Evidence map›Paper›PMID 33291556›Full record

ArticleCancers2020

Apigenin Increases SHIP-1 Expression, Promotes Tumoricidal Macrophages and Anti-Tumor Immune Responses in Murine Pancreatic Cancer.

Krystal Villalobos-Ayala, Ivannie Ortiz Rivera, Ciara Alvarez, Kazim Husain, DeVon DeLoach, Gerald Krystal, Margaret L Hibbs, Kun Jiang, Tomar Ghansah

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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, 40 citations in OpenAlex.

  1. Review
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  6. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
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  12. Article
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  14. The antitumoral activity of TLR7 ligands is corrupted by the microenvironment of pancreatic tumors.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  15. Article
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  19. Targeting Akt in cancer for precision therapy.Journal of hematology & oncology · 2021
    Review
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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 at 4 institutions in 3 countries.

Krystal Villalobos-AyalaDepartment of Molecular Medicine, Morsani College of Medicine at the University of South Florida, Tampa, FL 33612, USA.
Ivannie Ortiz RiveraDepartment of Molecular Medicine, Morsani College of Medicine at the University of South Florida, Tampa, FL 33612, USA.
Ciara AlvarezDepartment of Molecular Medicine, Morsani College of Medicine at the University of South Florida, Tampa, FL 33612, USA.
Kazim HusainDepartment of Molecular Medicine, Morsani College of Medicine at the University of South Florida, Tampa, FL 33612, USA.
DeVon DeLoachComparative Medicine at the University of South Florida, Tampa, FL 33612, USA.
Gerald KrystalThe Terry Fox Laboratory, BC Cancer, Vancouver, BC V5Z 1L3, Canada.
Margaret L HibbsDepartment of Immunology and Pathology, Central Clinical School, Monash University, Melbourne 3004, Australia.
Kun JiangAnatomic Pathology Department, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Tomar GhansahDepartment of Molecular Medicine, Morsani College of Medicine at the University of South Florida, Tampa, FL 33612, USA.
University of South Florida · USMoffitt Cancer Center · USMonash University · AUTerry Fox Research Institute · CA

Funding

The Role of SHIP-1 in the Modulation of Immunoregulatory Cells in Pancreatic CancR21CA179668 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI GHANSAH, TOMAR · 2014 to 2015
$397k
Florida Department of Health 8KJ09NCI NIH HHS 1R21 CA179668-01A1University of South Florida Bridge Funding
6 · The paper itself

Abstract

Pancreatic cancer (PC) has an extremely poor prognosis due to the expansion of immunosuppressive myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) in the inflammatory tumor microenvironment (TME), which halts the recruitment of effector immune cells and renders immunotherapy ineffective. Thus, the identification of new molecular targets that can modulate the immunosuppressive TME is warranted for PC intervention. Src Homology-2 (SH2) domain-containing Inositol 5'-Phosphatase-1 (SHIP-1) is a lipid signaling protein and a regulator of myeloid cell development and function. Herein, we used the bioflavonoid apigenin (API) to reduce inflammation in different PC models. Wild type mice harboring heterotopic or orthotopic PC were treated with API, which induced SHIP-1 expression, reduced inflammatory tumor-derived factors (TDF), increased the proportion of tumoricidal macrophages and enhanced anti-tumor immune responses, resulting in a reduction in tumor burden compared to vehicle-treated PC mice. In contrast, SHIP-1-deficient mice exhibited an increased tumor burden and displayed augmented proportions of pro-tumor macrophages. These results provide further support for the importance of SHIP-1 expression in promoting pro-tumor macrophage development in the pancreatic TME. Our findings suggest that agents augmenting SHIP-1 expression may provide novel therapeutic options for the treatment of PC.

Indexed as

apigeninmyeloid homeostasispancreatic cancerSHIP-1tumor immunity

Identifiers

PMID33291556
PMCPMC7761852
OpenAlexW3106820687

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.