Evidence map›Paper›PMID 27413117›Full record

ArticleOncotarget2016

Diabetes mellitus stimulates pancreatic cancer growth and epithelial-mesenchymal transition-mediated metastasis via a p38 MAPK pathway.

Lishan Wang, Ying-Ying Bai, Yang Yang, Fangfang Hu, Yonghui Wang, Zeqian Yu, Zhangjun Cheng, Jiahua Zhou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. TGF-β Alters the Proportion of Infiltrating Immune Cells in a Pancreatic Ductal Adenocarcinoma.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022
    Article
  8. Review
  9. Modeling pancreatic cancer in mice for experimental therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer.Journal of the Academy of Nutrition and Dietetics · 2018
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Lishan WangDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Ying-Ying BaiJiangsu Key Laboratory of Molecular and Functional Imaging, Department of Radiology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Yang YangDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Fangfang HuDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Yonghui WangDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Zeqian YuDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Zhangjun ChengDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Jiahua ZhouDepartment of General Surgery, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Zhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) and its accompanying chronic inflammation promote tumor progression. p38 mitogen-activated protein kinase (MAPK) is an essential kinase for inflammation. The effects of p38 MAPK on epithelial-mesenchymal transition (EMT)-mediated diabetic pancreatic cancer metastasis remain unclear. Here, we demonstrate that p38 MAPK phosphorylation was significantly increased in pancreatic cancer cells treated with high glucose and in pancreatic tumors from diabetic animals. A p38 MAPK inhibitor significantly suppressed the proliferation and invasion of pancreatic cancer cells under high-glucose conditions. Moreover, p38 MAPK inhibition not only significantly decreased both the tumor volume monitored by magnetic resonance imaging and EMT-related metastasis but also increased the survival of diabetic mice bearing pancreatic tumors. Furthermore, the inflammation in diabetic animals bearing pancreatic tumors was also significantly lower after therapy. Collectively, our findings reveal that p38 MAPK inhibitors may provide a novel intervention strategy for diabetic pancreatic cancer treatment.

Indexed as

MAP Kinase Signaling SystemAnimalsCell ProliferationDiabetes ComplicationsDiabetes Mellitus, ExperimentalDisease Models, AnimalDisease ProgressionEpithelial-Mesenchymal TransitionHumansMiceNeoplasm Metastasisp38 Mitogen-Activated Protein KinasesPancreatic NeoplasmsPhosphorylationp38 Mitogen-Activated Protein Kinasesdiabetes mellitusepithelial-mesenchymal transitioninflammationp38 MAPKpancreatic cancer

Identifiers

PMID27413117
PMCPMC5122409
OpenAlexW2408457517

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.