Evidence map›Paper›PMID 37109309›Full record

ReviewJournal of clinical medicine2023

Anti-Claudin Treatments in Gastroesophageal Adenocarcinoma: Mainstream and Upcoming Strategies.

Giulia Grizzi, Kostantinos Venetis, Nerina Denaro, Maria Bonomi, Andrea Celotti, Antonia Pagkali, Jens Claus Hahne, Gianluca Tomasello, Fausto Petrelli, Nicola Fusco and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% of its field
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. SEOM-GEMCAD-TTD clinical guideline for the diagnosis and treatment of gastric cancer (2023).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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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

11 authors at 6 institutions in 3 countries.

Giulia GrizziOperative Unit of Oncology, ASST of Cremona, 26100 Cremona, Italy.
Kostantinos VenetisDivision of Pathology, IEO, European Institute of Oncology IRCCS, 20141 Milan, Italy.
Nerina DenaroOncology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.ORCID 0000-0002-8605-4290
Maria BonomiOperative Unit of Oncology, ASST of Cremona, 26100 Cremona, Italy.
Andrea CelottiDepartment of Surgery, ASST of Cremona, 26100 Cremona, Italy.
Antonia PagkaliSchool of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-4240-2900
Jens Claus HahneDivision of Molecular Pathology, The Institute of Cancer Research, London SM2 5NG, UK.
Gianluca TomaselloOncology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.
Fausto PetrelliOncology Unit, Medical Sciences Department, ASST Bergamo Ovest, 24047 Bergamo, Italy.ORCID 0000-0001-9639-4486
Nicola FuscoDivision of Pathology, IEO, European Institute of Oncology IRCCS, 20141 Milan, Italy.ORCID 0000-0002-9101-9131
Michele GhidiniOncology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.ORCID 0000-0001-5435-1218
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITIstituti Ospitalieri di Cremona · ITUniversity of Milan · ITInstitute of Cancer Research · GBNational and Kapodistrian University of Athens · GRUniversity of Bergamo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Claudins (CLDNs) are a multigene family of proteins and the principal components of tight junctions (TJs), which normally mediate cell-cell adhesion and selectively allow the paracellular flux of ions and small molecules between cells. Downregulation of claudin proteins increases the paracellular permeability of nutrients and growth stimuli to malignant cells, which aids the epithelial transition. Claudin 18.2 (CLDN18.2) was identified as a promising target for the treatment of advanced gastroesophageal adenocarcinoma (GEAC), with high levels found in almost 30% of metastatic cases. CLDN18.2 aberrations, enriched in the genomically stable subgroup of GEAC and the diffuse histological subtype, are ideal candidates for monoclonal antibodies and CAR-T cells. Zolbetuximab, a highly specific anti-CLDN18.2 monoclonal antibody, demonstrated efficacy in phase II studies and, more recently, in the phase III SPOTLIGHT trial, with improvements in both PFS and OS with respect to standard chemotherapy. Anti-CLDN18.2 chimeric antigen receptor (CAR)-T cells showed a safety profile with a prevalence of hematologic toxicity in early phase clinical trials. The aim of this review is to present new findings in the treatment of CLDN18.2-positive GEAC, with a particular focus on the monoclonal antibody zolbetuximab and on the use of engineered anti-CLDN18.2 CAR-T cells.

Indexed as

anti-claudin 18.2car-T cellschemotherapyclaudinsesophageal cancergastric cancerzolbetuximab

Identifiers

PMID37109309
PMCPMC10142079
OpenAlexW4366582539

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.