ResearcherHarvard UniversityActive in the last 2 years
James M. Cleary
Matched on ORCID iD 0000-0001-7213-3951; OpenAlex author ID A5018655814. Sources: ClinicalTrials.gov.
Their work
- Papers
- 26 (first author 0, last author 5)
- Trials
- 3 (principal investigator on 3)
- Grants
- 0
- Labs led
- 1
- Collaborators
- 119
2014: 1 paper · 2015: none · 2016: none · 2017: none · 2018: 1 paper, 1 trial · 2019: none · 2020: none · 2021: 3 papers · 2022: 2 papers, 2 trials · 2023: 6 papers · 2024: 4 papers · 2025: 2 papers · 2026: 7 papers
Papers 26
- Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. Co-author DOI 10.1016/j.ccell.2026.04.005↗
- CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. Co-author DOI 10.1016/j.cell.2026.08.045↗
- Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomized, multiarm, run-in phase trial. Co-author DOI 10.1038/s43018-026-01165-8↗
- A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, BRCA2, PALB2, and CHEK2. Last author DOI 10.1158/1078-0432.ccr-24-3766↗
- Cell-free chromatin epigenomic profiling enables non-invasive pancreatic cancer cell-state identification Co-author DOI 10.64898/2026.04.02.26349987↗
- Immune and stromal features of durable complete response to radiation and dual immune checkpoint blockade in pancreatic cancer Co-author DOI 10.64898/2026.08.06.26359422↗
- Context-specific genetic interaction mapping reveals combinatorial KRAS/FGFR dependence in pancreatic cancer Co-author DOI 10.64898/2026.09.24.754062↗
- Pancreatic cancer-restricted cryptic antigens are targets for T cell recognition. Co-author DOI 10.1126/science.adk3487↗
- Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibition in Patients With Metastatic Pancreat… Co-author DOI 10.1200/po-25-00332↗
- Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer. Co-author DOI 10.1038/s41586-024-07379-z↗
- Author Correction: Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer. Co-author DOI 10.1038/s41586-024-08084-7↗
- Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-24-1164↗
- Blockade of IL1β and PD1 with Combination Chemotherapy Reduces Systemic Myeloid Suppression in Metastatic Pancreatic Cancer with Heterogeneous Effects in the T… Co-author DOI 10.1158/2326-6066.cir-23-1073↗
- Effect of a MUC5AC Antibody (NPC-1C) Administered With Second-Line Gemcitabine and Nab-Paclitaxel on the Survival of Patients With Advanced Pancreatic Ductal A… Last author DOI 10.1001/jamanetworkopen.2022.49720↗
- USP9X mediates an acute adaptive response to MAPK suppression in pancreatic cancer but creates multiple actionable therapeutic vulnerabilities. Co-author DOI 10.1016/j.xcrm.2023.101007↗
- Phase Ib and Expansion Study of Gemcitabine, Nab-Paclitaxel, and Ficlatuzumab in Patients With Metastatic Pancreatic Cancer. Co-author DOI 10.1093/oncolo/oyad002↗
- Spatially Resolved Single-Cell Assessment of Pancreatic Cancer Expression Subtypes Reveals Co-expressor Phenotypes and Extensive Intratumoral Heterogeneity. Co-author DOI 10.1158/0008-5472.can-22-3050↗
- Oncogenic Drivers and Therapeutic Vulnerabilities in KRAS Wild-Type Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-22-3930↗
- A Phase I Expansion Cohort Study Evaluating the Safety and Efficacy of the CHK1 Inhibitor LY2880070 with Low-dose Gemcitabine in Patients with Metastatic Pancr… Last author DOI 10.1158/1078-0432.ccr-23-2005↗
- Neoadjuvant Chemotherapy Is Associated with Altered Immune Cell Infiltration and an Anti-Tumorigenic Microenvironment in Resected Pancreatic Cancer. Co-author DOI 10.1158/1078-0432.ccr-22-1125↗
- Emerging Role of Targeted Therapy in Metastatic Pancreatic Adenocarcinoma. Last author DOI 10.3390/cancers14246223↗
- Microenvironment drives cell state, plasticity, and drug response in pancreatic cancer. Co-author DOI 10.1016/j.cell.2021.11.017↗
- Opportunities for Utilization of DNA Repair Inhibitors in Homologous Recombination Repair-Deficient and Proficient Pancreatic Adenocarcinoma. Co-author DOI 10.1158/1078-0432.ccr-21-1367↗
