ResearcherRoswell Park Comprehensive Cancer CenterActive in the last 2 years
Prasenjit Dey
Matched on ORCID iD 0000-0001-6678-503X; OpenAlex author ID A5058602189; NIH RePORTER profile ID 11968962. Sources: OpenAlex.
Their work
- Papers
- 11 (first author 1, last author 3)
- Trials
- 0
- Grants
- 3
- Labs led
- 1
- Collaborators
- 38
2017: 2 papers · 2018: none · 2019: 1 grant · 2020: 1 paper · 2021: 1 grant · 2022: 3 papers · 2023: 1 paper · 2024: 1 paper · 2025: 1 paper, 1 grant · 2026: 2 papers
Papers 11
- Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Co-author DOI 10.1038/s41586-026-10995-6↗
- Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Co-author DOI 10.1038/s41586-026-11134-x↗
- Pancreatic Steatosis as a Risk Factor for Pancreatic Ductal Adenocarcinoma: Pathogenesis and Clinical Implications. First author DOI 10.14309/ctg.0000000000000832↗
- The Extracellular Niche and Tumor Microenvironment Enhance KRAS Inhibitor Efficacy in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-23-2504↗
- Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable response in pancreatic cancer. Co-author DOI 10.1038/s43018-022-00500-z↗
- Fungal mycobiome drives IL-33 secretion and type 2 immunity in pancreatic cancer. Last author DOI 10.1016/j.ccell.2022.01.003↗
- Isolation and adoptive transfer of innate lymphoid cells 2 to a recipient mouse model of PDAC. Last author DOI 10.1016/j.xpro.2022.101563↗
- Fungal ablation and transplantation of specific fungal species into PDAC tumor-bearing mice. Last author DOI 10.1016/j.xpro.2022.101644↗
- Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment. Co-author DOI 10.1158/2159-8290.cd-19-0297↗
- Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Co-author DOI 10.1038/nature21052↗
- Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Co-author DOI 10.1038/nature21064↗
Grants 3
Closest collaborators
The 25 strongest of 38 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Huamin Wang · 7 shared papers, 2017–2026 · strength 0.81
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable respo… DOI 10.1038/s43018-022-00500-z↗
- Ronald Anthony Depinho · 7 shared papers, 2017–2026 · strength 0.81
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable respo… DOI 10.1038/s43018-022-00500-z↗
- Anirban Maitra · 7 shared papers, 2017–2026 · strength 0.81
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable respo… DOI 10.1038/s43018-022-00500-z↗
- Haoqiang Ying · 6 shared papers, 2017–2026 · strength 0.70
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable respo… DOI 10.1038/s43018-022-00500-z↗
- Giannicola Genovese · 5 shared papers, 2017–2026 · strength 0.57
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenviron… DOI 10.1158/2159-8290.cd-19-0297↗
- Aftab Alam · 3 shared papers, 2022 · strength 0.56
- Paper Isolation and adoptive transfer of innate lymphoid cells 2 to a recipient mouse model of PDAC. DOI 10.1016/j.xpro.2022.101563↗
- Paper Fungal ablation and transplantation of specific fungal species into PDAC tumor-bearing mice. DOI 10.1016/j.xpro.2022.101644↗
- Paper Fungal mycobiome drives IL-33 secretion and type 2 immunity in pancreatic cancer. DOI 10.1016/j.ccell.2022.01.003↗
- Andrea Viale · 4 shared papers, 2017–2026 · strength 0.49
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Jason B. Fleming · 4 shared papers, 2017–2026 · strength 0.49
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Giulio Francesco Draetta · 4 shared papers, 2017–2026 · strength 0.49
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Tony Gutschner · 4 shared papers, 2017–2026 · strength 0.49
- Paper Author Correction: Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/s41586-026-11134-x↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. DOI 10.1038/nature21052↗
- Zoi Papalamprakopoulou · 1 shared paper, 2025 · strength 0.37
- Christos K Fountzilas · 1 shared paper, 2025 · strength 0.37
- Lifeng Yang · 2 shared papers, 2017–2026 · strength 0.26
- Di Zhao · 2 shared papers, 2017–2026 · strength 0.26
- Ya’an Kang · 2 shared papers, 2017–2026 · strength 0.26
- Deepak Nagrath · 2 shared papers, 2017–2026 · strength 0.26
- Alessandro Carugo · 2 shared papers, 2017–2026 · strength 0.23
- Virginia Giuliani · 2 shared papers, 2017–2026 · strength 0.23
- Timothy Paul Heffernan · 2 shared papers, 2017–2026 · strength 0.23
- Marco Dal Molin · 2 shared papers, 2017–2026 · strength 0.23
- Laura DeLong Wood · 2 shared papers, 2017–2026 · strength 0.23
- Michael Goggins · 2 shared papers, 2017–2026 · strength 0.23
- Lynda Chin · 2 shared papers, 2017–2026 · strength 0.23
- Vishnu Muthuraj Kumarasamy · 1 shared paper, 2024 · strength 0.21
- Erik S. Knudsen · 1 shared paper, 2024 · strength 0.21
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.