ResearcherArmy Medical UniversityActive in the last 2 years

Wei Liu

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

Matched on ORCID iD 0000-0001-7118-815X; OpenAlex author ID A5100431658. Sources: OpenAlex.

Their work

Papers: 4
Trials: 0
Grants: 0
Labs led: 0
Collaborators: 11

Papers, trials and grants by year

2018: 1 paper · 2019: 1 paper · 2020: none · 2021: none · 2022: none · 2023: 1 paper · 2024: none · 2025: 1 paper

Papers 4

CALB2 facilitates macrophage M2 polarization to promote the growth and metastasis of pancreatic adenocarcinoma. Co-author DOI 10.1016/j.cellsig.2025.111887 ↗
CSTF2T facilitates pancreatic adenocarcinoma growth and metastasis by elevating H3K4Me1 methylation of CALB2 via ASH2L. Co-author DOI 10.1080/15384047.2023.2216041 ↗
ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. Co-author DOI 10.1186/s13046-019-1340-7 ↗
Kallikrein-related peptidase 7 is a potential target for the treatment of pancreatic cancer. Co-author DOI 10.18632/oncotarget.24132 ↗

Closest collaborators

The 11 strongest of 11 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

Zongjing Chen · 2 shared papers, 2023–2025 · strength 0.49
- Paper CALB2 facilitates macrophage M2 polarization to promote the growth and metastasis of pancreatic adenocarcinoma. DOI 10.1016/j.cellsig.2025.111887 ↗
- Paper CSTF2T facilitates pancreatic adenocarcinoma growth and metastasis by elevating H3K4Me1 methylation of CALB2 via ASH2L. DOI 10.1080/15384047.2023.2216041 ↗
Bo Xu · 2 shared papers, 2023–2025 · strength 0.49
- Paper CALB2 facilitates macrophage M2 polarization to promote the growth and metastasis of pancreatic adenocarcinoma. DOI 10.1016/j.cellsig.2025.111887 ↗
- Paper CSTF2T facilitates pancreatic adenocarcinoma growth and metastasis by elevating H3K4Me1 methylation of CALB2 via ASH2L. DOI 10.1080/15384047.2023.2216041 ↗
Dongwei Hu · 2 shared papers, 2023–2025 · strength 0.49
- Paper CALB2 facilitates macrophage M2 polarization to promote the growth and metastasis of pancreatic adenocarcinoma. DOI 10.1016/j.cellsig.2025.111887 ↗
- Paper CSTF2T facilitates pancreatic adenocarcinoma growth and metastasis by elevating H3K4Me1 methylation of CALB2 via ASH2L. DOI 10.1080/15384047.2023.2216041 ↗
Zhengde Wen · 1 shared paper, 2025 · strength 0.27
- Paper CALB2 facilitates macrophage M2 polarization to promote the growth and metastasis of pancreatic adenocarcinoma. DOI 10.1016/j.cellsig.2025.111887 ↗
Ping Bie · 1 shared paper, 2019 · strength 0.10
- Paper ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. DOI 10.1186/s13046-019-1340-7 ↗
Haisu Dai · 1 shared paper, 2019 · strength 0.10
- Paper ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. DOI 10.1186/s13046-019-1340-7 ↗
Yi Gong · 1 shared paper, 2019 · strength 0.10
- Paper ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. DOI 10.1186/s13046-019-1340-7 ↗
Anbin Wang · 1 shared paper, 2019 · strength 0.10
- Paper ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. DOI 10.1186/s13046-019-1340-7 ↗
Jian Ping Du · 1 shared paper, 2018 · strength 0.08
- Paper Kallikrein-related peptidase 7 is a potential target for the treatment of pancreatic cancer. DOI 10.18632/oncotarget.24132 ↗
Jun Zheng · 1 shared paper, 2018 · strength 0.08
- Paper Kallikrein-related peptidase 7 is a potential target for the treatment of pancreatic cancer. DOI 10.18632/oncotarget.24132 ↗
Xiao Tan · 1 shared paper, 2018 · strength 0.08
- Paper Kallikrein-related peptidase 7 is a potential target for the treatment of pancreatic cancer. DOI 10.18632/oncotarget.24132 ↗

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.