ReviewMedComm2026
Mesothelin as Biomarker and Therapeutic Target for Immunotherapy in Cancer.
Review in MedComm, 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
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer remains a critical global health concern due to late detection, drug resistance, and high mortality. Mesothelin (MSLN) is a glycoprotein highly expressed on the surface of various cancer cells, including those of ovarian, pancreatic, and gastric cancers. Thus, it could be a valuable target for both as a biomarker and for immunotherapy. This review summarizes MSLN biology in cancer, current immunotherapeutic strategies targeting MSLN, associated clinical challenges, and emerging avenues to enhance immunotherapy efficacy. During cancer progression, MSLN acts as a cellular accelerator, promoting cell division and survival. It activates several critical signaling pathways, including nuclear factor k-light-chain-enhancer of activated B cells (NF-κB), interleukin-6 and its soluble receptor (IL-6/sIL-6R), and c-Jun N-terminal kinase (JNK), thereby promoting epithelial-mesenchymal transition and angiogenesis. Various MSLN-targeting immunotherapies, including monoclonal antibodies, chimeric antigen receptor-T cells, cytokine therapies, and vaccines, have shown preclinical and early clinical efficacy. However, immune evasion, an immunosuppressive tumor microenvironment, antigen heterogeneity, tumor immune escape, and off-tumor toxicities continue to hinder the broad clinical success of these modalities. Nonetheless, rational combinations of MSLN-directed therapies with other immunomodulatory strategies, optimized patient stratification, and advances in vaccine and adoptive cell therapy design hold promise for overcoming resistance and improving patient outcomes.
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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.