- Durable clinical benefit from PARP inhibition in a platinum-sensitive, BRCA2-mutated pancreatic cancer patient after earlier progression on placebo treatment o… Last author DOI 10.21037/jgo-21-197↗
- Real-time Genomic Characterization of Advanced Pancreatic Cancer to Enable Precision Medicine. Co-author DOI 10.1158/2159-8290.cd-18-0275↗
- Phase II and pharmacodynamic study of autophagy inhibition using hydroxychloroquine in patients with metastatic pancreatic adenocarcinoma. Co-author DOI 10.1634/theoncologist.2014-0086↗
Trials 3
- Adavosertib and Gemcitabine in Advanced Pancreatic Principal investigator NCT05212025↗
- Switch Maintenance in Pancreatic Principal investigator NCT05419479↗
- Niraparib in Patients With Pancreatic Cancer Principal investigator NCT03601923↗
Closest collaborators
The 25 strongest of 119 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Brian Matthew Wolpin · 22 shared papers, 2014–2026 · strength 3.11
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Andrew J. Aguirre · 18 shared papers, 2021–2026 · strength 2.64
- Paper Context-specific genetic interaction mapping reveals combinatorial KRAS/FGFR dependence in pancreatic cancer DOI 10.64898/2026.09.24.754062↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Kimberly J. Perez · 16 shared papers, 2021–2026 · strength 2.31
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Harshabad Singh · 15 shared papers, 2021–2026 · strength 2.23
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Douglas Adam Rubinson · 16 shared papers, 2014–2026 · strength 2.15
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Jonathan Andrew Nowak · 13 shared papers, 2021–2026 · strength 1.92
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Brandon M. Huffman · 11 shared papers, 2021–2026 · strength 1.73
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Srivatsan Raghavan · 12 shared papers, 2021–2026 · strength 1.69
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Pancreatic cancer-restricted cryptic antigens are targets for T cell recognition. DOI 10.1126/science.adk3487↗
- Matthew B.B. Yurgelun · 7 shared papers, 2021–2026 · strength 1.03
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper Immune and stromal features of durable complete response to radiation and dual immune checkpoint blockade in pancreatic… DOI 10.64898/2026.08.06.26359422↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Kimmie Ng · 8 shared papers, 2014–2026 · strength 0.99
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Andressa Dias Costa · 7 shared papers, 2021–2026 · strength 0.95
- Paper Cell-free chromatin epigenomic profiling enables non-invasive pancreatic cancer cell-state identification DOI 10.64898/2026.04.02.26349987↗
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-24-1164↗
- Joseph Douglas Mancias · 6 shared papers, 2022–2026 · strength 0.94
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper Immune and stromal features of durable complete response to radiation and dual immune checkpoint blockade in pancreatic… DOI 10.64898/2026.08.06.26359422↗
- Thomas Adam Abrams · 6 shared papers, 2023–2026 · strength 0.91
- Paper Immune and stromal features of durable complete response to radiation and dual immune checkpoint blockade in pancreatic… DOI 10.64898/2026.08.06.26359422↗
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Stephanie K. Dougan · 6 shared papers, 2021–2026 · strength 0.90
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-24-1164↗
- Rishi Surana · 6 shared papers, 2022–2026 · strength 0.89
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Paper Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-24-1164↗
- Thomas E. Clancy · 6 shared papers, 2021–2026 · strength 0.80
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper Oncogenic Drivers and Therapeutic Vulnerabilities in KRAS Wild-Type Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-22-3930↗
