A5019257615- Pancreatic and Hepatic Oncology Research
- Pancreatitis Pathology and Treatment
- Metabolism, Diabetes, and Cancer
- Hippo pathway signaling and YAP/TAZ
- Phagocytosis and Immune Regulation
- Inflammatory mediators and NSAID effects
- Cell death mechanisms and regulation
- Cancer, Hypoxia, and Metabolism
- Cancer, Stress, Anesthesia, and Immune Response
- Electrolyte and hormonal disorders
- Pancreatic function and diabetes
- PI3K/AKT/mTOR signaling in cancer
- Cancer Research and Treatments
- Cancer, Lipids, and Metabolism
- Growth Hormone and Insulin-like Growth Factors
- Chemokine receptors and signaling
- Estrogen and related hormone effects
- Liver Disease Diagnosis and Treatment
- Adipokines, Inflammation, and Metabolic Diseases
- Renal function and acid-base balance
- Neuroendocrine Tumor Research Advances
- FOXO transcription factor regulation
- Angiogenesis and VEGF in Cancer
- Eicosanoids and Hypertension Pharmacology
- Cancer-related Molecular Pathways
University of California, Los Angeles
2015-2024
Digestive Care (United States)
2019
Hirshberg Foundation for Pancreatic Cancer Research
2006-2018
University of Michigan
2018
VA Tennessee Valley Healthcare System
2018
Vanderbilt University
2018
UCLA Health
2015
Cedars-Sinai Medical Center
2014
Center for Excellence in Education
2011
University of Colorado Cancer Center
2010
The relationships between diabetes and pancreatic ductal adenocarcinoma (PDAC) are complex. Longstanding type 2 (T2DM) is a risk factor for cancer, but increasing epidemiological data point to PDAC as also cause of due unknown mechanisms. New-onset particular interest the oncology community differentiation new-onset caused by distinct from T2DM may allow earlier diagnosis PDAC. To address these raise awareness diabetes, symposium entitled Diabetes, Pancreatogenic Pancreatic Cancer was held...
Abstract Recently, we identified a novel crosstalk between insulin and G protein–coupled receptor (GPCR) signaling pathways in human pancreatic cancer cells. Insulin enhanced GPCR through rapamycin-sensitive mTOR-dependent pathway. Metformin, the most widely used drug treatment of type 2 diabetes, activates AMP kinase (AMPK), which negatively regulates mTOR. Here, determined whether metformin disrupts Treatment cells (PANC-1, MIAPaCa-2, BxPC-3) with (10 ng/mL) for 5 minutes markedly increase...
Pancreatic ductal adenocarcinoma (PDAC) is generally a fatal disease with no efficacious treatment modalities. Elucidation of signaling mechanisms that will lead to the identification novel targets for therapy and chemoprevention urgently needed. Here, we review role Yes-associated protein (YAP) WW-domain-containing Transcriptional co-Activator PDZ-binding motif (TAZ) in development PDAC. These oncogenic proteins are at center network involves multiple upstream signals downstream...
Epidemiologic data has linked obesity to a higher risk of pancreatic cancer, but the underlying mechanisms are poorly understood. To allow for detailed mechanistic studies in relevant model mimicking diet-induced and high-fat, high-calorie diet (HFCD) was given P48+/Cre;LSL-KRASG12D (KC) mice carrying pancreas-specific oncogenic Kras mutation. The were randomly allocated HFCD or control (CD). Cohorts sacrificed at 3, 6, 9 months tissues harvested further analysis. Compared CD-fed mice,...
Pancreatic ductal adenocarcinomas are thought to arise from noninvasive, intraductal precursor lesions called pancreatic intraepithelial neoplasias (PanIN). The study of PanINs holds great promise for the identification early detection markers and effective cancer-preventing strategies. Cyclooxygenase-2 (COX-2) represents an intriguing target therapeutic preventive approaches in various human malignancies. aim present was evaluate efficacy a selective COX-2 inhibitor prevent progression...
Pancreatic ductal adenocarcinoma is a devastating disease, with an overall 5-year survival rate of only 3% to 5%. As the current therapies offer very limited benefits, novel therapeutic strategies are urgently required treat this disease. Here, we determined whether metformin administration inhibits growth PANC-1 and MiaPaCa-2 tumor xenografts in vivo.Different xenograft models, including orthotopic implantation, were used determine intraperitoneal or oral pancreatic cancer vivo.We...
Abstract Substance P analogues, including [D-Arg1,D-Trp5,7,9,Leu11]SP (SPA) are broad-spectrum G protein–coupled receptor (GPCR) antagonists that have potential antitumorigenic activities, although the mechanism(s) not completely understood. Here, we examined effects of SPA in ductal pancreatic cancers express multiple GPCRs for mitogenic agonists and also produce proangiogenic chemokines. Using HPAF-II, a well-differentiated cancer cell line as our model system, showed inhibited...
Saliva (oral fluids) is an emerging biofluid poised for detection of clinical diseases. Although the rationale oral diseases applications (e.g. cancer) intuitive, and relationship between systemic saliva biomarkers are unclear.In this study, we used mouse models melanoma non-small cell lung cancer compared transcriptome biomarker profiles tumor-bearing mice to those control mice. Microarray analysis showed that salivary transcriptomes were significantly altered in vs. controls. Significant...
Natural products represent a rich reservoir of potential small chemical molecules exhibiting anti-proliferative and chemopreventive properties. Here, we show that treatment pancreatic ductal adenocarcinoma (PDAC) cells (PANC-1, MiaPaCa-2) with the isoquinoline alkaloid berberine (0.3–6 µM) inhibited DNA synthesis proliferation these delay progression their cell cycle in G1. Berberine also reduced (by 70%) growth MiaPaCa-2 when implanted into flanks nu/nu mice. Mechanistic studies revealed...
Epidemiological studies support strong links between obesity, diabetes, and pancreatic disorders including pancreatitis adenocarcinoma (PDAC). Type 2 diabetes (T2DM) is associated with insulin resistance, hyperglycemia, hyperinsulinemia, the latter due to increased secretion by beta-cells. We reported that high-fat diet-induced PDAC progression in mice activation of stellate cells (PaSC). investigated here effects high concentrations glucose on mouse human PaSC growth fibrosing responses....
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with low survival rates and limited therapeutic options. Thus elucidation of signaling pathways involved in PDAC pathogenesis essential for identifying novel potential gene targets. Here, we used a systems approach to elucidate those by integrating microRNA profiling analyses together CRISPR/Cas9 technology identify transcription factors pathogenesis. FOXA2 factor was found be significantly downregulated relative control...