ResearcherFirst Affiliated Hospital of Soochow UniversityActive in the last 2 years
Kai Chen
Matched on ORCID iD 0009-0001-4594-1053; OpenAlex author ID A5102029891. Sources: OpenAlex.
Their work
- Papers
- 12 (first author 0, last author 2)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 32
2011: 1 paper · 2012: none · 2013: none · 2014: none · 2015: 2 papers · 2016: 3 papers · 2017: none · 2018: 1 paper · 2019: 1 paper · 2020: none · 2021: 1 paper · 2022: none · 2023: 1 paper · 2024: none · 2025: 2 papers
Papers 12
- Development and validation of an MBD3/UHRF1 methylation-regulator-based prognostic model for pancreatic cancer survival. Last author DOI 10.21037/tcr-24-1887↗
- Multi-omics analyses inform mechanisms of immunotherapy response in pancreatic cancer. Co-author DOI 10.3389/fimmu.2025.1673098↗
- Prognostic evaluation of pancreatic cancer based on the model of chemo-radiotherapy resistance-related genes. Last author DOI 10.21037/jgo-23-308↗
- Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mRNA. Co-author DOI 10.1038/s41598-021-84394-4↗
- Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. Co-author DOI 10.1097/mpa.0000000000001386↗
- The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic cancer. Co-author DOI 10.1038/s41389-018-0102-2↗
- Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression of PP2Ac. Co-author DOI 10.1080/15384101.2015.1127468↗
- FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. Co-author DOI 10.18632/oncotarget.9975↗
- B7-H3 and B7-H4 are independent predictors of a poor prognosis in patients with pancreatic cancer. Co-author DOI 10.3892/ol.2016.4128↗
- Effect of Diabetes Mellitus on Survival in Patients with Pancreatic Cancer: A Systematic Review and Meta-analysis. Co-author DOI 10.1038/srep17102↗
- FH535 inhibited metastasis and growth of pancreatic cancer cells. Co-author DOI 10.2147/ott.s82718↗
- Growth of the pancreatic cancer cell line PANC-1 is inhibited by protein phosphatase 2A inhibitors through overactivation of the c-Jun N-terminal kinase pathwa… Co-author DOI 10.1016/j.ejca.2011.08.014↗
Closest collaborators
The 25 strongest of 32 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Min Tao · 8 shared papers, 2011–2021 · strength 0.51
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. DOI 10.1097/mpa.0000000000001386↗
- Paper The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic c… DOI 10.1038/s41389-018-0102-2↗
- Mengyao Wu · 4 shared papers, 2016–2025 · strength 0.48
- Paper Multi-omics analyses inform mechanisms of immunotherapy response in pancreatic cancer. DOI 10.3389/fimmu.2025.1673098↗
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. DOI 10.18632/oncotarget.9975↗
- Mengdan Xu · 3 shared papers, 2018–2025 · strength 0.40
- Paper Multi-omics analyses inform mechanisms of immunotherapy response in pancreatic cancer. DOI 10.3389/fimmu.2025.1673098↗
- Paper Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. DOI 10.1097/mpa.0000000000001386↗
- Paper The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic c… DOI 10.1038/s41389-018-0102-2↗
- Qiaoming Zhi · 5 shared papers, 2016–2021 · strength 0.39
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. DOI 10.1097/mpa.0000000000001386↗
- Paper The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic c… DOI 10.1038/s41389-018-0102-2↗
- Xue Cheng · 1 shared paper, 2025 · strength 0.37
- Chunbin Wang · 1 shared paper, 2025 · strength 0.37
- Meng Shen · 5 shared papers, 2015–2021 · strength 0.36
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. DOI 10.1097/mpa.0000000000001386↗
- Paper FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. DOI 10.18632/oncotarget.9975↗
- Jinming Cao · 1 shared paper, 2025 · strength 0.25
- Dapeng Li · 1 shared paper, 2025 · strength 0.25
- Yecheng Li · 1 shared paper, 2025 · strength 0.25
- Ge Li · 1 shared paper, 2025 · strength 0.25
- Wěi Li · 1 shared paper, 2023 · strength 0.20
- Hui‐Chuan Sun · 1 shared paper, 2023 · strength 0.20
- Mengyao Wu · 3 shared papers, 2015–2019 · strength 0.20
- Paper Inflammation Promotes Progression of Pancreatic Cancer Through WNT/β-Catenin Pathway-Dependent Manner. DOI 10.1097/mpa.0000000000001386↗
- Paper The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic c… DOI 10.1038/s41389-018-0102-2↗
- Paper FH535 inhibited metastasis and growth of pancreatic cancer cells. DOI 10.2147/ott.s82718↗
- Daoming Li · 3 shared papers, 2011–2021 · strength 0.20
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper FH535 inhibited metastasis and growth of pancreatic cancer cells. DOI 10.2147/ott.s82718↗
- Paper Growth of the pancreatic cancer cell line PANC-1 is inhibited by protein phosphatase 2A inhibitors through overactivati… DOI 10.1016/j.ejca.2011.08.014↗
- Wei Li · 2 shared papers, 2016–2021 · strength 0.18
- Paper Author Correction: Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mR… DOI 10.1038/s41598-021-84394-4↗
- Paper Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression … DOI 10.1080/15384101.2015.1127468↗
- Wei Li · 3 shared papers, 2015–2018 · strength 0.17
- Paper The combination of cantharidin and antiangiogenic therapeutics presents additive antitumor effects against pancreatic c… DOI 10.1038/s41389-018-0102-2↗
- Paper FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. DOI 10.18632/oncotarget.9975↗
- Paper FH535 inhibited metastasis and growth of pancreatic cancer cells. DOI 10.2147/ott.s82718↗
- Weiming Duan · 3 shared papers, 2011–2016 · strength 0.12
- Paper FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. DOI 10.18632/oncotarget.9975↗
- Paper FH535 inhibited metastasis and growth of pancreatic cancer cells. DOI 10.2147/ott.s82718↗
- Paper Growth of the pancreatic cancer cell line PANC-1 is inhibited by protein phosphatase 2A inhibitors through overactivati… DOI 10.1016/j.ejca.2011.08.014↗
- Yixiang Mao · 2 shared papers, 2015–2016 · strength 0.12
- Lian Lian · 2 shared papers, 2015–2016 · strength 0.10
- Wei Li · 1 shared paper, 2019 · strength 0.08
- Rui Ren · 1 shared paper, 2019 · strength 0.08
- Wei Li · 1 shared paper, 2016 · strength 0.06
- Hong Xu · 1 shared paper, 2016 · strength 0.06
- Hongwei Tang · 1 shared paper, 2015 · strength 0.06
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.