Evidence map›Paper›PMID 37322295›Full record

ArticleBrain tumor pathology2023

A clinicopathological analysis of supratentorial ependymoma, ZFTA fusion-positive: utility of immunohistochemical detection of CDKN2A alterations and characteristics of the immune microenvironment.

Naohito Hashimoto, Tomonari Suzuki, Keisuke Ishizawa, Sumihito Nobusawa, Hideaki Yokoo, Ryo Nishikawa, Masanori Yasuda, Atsushi Sasaki

Open access · hybridAbstract read
In one paragraph

Article in Brain tumor pathology, 2023. 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
1.2field-weighted citation impact, top 20% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Frontiers in oncology · 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

8 authors at 3 institutions in 1 country.

Naohito HashimotoDepartment of Pathology, Saitama Medical University Hospital, 38 Morohongou, Moroyama, Saitama, 350-0495, Japan.
Tomonari SuzukiDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Keisuke IshizawaDepartment of Pathology, Saitama Medical University Hospital, 38 Morohongou, Moroyama, Saitama, 350-0495, Japan.
Sumihito NobusawaDepartment of Human Pathology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Hideaki YokooDepartment of Human Pathology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Ryo NishikawaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Masanori YasudaDepartment of Pathology, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Atsushi SasakiDepartment of Pathology, Saitama Medical University Hospital, 38 Morohongou, Moroyama, Saitama, 350-0495, Japan. asasaki@saitama-med.ac.jp.ORCID http://orcid.org/0000-0002-1333-9391
Saitama Medical University · JPSaitama Medical University Hospital · JPGunma University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EPN-ZFTA is a rare brain tumor where prognostic factors remain unclear and no effective immunotherapy or chemotherapy is currently available. Therefore, this study investigated its clinicopathological features, evaluated the utility of MTAP and p16 IHC as surrogate markers of CDKN2A alterations, and characterized the immune microenvironment of EPN-ZFTA. Thirty surgically removed brain tumors, including 10 EPN-ZFTA, were subjected to IHC. MLPA was performed for CDKN2A HD in 20 ependymal tumors, including EPN-ZFTA. The 5-years OS and PFS of EPN-ZFTA were 90% and 60%, respectively. CDKN2A HD was detected in two cases of EPN-ZFTA; these cases were immunohistochemically negative for both MTAP and p16 and recurred earlier after surgery. As for the immune microenvironment of EPN-ZFTA, B7-H3, but not PD-L1, was positive in all cases of EPN-ZFTA; Iba-1-positive or CD204-positive macrophages were large, while infiltrating lymphocytes were small, in number in EPN-ZFTA. Collectively, these results indicate the potential of MTAP and p16 IHC as useful surrogate markers of CDKN2A HD in EPN-ZFTA, and tumor-associated macrophages, including the M2 type, may contribute to its immune microenvironment. Furthermore, the expression of B7-H3 in EPN-ZFTA may indicate the usefulness of B7-H3 as a target of immune checkpoint chemotherapy for EPN-ZFTA via B7-H3 pathway.

Indexed as

Brain NeoplasmsEpendymomaCyclin-Dependent Kinase Inhibitor p16HumansTumor MicroenvironmentCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16CDKN2A homozygous deletionMTAP-p16-supratentorial ependymomaTumor-associated macrophagesZFTA fusion-positive

Identifiers

PMID37322295
PMCPMC10314846
OpenAlexW4380869806

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.