Paul M. Grandgenett
- Pancreatic and Hepatic Oncology Research
- Glycosylation and Glycoproteins Research
- Cancer Genomics and Diagnostics
- Monoclonal and Polyclonal Antibodies Research
- Radiopharmaceutical Chemistry and Applications
- Cancer Research and Treatments
- Cancer Cells and Metastasis
- Proteoglycans and glycosaminoglycans research
- Cell Adhesion Molecules Research
- Cancer, Hypoxia, and Metabolism
- Pancreatic function and diabetes
- Epigenetics and DNA Methylation
- Renal cell carcinoma treatment
- Galectins and Cancer Biology
- Ferroptosis and cancer prognosis
- Cancer Immunotherapy and Biomarkers
- Immune Cell Function and Interaction
- Extracellular vesicles in disease
- Peptidase Inhibition and Analysis
- Synthesis and Biological Evaluation
- Osteoarthritis Treatment and Mechanisms
- Radiomics and Machine Learning in Medical Imaging
- Phagocytosis and Immune Regulation
- Trypanosoma species research and implications
- RNA modifications and cancer
University of Nebraska Medical Center
2016-2025
Nebraska Medical Center
2010-2025
University of Nebraska at Omaha
2020
University of Nebraska–Lincoln
2013
University of California, San Francisco
2011
University of Iowa
2000-2007
Pancreatic cancer is the most lethal common solid malignancy. Systemic therapies are often ineffective, and predictive biomarkers to guide treatment urgently needed. We generated a pancreatic patient-derived organoid (PDO) library that recapitulates mutational spectrum transcriptional subtypes of primary cancer. New driver oncogenes were nominated transcriptomic analyses revealed unique clusters. PDOs exhibited heterogeneous responses standard-of-care chemotherapeutics investigational...
Abstract The ability of tumour cells to thrive in harsh microenvironments depends on the utilization nutrients available milieu. Here we show that pancreatic cancer-associated fibroblasts (CAFs) regulate cell metabolism through secretion acetate, which can be blocked by silencing ATP citrate lyase (ACLY) CAFs. We further acetyl-CoA synthetase short-chain family member 2 (ACSS2) channels exogenous acetate dynamic cancer epigenome and transcriptome, thereby facilitating survival an acidic...
Abstract Purpose: To evaluate the nature of cyclin-dependent kinase 5 (CDK5) hyperactivity in pancreatic cancer progression. Experimental Design: We used genetic, biochemical, and molecular biology methods to investigate function overexpression CDK5 its activators p35 p39 during progression cancer. Results: Amplification gene or either main activators, p39, was observed 67% human ductal adenocarcinoma (PDAC). CDK5, p35, were rarely expressed ducts whereas more than 90% PDACs had increased...
Abstract Purpose: Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic disease that can be separated into distinct subtypes based on molecular signatures. Identifying PDAC subtype-specific therapeutic vulnerabilities necessary to develop precision medicine approaches treat PDAC. Experimental Design: A total of 56 liver metastases were obtained from the UNMC Rapid Autopsy Program and analyzed with quantitative proteomics. identified by principal component analysis protein expression...
Many tumors express proteoglycans modified with oncofetal chondroitin sulfate glycosaminoglycan chains (ofCS), which are normally restricted to the placenta. However, role of ofCS in cancer is largely unknown. The function was analyzed using recombinant ofCS-binding VAR2CSA protein (rVAR2) derived from malaria parasite, Plasmodium falciparum We demonstrate that plays a key tumor cell motility by affecting canonical integrin signaling pathways. Binding rVAR2 cells inhibited interaction...
Approximately one third of cancer patients die due to complexities related cachexia. However, the mechanisms cachexia and potential therapeutic interventions remain poorly studied. We observed a significant positive correlation between SIRT1 expression muscle fiber cross-sectional area in pancreatic patients. Rescuing Sirt1 by exogenous or pharmacological agents reverted cell–induced myotube wasting culture conditions mouse models. RNA-seq follow-up analyses showed cell–mediated loss induced...
Pancreatic cancer is one of the most aggressive malignant diseases. We recently reported that N-cadherin plays a key role in tumor progression and metastasis pancreatic cancer. For this study, we sought to determine if an N-cadherin-blocking peptide (ADH-1) could prevent N-cadherin-mediated mouse model for The effect ADH-1 on cell scattering migration collagen I was examined using cells. also influence apoptosis. Furthermore, vivo animal studies were performed orthotopic injection...