ResearcherShanghai Jiao Tong UniversityActive in the last 2 years

Xuqing Shen

ORCID-verified (high confidence, 0.95), identity_conf@1As of 7 November 2026

Matched on ORCID iD 0000-0002-1022-7634; OpenAlex author ID A5020956186. Sources: OpenAlex.

Their work

Papers: 6 (first author 1, last author 0)
Trials: 0
Grants: 0
Labs led: 0
Collaborators: 29

Papers, trials and grants by year

2022: 2 papers · 2023: 2 papers · 2024: 1 paper · 2025: 1 paper

Papers 6

Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. Co-author DOI 10.1016/j.xcrm.2025.101928 ↗
Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically support pancreatic cancer. First author DOI 10.1016/j.ccell.2024.03.005 ↗
Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinoma. Co-author DOI 10.1007/s13402-023-00831-8 ↗
Oncogenic KRAS triggers metabolic reprogramming in pancreatic ductal adenocarcinoma. Co-author DOI 10.2478/jtim-2022-0022 ↗
Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-deficient pancreatic cancer. Co-author DOI 10.1016/j.bbrc.2022.05.047 ↗
SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. Co-author DOI 10.1016/j.canlet.2022.215693 ↗

Closest collaborators

The 25 strongest of 29 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

Jing Xue · 6 shared papers, 2022–2025 · strength 1.17
- Paper Oncogenic KRAS triggers metabolic reprogramming in pancreatic ductal adenocarcinoma. DOI 10.2478/jtim-2022-0022 ↗
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
- Paper Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinom… DOI 10.1007/s13402-023-00831-8 ↗
Ningning Niu · 5 shared papers, 2022–2025 · strength 0.96
- Paper Oncogenic KRAS triggers metabolic reprogramming in pancreatic ductal adenocarcinoma. DOI 10.2478/jtim-2022-0022 ↗
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Ping Lu · 4 shared papers, 2022–2025 · strength 0.66
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
- Paper Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-de… DOI 10.1016/j.bbrc.2022.05.047 ↗
Yongwei Sun · 3 shared papers, 2022–2024 · strength 0.43
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
- Paper Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-de… DOI 10.1016/j.bbrc.2022.05.047 ↗
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Yingying Tang · 2 shared papers, 2024–2025 · strength 0.39
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Minwei Yang · 2 shared papers, 2022–2024 · strength 0.29
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Tiebo Mao · 1 shared paper, 2025 · strength 0.22
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
Liwei Wang · 1 shared paper, 2025 · strength 0.22
- Paper Targeting pancreatic cancer glutamine dependency confers vulnerability to GPX4-dependent ferroptosis. DOI 10.1016/j.xcrm.2025.101928 ↗
Zhengyan Zhang · 1 shared paper, 2023 · strength 0.20
- Paper Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinom… DOI 10.1007/s13402-023-00831-8 ↗
Junyi Xu · 1 shared paper, 2023 · strength 0.20
- Paper Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinom… DOI 10.1007/s13402-023-00831-8 ↗
Xiaotong Yang · 1 shared paper, 2023 · strength 0.20
- Paper Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinom… DOI 10.1007/s13402-023-00831-8 ↗
Wei Wang · 1 shared paper, 2023 · strength 0.20
- Paper Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinom… DOI 10.1007/s13402-023-00831-8 ↗
Zipeng Lu · 1 shared paper, 2024 · strength 0.17
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Liwei Wang · 1 shared paper, 2024 · strength 0.17
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Jiabin Jin · 1 shared paper, 2024 · strength 0.17
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Kuirong Jiang · 1 shared paper, 2024 · strength 0.17
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Baiyong Shen · 1 shared paper, 2024 · strength 0.17
- Paper Tumor cell-intrinsic epigenetic dysregulation shapes cancer-associated fibroblasts heterogeneity to metabolically suppo… DOI 10.1016/j.ccell.2024.03.005 ↗
Juanjuan Shi · 1 shared paper, 2022 · strength 0.14
- Paper Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-de… DOI 10.1016/j.bbrc.2022.05.047 ↗
Hong‐Fei Yao · 1 shared paper, 2022 · strength 0.14
- Paper Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-de… DOI 10.1016/j.bbrc.2022.05.047 ↗
Ruizhe He · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Jian‐Yu Yang · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Juanjuan Shi · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Xueliang Fu · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Yongsheng Jiang · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗
Jian Yang · 1 shared paper, 2022 · strength 0.12
- Paper SULF2 enhances GDF15-SMAD axis to facilitate the initiation and progression of pancreatic cancer. DOI 10.1016/j.canlet.2022.215693 ↗

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.