ResearcherJesse Brown VA Medical CenterActive in the last 2 years
Ajay Nmn Rana
Matched on ORCID iD 0000-0003-0951-2566; OpenAlex author ID A5081839578; NIH RePORTER profile ID 1973958. Sources: OpenAlex.
Their work
- Papers
- 10 (first author 1, last author 8)
- Trials
- 0
- Grants
- 3
- Labs led
- 1
- Collaborators
- 19
2018: 1 paper · 2019: 1 paper, 1 grant · 2020: 1 paper · 2021: 3 papers · 2022: 3 papers · 2023: 1 paper · 2024: none · 2025: none · 2026: 2 grants
Papers 10
- Interplay between MAP kinases and tumor microenvironment: Opportunity for immunotherapy in pancreatic cancer. Last author DOI 10.1016/bs.acr.2023.02.003↗
- XP-524 is a dual-BET/EP300 inhibitor that represses oncogenic KRAS and potentiates immune checkpoint inhibition in pancreatic cancer. Last author DOI 10.1073/pnas.2116764119↗
- Calcium channel blockers potentiate gemcitabine chemotherapy in pancreatic cancer. Last author DOI 10.1073/pnas.2200143119↗
- Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. Last author DOI 10.3389/fonc.2022.806963↗
- Trials and tribulations of pancreatic cancer immunotherapy. Last author DOI 10.1016/j.canlet.2021.01.031↗
- Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer development. Last author DOI 10.1016/j.canlet.2021.04.015↗
- The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy. Last author DOI 10.3389/fonc.2021.688377↗
- Updated risk factors to inform early pancreatic cancer screening and identify high risk patients. First author DOI 10.1016/j.canlet.2020.04.022↗
- TGFβ Blockade Augments PD-1 Inhibition to Promote T-Cell-Mediated Regression of Pancreatic Cancer. Last author DOI 10.1158/1535-7163.mct-18-0850↗
- KRAS G12D and TP53R167H Cooperate to Induce Pancreatic Ductal Adenocarcinoma in Sus scrofa Pigs. Co-author DOI 10.1038/s41598-018-30916-6↗
Grants 3
Closest collaborators
The 19 strongest of 19 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Daniel R. Principe · 9 shared papers, 2018–2022 · strength 1.27
- Paper Updated risk factors to inform early pancreatic cancer screening and identify high risk patients. DOI 10.1016/j.canlet.2020.04.022↗
- Paper Trials and tribulations of pancreatic cancer immunotherapy. DOI 10.1016/j.canlet.2021.01.031↗
- Paper Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. DOI 10.3389/fonc.2022.806963↗
- Hidayatullah G. Munshi · 7 shared papers, 2018–2022 · strength 0.92
- Paper Trials and tribulations of pancreatic cancer immunotherapy. DOI 10.1016/j.canlet.2021.01.031↗
- Paper Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. DOI 10.3389/fonc.2022.806963↗
- Paper The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy. DOI 10.3389/fonc.2021.688377↗
- Patrick W. Underwood · 4 shared papers, 2021–2022 · strength 0.59
- Paper Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. DOI 10.3389/fonc.2022.806963↗
- Paper The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy. DOI 10.3389/fonc.2021.688377↗
- Paper Calcium channel blockers potentiate gemcitabine chemotherapy in pancreatic cancer. DOI 10.1073/pnas.2200143119↗
- Sandeep Kumar · 4 shared papers, 2019–2022 · strength 0.51
- Paper Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. DOI 10.3389/fonc.2022.806963↗
- Paper Calcium channel blockers potentiate gemcitabine chemotherapy in pancreatic cancer. DOI 10.1073/pnas.2200143119↗
- Paper Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer develop… DOI 10.1016/j.canlet.2021.04.015↗
- Jose Gilberto Trevino · 3 shared papers, 2021–2022 · strength 0.45
- Paper Loss of SMAD4 Is Associated With Poor Tumor Immunogenicity and Reduced PD-L1 Expression in Pancreatic Cancer. DOI 10.3389/fonc.2022.806963↗
- Paper The Current Treatment Paradigm for Pancreatic Ductal Adenocarcinoma and Barriers to Therapeutic Efficacy. DOI 10.3389/fonc.2021.688377↗
- Paper XP-524 is a dual-BET/EP300 inhibitor that represses oncogenic KRAS and potentiates immune checkpoint inhibition in panc… DOI 10.1073/pnas.2116764119↗
- Murray Korc · 2 shared papers, 2021 · strength 0.33
- Suneel Deepak Kamath · 2 shared papers, 2021–2022 · strength 0.30
- Paul J. Grippo · 3 shared papers, 2018–2021 · strength 0.27
- Paper Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer develop… DOI 10.1016/j.canlet.2021.04.015↗
- Paper TGFβ Blockade Augments PD-1 Inhibition to Promote T-Cell-Mediated Regression of Pancreatic Cancer. DOI 10.1158/1535-7163.mct-18-0850↗
- Paper KRAS G12D and TP53R167H Cooperate to Induce Pancreatic Ductal Adenocarcinoma in Sus scrofa Pigs. DOI 10.1038/s41598-018-30916-6↗
- Thao D. Pham · 2 shared papers, 2022 · strength 0.27
- Sandeep Kumar · 1 shared paper, 2023 · strength 0.22
- Navin Viswakarma · 2 shared papers, 2019–2021 · strength 0.21
- Paper Mixed Lineage Kinase 3 phosphorylates prolyl-isomerase PIN1 and potentiates GLI1 signaling in pancreatic cancer develop… DOI 10.1016/j.canlet.2021.04.015↗
- Paper TGFβ Blockade Augments PD-1 Inhibition to Promote T-Cell-Mediated Regression of Pancreatic Cancer. DOI 10.1158/1535-7163.mct-18-0850↗
- Carolina Torres · 2 shared papers, 2018–2019 · strength 0.16
- Jose Trevino · 1 shared paper, 2022 · strength 0.14
- Dinesh Thummuri · 1 shared paper, 2022 · strength 0.13
- Daohong Zhou · 1 shared paper, 2022 · strength 0.13
- Pier Cristoforo Giulianotti · 1 shared paper, 2021 · strength 0.12
- Ajay V. Maker · 1 shared paper, 2018 · strength 0.07
- David W. Dawson · 1 shared paper, 2018 · strength 0.07
- Lawrence B. Schook · 1 shared paper, 2018 · strength 0.07
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.