Evidence map›Paper›PMID 42857022›Full record

ReviewFrontiers in molecular medicine2026

CLDN18 and FGFR2 splicing variants are emerging tumor-associated antigens for cancer therapy.

Masuko Katoh, Masaru Katoh

Abstract readReview
In one paragraph

Review in Frontiers in molecular medicine, 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

2 authors.

Masuko KatohDepartment of Global Network, M & M Precision Medicine, Tokyo, Japan.
Masaru KatohDepartment of Global Network, M & M Precision Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative splicing and alternative promoters generate splicing variants to expand proteomic and transcriptional diversity to orchestrate physiological activities and dictate tumorigenesis. Splicing variants are attractive tumor-associated antigens (TAAs) for the clinical development of cancer therapies. Here, recent progress in claudin-18 isoform 2 (CLDN18.2)- and fibroblast growth factor receptor 2 isoform b (FGFR2b)-targeted therapeutics is summarized, and perspectives in this field are discussed. Zolbetuximab and bemarituzumab are first-generation monoclonal antibodies (mAbs) targeting CLDN18.2 and FGFR2b, respectively, while next-generation biologics targeting these TAAs are emerging. Single-agent objective response rates of CLDN18.2-targeting mAb (omectatug), antibody-drug conjugates (ADCs, arcotatug tavatecan, BL-M05D1, garetatug rezetecan, JS107, sonesitatug vedotin and tecotabart vedotin), bispecific antibodies (emaretamig and givastomig) and chimeric antigen receptor T (CAR-T) cells (IMC002) were higher than that of zolbetuximab. Gastrointestinal toxicity, nausea and vomiting are common on-target/off-tumor adverse effects of CLDN18.2-targeted biologics, which are mitigated for arcotatug tavatecan and givastomig as a result of antibody engineering. Combination therapy of zolbetuximab plus chemotherapy is approved for the treatment of gastric and gastroesophageal junction cancer patients, while results of other CLDN18.2-targeting biologics in phase 3 clinical trials are anticipated with expectations for improved clinical activities and mitigated adverse events. Diagnostics detecting alternative isoforms and combination strategies using immune checkpoint inhibitors would address resistance mechanisms, such as epitope-losing isoform switching and immune evasion. Comparative studies on ADC monotherapy versus combination mAb-chemotherapy as well as the clinical development of bispecific ADCs and allogeneic CAR-T cells should further improve the clinical benefits of CLDN18.2- and FGFR2b-targeted therapies.

Indexed as

clinical immunohistochemistryepithelial–mesenchymal plasticityextrachromosomal DNA amplificationimmune checkpoint inhibitorimmunosuppressive tumor microenvironmentintertumor heterogeneityreceptor tyrosine kinasetight junction

Identifiers

PMID42857022
PMCPMC13650739

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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.