ResearcherUniversity of MichiganActive in the last 2 years
Ronald Anthony Depinho
Matched on ORCID iD 0000-0002-5625-577X; OpenAlex author ID A5008120994; NIH RePORTER profile ID 1863036. Sources: OpenAlex.
Their work
- Papers
- 28 (first author 1, last author 10)
- Trials
- 0
- Grants
- 2
- Labs led
- 1
- Collaborators
- 111
2011: 1 paper · 2012: none · 2013: 2 papers · 2014: 3 papers · 2015: 1 paper · 2016: 1 paper · 2017: 4 papers · 2018: none · 2019: 1 paper · 2020: 2 papers · 2021: 2 papers · 2022: 2 papers, 1 grant · 2023: 2 papers · 2024: 1 paper · 2025: 3 papers, 1 grant · 2026: 3 papers
Papers 28
- Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Co-author DOI 10.1038/s41586-026-10488-6↗
- 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. Last author DOI 10.1038/s41586-026-11134-x↗
- Genetics and biology of pancreatic ductal adenocarcinoma. Last author DOI 10.1101/gad.351863.124↗
- KRAS Inhibition Activates an Actionable CD24 "Do Not Eat Me" Signal in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-25-2024↗
- Combined KRAS Inhibition and Immune Therapy Generates Durable Complete Responses in an Autochthonous PDAC Model. Last author DOI 10.1158/2159-8290.cd-24-0489↗
- Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer. Co-author DOI 10.1038/s41421-024-00720-w↗
- Elimination of oncogenic KRAS in genetic mouse models eradicates pancreatic cancer by inducing FAS-dependent apoptosis by CD8+ T cells. Co-author DOI 10.1016/j.devcel.2023.07.025↗
- Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable response in pancreatic cancer. Last author DOI 10.1038/s43018-022-00500-z↗
- Fungal mycobiome drives IL-33 secretion and type 2 immunity in pancreatic cancer. Co-author DOI 10.1016/j.ccell.2022.01.003↗
- 3D imaging analysis on an organoid-based platform guides personalized treatment in pancreatic ductal adenocarcinoma. Co-author DOI 10.1172/jci151604↗
- Single-cell RNA sequencing in pancreatic cancer. First author DOI 10.1038/s41575-021-00471-z↗
- USP21 deubiquitinase elevates macropinocytosis to enable oncogenic KRAS bypass in pancreatic cancer. Last author DOI 10.1101/gad.348787.121↗
- Oncogenic KRAS-Driven Metabolic Reprogramming in Pancreatic Cancer Cells Utilizes Cytokines from the Tumor Microenvironment. Last author DOI 10.1158/2159-8290.cd-19-0297↗
- Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer. Last author DOI 10.1158/2159-8290.cd-19-0597↗
- Syndecan 1 is a critical mediator of macropinocytosis in pancreatic cancer. Co-author DOI 10.1038/s41586-019-1062-1↗
- Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Last author DOI 10.1038/nature21052↗
- Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Co-author DOI 10.1038/nature21064↗
- Mutant Kras- and p16-regulated NOX4 activation overcomes metabolic checkpoints in development of pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/ncomms14437↗
- A tumor vessel-targeting fusion protein elicits a chemotherapeutic bystander effect in pancreatic ductal adenocarcinoma. Co-author PMID 28401019↗
- In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determinant of Pancreatic Cancer. Co-author DOI 10.1016/j.celrep.2016.05.063↗
- Genetic events that limit the efficacy of MEK and RTK inhibitor therapies in a mouse model of KRAS-driven pancreatic cancer. Co-author DOI 10.1158/0008-5472.can-14-1854↗
- Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Last author DOI 10.1016/j.cell.2014.06.003↗
- Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Co-author DOI 10.1038/nature13611↗
- Neuroplastic changes occur early in the development of pancreatic ductal adenocarcinoma. Co-author DOI 10.1158/0008-5472.can-13-2050↗
- Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway. Co-author DOI 10.1038/nature12040↗
- Targeting cathepsin E in pancreatic cancer by a small molecule allows in vivo detection. Co-author DOI 10.1593/neo.13276↗
- PTEN is a major tumor suppressor in pancreatic ductal adenocarcinoma and regulates an NF-κB-cytokine network. Last author DOI 10.1158/2159-8290.cd-11-0031↗
Grants 2
Closest collaborators
The 25 strongest of 111 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Anirban Maitra · 14 shared papers, 1 shared grant, 2016–2026 · strength 2.28
