Evidence map›Paper›PMID 39219271›Full record

ReviewOncology reports2024

Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).

Wanli Liu, Xianze Wang, Wenming Wu

Abstract readReview
In one paragraph

Review in Oncology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Construction ofiScience · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Updates in Immunotherapy for Pancreatic Cancer.Journal of clinical medicine · 2024
    Review
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

3 authors.

Wanli Liu *Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, P.R. China.
Xianze Wang *Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, P.R. China.
Wenming WuDepartment of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin‑17 (IL‑17), an inflammatory cytokine primarily secreted by T helper 17 cells, serves a crucial role in numerous inflammatory diseases and malignancies via its receptor, IL‑17R. In addition to stimulating inflammatory responses, IL‑17 exhibits dual functions in tumors, exerting both pro‑ and antitumor effects. Pancreatic ductal adenocarcinoma (PDAC) is the most common pancreatic malignancy and accounts for >90% of pancreatic cancer cases. PDAC is characterized by a prominent stromal microenvironment with significant heterogeneity, which contributes to treatment resistance. IL‑17/IL‑17R signaling has a notable effect on tumorigenesis, the tumor microenvironment and treatment efficacy in various cancer types, including PDAC. However, the specific mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer remain uncertain. This review presents a brief overview of the current knowledge and recent advances in the role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer. Furthermore, the potential of IL‑17‑targeted therapeutic strategies for PDAC treatment is also discussed.

Indexed as

Carcinoma, Pancreatic DuctalInterleukin-17Pancreatic NeoplasmsReceptors, Interleukin-17Signal TransductionTumor MicroenvironmentAnimalsHumansIL17RA protein, humanInterleukin-17Receptors, Interleukin-17cytokinesIL‑17immunotherapypancreatic cancerTME

Identifiers

PMID39219271
PMCPMC11378154

What OpenQuestion holds

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Registered trials

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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.