Pancreatic Cancer Research

ResearcherUniversity of North Carolina at Chapel HillActive in the last 2 years

Adrienne D. Cox

ORCID-verified (high confidence, 0.95), identity_conf@1As of 6 November 2026

Matched on ORCID iD 0000-0002-4901-2454; OpenAlex author ID A5005839868; NIH RePORTER profile ID 1886390. Sources: OpenAlex.

Their work

Papers
20 (first author 0, last author 1)
Trials
0
Grants
2
Labs led
1
Collaborators
59
Papers, trials and grants by year

2011: 1 paper · 2012: 1 paper · 2013: none · 2014: none · 2015: none · 2016: 1 paper · 2017: none · 2018: none · 2019: 2 papers, 1 grant · 2020: 2 papers, 1 grant · 2021: 3 papers · 2022: 2 papers · 2023: 2 papers · 2024: none · 2025: 4 papers · 2026: 2 papers

Papers 20

  1. Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition. Co-author DOI 10.1016/j.celrep.2026.117627↗
  2. CRISPR-Cas9 Screening Identifies Resistance Mechanisms to KRAS Inhibition in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-25-1835↗
  3. Defining the MYC-regulated transcriptome and kinome that support KRAS- and ERK-dependent growth of pancreatic cancer. Co-author DOI 10.1126/scisignal.adu7145↗
  4. Concurrent Inhibition of the RAS-MAPK Pathway and PIKfyve Is a Therapeutic Strategy for Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-24-1757↗
  5. Combination of the MTA-Cooperative PRMT5 Inhibitor BMS-986504 and KRAS Inhibitors Is an Effective Treatment Strategy for MTAP-Deleted KRAS-Mutant Pancreatic Ca… Co-author DOI 10.1158/0008-5472.can-25-1507↗
  6. Dordaviprone/ONC201 Activation of the ClpP Mitochondrial Protease Inhibits the Growth of KRAS-Mutant Pancreatic Cancer and Overcomes RAS Inhibitor Resistance Co-author DOI 10.64898/2025.12.01.691471↗
  7. Combination Therapies with CDK4/6 Inhibitors to Treat KRAS-Mutant Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-22-0391↗
  8. VCP/p97, a pleiotropic protein regulator of the DNA damage response and proteostasis, is a potential therapeutic target in KRAS-mutant pancreatic cancer. Last author DOI 10.18632/genesandcancer.231↗
  9. Targeting the ERK mitogen-activated protein kinase cascade for the treatment of KRAS-mutant pancreatic cancer. Co-author DOI 10.1016/bs.acr.2021.07.008↗
  10. Concurrent Inhibition of IGF1R and ERK Increases Pancreatic Cancer Sensitivity to Autophagy Inhibitors. Co-author DOI 10.1158/0008-5472.can-21-1443↗
  11. Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition. Co-author DOI 10.1016/j.celrep.2021.109291↗
  12. CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment. Co-author DOI 10.1016/j.celrep.2021.110060↗
  13. The KRAS-regulated kinome identifies WEE1 and ERK coinhibition as a potential therapeutic strategy in KRAS-mutant pancreatic cancer. Co-author DOI 10.1016/j.jbc.2021.101335↗
  14. Author Correction: Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-020-0947-8↗
  15. Atypical KRAS G12R Mutant Is Impaired in PI3K Signaling and Macropinocytosis in Pancreatic Cancer. Co-author DOI 10.1158/2159-8290.cd-19-1006↗
  16. Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. Co-author DOI 10.1038/s41591-019-0368-8↗
  17. Application of a MYC degradation screen identifies sensitivity to CDK9 inhibitors in KRAS-mutant pancreatic cancer. Co-author DOI 10.1126/scisignal.aav7259↗
  18. Long-Term ERK Inhibition in KRAS-Mutant Pancreatic Cancer Is Associated with MYC Degradation and Senescence-like Growth Suppression. Co-author DOI 10.1016/j.ccell.2015.11.011↗
  19. Silencing the killers: paracrine immune suppression in pancreatic cancer. Co-author DOI 10.1016/j.ccr.2012.05.029↗
  20. The oncogenic kinase Pim-1 is modulated by K-Ras signaling and mediates transformed growth and radioresistance in human pancreatic ductal adenocarcinoma cells. Co-author DOI 10.1093/carcin/bgr007↗

Grants 2

  1. Project 3: Mechanisms and therapeutic targeting of NRAS in melanoma P01CA203657↗
  2. Identification of synthetic lethal interactors in pancreatic cancer U01CA199235↗

Closest collaborators

The 25 strongest of 59 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Channing J. Der · 18 shared papers, 2 shared grants, 2016–2026 · strength 3.27
  2. Clint A. Stalnecker · 13 shared papers, 2019–2026 · strength 1.92
  3. Kirsten L. Bryant · 13 shared papers, 2016–2026 · strength 1.76
  4. Craig M. Goodwin · 9 shared papers, 2020–2026 · strength 1.27
  5. Jennifer E. Klomp · 10 shared papers, 2019–2026 · strength 1.18
  6. Andrew M. Waters · 9 shared papers, 2019–2026 · strength 1.11
  7. Mariaelena Pierobon · 10 shared papers, 2016–2025 · strength 1.08
  8. J. Nathaniel Diehl · 9 shared papers, 2019–2026 · strength 1.05
  9. Kristina Drizyte‐Miller · 6 shared papers, 2021–2025 · strength 0.99
  10. Bjoern Papke · 9 shared papers, 2019–2026 · strength 0.95
  11. Lee M. Graves · 6 shared papers, 2019–2026 · strength 0.84
  12. A. Cole Edwards · 5 shared papers, 2021–2026 · strength 0.80
  13. Emanuel F. Petricoin · 8 shared papers, 2016–2025 · strength 0.79
  14. Priya S. Hibshman · 5 shared papers, 2021–2026 · strength 0.74
  15. G. Aaron Hobbs · 6 shared papers, 2019–2026 · strength 0.70
  16. Emanuel F. Petricoin · 4 shared papers, 2023–2025 · strength 0.69
  17. Andrew J. Aguirre · 4 shared papers, 2020–2026 · strength 0.57
  18. Jonathan M. DeLiberty · 4 shared papers, 2020–2025 · strength 0.49
  19. Tikvah K. Hayes · 5 shared papers, 2016–2026 · strength 0.46
  20. Devon R. Blake · 4 shared papers, 2019–2026 · strength 0.46
  21. Sarah E. Ackermann · 2 shared papers, 2025–2026 · strength 0.40
  22. Ryan N. Robb · 2 shared papers, 2025 · strength 0.37
  23. Mallory K. Roach · 2 shared papers, 2025 · strength 0.37
  24. Naim U. Rashid · 2 shared papers, 2021–2025 · strength 0.29
  25. William C. Hahn · 2 shared papers, 2021–2026 · strength 0.28

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.