Pankaj Singh
University of Oklahoma-Health Sciences Center, OK·Biochemistry
Pancreatic ductal adenocarcinoma (PDAC), the most common pancreatic cancer, has a very poor outlook. It spreads early, invades nearby tissue, is found late and responds poorly to chemotherapy.
- Fields
Biochemistry
Pharmacology
Medicine & Clinical Research
- Topics
pancreatic cancer
pancreatic ductal adenocarcinoma
cancer metabolism
- Grants
- 5 known grants, through Apr 2031
What they work on
- Test whether blocking PADI1, an enzyme that chemically modifies arginine in proteins, or its downstream metabolic pathways prevents FOLFIRINOX resistance in pancreatic cancer cells, organoids and patient-derived xenografts.
- Determine how PADI1 drives tumor-cell metabolic rewiring toward glycolysis, a fast sugar-burning pathway, and how this reshapes surrounding immune and non-immune stroma, and check clinical links in human tissue.
- Provide center-wide metabolomics, lipidomics, carbon-13 isotope tracing of nutrient flow, and Seahorse assays of cell respiration on cells, organoids, exosomes and tumors, plus drug pharmacokinetic measurements.
- Use genetically engineered mice to determine how loss of ME2, a metabolic enzyme deleted with SMAD4 in up to 30% of PDAC, affects pancreatic cancer initiation, progression and metastasis.
- Define the signaling changes caused by ME2 loss and test personalized therapies and response biomarkers for ME2-deficient tumors in spontaneous mouse models and patient-derived xenografts.
- Determine how the PHGDH-made metabolite D-2-hydroxyglutarate, secreted by tumor cells, reprograms stellate cells, and whether halting this crosstalk slows pancreatic cancer progression and metastasis.
- Test therapies that block tumor–stellate cell metabolic crosstalk supporting tumor survival under low glucose, building on the finding that MUC1 loss raises PHGDH.
More about the research
Even tumors that respond at first usually become resistant. The research centers on cancer metabolism, the way tumor cells rewire how they use nutrients and energy, and asks how this rewiring drives tumor growth, spread and drug resistance. A common thread is the stroma: the non-cancer cells around a tumor, including immune cells and stellate cells, which build its dense scar-like tissue. The projects study how tumor cells and stroma exchange metabolic signals, and how specific genes and enzymes could be targeted with new drug combinations.
Why it matters
Most patients with pancreatic cancer have few effective options because tumors resist chemotherapy. This work could reveal new drug targets, such as PADI1, pathways switched on by ME2 loss, or tumor–stroma metabolic exchange, that could be combined with FOLFIRINOX or other standard treatments. It may also yield biomarkers to match patients with ME2-deficient or similar tumors to personalized therapies, with the long-term goal of improving survival.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Wantong Yao
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Define the molecular pathways through which a newly identified stress-response regulator helps pancreatic ductal adenocarcinoma (PDAC) cells survive nutrient shortage, low oxygen and oxidative stress, and evade the immune system.
Nicholas Woods
University of Nebraska Medical Center, NE·Medicine & Clinical Research
Test whether Tazemetostat, which blocks the gene-silencing complex PRC2, prevents chemotherapy-induced shifts in tumor subtype, using organoids grown from tumors of Black and White PDAC patients.
Saunjoo Yoon
University of Florida, FL·Pharmacology
Test the effectiveness of 4NSGnpcetu, anti-EGFR antibody-coated nanoparticles carrying a modified gemcitabine, in patient-derived pancreatic cancer organoids with stroma and in primary tumor cells from patients.
The school
University of Oklahoma-Health Sciences Center: 11 labs on PI Pages, $474M a year on research, 31 research doctorates a year.
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