- Haoqiang Ying · 20 shared papers, 2011–2026 · strength 2.01
- Paper Genetics and biology of pancreatic ductal adenocarcinoma. DOI 10.1101/gad.351863.124↗
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Huamin Wang · 17 shared papers, 2014–2026 · strength 1.68
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Andrea Viale · 11 shared papers, 2014–2026 · strength 1.05
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Jason B. Fleming · 11 shared papers, 2013–2026 · strength 0.99
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Raghu Kalluri · 3 shared papers, 1 shared grant, 2020–2025 · strength 0.99
- Giulio Francesco Draetta · 10 shared papers, 2014–2026 · strength 0.88
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Giannicola Genovese · 9 shared papers, 2014–2026 · strength 0.87
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Prasenjit Dey · 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↗
- Timothy Paul Heffernan · 9 shared papers, 2014–2026 · strength 0.79
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper KRAS Inhibition Activates an Actionable CD24 "Do Not Eat Me" Signal in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-2024↗
- Alec C. Kimmelman · 6 shared papers, 2011–2026 · strength 0.69
- Paper Genetics and biology of pancreatic ductal adenocarcinoma. DOI 10.1101/gad.351863.124↗
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper USP21 deubiquitinase elevates macropinocytosis to enable oncogenic KRAS bypass in pancreatic cancer. DOI 10.1101/gad.348787.121↗
- Ya’an Kang · 7 shared papers, 2013–2026 · strength 0.67
- 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: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper 3D imaging analysis on an organoid-based platform guides personalized treatment in pancreatic ductal adenocarcinoma. DOI 10.1172/jci151604↗
- Wantong Yao · 8 shared papers, 2014–2026 · strength 0.67
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper KRAS Inhibition Activates an Actionable CD24 "Do Not Eat Me" Signal in Pancreatic Cancer. DOI 10.1158/0008-5472.can-25-2024↗
- Paper USP21 deubiquitinase elevates macropinocytosis to enable oncogenic KRAS bypass in pancreatic cancer. DOI 10.1101/gad.348787.121↗
- Jincheng Han · 3 shared papers, 2021–2025 · strength 0.60
- Paper Combined KRAS Inhibition and Immune Therapy Generates Durable Complete Responses in an Autochthonous PDAC Model. DOI 10.1158/2159-8290.cd-24-0489↗
- Paper Single-cell RNA sequencing in pancreatic cancer. DOI 10.1038/s41575-021-00471-z↗
- 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↗
- Alessandro Carugo · 7 shared papers, 2014–2026 · strength 0.59
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Syndecan 1 is a critical mediator of macropinocytosis in pancreatic cancer. DOI 10.1038/s41586-019-1062-1↗
- Virginia Giuliani · 5 shared papers, 2014–2026 · strength 0.49
- Paper Author Correction: Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. DOI 10.1038/s41586-026-10488-6↗
- Paper Author Correction: Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/s41586-026-10995-6↗
- Paper Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. DOI 10.1038/nature21064↗
- Gerald C Chu · 2 shared papers, 1 shared grant, 2011–2025 · strength 0.49
- Grant Core C-Computational Core P01CA117969↗
- Paper Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. DOI 10.1016/j.cell.2014.06.003↗
- Paper PTEN is a major tumor suppressor in pancreatic ductal adenocarcinoma and regulates an NF-κB-cytokine network. DOI 10.1158/2159-8290.cd-11-0031↗
- 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↗
- Ralph Weissleder · 1 shared paper, 1 shared grant, 2013–2025 · strength 0.48
- Sarah P. Thayer · 1 shared paper, 1 shared grant, 2011–2025 · strength 0.46
- Cyril Henri Benes · 1 shared grant, 2025 · strength 0.45
- Phillip Andrew Futreal · 1 shared grant, 2025 · strength 0.45
- NABEEL El-BARDEESY · 1 shared grant, 2025 · strength 0.45
- Lewis C. Cantley · 1 shared grant, 2025 · strength 0.45
- James wesley Horner · 1 shared grant, 2025 · strength 0.45
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.