Pancreatic Cancer Research

ResearcherDuke UniversityActive in the last 2 years

Hui Wang

Matched on ORCID iD 0000-0001-5484-4071; OpenAlex author ID A5100460663. Sources: OpenAlex.

Their work

Papers
13 (first author 3, last author 0)
Trials
0
Grants
0
Labs led
0
Collaborators
16
Papers, trials and grants by year

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

Papers 13

  1. COL11A1 Inhibits Ferroptosis in Pancreatic Cancer by Regulating AKT/Beclin 1 Dependent Autophagy. Co-author DOI 10.31083/fbl49200↗
  2. Apolipoprotein E2 inhibits mitochondrial apoptosis in pancreatic cancer cells through ERK1/2/CREB/BCL-2 signaling. Co-author DOI 10.1016/j.hbpd.2022.09.010↗
  3. COL11A1-Driven Epithelial-Mesenchymal Transition and Stemness of Pancreatic Cancer Cells Induce Cell Migration and Invasion by Modulating the AKT/GSK-3β/Snail … Co-author DOI 10.3390/biom12030391↗
  4. The COL11A1/Akt/CREB signaling axis enables mitochondrial-mediated apoptotic evasion to promote chemoresistance in pancreatic cancer cells through modulating B… Co-author DOI 10.7150/jca.47032↗
  5. LAMC2 modulates the acidity of microenvironments to promote invasion and migration of pancreatic cancer cells via regulating AKT-dependent NHE1 activity. Co-author DOI 10.1016/j.yexcr.2020.111984↗
  6. Apolipoprotein E2 modulates cell cycle function to promote proliferation in pancreatic cancer cells via regulation of the c-Myc-p21Waf1 signalling pathway. First author DOI 10.1139/bcb-2018-0230↗
  7. Apolipoprotein E2 Promotes the Migration and Invasion of Pancreatic Cancer Cells via Activation of the ERK1/2 Signaling Pathway. Co-author DOI 10.2147/cmar.s284115↗
  8. Artemin regulates CXCR4 expression to induce migration and invasion in pancreatic cancer cells through activation of NF-κB signaling. First author DOI 10.1016/j.yexcr.2018.02.008↗
  9. Tenascin-C Modulates Cell Cycle Progression to Enhance Tumour Cell Proliferation through AKT/FOXO1 Signalling in Pancreatic Cancer. Co-author DOI 10.7150/jca.25926↗
  10. Fractalkine/CX3CR1 induces apoptosis resistance and proliferation through the activation of the AKT/NF-κB cascade in pancreatic cancer cells. Co-author DOI 10.1002/cbf.3278↗
  11. TM4SF1 Promotes Metastasis of Pancreatic Cancer via Regulating the Expression of DDR1. Co-author DOI 10.1038/srep45895↗
  12. Tenascin-C induces migration and invasion through JNK/c-Jun signalling in pancreatic cancer. Co-author DOI 10.18632/oncotarget.20160↗
  13. A PK2/Bv8/PROK2 antagonist suppresses tumorigenic processes by inhibiting angiogenesis in glioma and blocking myeloid cell infiltration in pancreatic cancer. First author DOI 10.1371/journal.pone.0054916↗

Closest collaborators

The 16 strongest of 16 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Xiaohong Shen · 10 shared papers, 2017–2023 · strength 1.34
  2. Shaoxia Du · 9 shared papers, 2017–2023 · strength 1.11
  3. Jun Cai · 8 shared papers, 2017–2021 · strength 0.90
  4. Dongdong Li · 1 shared paper, 2026 · strength 0.32
  5. Na Gu · 1 shared paper, 2026 · strength 0.32
  6. Juan Wang · 3 shared papers, 2017–2020 · strength 0.30
  7. Beibei Xin · 3 shared papers, 2017–2018 · strength 0.23
  8. Wei Wei · 2 shared papers, 2017–2020 · strength 0.20
  9. Wei Wei · 1 shared paper, 2020 · strength 0.15
  10. Jia-Chun Yang · 1 shared paper, 2017 · strength 0.07
  11. Jia Cao · 1 shared paper, 2017 · strength 0.07
  12. Leiming Xu · 1 shared paper, 2017 · strength 0.07
  13. Mingming Li · 1 shared paper, 2017 · strength 0.07
  14. Yi Zhang · 1 shared paper, 2017 · strength 0.07
  15. Xiao‐Fan Wang · 1 shared paper, 2013 · strength 0.04
  16. Valerie F. Curtis · 1 shared paper, 2013 · strength 0.04

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.