ResearcherAlbert Einstein College of MedicineActive in the last 2 years
Samarth Hegde
Matched on ORCID iD 0000-0001-6319-0372; OpenAlex author ID A5036013721; NIH RePORTER profile ID 16324865. Sources: OpenAlex.
Their work
- Papers
- 5
- Trials
- 0
- Grants
- 4
- Labs led
- 1
- Collaborators
- 24
2018: 1 grant · 2019: 1 paper · 2020: 2 papers · 2021: 1 paper · 2022: none · 2023: 1 grant · 2024: none · 2025: 1 paper, 1 grant · 2026: 1 grant
Papers 5
- Distinct immune cell infiltration patterns in pancreatic ductal adenocarcinoma (PDAC) exhibit divergent immune cell selection and immunosuppressive mechanisms. Co-author DOI 10.1038/s41467-024-55424-2↗
- Pancreatic Cancer Immuno-oncology in the Era of Precision Medicine. Co-author DOI 10.1007/s13193-020-01192-6↗
- Dendritic Cell Paucity Leads to Dysfunctional Immune Surveillance in Pancreatic Cancer. Co-author DOI 10.1016/j.ccell.2020.02.008↗
- Development of resistance to FAK inhibition in pancreatic cancer is linked to stromal depletion. Co-author DOI 10.1136/gutjnl-2018-317424↗
- Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies. Co-author DOI 10.1126/scitranslmed.aau9240↗
Grants 4
- Deconstructing pathogenic myelopoiesis in cancer immunosuppression and treatment resistance R00CA293148↗
- Deconstructing pathogenic myelopoiesis in cancer immunosuppression and treatment resistance K99CA293148↗
- Defining the barriers to immune surveillance in solid tumors K00CA223043↗
- Defining the barriers to immune surveillance in solid tumors F99CA223043↗
Closest collaborators
The 24 strongest of 24 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Ryan C Fields · 3 shared papers, 2019–2020 · strength 0.27
- Paper Development of resistance to FAK inhibition in pancreatic cancer is linked to stromal depletion. DOI 10.1136/gutjnl-2018-317424↗
- Paper Dendritic Cell Paucity Leads to Dysfunctional Immune Surveillance in Pancreatic Cancer. DOI 10.1016/j.ccell.2020.02.008↗
- Paper Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies. DOI 10.1126/scitranslmed.aau9240↗
- David G DeNardo · 3 shared papers, 2019–2020 · strength 0.27
- Paper Development of resistance to FAK inhibition in pancreatic cancer is linked to stromal depletion. DOI 10.1136/gutjnl-2018-317424↗
- Paper Dendritic Cell Paucity Leads to Dysfunctional Immune Surveillance in Pancreatic Cancer. DOI 10.1016/j.ccell.2020.02.008↗
- Paper Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies. DOI 10.1126/scitranslmed.aau9240↗
- Julie Kristina Schwarz · 2 shared papers, 2019–2020 · strength 0.17
- Graham D. Hogg · 2 shared papers, 2019–2020 · strength 0.17
- William G. Hawkins · 2 shared papers, 2019–2020 · strength 0.17
- Chong Zuo · 2 shared papers, 2019–2020 · strength 0.17
- Miriam Merad · 1 shared paper, 2025 · strength 0.16
- Lara Rosaline Heij · 1 shared paper, 2025 · strength 0.16
- Rachael J. M. Bashford-Rogers · 1 shared paper, 2025 · strength 0.16
- Georg J. Wiltberger · 1 shared paper, 2025 · strength 0.16
- Ashwin Jainarayanan · 1 shared paper, 2025 · strength 0.16
- Michael Loran Dustin · 1 shared paper, 2025 · strength 0.16
- Shihong Wu · 1 shared paper, 2025 · strength 0.16
- Adam Enver Frampton · 1 shared paper, 2025 · strength 0.16
- Shivan Sivakumar · 1 shared paper, 2025 · strength 0.16
- Hongmei Jiang · 1 shared paper, 2020 · strength 0.11
- Hong Jiang · 1 shared paper, 2020 · strength 0.11
- Kian‐Huat Lim · 1 shared paper, 2020 · strength 0.11
- Brett H. Herzog · 1 shared paper, 2020 · strength 0.09
- Varintra E. Lander · 1 shared paper, 2020 · strength 0.09
- John M. Baer · 1 shared paper, 2020 · strength 0.09
- Carl DeSelm · 1 shared paper, 2020 · strength 0.09
- Roheena Z. Panni · 1 shared paper, 2019 · strength 0.08
- Xiaobo Li · 1 shared paper, 2019 · strength 0.08
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.