Evidence map›Paper›PMID 31831007›Full record

ReviewMolecular cancer2019

The reciprocal regulation between host tissue and immune cells in pancreatic ductal adenocarcinoma: new insights and therapeutic implications.

Xiaomeng Liu, Jin Xu, Bo Zhang, Jiang Liu, Chen Liang, Qingcai Meng, Jie Hua, Xianjun Yu, Si Shi

Abstract readReview
In one paragraph

Review in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed.

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  13. WTAP Accelerates Exhaustion of CD8Mediators of inflammation · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Panoramic tumor microenvironment in pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  18. Review
  19. The Neuroimmune Axis and Its Therapeutic Potential for Primary Liver Cancer.International journal of molecular sciences · 2024
    Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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

9 authors.

Xiaomeng LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jiang LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Chen LiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qingcai MengDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jie HuaDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. yuxianjun@fudanpci.org.ORCID 0000-0002-7039-9024
Si ShiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. shisi@fudanpci.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related death and is one of the most difficult-to-treat cancers. Surgical resection and adjuvant therapy have limited effects on the overall survival of PDAC patients. PDAC exhibits an immunosuppressive microenvironment, the immune response predicts survival, and activation of immune system has the potential to produce an efficacious PDAC therapy. However, chimeric antigen receptor T (CAR-T) cell immunotherapy and immune checkpoint blockade (ICB), which have produced unprecedented clinical benefits in a variety of different cancers, produce promising results in only some highly selected patients with PDAC. This lack of efficacy may be because existing immunotherapies mainly target the interactions between cancer cells and immune cells. However, PDAC is characterized by an abundant tumor stroma that includes a heterogeneous mixture of immune cells, fibroblasts, endothelial cells, neurons and some molecular events. Immune cells engage in extensive and dynamic crosstalk with stromal components in the tumor tissue in addition to tumor cells, which subsequently impacts tumor suppression or promotion to a large extent. Therefore, exploration of the interactions between the stroma and immune cells may offer new therapeutic opportunities for PDAC. In this review, we discuss how infiltrating immune cells influence PDAC development and explore the contributions of complex components to the immune landscape of tumor tissue. The roles of stromal constituents in immune modulation are emphasized. We also predict potential therapeutic strategies to target signals in the immune network in the abundant stromal microenvironment of PDAC.

Indexed as

Disease SusceptibilityAnimalsCarcinoma, Pancreatic DuctalHumansImmune SystemLymphocytes, Tumor-InfiltratingLymphocyte SubsetsPancreatic NeoplasmsStromal CellsTumor MicroenvironmentImmune infiltrateImmunotherapyPancreatic ductal adenocarcinomaStromal cells

Identifiers

PMID31831007
PMCPMC6909567

What OpenQuestion holds

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LicenceCC BY
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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.