Evidence map›Paper›PMID 39230026›Full record

ArticleThoracic cancer2024

Anti-Müllerian hormone type II receptor protein expression in non-small cell lung cancer and the effect of AMH/AMHR2 signaling on cancer cell proliferation.

Yoshika Koinuma, Yoichiro Mitsuishi, Wira Winardi, Moulid Hidayat, Aditya Wirawan, Daisuke Hayakawa, Koichiro Kanamori, Naohisa Matsumoto, Takuo Hayashi, Naoko Shimada and 5 more

Abstract read
In one paragraph

Article in Thoracic cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Yoshika KoinumaDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Yoichiro MitsuishiDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Wira WinardiDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Moulid HidayatDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Aditya WirawanDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Daisuke HayakawaDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.ORCID 0000-0002-2116-5264
Koichiro KanamoriDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Naohisa MatsumotoDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Takuo HayashiDepartment of Human Pathology, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Naoko ShimadaDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Ken TajimaDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Kazuya TakamochiDepartment of General Thoracic Surgery, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Fumiyuki TakahashiDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Kenji SuzukiDepartment of General Thoracic Surgery, Juntendo University, Graduate School of Medicine, Tokyo, Japan.
Kazuhisa TakahashiDepartment of Respiratory Medicine, Juntendo University, Graduate School of Medicine, Tokyo, Japan.

Funding

Institute for Environmental and Gender-specific MedicineJapan Society for the Promotion of Science 15K09230Japan Society for the Promotion of Science 23K07636
6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths worldwide despite advances in cancer therapeutics. In several gynecological cancers, anti-Müllerian hormone receptor type 2 (AMHR2) mediates AMH-induced growth inhibition and is expressed at high levels. Furthermore, 5%-8% of NSCLCs exhibit high AMHR2 expression, suggesting that AMH may inhibit the progression of some lung cancers. However, the clinical relevance of AMHR2 expression and its role in lung cancer is not fully clarified.

methodsImmunostaining was performed on 79 surgical specimens of NSCLC. The Cancer Genome Atlas RNA-seq data for lung adenocarcinoma were analyzed, and gene ontology and gene set enrichment analyses were performed. In cellular experiments, AMHR2-overexpressing NSCLC cell lines were established, and the role of the AMH-AMHR2 pathway in cell proliferation with recombinant human AMH protein treatment was examined.

resultsA total of 13 cases (16.5%) were positive for immunostaining in lung adenocarcinoma tissues; no positive signals were detected in lung squamous carcinoma tissues. Gene expression variation analysis using The Cancer Genome Atlas data showed that the expression of genes related to the cell cycle was downregulated in the AMHR2-high group. Cellular experiments showed that activation of the AMH-AMHR2 pathway suppressed cell proliferation.

conclusionIn lung adenocarcinoma tissues with high expression of AMHR2, activation of the AMH-AMHR2 pathway may suppress cell proliferation.

Indexed as

Anti-Mullerian HormoneCarcinoma, Non-Small-Cell LungCell ProliferationLung NeoplasmsReceptors, PeptideSignal TransductionAgedCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedReceptors, Transforming Growth Factor betaAnti-Mullerian Hormoneanti-Mullerian hormone receptorReceptors, PeptideReceptors, Transforming Growth Factor betaAMH‐AMHR2 pathwaycell cyclecell proliferationnon‐small cell lung cancer

Identifiers

PMID39230026
PMCPMC11471453

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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.