Evidence map›Paper›PMID 36603850›Full record

ArticleJournal of gynecologic oncology2023

Interleukin-34 cancels anti-tumor immunity by PARP inhibitor.

Takayoshi Nakamura, Nabeel Kajihara, Naoki Hama, Takuto Kobayashi, Ryo Otsuka, Nanumi Han, Haruka Wada, Yoshinori Hasegawa, Nao Suzuki, Ken-Ichiro Seino

Open access · diamondAbstract read
In one paragraph

Article in Journal of gynecologic oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
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  4. 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

10 authors at 3 institutions in 1 country.

Takayoshi NakamuraDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-6968-2893
Nabeel KajiharaDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-0822-3391
Naoki HamaDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-4318-8448
Takuto KobayashiDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-0096-6038
Ryo OtsukaDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-3730-9867
Nanumi HanDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-9524-1808
Haruka WadaDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-5526-3647
Yoshinori HasegawaDepartment of Applied Genomics, Kazusa DNA Research Institute, Kisarazu, Japan.ORCID 0000-0003-2904-6611
Nao SuzukiDepartment of Obstetrics and Gynecology, St. Marianna University School of Medicine, Kawasaki, Japan.ORCID 0000-0002-7440-8127
Ken-Ichiro SeinoDivision of Immunobiology, Graduate School of Medicine, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan. seino@igm.hokudai.ac.jp.ORCID 0000-0003-4122-1718
Hokkaido University · JPSt. Marianna University School of Medicine · JPKazusa DNA Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBreast cancer susceptibility gene 1 (BRCA1)-associated ovarian cancer patients have been treated with A poly (ADP-ribose) polymerase (PARP) inhibitor, extending the progression-free survival; however, they finally acquire therapeutic resistance. Interleukin (IL)-34 has been reported as a poor prognostic factor in several cancers, including ovarian cancer, and it contributes to the therapeutic resistance of chemotherapies. IL-34 may affect the therapeutic effect of PARP inhibitor through the regulation of tumor microenvironment (TME).

methodsIn this study, The Cancer Genome Atlas (TCGA) data set was used to evaluate the prognosis of IL-34 and human ovarian serous carcinoma. We also used CRISPR-Cas9 genome editing technology in a mouse model to evaluate the efficacy of PARP inhibitor therapy in the presence or absence of IL-34.

resultsWe found that

conclusionThese results suggest that tumor-derived IL-34 benefits tumors by creating an immunosuppressive TME and conferring PARP inhibitor therapeutic resistance. Thus, we showed the pathological effect of IL-34 and the need for it as a therapeutic target in ovarian cancer.

Indexed as

Antineoplastic AgentsCarcinomaOvarian NeoplasmsAnimalsFemaleHumansInterleukinsMicePoly(ADP-ribose) Polymerase InhibitorsTumor MicroenvironmentAntineoplastic AgentsInterleukinsPoly(ADP-ribose) Polymerase InhibitorsBRCA1-Associated CancerCD8Interleukin-34PARP InhibitorTherapeutic ResistanceXCR1

Identifiers

PMID36603850
PMCPMC10157335
OpenAlexW4313580303

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.