologic inhibition leads increased reactive oxygen species, DNA damage, metabolic defect leading decreased mitochondrial oxidative...
Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising anticancer activity, but their efficacy in brain tumor glioblastoma multiforme (GBM) other solid tumors has been modest. We hypothesized multiple RTKs are coactivated these redundant inputs drive maintain signaling, thereby limiting of targeting single RTKs. Tumor cell lines, xenotransplants, primary indeed show concomitantly...
Pancreatic ductal adenocarcinoma is refractory to available therapies. We have previously shown that these tumors elevated autophagy and inhibition of leads decreased tumor growth. Using an autochthonous model pancreatic cancer driven by oncogenic Kras the stochastic LOH Trp53, we demonstrate although genetic ablation in pancreas increased initiation, premalignant lesions are impaired their ability progress invasive cancer, leading prolonged survival. In addition, mouse cell lines with...
Kruppel-like factor 6 ( KLF6 ) is a zinc finger transcription of unknown function. Here, we show that the gene mutated in subset human prostate cancer. Loss-of-heterozygosity analysis revealed one allele deleted 77% (17 22) primary tumors. Sequence retained mutations 71% these Functional studies confirm whereas wild-type up-regulates p21 (WAF1/CIP1) p53-independent manner and significantly reduces cell proliferation, tumor-derived mutants do not. Our data suggest tumor suppressor involved
NCOA4 is a selective cargo receptor for the autophagic turnover of ferritin, process critical regulation intracellular iron bioavailability. However, how ferritinophagy flux controlled and roles in iron-dependent processes are poorly understood. Through analysis NCOA4-FTH1 interaction, we demonstrate that direct association via key surface arginine FTH1 C-terminal element required delivery ferritin to lysosome autophagosomes. Moreover, abundance under dual control autophagy ubiquitin...