ArticleMolecular therapy. Oncology2026
A monoclonal antibody W1 blocks mesothelin-mediated tumor progression.
Article in Molecular therapy. Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesothelin (MSLN) represents an attractive and potential biomarker for targeted cancer therapy. Although MSLN has been implicated in mediating tumorigenesis, its precise physiological function remains incompletely elucidated. Moreover, only a limited number of antibodies have been reported to directly inhibit its function in tumor progression. In this study, we confirmed that the N-terminal domain 1 (D1) of MSLN serves as the key region responsible for mediating binding to tumor cells and promoting migration and invasion through the activation of the matrix metalloproteinase-7 (MMP7) pathway. We further identified two monoclonal antibodies, W1 and A12H, which specifically bind to D1 and domain 3 (D3) of MSLN, respectively. W1 effectively inhibits the interaction between D1 and tumor cells, thereby suppressing cell migration and invasion via interference with MSLN-mediated signaling pathways. In contrast, A12H, which targets D3, does not exhibit a similar functional blockade. Additionally, W1 significantly reduces the tumor burden in mice bearing MSLN-positive tumor cells. Together, these findings provide mechanistic insights into the role of D1 in driving tumor progression and reinforce the potential of MSLN as a therapeutic biomarker. The antibody W1 emerges as a promising candidate, offering novel perspectives for developing immunotherapeutic strategies against MSLN-related cancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.