Pancreatic Cancer Research

ResearcherTongji UniversityNo recent work listed

Qiangsheng Hu

ORCID-verified (high confidence, 0.95), identity_conf@1As of 8 November 2026

Matched on ORCID iD 0000-0001-7469-1359; OpenAlex author ID A5021423929. Sources: OpenAlex.

Their work

Papers
25 (first author 5, last author 0)
Trials
0
Grants
0
Labs led
0
Collaborators
42
Papers, trials and grants by year

2016: 2 papers · 2017: 4 papers · 2018: 4 papers · 2019: 5 papers · 2020: 3 papers · 2021: 6 papers · 2022: none · 2023: 1 paper

Papers 25

  1. SETD8 inhibits ferroptosis in pancreatic cancer by inhibiting the expression of RRAD. First author DOI 10.1186/s12935-023-02899-6↗
  2. Improved tumor control with antiangiogenic therapy after treatment with gemcitabine and nab-paclitaxel in pancreatic cancer. Co-author DOI 10.1002/ctm2.398↗
  3. SETD8 potentiates constitutive ERK1/2 activation via epigenetically silencing DUSP10 expression in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2020.11.023↗
  4. FBW7-NRA41-SCD1 axis synchronously regulates apoptosis and ferroptosis in pancreatic cancer cells. Co-author DOI 10.1016/j.redox.2020.101807↗
  5. FGFBP1-mediated crosstalk between fibroblasts and pancreatic cancer cells via FGF22/FGFR2 promotes invasion and metastasis of pancreatic cancer. Co-author DOI 10.1093/abbs/gmab074↗
  6. SETD8 induces stemness and epithelial-mesenchymal transition of pancreatic cancer cells by regulating ROR1 expression. Co-author DOI 10.1093/abbs/gmab140↗
  7. MTAP Deficiency-Induced Metabolic Reprogramming Creates a Vulnerability to Cotargeting De Novo Purine Synthesis and Glycolysis in Pancreatic Cancer. Co-author DOI 10.1158/0008-5472.can-20-0414↗
  8. Oncogenic function of TRIM2 in pancreatic cancer by activating ROS-related NRF2/ITGB7/FAK axis. Co-author DOI 10.1038/s41388-020-01452-3↗
  9. Pin1 promotes pancreatic cancer progression and metastasis by activation of NF-κB-IL-18 feedback loop. Co-author DOI 10.1111/cpr.12816↗
  10. Abrogation of ARF6 promotes RSL3-induced ferroptosis and mitigates gemcitabine resistance in pancreatic cancer cells. First author PMID 32368394↗
  11. UHRF1 promotes aerobic glycolysis and proliferation via suppression of SIRT4 in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2019.03.024↗
  12. Homeodomain-interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer. First author DOI 10.1111/cpr.12603↗
  13. Role of hepatocyte nuclear factor 4 alpha in cell proliferation and gemcitabine resistance in pancreatic adenocarcinoma. Co-author DOI 10.1186/s12935-019-0767-4↗
  14. PRMT5 enhances tumorigenicity and glycolysis in pancreatic cancer via the FBW7/cMyc axis. First author DOI 10.1186/s12964-019-0344-4↗
  15. FGFBP1, a downstream target of the FBW7/c-Myc axis, promotes cell proliferation and migration in pancreatic cancer. Co-author PMID 31911852↗
  16. TCF7L2 positively regulates aerobic glycolysis via the EGLN2/HIF-1α axis and indicates prognosis in pancreatic cancer. First author DOI 10.1038/s41419-018-0367-6↗
  17. SNX6 predicts poor prognosis and contributes to the metastasis of pancreatic cancer cells via activating epithelial-mesenchymal transition. Co-author DOI 10.1093/abbs/gmy110↗
  18. dCK negatively regulates the NRF2/ARE axis and ROS production in pancreatic cancer. Co-author DOI 10.1111/cpr.12456↗
  19. The impact of cancer-associated fibroblasts on major hallmarks of pancreatic cancer. Co-author DOI 10.7150/thno.26546↗
  20. ARF6, induced by mutant Kras, promotes proliferation and Warburg effect in pancreatic cancer. Co-author DOI 10.1016/j.canlet.2016.12.014↗
  21. Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1158/1541-7786.mcr-16-0296↗
  22. A new facet of NDRG1 in pancreatic ductal adenocarcinoma: Suppression of glycolytic metabolism. Co-author DOI 10.3892/ijo.2017.3938↗
  23. FBW7 increases the chemosensitivity of pancreatic cancer cells to gemcitabine through upregulation of ENT1. Co-author DOI 10.3892/or.2017.5856↗
  24. Metabolic plasticity in heterogeneous pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.bbcan.2016.09.001↗
  25. Energy sources identify metabolic phenotypes in pancreatic cancer. Co-author DOI 10.1093/abbs/gmw097↗

Closest collaborators

The 25 strongest of 42 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Yi Qin · 24 shared papers, 2016–2023 · strength 2.11
  2. Shunrong Ji · 23 shared papers, 2016–2023 · strength 2.07
  3. Xianjun Yu · 23 shared papers, 2016–2021 · strength 1.97
  4. Wensheng Liu · 18 shared papers, 2017–2021 · strength 1.71
  5. Wenyan Xu · 20 shared papers, 2016–2021 · strength 1.67
  6. Xiaowu Xu · 15 shared papers, 2019–2023 · strength 1.60
  7. Zheng Zhang · 13 shared papers, 2018–2021 · strength 1.27
  8. Mengqi Liu · 9 shared papers, 2019–2021 · strength 0.93
  9. Qiqing Sun · 10 shared papers, 2018–2020 · strength 0.89
  10. Qifeng Zhuo · 8 shared papers, 2020–2021 · strength 0.87
  11. Quanxing Ni · 11 shared papers, 2016–2019 · strength 0.74
  12. Jin Xu · 11 shared papers, 2016–2019 · strength 0.73
  13. Ye Zeng · 6 shared papers, 2020–2021 · strength 0.65
  14. Jinfeng Xiang · 8 shared papers, 2016–2018 · strength 0.48
  15. Ye Zeng · 4 shared papers, 2019–2021 · strength 0.43
  16. Chen Liang · 7 shared papers, 2016–2018 · strength 0.41
  17. Dingkong Liang · 7 shared papers, 2016–2018 · strength 0.41
  18. Si Shi · 7 shared papers, 2016–2018 · strength 0.41
  19. Bo Zhang · 4 shared papers, 2017–2019 · strength 0.30
  20. Wenyan Xu · 2 shared papers, 2019–2021 · strength 0.21
  21. Zekun Lu · 1 shared paper, 2023 · strength 0.17
  22. Bingkai Xiao · 1 shared paper, 2023 · strength 0.17
  23. Xuemin Chen · 1 shared paper, 2023 · strength 0.17
  24. Pengfei Hu · 2 shared papers, 2017–2018 · strength 0.13
  25. Qingcai Meng · 2 shared papers, 2017–2018 · strength 0.12

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.