Pancreatic Cancer Research

ResearcherPennsylvania State UniversityActive in the last 2 years

Shengyu Yang

Matched on ORCID iD 0000-0001-7154-6850; OpenAlex author ID A5044453840, A5100527969, A5123516836. Sources: OpenAlex.

Their work

Papers
33 (first author 0, last author 2)
Trials
0
Grants
0
Labs led
0
Collaborators
74
Papers, trials and grants by year

2014: 1 paper · 2015: 1 paper · 2016: 2 papers · 2017: 3 papers · 2018: 1 paper · 2019: 3 papers · 2020: 2 papers · 2021: 2 papers · 2022: 5 papers · 2023: 4 papers · 2024: 4 papers · 2025: 3 papers · 2026: 2 papers

Papers 33

  1. Mitochondrial Calcium Uniporter Drives Chemoresistance in Pancreatic Cancer via Glutathione-Mediated Stemness Maintenance. Co-author DOI 10.1002/advs.202507346↗
  2. Senescent Cancer-Associated Fibroblasts Drive Early-Stage Lymph Node Metastasis in Pancreatic Cancer through Lactate-Mediated Metabolic-Epigenetic Rewiring. Co-author DOI 10.1158/2159-8290.cd-25-1627↗
  3. Adaptation to cystine limitation stress confers a targetable lipid metabolism vulnerability in pancreatic ductal adenocarcinoma. Last author DOI 10.1038/s41467-025-68099-0↗
  4. Endothelial-like cancer-associated fibroblasts facilitate pancreatic cancer metastasis via vasculogenic mimicry and paracrine signalling. Co-author DOI 10.1136/gutjnl-2024-333638↗
  5. CLT-003 exerts anti-tumor activity in pancreatic cancer by blocking the PI3K/AKT/HIF-1α pathway. Co-author DOI 10.20892/j.issn.2095-3941.2025.0058↗
  6. Tumor-derived interleukin 35 mediates the dissemination of gemcitabine resistance in pancreatic adenocarcinoma. Co-author DOI 10.1038/s41388-024-02938-0↗
  7. Correction: BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis. Co-author DOI 10.1038/s41392-023-01721-z↗
  8. Targeting ESE3/EHF With Nifurtimox Inhibits CXCR2+ Neutrophil Infiltration and Overcomes Pancreatic Cancer Resistance to Chemotherapy and Immunotherapy. Co-author DOI 10.1053/j.gastro.2024.02.046↗
  9. BICC1 drives pancreatic cancer stemness and chemoresistance by facilitating tryptophan metabolism. Co-author DOI 10.1126/sciadv.adj8650↗
  10. BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis. Co-author DOI 10.1038/s41392-023-01478-5↗
  11. SDCBP promotes pancreatic cancer progression by preventing YAP1 from β-TrCP-mediated proteasomal degradation. Co-author DOI 10.1136/gutjnl-2022-327492↗
  12. Irbesartan overcomes gemcitabine resistance in pancreatic cancer by suppressing stemness and iron metabolism via inhibition of the Hippo/YAP1/c-Jun axis. Co-author DOI 10.1186/s13046-023-02671-8↗
  13. Nuclear PLD1 combined with NPM1 induces gemcitabine resistance through tumorigenic IL7R in pancreatic adenocarcinoma. Co-author DOI 10.20892/j.issn.2095-3941.2023.0039↗
  14. ESE3-positive PSCs drive pancreatic cancer fibrosis, chemoresistance and poor prognosis via tumour-stromal IL-1β/NF-κB/ESE3 signalling axis. Co-author DOI 10.1038/s41416-022-01927-y↗
  15. BZW1 Facilitates Glycolysis and Promotes Tumor Growth in Pancreatic Ductal Adenocarcinoma Through Potentiating eIF2α Phosphorylation. Co-author DOI 10.1053/j.gastro.2021.12.249↗
  16. ESE3/EHF, a promising target of rosiglitazone, suppresses pancreatic cancer stemness by downregulating CXCR4. Co-author DOI 10.1136/gutjnl-2020-321952↗
  17. Mitochondrial Calcium Uniporter Drives Metastasis and Confers a Targetable Cystine Dependency in Pancreatic Cancer. Last author DOI 10.1158/0008-5472.can-21-3230↗
  18. SOX8 Affects Tumoral SPARC Expression by Regulating EZH2 to Attenuate Effectiveness of albumin-bound paclitaxel in PDAC. Co-author DOI 10.7150/ijbs.64752↗
  19. Serum insulin-like growth factor binding protein 2 levels as biomarker for pancreatic ductal adenocarcinoma-associated malnutrition and muscle wasting. Co-author DOI 10.1002/jcsm.12692↗
  20. CD73 induces gemcitabine resistance in pancreatic ductal adenocarcinoma: A promising target with non-canonical mechanisms. Co-author DOI 10.1016/j.canlet.2021.07.024↗
  21. PD-L1 is a direct target of cancer-FOXP3 in pancreatic ductal adenocarcinoma (PDAC), and combined immunotherapy with antibodies against PD-L1 and CCL5 is effec… Co-author DOI 10.1038/s41392-020-0144-8↗
  22. IL-37/ STAT3/ HIF-1α negative feedback signaling drives gemcitabine resistance in pancreatic cancer. Co-author DOI 10.7150/thno.42416↗
  23. Tumoral EHF predicts the efficacy of anti-PD1 therapy in pancreatic ductal adenocarcinoma. Co-author DOI 10.1084/jem.20180749↗
  24. LIMS1 Promotes Pancreatic Cancer Cell Survival under Oxygen-Glucose Deprivation Conditions by Enhancing HIF1A Protein Translation. Co-author DOI 10.1158/1078-0432.ccr-18-3533↗
  25. Fendiline Enhances the Cytotoxic Effects of Therapeutic Agents on PDAC Cells by Inhibiting Tumor-Promoting Signaling Events: A Potential Strategy to Combat PDA… Co-author DOI 10.3390/ijms20102423↗
  26. Interleukin 35 Expression Correlates With Microvessel Density in Pancreatic Ductal Adenocarcinoma, Recruits Monocytes, and Promotes Growth and Angiogenesis of … Co-author DOI 10.1053/j.gastro.2017.09.039↗
  27. Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression. Co-author DOI 10.1038/ncomms14035↗
  28. Cancer-FOXP3 directly activated CCL5 to recruit FOXP3+Treg cells in pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/onc.2016.458↗
  29. ESE3 Inhibits Pancreatic Cancer Metastasis by Upregulating E-Cadherin. Co-author DOI 10.1158/0008-5472.can-16-2170↗
  30. Arsenic trioxide plus PX-478 achieves effective treatment in pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.canlet.2016.05.016↗
  31. Single nucleotide polymorphism in the microRNA-199a binding site of HIF1A gene is associated with pancreatic ductal adenocarcinoma risk and worse clinical outc… Co-author DOI 10.18632/oncotarget.7263↗
  32. Fendiline inhibits proliferation and invasion of pancreatic cancer cells by interfering with ADAM10 activation and β-catenin signaling. Co-author DOI 10.18632/oncotarget.5933↗
  33. Hypoxia-inducible factor-1 promotes pancreatic ductal adenocarcinoma invasion and metastasis by activating transcription of the actin-bundling protein fascin. Co-author DOI 10.1158/0008-5472.can-13-3009↗

