Pancreatic Cancer Research

ResearcherFirst Affiliated Hospital of Anhui Medical UniversityActive in the last 2 years

Weiwei Sheng

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

Matched on ORCID iD 0000-0003-2311-7140; OpenAlex author ID A5089402455. Sources: OpenAlex.

Their work

Papers
38 (first author 3, last author 7)
Trials
0
Grants
0
Labs led
2
Collaborators
44
Papers, trials and grants by year

2012: 1 paper · 2013: 4 papers · 2014: 6 papers · 2015: 2 papers · 2016: 2 papers · 2017: 3 papers · 2018: 2 papers · 2019: 2 papers · 2020: 5 papers · 2021: 1 paper · 2022: 6 papers · 2023: none · 2024: 1 paper · 2025: 2 papers · 2026: 1 paper

Papers 38

  1. GATA6-CRT axis promotes stress-associated autophagy, EMT, and stemness-associated traits in pancreatic cancer. Last author DOI 10.1038/s41419-026-08914-8↗
  2. A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer. Last author DOI 10.1111/cas.70019↗
  3. Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2. Last author DOI 10.7150/ijbs.102381↗
  4. ZNF263 cooperates with ZNF31 to promote the drug resistance and EMT of pancreatic cancer through transactivating RNF126. Last author DOI 10.1002/jcp.31259↗
  5. Numb-PRRL promotes TGF-β1- and EGF-induced epithelial-to-mesenchymal transition in pancreatic cancer. Co-author DOI 10.1038/s41419-022-04609-y↗
  6. Correction: Musashi2 promotes the development and progression of pancreatic cancer by down-regulating Numb protein. Co-author DOI 10.18632/oncotarget.28157↗
  7. Calreticulin promotes EMT in pancreatic cancer by enhancing endoplasmic reticulum stress-induced autophagy Last author DOI 10.21203/rs.3.rs-1963841/v1↗
  8. [Corrigendum] Expression and prognostic significance of TRPV6 in the development and progression of pancreatic cancer. Co-author DOI 10.3892/or.2022.8395↗
  9. Down-regulation of MSMO1 promotes the development and progression of pancreatic cancer. Co-author DOI 10.7150/jca.73112↗
  10. ATP11A promotes EMT by regulating Numb PRR L in pancreatic cancer cells. Co-author DOI 10.7717/peerj.13172↗
  11. GINS2 promotes EMT in pancreatic cancer via specifically stimulating ERK/MAPK signaling. Last author DOI 10.1038/s41417-020-0206-7↗
  12. Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. First author DOI 10.1111/jcmm.15676↗
  13. Integrated analysis identifies a pathway-related competing endogenous RNA network in the progression of pancreatic cancer. Co-author DOI 10.1186/s12885-020-07470-4↗
  14. Correction to: Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. Co-author DOI 10.1186/s13046-020-01663-2↗
  15. Calreticulin promotes EMT in pancreatic cancer via mediating Ca2+ dependent acute and chronic endoplasmic reticulum stress. Co-author DOI 10.1186/s13046-020-01702-y↗
  16. Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. Co-author DOI 10.1186/s13046-020-1521-4↗
  17. C6orf106 accelerates pancreatic cancer cell invasion and proliferation via activating ERK signaling pathway. Last author DOI 10.1007/s11010-018-3455-0↗
  18. Serine/arginine protein-specific kinase 2 promotes the development and progression of pancreatic cancer by downregulating Numb and p53. First author DOI 10.1111/febs.14778↗
  19. Silencing Tspan1 inhibits migration and invasion, and induces the apoptosis of human pancreatic cancer cells. Co-author DOI 10.3892/mmr.2018.9331↗
  20. Expression and prognostic significance of TRPV6 in the development and progression of pancreatic cancer. Co-author DOI 10.3892/or.2018.6216↗
  21. Calreticulin promotes EGF-induced EMT in pancreatic cancer cells via Integrin/EGFR-ERK/MAPK signaling pathway. Co-author DOI 10.1038/cddis.2017.547↗
  22. Cooperation of Musashi-2, Numb, MDM2, and P53 in drug resistance and malignant biology of pancreatic cancer. Co-author DOI 10.1096/fj.201601240r↗
  23. Musashi2 promotes the development and progression of pancreatic cancer by down-regulating Numb protein. Co-author DOI 10.18632/oncotarget.8736↗
  24. Roles of Carbonic Anhydrase IX in Development of Pancreatic Cancer. Co-author DOI 10.1007/s12253-015-9935-6↗
  25. Co-expression of FOXL1 and PP2A inhibits proliferation inducing apoptosis in pancreatic cancer cells via promoting TRAIL and reducing phosphorylated MYC. Co-author DOI 10.3892/or.2016.4592↗
  26. Gli1 promotes transforming growth factor-beta1- and epidermal growth factor-induced epithelial to mesenchymal transition in pancreatic cancer cells. First author DOI 10.1016/j.surg.2015.03.016↗
  27. Expression of vitamin D receptor as a potential prognostic factor and therapeutic target in pancreatic cancer. Co-author DOI 10.1111/his.12663↗
  28. Overexpression of calreticulin contributes to the development and progression of pancreatic cancer. Co-author DOI 10.1002/jcp.24519↗
  29. The clinicopathological significance and relationship of Gli1, MDM2 and p53 expression in resectable pancreatic cancer. Co-author DOI 10.1111/his.12273↗
  30. [Expression and significance of leukemia inhibitory factor in human pancreatic cancer]. Co-author PMID 24721346↗
  31. [The role of Gli1 in the invasion and migration of pancreatic cancer cells]. Co-author PMID 25262609↗
  32. [The relationship and clinicopathological significance of Numb,MDM2 and p53 expression in human pancreatic cancer]. Co-author PMID 25410780↗
  33. [Expression and clinical significance of Tspan 1 and Integrin α6 in human pancreatic ductal adenocarcinoma]. Co-author PMID 25573220↗
  34. Down regulation of CAII is associated with tumor differentiation and poor prognosis in patients with pancreatic cancer. Co-author DOI 10.1002/jso.23282↗
  35. Cooperation among Numb, MDM2 and p53 in the development and progression of pancreatic cancer. Co-author DOI 10.1007/s00441-013-1679-6↗
  36. [Clinicopathological significance of the expression of calreticulin in human pancreatic cancer]. Co-author PMID 23578430↗
  37. [Correlation between Gli1 expression and clinicopathological significance in human pancreatic cancer]. Co-author PMID 24433772↗
  38. [Clinicopathological significance of the expression of carbonic anhydrase I and II in human pancreatic cancer]. Co-author PMID 23327700↗

