Evidence map›Paper›PMID 42145875›Full record

ArticleNeuro-oncology advances

Cerebrospinal fluid soluble protein tyrosine phosphatase receptor type Z detected with human natural killer-1 antibody as a practical biomarker for glioma diagnosis.

Yu Naruse, Masazumi Fujii, Kenichiro Nagai, Ryo Hiruta, Toshie Sakagami, Takuru Kobayashi, Kazuto Takahashi, Junko Iijima, Hideaki Suzuki, Kasumi Hattori and 17 more

Abstract read
In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

27 authors.

Yu NaruseDepartment of Neurosurgery, Fukushima Medical University, Fukushima, Japan.
Masazumi FujiiDepartment of Neurosurgery, Fukushima Medical University, Fukushima, Japan.
Kenichiro NagaiDepartment of Neurosurgery, Fukushima Medical University, Fukushima, Japan.
Ryo HirutaDepartment of Neurosurgery, Fukushima Medical University, Fukushima, Japan.
Toshie SakagamiDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Takuru KobayashiDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Kazuto TakahashiDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Junko IijimaDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Hideaki SuzukiDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Kasumi HattoriDepartment of Neurology, Fukushima Medical University, Fukushima, Japan.
Kazuaki KanaiDepartment of Neurology, Fukushima Medical University, Fukushima, Japan.
Yuka OkaDepartment of Diagnostic Pathology, Fukushima Medical University, Fukushima, Japan.
Yuko HashimotoDepartment of Diagnostic Pathology, Fukushima Medical University, Fukushima, Japan.
Shunichi KoriyamaDepartment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Taiichi SaitoDepartment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Yoshihiro MuragakiDepartment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Takakazu KawamataDepartment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-6076-7065
Takashi SasayamaDepartment of Neurosurgery, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID https://orcid.org/0000-0002-5593-9045
Jun YasudaDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Miwa UzukiDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.
Yasushi KawaguchiDepartment of Infectious Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kentaro KawataIntegrated Research Center for Self-Care Technology, National Institute of Advanced Industrial Science and Technology (AIST), Kagawa, Japan.
Yoshiki YamaguchiDepartment of Medical Device Engineering, Kobe University Graduate School of Medicine, Kobe, Japan.
Shiori GoInstitute for Glyco-core Research (iGCORE), Nagoya University, Furo-cho, Chikusa, Nagoya, Japan.
Hiromu ArakawaInstitute for Glyco-core Research (iGCORE), Nagoya University, Furo-cho, Chikusa, Nagoya, Japan.
Hiroyuki KajiInstitute for Glyco-core Research (iGCORE), Nagoya University, Furo-cho, Chikusa, Nagoya, Japan.
Shinobu KitazumeDepartment of Clinical Laboratory Sciences, Graduate School of Health Sciences, Fukushima Medical University, Fukushima, Japan.ORCID https://orcid.org/0000-0003-4757-723X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: A major challenge in managing gliomas is the lack of reliable and clinically applicable biomarkers. Imaging alone is often insufficient to distinguish gliomas from primary central nervous system lymphoma (PCNSL), necessitating invasive biopsy. Soluble protein tyrosine phosphatase receptor type Z (sPTPRZ) in cerebrospinal fluid (CSF) has recently emerged as a promising candidate. We evaluated the diagnostic utility of CSF sPTPRZ in differentiating gliomas from PCNSL. Methods: We developed an anti-HNK-1 antibody-based ELISA for CSF sPTPRZ and analyzed 51 glioma, 15 PCNSL, and 20 control patients. Complementary assays included western blotting, immunohistochemistry, qPCR. sPTPRZ immunopurified from glioma CSF was used to determine HNK-1 epitope sites. RNA-seq data from the C-CAT database were used to identify PTPRZ gene fusions. Results: CSF sPTPRZ levels were significantly elevated in glioma patients compared with both controls and PCNSL, demonstrating robust discrimination between these entities (AUC = 0.910 vs controls; AUC = 0.805 vs PCNSL; Conclusion: CSF sPTPRZ detection with anti-HNK-1 antibody is a minimally invasive biomarker for glioma. It significantly improves diagnostic discrimination from PCNSL, and provides a molecular rationale for biomarker-negative glioma subsets with PTPRZ-MET fusions.

Indexed as

biomarkergliomaHNK-1primary CNS lymphomaPTPRZ

Identifiers

PMID42145875
PMCPMC13175180

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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.