Pancreatic Cancer Research

ResearcherTongji UniversityNo recent work listed

Guoyong Hu

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

Matched on ORCID iD 0000-0003-3550-6127; OpenAlex author ID A5042452122. Sources: OpenAlex.

Their work

Papers
12 (first author 0, last author 6)
Trials
0
Grants
0
Labs led
1
Collaborators
20
Papers, trials and grants by year

2011: 2 papers · 2012: none · 2013: none · 2014: none · 2015: none · 2016: 3 papers · 2017: 2 papers · 2018: 1 paper · 2019: none · 2020: none · 2021: none · 2022: 1 paper · 2023: 3 papers

Papers 12

  1. Retraction Note: Transcriptional repression of SOCS3 mediated by IL-6/STAT3 signaling via DNMT1 promotes pancreatic cancer growth and metastasis. Co-author DOI 10.1186/s13046-023-02595-3↗
  2. Corrigendum: Systematic characterization of the clinical relevance of KPNA4 in pancreatic ductal adenocarcinoma. Last author DOI 10.3389/fonc.2023.1282120↗
  3. Erratum: Shikonin induces apoptosis and necroptosis in pancreatic cancer via regulating the expression of RIP1/RIP3 and synergizes the activity of gemcitabine. Last author PMID 38074805↗
  4. Systematic Characterization of the Clinical Relevance of KPNA4 in Pancreatic Ductal Adenocarcinoma. Last author DOI 10.3389/fonc.2022.834728↗
  5. Identification of Sox6 as a regulator of pancreatic cancer development. Co-author DOI 10.1111/jcmm.13470↗
  6. Thalidomide inhibits proliferation and epithelial-mesenchymal transition by modulating CD133 expression in pancreatic cancer cells. Last author DOI 10.3892/ol.2017.7213↗
  7. Shikonin induces apoptosis and necroptosis in pancreatic cancer via regulating the expression of RIP1/RIP3 and synergizes the activity of gemcitabine. Last author PMID 29312502↗
  8. The circadian clock gene Bmal1 acts as a potential anti-oncogene in pancreatic cancer by activating the p53 tumor suppressor pathway. Co-author DOI 10.1016/j.canlet.2015.12.002↗
  9. HIC1 attenuates invasion and metastasis by inhibiting the IL-6/STAT3 signalling pathway in human pancreatic cancer. Last author DOI 10.1016/j.canlet.2016.04.013↗
  10. Transcriptional repression of SOCS3 mediated by IL-6/STAT3 signaling via DNMT1 promotes pancreatic cancer growth and metastasis. Co-author DOI 10.1186/s13046-016-0301-7↗
  11. Identification of RegIV as a novel GLI1 target gene in human pancreatic cancer. Co-author DOI 10.1371/journal.pone.0018434↗
  12. Expression of DNMT1 and DNMT3a are regulated by GLI1 in human pancreatic cancer. Co-author DOI 10.1371/journal.pone.0027684↗

Closest collaborators

The 20 strongest of 20 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Congying Chen · 7 shared papers, 2016–2023 · strength 0.70
  2. Lijuan Yang · 7 shared papers, 2011–2023 · strength 0.59
  3. Rong Wan · 7 shared papers, 2016–2023 · strength 0.58
  4. Xingpeng Wang · 7 shared papers, 2011–2023 · strength 0.46
  5. Li Huang · 2 shared papers, 2023 · strength 0.36
  6. Bin Li · 2 shared papers, 2022–2023 · strength 0.36
  7. Jingpiao Bao · 2 shared papers, 2022–2023 · strength 0.36
  8. Li Huang · 4 shared papers, 2016–2018 · strength 0.26
  9. Weiliang Jiang · 4 shared papers, 2016–2018 · strength 0.24
  10. Yue Zeng · 1 shared paper, 2023 · strength 0.17
  11. Bin Hu · 2 shared papers, 2016 · strength 0.11
  12. Qiong-Ying Yuan · 1 shared paper, 2018 · strength 0.08
  13. Lijuan Yang · 1 shared paper, 2018 · strength 0.08
  14. Xiaohua Jiang · 1 shared paper, 2016 · strength 0.05
  15. Xuanfu Xu · 2 shared papers, 2011 · strength 0.05
  16. Shanshan He · 2 shared papers, 2011 · strength 0.05
  17. Feng Wang · 2 shared papers, 2011 · strength 0.05
  18. Chuanyong Guo · 2 shared papers, 2011 · strength 0.05
  19. Yinshi Huang · 1 shared paper, 2011 · strength 0.02
  20. Wenhui Mo · 1 shared paper, 2011 · strength 0.02

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.