ResearcherUniversity of MichiganActive in the last 2 years
Christopher J. Halbrook
Matched on ORCID iD 0000-0002-3376-3114; OpenAlex author ID A5005221333; NIH RePORTER profile ID 12098579. Sources: OpenAlex.
Their work
- Papers
- 23 (first author 3, last author 2)
- Trials
- 0
- Grants
- 5
- Labs led
- 1
- Collaborators
- 105
2016: 1 paper · 2017: 1 paper · 2018: 2 papers · 2019: 2 papers, 1 grant · 2020: 1 paper, 1 grant · 2021: 4 papers · 2022: 3 papers, 1 grant · 2023: 4 papers · 2024: none · 2025: 2 papers · 2026: 3 papers, 2 grants
Papers 23
- Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. Last author DOI 10.1016/j.jcmgh.2026.101872↗
- Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. Last author DOI 10.1053/j.gastro.2026.09.027↗
- ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-26-0138↗
- Homologous Repair-Deficient Pancreatic Cancer: Refined Targeting of DNA Damage Response is an Effective Therapeutic Strategy. First author DOI 10.1002/ueg2.12773↗
- Tumor nutrient stress gives rise to a drug tolerant cell state in pancreatic cancer Co-author DOI 10.1101/2025.09.04.673818↗
- Pancreatic cancer: Advances and challenges. Co-author DOI 10.1016/j.cell.2023.02.014↗
- Uridine-derived ribose fuels glucose-restricted pancreatic cancer. Co-author DOI 10.1038/s41586-023-06073-w↗
- Barriers and opportunities for gemcitabine in pancreatic cancer therapy. First author DOI 10.1152/ajpcell.00331.2022↗
- Arginase 1 is a key driver of immune suppression in pancreatic cancer. Co-author DOI 10.7554/elife.80721↗
- Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic adenocarcinoma cells. Co-author DOI 10.1038/s43018-022-00463-1↗
- Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. Co-author DOI 10.7554/elife.73245↗
- Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF-PI3K pathway. Co-author DOI 10.7554/elife.73796↗
- GOT1 inhibition promotes pancreatic cancer cell death by ferroptosis. Co-author DOI 10.1038/s41467-021-24859-2↗
- Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 Co-author DOI 10.1101/2021.06.07.447448↗
- Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-20-3715↗
- Hyaluronic acid fuels pancreatic cancer cell growth. First author DOI 10.7554/elife.62645↗
- Clonal Heterogeneity Supports Mitochondrial Metabolism in Pancreatic Cancer Co-author DOI 10.1101/2020.05.15.098368↗
- Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. Co-author DOI 10.1016/j.cmet.2019.02.001↗
- Metabolism and epigenetics of pancreatic cancer stem cells. Co-author DOI 10.1016/j.semcancer.2018.09.008↗
- Tumor cross-talk networks promote growth and support immune evasion in pancreatic cancer. Co-author DOI 10.1152/ajpgi.00416.2017↗
- Mutant p53R270H drives altered metabolism and increased invasion in pancreatic ductal adenocarcinoma. Co-author DOI 10.1172/jci.insight.97422↗
- Employing Metabolism to Improve the Diagnosis and Treatment of Pancreatic Cancer. Co-author DOI 10.1016/j.ccell.2016.12.006↗
- PDX1 dynamically regulates pancreatic ductal adenocarcinoma initiation and maintenance. Co-author DOI 10.1101/gad.291021.116↗
Grants 5
- Harnessing Nutritional Modulation to Enhance Cancer Drug Potency R21CA307778↗
- Targeting Metabolic Crosstalk in Pancreatic Cancer R37CA283575↗
- Disrupting macrophage metabolism to reduce immunosuppression and enhance therapy in pancreatic cancer R00CA241357↗
- Disrupting macrophage metabolism to reduce immunosuppression and enhance therapy in pancreatic cancer K99CA241357↗
- Targeting Epithelial-Immune Cell Crosstalk to Improve Therapy in Pancreatic Cancer F32CA228328↗
Closest collaborators
The 25 strongest of 105 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Costas Andreas Lyssiotis · 16 shared papers, 2017–2023 · strength 1.87
- Paper Pancreatic cancer: Advances and challenges. DOI 10.1016/j.cell.2023.02.014↗
- Paper Employing Metabolism to Improve the Diagnosis and Treatment of Pancreatic Cancer. DOI 10.1016/j.ccell.2016.12.006↗
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Marina Pasca di Magliano · 13 shared papers, 2018–2023 · strength 1.51
- Paper Pancreatic cancer: Advances and challenges. DOI 10.1016/j.cell.2023.02.014↗
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Tumor cross-talk networks promote growth and support immune evasion in pancreatic cancer. DOI 10.1152/ajpgi.00416.2017↗
- Peter Kaiser · 1 shared grant, 2026 · strength 1.26
- Rima Singh · 5 shared papers, 2022–2026 · strength 0.84
- Paper Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. DOI 10.1016/j.jcmgh.2026.101872↗
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer. DOI 10.1158/0008-5472.can-26-0138↗
- Alica K. Michels · 4 shared papers, 2025–2026 · strength 0.79
- Paper Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. DOI 10.1016/j.jcmgh.2026.101872↗
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper Tumor nutrient stress gives rise to a drug tolerant cell state in pancreatic cancer DOI 10.1101/2025.09.04.673818↗
- Li Zhang · 7 shared papers, 2019–2023 · strength 0.74
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Paper Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 DOI 10.1101/2021.06.07.447448↗