- Geoffrey Ira Shapiro · 6 shared papers, 2021–2026 · strength 0.76
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper A Phase I Expansion Cohort Study Evaluating the Safety and Efficacy of the CHK1 Inhibitor LY2880070 with Low-dose Gemci… DOI 10.1158/1078-0432.ccr-23-2005↗
- Paper Opportunities for Utilization of DNA Repair Inhibitors in Homologous Recombination Repair-Deficient and Proficient Panc… DOI 10.1158/1078-0432.ccr-21-1367↗
- Hannah L. Williams · 5 shared papers, 2021–2025 · strength 0.61
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Paper Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-24-1164↗
- Paper Spatially Resolved Single-Cell Assessment of Pancreatic Cancer Expression Subtypes Reveals Co-expressor Phenotypes and … DOI 10.1158/0008-5472.can-22-3050↗
- Leah H. Biller · 4 shared papers, 2023–2026 · strength 0.60
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Paper Blockade of IL1β and PD1 with Combination Chemotherapy Reduces Systemic Myeloid Suppression in Metastatic Pancreatic Ca… DOI 10.1158/2326-6066.cir-23-1073↗
- Alan D. D’Andrea · 4 shared papers, 2021–2026 · strength 0.56
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper A Phase I Expansion Cohort Study Evaluating the Safety and Efficacy of the CHK1 Inhibitor LY2880070 with Low-dose Gemci… DOI 10.1158/1078-0432.ccr-23-2005↗
- Paper Opportunities for Utilization of DNA Repair Inhibitors in Homologous Recombination Repair-Deficient and Proficient Panc… DOI 10.1158/1078-0432.ccr-21-1367↗
- ANDREA C Enzinger · 3 shared papers, 2025–2026 · strength 0.52
- Paper A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, … DOI 10.1158/1078-0432.ccr-24-3766↗
- Paper Gemcitabine and nab-paclitaxel with or without the VDR agonist paricalcitol for metastatic pancreatic cancer: a randomi… DOI 10.1038/s43018-026-01165-8↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Michael Lawrence Dougan · 3 shared papers, 2024–2026 · strength 0.51
- Paper Dendritic cell redundancy enables priming of anti-tumor CD4+ T cells in pancreatic cancer. DOI 10.1016/j.ccell.2026.04.005↗
- Paper CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer. DOI 10.1016/j.cell.2026.08.045↗
- Paper Blockade of IL1β and PD1 with Combination Chemotherapy Reduces Systemic Myeloid Suppression in Metastatic Pancreatic Ca… DOI 10.1158/2326-6066.cir-23-1073↗
- Chen Yuan · 4 shared papers, 2022–2024 · strength 0.50
- Paper Clinical and Genomic Features of Classical and Basal Transcriptional Subtypes in Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-24-1164↗
- Paper Oncogenic Drivers and Therapeutic Vulnerabilities in KRAS Wild-Type Pancreatic Cancer. DOI 10.1158/1078-0432.ccr-22-3930↗
- Paper Spatially Resolved Single-Cell Assessment of Pancreatic Cancer Expression Subtypes Reveals Co-expressor Phenotypes and … DOI 10.1158/0008-5472.can-22-3050↗
- Colin D. Weekes · 3 shared papers, 2023–2026 · strength 0.47
- Paper Immune and stromal features of durable complete response to radiation and dual immune checkpoint blockade in pancreatic… DOI 10.64898/2026.08.06.26359422↗
- Paper Open-Label, Phase II Trial of Extracellular Regulated Kinase Inhibition Alone and in Combination With Autophagy Inhibit… DOI 10.1200/po-25-00332↗
- Paper Phase Ib and Expansion Study of Gemcitabine, Nab-Paclitaxel, and Ficlatuzumab in Patients With Metastatic Pancreatic Ca… DOI 10.1093/oncolo/oyad002↗
- William A. Freed-Pastor · 3 shared papers, 2022–2025 · strength 0.42
- Paper Pancreatic cancer-restricted cryptic antigens are targets for T cell recognition. DOI 10.1126/science.adk3487↗
- Paper Emerging Role of Targeted Therapy in Metastatic Pancreatic Adenocarcinoma. DOI 10.3390/cancers14246223↗
- Paper Neoadjuvant Chemotherapy Is Associated with Altered Immune Cell Infiltration and an Anti-Tumorigenic Microenvironment i… DOI 10.1158/1078-0432.ccr-22-1125↗
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.