Closest collaborators

The 25 strongest of 74 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Jihui Hao · 29 shared papers, 2014–2026 · strength 3.59
  2. Xiuchao Wang · 26 shared papers, 2016–2026 · strength 3.21
  3. Tiansuo Zhao · 23 shared papers, 2016–2026 · strength 2.88
  4. Chongbiao Huang · 23 shared papers, 2016–2026 · strength 2.82
  5. Song Gao · 18 shared papers, 2014–2026 · strength 2.35
  6. Jing Liu · 13 shared papers, 2019–2026 · strength 1.91
  7. Tianxing Zhou · 9 shared papers, 2019–2026 · strength 1.43
  8. Yongjie Xie · 8 shared papers, 2022–2026 · strength 1.35
  9. Chao Xu · 5 shared papers, 2023–2026 · strength 0.90
  10. Zengxun Li · 7 shared papers, 2017–2024 · strength 0.85
  11. Danqi Fu · 6 shared papers, 2019–2025 · strength 0.85
  12. Wenna Jiang · 6 shared papers, 2017–2024 · strength 0.69
  13. Huizhi Sun · 4 shared papers, 2023–2024 · strength 0.66
  14. Chuntao Gao · 4 shared papers, 2021–2025 · strength 0.59
  15. Liangliang Wu · 4 shared papers, 2021–2025 · strength 0.54
  16. Yunzhan Li · 2 shared papers, 2025–2026 · strength 0.41
  17. Jie Dong · 4 shared papers, 2017–2022 · strength 0.40
  18. Yukuan Feng · 2 shared papers, 2024–2026 · strength 0.37
  19. Bo Ni · 2 shared papers, 2024–2025 · strength 0.34
  20. Wenrun Cai · 2 shared papers, 2022–2025 · strength 0.33
  21. Pankaj Kumar Singh · 2 shared papers, 2022–2025 · strength 0.31
  22. Shuai Yuan · 2 shared papers, 2022–2023 · strength 0.28
  23. He Ren · 4 shared papers, 2014–2020 · strength 0.28
  24. Mingxiao Lang · 3 shared papers, 2016–2022 · strength 0.26
  25. He Ren · 4 shared papers, 2016–2019 · strength 0.26

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.