Evidence map›Paper›PMID 40664444›Full record

ArticleJournal for immunotherapy of cancer2025

Allogeneic cetuximab-armed gamma delta T cells using antibody-cell conjugation technology for the treatment of EGFR-expressing solid tumors.

Hao-Kang Li, Tai-Sheng Wu, Ying Ru, Yi-Chiu Kuo, Chia-Yun Lee, Pei-Ju Leng, Yi-Chun Hsieh, Yun-Jung Chiang, Zih-Fei Cheng, Yan-Liang Lin and 2 more

Abstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 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. γδ T cells and cancer.The Journal of clinical investigation · 2026
    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

12 authors.

Hao-Kang LiAcepodia Biotech Inc, Alameda, California, USA.ORCID http://orcid.org/0009-0003-7790-3443
Tai-Sheng WuAcepodia Biotech Inc, Alameda, California, USA.
Ying RuAcepodia Biotech Inc, Alameda, California, USA.
Yi-Chiu KuoAcepodia Biotech Inc, Alameda, California, USA.
Chia-Yun LeeAcepodia Biotech Inc, Alameda, California, USA.
Pei-Ju LengAcepodia Biotech Inc, Alameda, California, USA.
Yi-Chun HsiehAcepodia Biotech Inc, Alameda, California, USA.
Yun-Jung ChiangAcepodia Biotech Inc, Alameda, California, USA.
Zih-Fei ChengAcepodia Biotech Inc, Alameda, California, USA.
Yan-Liang LinAcepodia Biotech Inc, Alameda, California, USA.
Shih-Chia HsiaoAcepodia Biotech Inc, Alameda, California, USA saiwen@acepodiabio.com sonny@acepodiabio.com.
Sai-Wen TangAcepodia Biotech Inc, Alameda, California, USA saiwen@acepodiabio.com sonny@acepodiabio.com.ORCID http://orcid.org/0000-0001-8577-2461

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTargeting epidermal growth factor receptor (EGFR) has become a strategic approach in cancer therapy, using various modalities including chimeric antigen receptor (CAR)-αβT cell therapies. Despite significant advancements in autologous CAR-αβT cell therapies in B-cell lymphoma, current cell therapies face challenges such as potential risks associated with genetic engineering, waiting time and high costs of autologous CAR-αβT cell therapies. Innovations in click chemistry and bioorthogonal chemistry have enabled the development of antibody-cell conjugation (ACC) technology, which links cancer-targeting antibodies to immune cells without genetic modifications, potentially providing a safer profile.

methodsIn this study, we introduce ACE2016, an innovative allogeneic cell therapy targeting EGFR. ACE2016 is generated by ACC technology to conjugate donor-derived γδ2 T cells with the EGFR-specific antibody cetuximab.

resultsOur preclinical studies demonstrate that ACE2016 exhibits superior cytotoxicity against various EGFR-expressing cancer cell lines and minimal cytotoxic effects on normal cells. Mechanistic studies revealed that ACE2016 enhances cytotoxicity through increased capacity towards EGFR-expressing cancer cells, enhanced levels of cytotoxic cytokines and recruitment of peripheral cytotoxic cells, reflecting significant tumor suppression and prolonged survival in ACE2016-treated groups without causing treatment-related toxicity in vivo.

conclusionsThese findings support the clinical potential of ACE2016 as an off-the-shelf γδ2 T-cell therapy for EGFR-expressing cancers, offering a combination of specificity, scalability, and safety in the development of solid tumor therapy.

Indexed as

Antineoplastic Agents, ImmunologicalCetuximabImmunotherapy, AdoptiveIntraepithelial LymphocytesNeoplasmsReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesAnimalsCell Line, TumorErbB ReceptorsFemaleHumansMiceXenograft Model Antitumor AssaysAntineoplastic Agents, ImmunologicalCetuximabEGFR protein, humanErbB ReceptorsReceptors, Antigen, T-Cell, gamma-deltaAdoptive cell therapy - ACTInnateSolid tumorT cell

Identifiers

PMID40664444
PMCPMC12265807

What OpenQuestion holds

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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.