Evidence map›Paper›PMID 41469420›Full record

ArticleScientific reports2025

Novel anti-ITGA4 monoclonal antibody induces cell death via large pore formation in NK/T-cell lymphoma cells.

Shiori Takeuchi, Yasuhiko Ito, Shuji Matsuoka, Masaaki Abe, Hiromichi Tsurui, Yoshiya Horimoto, Takeshi Fukuhara, Takeshi Hirano, Natsuko Mizutani, Takumi Ito and 11 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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. Review
  2. 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

21 authors.

Shiori TakeuchiDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Yasuhiko ItoDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Shuji MatsuokaDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. matsuoka@juntendo.ac.jp.ORCID 0000-0002-8497-0973
Masaaki AbeDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Hiromichi TsuruiDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Yoshiya HorimotoDepartment of Breast Surgery and Oncology, Tokyo Medical University, Tokyo, Japan.
Takeshi FukuharaNeurodegenerative Disorders Collaboration Laboratory, RIKEN Center for Brain Science, Wako, Japan.
Takeshi HiranoDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Natsuko MizutaniDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Takumi ItoDepartment of Therapy Development and Innovation for Immune Disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Ryo HatanoDepartment of Therapy Development and Innovation for Immune Disorders and Cancers, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Atsuhito NakaoDepartment of Immunology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Yasuhisa TeraoDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Mari KitadeDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Yoshitomo HamanoDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Hiroyuki TakamatsuFaculty of Transdisciplinary Sciences for Innovation, Institute of Transdisciplinary Sciences for Innovation, Kanazawa University, Kanazawa, Japan.
Hiroshi MatsuokaDivision of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tetsuya NakatsuraDivision of Cancer Immunotherapy, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center, Kashiwa, Chiba, Japan.
Hideo YagitaDepartment of Immunological Diagnosis, Graduate School of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Ko OkumuraAtopy (Allergy) Research Center, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Atsuo ItakuraDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Juntendo University, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer (NK)/T-cell lymphomas are a highly aggressive lymphoma subtype common in East Asia and Latin America. To develop a therapeutic monoclonal antibody (mAb) against it, BALB/c mice were alternately immunized with two vigorous NK lymphoma cell lines. After hybridization, culture supernatants of the hybridoma clones were added to a third NK lymphoma cell line not used for immunization, and the antibodies were screened for direct cytolytic activity. Results showed that the newly established mAb, named mAb ANAP, induced immediate cell death against NK lymphoma cells in a cytoskeleton-dependent manner, which was also complement-, antibody-dependent cell-mediated cytotoxicity-, and caspase-independent, forming large pores on target cell surface within 20 min; mAb ANAP did not injure normal cells and could bind to the ITGA4 (CD49d). Contrary to existing anti-ITGA4 antibodies, which did not exhibit any destructive activity against NK lymphoma, ANAP antibody has promising potential as a therapeutic agent for NK lymphoma.

Indexed as

Antibodies, MonoclonalKiller Cells, NaturalLymphoma, T-CellAnimalsAntibody-Dependent Cell CytotoxicityCell DeathCell Line, TumorHumansMiceMice, Inbred BALB CAntibodies, Monoclonal

Identifiers

PMID41469420
PMCPMC12753658

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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.