Pancreatic Cancer Research

ResearcherMassachusetts Institute of TechnologyActive in the last 2 years

Tyler Jacks

Matched on ORCID iD 0000-0001-5785-8911; OpenAlex author ID A5071936673; NIH RePORTER profile ID 3128332. Sources: funder_awards.

Their work

Papers
20 (first author 0, last author 3)
Trials
0
Grants
4
Labs led
1
Collaborators
108
Papers, trials and grants by year

2012: 1 grant · 2013: none · 2014: none · 2015: 1 paper · 2016: none · 2017: 1 paper · 2018: 4 papers · 2019: 1 paper · 2020: 3 papers · 2021: 2 papers · 2022: 1 paper · 2023: none · 2024: 2 papers · 2025: 2 papers, 1 grant · 2026: 3 papers, 1 grant

Papers 20

  1. GLIS3 marks a neural-like progenitor cell state that drives metastasis in pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.celrep.2026.117314↗
  2. Author Correction: Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarc… Co-author DOI 10.1038/s41591-026-04234-8↗
  3. Pancreatic cancer-associated organ dysfunction promotes muscle autophagy and contributes to peripheral tissue wasting Co-author DOI 10.64898/2026.02.27.708635↗
  4. The Pdgfd-Pdgfrb axis orchestrates tumor-nerve crosstalk in pancreatic cancer Co-author DOI 10.1101/2025.08.26.672505↗
  5. Pancreatic cancer-restricted cryptic antigens are targets for T cell recognition. Co-author DOI 10.1126/science.adk3487↗
  6. Spatially resolved analysis of pancreatic cancer identifies therapy-associated remodeling of the tumor microenvironment. Co-author DOI 10.1038/s41588-024-01890-9↗
  7. Author Correction: Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarc… Co-author DOI 10.1038/s41591-024-03054-y↗
  8. Single-nucleus and spatial transcriptome profiling of pancreatic cancer identifies multicellular dynamics associated with neoadjuvant treatment. Co-author DOI 10.1038/s41588-022-01134-8↗
  9. The CD155/TIGIT axis promotes and maintains immune evasion in neoantigen-expressing pancreatic cancer. Last author DOI 10.1016/j.ccell.2021.07.007↗
  10. Microenvironment drives cell state, plasticity, and drug response in pancreatic cancer. Co-author DOI 10.1016/j.cell.2021.11.017↗
  11. Endocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1016/j.cell.2020.03.062↗
  12. Single-nucleus and spatial transcriptomics of archival pancreatic cancer reveals multi-compartment reprogramming after neoadjuvant treatment Co-author DOI 10.1101/2020.08.25.267336↗
  13. Dissecting cell-type-specific metabolism in pancreatic ductal adenocarcinoma. Co-author DOI 10.7554/elife.56782↗
  14. Endocrine-exocrine signaling drives obesity-associated pancreatic ductal adenocarcinoma Co-author DOI 10.1101/663583↗
  15. Differences in Nanoparticle Uptake in Transplanted and Autochthonous Models of Pancreatic Cancer. Co-author DOI 10.1021/acs.nanolett.7b04043↗
  16. Intercepting Pancreatic Cancer: Our Dream Team's Resolve to Stop Pancreatic Cancer. Co-author DOI 10.1097/mpa.0000000000001165↗
  17. Adaptive and Reversible Resistance to Kras Inhibition in Pancreatic Cancer Cells. Last author DOI 10.1158/0008-5472.can-17-2129↗
  18. iRGD-guided Tumor-penetrating Nanocomplexes for Therapeutic siRNA Delivery to Pancreatic Cancer. Co-author DOI 10.1158/1535-7163.mct-17-1090↗
  19. Survival of pancreatic cancer cells lacking KRAS function. Last author DOI 10.1038/s41467-017-00942-5↗
  20. Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/nm.3952↗

Grants 4

  1. Studying factors controlling cancer progression and immune recognition in mouse models R35CA274464↗
  2. Core C-Computational Core P01CA117969↗
  3. Mechanisms of K-RAS Independent Growth in Pancreatic Cancer AWARD pancan:2012-tyler-jacks-phd-mechanisms-of-k-ras-independent-growth-i
  4. Lustgarten Laboratory at MIT AWARD lustgarten:na-tyler-jacks-lustgarten-laboratory-at-mit

Closest collaborators

The 25 strongest of 108 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Brian Matthew Wolpin · 7 shared papers, 2018–2026 · strength 0.90
  2. Ralph Weissleder · 2 shared papers, 1 shared grant, 2024–2025 · strength 0.75
  3. William L. Hwang · 5 shared papers, 2020–2026 · strength 0.68
  4. Jonathan Andrew Nowak · 5 shared papers, 2019–2026 · strength 0.66
  5. Andrew J. Aguirre · 5 shared papers, 2018–2026 · strength 0.61
  6. Jimmy A. Guo · 4 shared papers, 2020–2026 · strength 0.59
  7. Mari A. Mino-Kenudson · 4 shared papers, 2020–2026 · strength 0.59
  8. William A. Freed-Pastor · 4 shared papers, 2020–2026 · strength 0.56
  9. Anirban Maitra · 1 shared paper, 1 shared grant, 2018–2025 · strength 0.54
  10. Nicholas J Caldwell · 3 shared papers, 2024–2026 · strength 0.52
  11. Dennis H. Gong · 3 shared papers, 2024–2026 · strength 0.52
  12. Carina Shiau · 3 shared papers, 2024–2026 · strength 0.52
  13. Cyril Henri Benes · 1 shared grant, 2025 · strength 0.45
  14. Gerald C Chu · 1 shared grant, 2025 · strength 0.45
  15. Phillip Andrew Futreal · 1 shared grant, 2025 · strength 0.45
  16. Ronald Anthony Depinho · 1 shared grant, 2025 · strength 0.45
  17. NABEEL El-BARDEESY · 1 shared grant, 2025 · strength 0.45
  18. Lewis C. Cantley · 1 shared grant, 2025 · strength 0.45
  19. Raghu Kalluri · 1 shared grant, 2025 · strength 0.45
  20. Sarah P. Thayer · 1 shared grant, 2025 · strength 0.45
  21. James wesley Horner · 1 shared grant, 2025 · strength 0.45
  22. Huamin Wang · 1 shared grant, 2025 · strength 0.45
  23. Mandar Deepak Muzumdar · 6 shared papers, 2017–2020 · strength 0.43
  24. Marija Trajkovic‐Arsic · 3 shared papers, 2015–2026 · strength 0.37
  25. Stephano S. Mello · 3 shared papers, 2015–2026 · strength 0.37

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.