Closest collaborators

The 25 strongest of 44 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.

  1. Ming Dong · 27 shared papers, 2012–2022 · strength 2.68
  2. Jianping Zhou · 19 shared papers, 2012–2022 · strength 1.34
  3. Qi Dong · 13 shared papers, 2013–2022 · strength 0.99
  4. Guosen Wang · 7 shared papers, 2017–2025 · strength 0.85
  5. Rongxian Cao · 6 shared papers, 2020–2022 · strength 0.80
  6. Jian Hua Sun · 5 shared papers, 2020–2022 · strength 0.63
  7. Fuqiang Zu · 3 shared papers, 2020–2026 · strength 0.60
  8. Qingfeng Liu · 7 shared papers, 2013–2022 · strength 0.51
  9. Bernhard Willibald Renz · 2 shared papers, 2025–2026 · strength 0.47
  10. Chao Jia · 4 shared papers, 2020 · strength 0.43
  11. Hong-jia Wu · 2 shared papers, 2022–2026 · strength 0.40
  12. Matthias Ilmer · 2 shared papers, 2022–2025 · strength 0.38
  13. Yuji Li · 4 shared papers, 2012–2017 · strength 0.27
  14. Ming-qing Wang · 1 shared paper, 2026 · strength 0.24
  15. Hua‐Qin Wang · 1 shared paper, 2026 · strength 0.24
  16. Longping Huang · 2 shared papers, 2016–2021 · strength 0.24
  17. Jiabin Jin · 1 shared paper, 2025 · strength 0.24
  18. Guopei Luo · 1 shared paper, 2025 · strength 0.23
  19. Shiyang Wang · 1 shared paper, 2024 · strength 0.23
  20. Jiawei Zhang · 1 shared paper, 2024 · strength 0.23
  21. Feng Li · 4 shared papers, 2013–2015 · strength 0.19
  22. Lin Chen · 1 shared paper, 2022 · strength 0.19
  23. Song He · 1 shared paper, 2022 · strength 0.19
  24. Wei Gao · 1 shared paper, 2022 · strength 0.19
  25. Song He · 2 shared papers, 2017–2018 · strength 0.17

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.