Pancreatic Cancer Research

ResearcherFirst Affiliated Hospital of Xi'an Jiaotong UniversityActive in the last 2 years

Wunai Zhang

ORCID-verified (high confidence, 0.95), identity_conf@1As of 7 November 2026

Matched on ORCID iD 0000-0001-9023-5580; OpenAlex author ID A5066919986. Sources: OpenAlex.

Their work

Papers
11 (first author 1, last author 0)
Trials
0
Grants
0
Labs led
0
Collaborators
38
Papers, trials and grants by year

2020: 1 paper · 2021: 1 paper · 2022: 6 papers · 2023: 1 paper · 2024: none · 2025: 1 paper · 2026: 1 paper

Papers 11

  1. MUC15 loss promotes perineural invasion in pancreatic cancer by activating the IGF1R/STAT3/NGF pathway. Co-author DOI 10.1016/j.canlet.2026.218362↗
  2. Elevated SREBP1 accelerates the initiation and growth of pancreatic cancer by targeting SOX9. Co-author DOI 10.1186/s13062-025-00595-1↗
  3. Mutant p53 driven-LINC00857, a protein scaffold between FOXM1 and deubiquitinase OTUB1, promotes the metastasis of pancreatic cancer. Co-author DOI 10.1016/j.canlet.2022.215976↗
  4. Thiostrepton induces ferroptosis in pancreatic cancer cells through STAT3/GPX4 signalling. Co-author DOI 10.1038/s41419-022-05082-3↗
  5. Correction: Thiostrepton induces ferroptosis in pancreatic cancer cells through STAT3/GPX4 signalling. Co-author DOI 10.1038/s41419-022-05236-3↗
  6. Autophagic Schwann cells promote perineural invasion mediated by the NGF/ATG7 paracrine pathway in pancreatic cancer. Co-author DOI 10.1186/s13046-021-02198-w↗
  7. Huaier suppresses pancreatic cancer progression via activating cell autophagy induced ferroptosis. Co-author DOI 10.3389/fonc.2022.960858↗
  8. High‑glucose microenvironment promotes perineural invasion of pancreatic cancer via activation of hypoxia inducible factor 1α. First author DOI 10.3892/or.2022.8275↗
  9. RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma. Co-author DOI 10.7150/ijbs.72204↗
  10. Honokiol Suppresses Perineural Invasion of Pancreatic Cancer by Inhibiting SMAD2/3 Signaling. Co-author DOI 10.3389/fonc.2021.728583↗
  11. The JAM-B/c-src/MMP9 pathway is associated with progression and regulates the invasion of pancreatic cancer. Co-author DOI 10.7150/jca.40953↗

Closest collaborators

The 25 strongest of 38 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Zeen Zhu · 8 shared papers, 2021–2026 · strength 1.28
  2. Simei Zhang · 8 shared papers, 2021–2026 · strength 1.22
  3. Weikun Qian · 7 shared papers, 2022–2026 · strength 1.19
  4. Qingyong Ma · 7 shared papers, 2021–2025 · strength 1.05
  5. Zheng Wang · 5 shared papers, 2022–2026 · strength 0.82
  6. Zheng Wu · 5 shared papers, 2022–2025 · strength 0.80
  7. Weifan Zhang · 5 shared papers, 2022–2023 · strength 0.71
  8. Yangyang Yue · 2 shared papers, 2022–2026 · strength 0.39
  9. Cancan Zhou · 2 shared papers, 2023–2025 · strength 0.37
  10. Tao Qin · 2 shared papers, 2021–2026 · strength 0.36
  11. Shuai Wu · 2 shared papers, 2022–2025 · strength 0.35
  12. Jiantao Mo · 2 shared papers, 2022 · strength 0.28
  13. Bo Zhang · 2 shared papers, 2022 · strength 0.28
  14. Wenbin Yang · 2 shared papers, 2020–2022 · strength 0.26
  15. Junhui Li · 2 shared papers, 2020–2022 · strength 0.26
  16. Zheng Wang · 2 shared papers, 2021–2022 · strength 0.25
  17. Yiqun Song · 1 shared paper, 2026 · strength 0.25
  18. Jie Hao · 1 shared paper, 2025 · strength 0.22
  19. Ruiqi Cao · 1 shared paper, 2025 · strength 0.22
  20. Xuqi Li · 1 shared paper, 2025 · strength 0.22
  21. Zhengdong Jiang · 1 shared paper, 2023 · strength 0.16
  22. Jingtao Gu · 1 shared paper, 2023 · strength 0.16
  23. Weili Min · 1 shared paper, 2022 · strength 0.16
  24. Xin Zhang · 1 shared paper, 2022 · strength 0.16
  25. Wěi Li · 1 shared paper, 2022 · strength 0.16

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.