- Alica K. Beutel · 3 shared papers, 2022–2025 · strength 0.73
- Paper Barriers and opportunities for gemcitabine in pancreatic cancer therapy. DOI 10.1152/ajpcell.00331.2022↗
- Paper Homologous Repair-Deficient Pancreatic Cancer: Refined Targeting of DNA Damage Response is an Effective Therapeutic Str… DOI 10.1002/ueg2.12773↗
- Paper Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic … DOI 10.1038/s43018-022-00463-1↗
- Nina G. Steele · 5 shared papers, 2021–2026 · strength 0.65
- Paper Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. DOI 10.1016/j.jcmgh.2026.101872↗
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Zeribe C. Nwosu · 6 shared papers, 2021–2023 · strength 0.65
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Paper Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 DOI 10.1101/2021.06.07.447448↗
- Howard C. Crawford · 7 shared papers, 2016–2023 · strength 0.63
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Paper Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic … DOI 10.1038/s43018-022-00463-1↗
- Alexander Kleger · 3 shared papers, 2025–2026 · strength 0.62
- Paper Homologous Repair-Deficient Pancreatic Cancer: Refined Targeting of DNA Damage Response is an Effective Therapeutic Str… DOI 10.1002/ueg2.12773↗
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer. DOI 10.1158/0008-5472.can-26-0138↗
- Thomas Theodor Werner Seufferlein · 3 shared papers, 2025–2026 · strength 0.62
- Paper Homologous Repair-Deficient Pancreatic Cancer: Refined Targeting of DNA Damage Response is an Effective Therapeutic Str… DOI 10.1002/ueg2.12773↗
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer. DOI 10.1158/0008-5472.can-26-0138↗
- Austin D. Silva · 3 shared papers, 2026 · strength 0.61
- Paper Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. DOI 10.1016/j.jcmgh.2026.101872↗
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper ATM Deficiency Induces TGFβ-Mediated Stromal Programming in Pancreatic Cancer. DOI 10.1158/0008-5472.can-26-0138↗
- Eileen S. Carpenter · 5 shared papers, 2021–2023 · strength 0.55
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Paper Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 DOI 10.1101/2021.06.07.447448↗
- Yaqing Zhang · 5 shared papers, 2019–2023 · strength 0.53
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Alexander Muir · 3 shared papers, 2023–2026 · strength 0.51
- Paper Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer. DOI 10.1053/j.gastro.2026.09.027↗
- Paper Tumor nutrient stress gives rise to a drug tolerant cell state in pancreatic cancer DOI 10.1101/2025.09.04.673818↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Jennifer P. Morton · 4 shared papers, 2018–2026 · strength 0.46
- Paper Comparative Analysis of Primary and Liver Fibroblasts Reveals MET as a Potent Target in Pancreatic Cancer Metastasis. DOI 10.1016/j.jcmgh.2026.101872↗
- Paper Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic … DOI 10.1038/s43018-022-00463-1↗
- Paper Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. DOI 10.1016/j.cmet.2019.02.001↗
- Élodie Roger · 2 shared papers, 2025–2026 · strength 0.42
- Johann Gout · 2 shared papers, 2025–2026 · strength 0.42
- Lukas Perkhofer · 2 shared papers, 2025–2026 · strength 0.42
- Samuel Andrew Kerk · 4 shared papers, 2021–2022 · strength 0.39
- Paper Metabolic requirement for GOT2 in pancreatic cancer depends on environmental context. DOI 10.7554/elife.73245↗
- Paper Differential integrated stress response and asparagine production drive symbiosis and therapy resistance of pancreatic … DOI 10.1038/s43018-022-00463-1↗
- Paper Hyaluronic acid fuels pancreatic cancer cell growth. DOI 10.7554/elife.62645↗
- Rosa Elena Menjivar · 3 shared papers, 2021–2023 · strength 0.38
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Paper Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 DOI 10.1101/2021.06.07.447448↗
- Matthew H. Ward · 3 shared papers, 2021–2023 · strength 0.37
- Paper Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic progra… DOI 10.7554/elife.73796↗
- Paper Uridine-derived ribose fuels glucose-restricted pancreatic cancer. DOI 10.1038/s41586-023-06073-w↗
- Paper Nutrient profiling reveals extracellular uridine as a fuel for pancreatic cancer through uridine phosphorylase 1 DOI 10.1101/2021.06.07.447448↗
- Filip Bednar · 3 shared papers, 2019–2023 · strength 0.33
- Paper Arginase 1 is a key driver of immune suppression in pancreatic cancer. DOI 10.7554/elife.80721↗
- Paper Metabolism and epigenetics of pancreatic cancer stem cells. DOI 10.1016/j.semcancer.2018.09.008↗
- Paper Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-20-3715↗
- Daniel M. Kremer · 4 shared papers, 2018–2021 · strength 0.32
- Paper Hyaluronic acid fuels pancreatic cancer cell growth. DOI 10.7554/elife.62645↗
- Paper GOT1 inhibition promotes pancreatic cancer cell death by ferroptosis. DOI 10.1038/s41467-021-24859-2↗
- Paper Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer. DOI 10.1016/j.cmet.2019.02.001↗
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.