Evidence map›Paper›PMID 42130710›Full record

ReviewACS pharmacology & translational science2026

Chimeric Antigen Receptor T‑Cell Therapy Targeting Tumor Necrosis Factor Receptor Superfamily Member 8 (CD30) for Relapsed or Refractory Anaplastic Large Cell Lymphoma: Rationale, Strategies, and Emerging Clinical Evidence.

Alberto Boretti

Abstract readReview
In one paragraph

Review in ACS pharmacology & translational science, 2026. 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

1 author.

Alberto BorettiIndependent Scientist, 6 Johnsonville Road, Johnsonville, Wellington 6037, New Zealand.ORCID https://orcid.org/0000-0002-3374-0238

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chimeric Antigen Receptor (CAR) T-cell therapy has fundamentally altered the treatment paradigm for relapsed or refractory (R/R) B-cell malignancies. However, translating this success to T-cell lymphomas has been impeded by a critical biological barrier: fratricide. This process describes the self-destruction of therapeutic T-cells caused by their shared expression of target antigens, such as Tumor Necrosis Factor Receptor Superfamily Member 8 (CD30), following activation. Anaplastic Large Cell Lymphoma (ALCL), characterized by its uniform and high-level expression of CD30, represents both an ideal candidate for this approach and a significant scientific challenge. This comprehensive review begins by outlining the established landscape of approved CD19- and BCMA-directed CAR-T therapies to provide context. It then focuses specifically on the application of anti-CD30 CAR-T therapy for ALCL, examining the molecular mechanisms that drive fratricide. We explore the innovative engineering and manufacturing strategies developed to overcome this obstacle, including ultrarapid production protocols, the selection of virus-specific T-cells, and precise genetic disruption of the

Indexed as

Anaplastic Large Cell Lymphoma (ALCL)CD30cellular immunotherapyChimeric Antigen Receptor T-Cell (CAR-T)molecular immunologyT-cell lymphoma

Identifiers

PMID42130710
PMCPMC13162160

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.