Pancreatic Cancer Research

ResearcherChinese Academy of Medical Sciences & Peking Union Medical CollegeActive in the last 2 years

Shuangni Yu

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

Matched on ORCID iD 0000-0002-3745-1097; OpenAlex author ID A5009562986. Sources: OpenAlex.

Their work

Papers
23 (first author 4, last author 0)
Trials
0
Grants
0
Labs led
0
Collaborators
33
Papers, trials and grants by year

2011: 1 paper · 2012: 1 paper · 2013: 2 papers · 2014: none · 2015: 4 papers · 2016: 1 paper · 2017: 1 paper · 2018: 2 papers · 2019: none · 2020: 1 paper · 2021: 1 paper · 2022: 4 papers · 2023: 3 papers · 2024: 1 paper · 2025: 1 paper

Papers 23

  1. Tumor-stroma ratio combined with PD-L1 identifies pancreatic ductal adenocarcinoma patients at risk for lymph node metastases. Co-author DOI 10.1038/s41416-025-03019-z↗
  2. Analysis of PD-L1 promoter methylation combined with immunogenic context in pancreatic ductal adenocarcinoma. First author DOI 10.1007/s00262-024-03745-y↗
  3. Targeting N-glycosylation of 4F2hc mediated by glycosyltransferase B3GNT3 sensitizes ferroptosis of pancreatic ductal adenocarcinoma. Co-author DOI 10.1038/s41418-023-01188-z↗
  4. Prognostic Value of Programmed Death Ligand-1 in Discriminating Patients With Lymph Node-Negative, p53-Wild-Type, or Low-BRCA1/2-Expression Pancreatic Ductal A… Co-author DOI 10.5858/arpa.2021-0471-oa↗
  5. The spatial coexistence of TIGIT/CD155 defines poorer survival and resistance to adjuvant chemotherapy in pancreatic ductal adenocarcinoma. Co-author DOI 10.7150/thno.86547↗
  6. PD-L1 and PD-L2 expression in pancreatic ductal adenocarcinoma and their correlation with immune infiltrates and DNA damage response molecules. Co-author DOI 10.1002/cjp2.259↗
  7. Analysis of a novel immune checkpoint, Siglec-15, in pancreatic ductal adenocarcinoma. Co-author DOI 10.1002/cjp2.260↗
  8. Intratumoral neutrophil extracellular traps are associated with unfavorable clinical outcomes and immunogenic context in pancreatic ductal adenocarcinoma. Co-author DOI 10.3389/fimmu.2022.1027459↗
  9. Analysis of the OX40/OX40L immunoregulatory axis combined with alternative immune checkpoint molecules in pancreatic ductal adenocarcinoma. Co-author DOI 10.3389/fimmu.2022.942154↗
  10. Upregulated MicroRNA-483-3p is an Early Event in Pancreatic Ductal Adenocarcinoma (PDAC) and as a Powerful Liquid Biopsy Biomarker in PDAC. Co-author DOI 10.2147/ott.s288936↗
  11. Development of a four-gene prognostic model for pancreatic cancer based on transcriptome dysregulation. Co-author DOI 10.18632/aging.102844↗
  12. Loss of ARID1A Expression Correlates With Tumor Differentiation and Tumor Progression Stage in Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1177/1533034618754475↗
  13. Establishment of a non‑coding RNAomics screening platform for the regulation of KRAS in pancreatic cancer by RNA sequencing. First author DOI 10.3892/ijo.2018.4560↗
  14. RUNX1 promote invasiveness in pancreatic ductal adenocarcinoma through regulating miR-93. Co-author DOI 10.18632/oncotarget.20433↗
  15. KRAS-related noncoding RNAs in pancreatic ductal adenocarcinoma. Co-author DOI 10.1016/j.cdtm.2016.11.012↗
  16. Elevated miR-483-3p expression is an early event and indicates poor prognosis in pancreatic ductal adenocarcinoma. Co-author DOI 10.1007/s13277-015-3690-x↗
  17. MiRNA-615-5p functions as a tumor suppressor in pancreatic ductal adenocarcinoma by targeting AKT2. Co-author DOI 10.1371/journal.pone.0119783↗
  18. Deregulation of the MiR-193b-KRAS Axis Contributes to Impaired Cell Growth in Pancreatic Cancer. Co-author DOI 10.1371/journal.pone.0125515↗
  19. Correction: MiRNA-615-5p Functions as a Tumor Suppressor in Pancreatic Ductal Adenocarcinoma by Targeting AKT2. Co-author DOI 10.1371/journal.pone.0128257↗
  20. Targeted degradation of KRAS by an engineered ubiquitin ligase suppresses pancreatic cancer cell growth in vitro and in vivo. Co-author DOI 10.1158/1535-7163.mct-12-0650↗
  21. [Target prediction and verification of miR-27a in pancreatic cancer]. Co-author DOI 10.3760/cma.j.issn.0529-5807.2013.06.008↗
  22. [Effects of ezrin silencing on pancreatic cancer cell line Panc-1]. First author DOI 10.3760/cma.j.issn.0529-5807.2012.12.009↗
  23. [Research advances in microRNA in pancreatic ductal adenocarcinoma]. First author PMID 22338146↗

Closest collaborators

The 25 strongest of 33 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Xianlong Chen · 9 shared papers, 2022–2025 · strength 1.97
  2. Jie Chen · 11 shared papers, 2013–2023 · strength 1.49
  3. Yue Zhang · 3 shared papers, 2022–2023 · strength 0.53
  4. Congwei Jia · 6 shared papers, 2013–2020 · strength 0.47
  5. Heng Ma · 2 shared papers, 2023 · strength 0.36
  6. Xinyuan Chen · 1 shared paper, 2024 · strength 0.36
  7. Cuiping Wang · 5 shared papers, 2015–2018 · strength 0.34
  8. Yang Sun · 6 shared papers, 2013–2017 · strength 0.33
  9. Xinyuan Chen · 1 shared paper, 2025 · strength 0.33
  10. Jie Chen · 4 shared papers, 2013–2017 · strength 0.23
  11. Xianglan Jin · 4 shared papers, 2015–2016 · strength 0.23
  12. Jie Chen · 1 shared paper, 2023 · strength 0.18
  13. Y. Liu · 1 shared paper, 2023 · strength 0.18
  14. Wei‐Min Tong · 1 shared paper, 2023 · strength 0.18
  15. Yue Zhang · 1 shared paper, 2022 · strength 0.17
  16. Tingting Zhang · 3 shared papers, 2013–2015 · strength 0.15
  17. Li Zhang · 2 shared papers, 2015–2018 · strength 0.14
  18. Jie Yan · 1 shared paper, 2020 · strength 0.13
  19. Yue Zhang · 1 shared paper, 2021 · strength 0.12
  20. Jie Chen · 1 shared paper, 2021 · strength 0.12
  21. Huilin Shao · 1 shared paper, 2021 · strength 0.12
  22. Jie Chen · 2 shared papers, 2015–2016 · strength 0.12
  23. Pingping Liu · 2 shared papers, 2015–2016 · strength 0.11
  24. Yihui Ma · 2 shared papers, 2013–2016 · strength 0.11
  25. Li Zhang · 1 shared paper, 2018 · strength 0.09

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.