ReviewOncoscience2026
Engineering CAR-T cells for solid tumors: Overcoming the microenvironment through integrated design and clinical translation.
Review in Oncoscience, 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
Chimeric antigen receptor T-cell (CAR-T) therapy has produced remarkable therapeutic results in blood cancers, while its application to solid malignancies remains limited by a pooled objective response rate of approximately 9%. This gap stems from core biological obstacles: heterogeneous antigen expression, physical inaccessibility within dense stromal architectures, and immunosuppressive microenvironments that drive T-cell exhaustion through epigenetically fixed transcriptional programs. The period spanning 2024-2025 represents a pivotal turning point. GD2-targeting CAR-T cells delivered intracerebroventricularly achieved durable complete responses (including one sustained beyond 30 months) in H3K27M-mutated diffuse midline gliomas. CLDN18.2-targeting satricabtagene autoleucel demonstrated randomized superiority over physician's choice in advanced gastric cancer (progression-free survival HR 0.37). GPC3-targeting CAR-T cells armored with a dominant-negative TGF-β receptor achieved objective response rates of 50-57% in hepatocellular carcinoma, representing a three- to four-fold improvement over unarmored predecessors. These breakthroughs reflect a paradigm shift from potency-driven engineering toward resilience-based design: metabolic armoring via autocrine IL-10 and IL-15, epigenetic protection through DNMT3A disruption and c-Jun overexpression, logic-gated targeting via synNotch circuits, and microenvironmental shielding through dominant-negative receptors. Beyond the local microenvironment, emerging recognition of systemic neuroendocrine-immune dysregulation further informs CAR-T persistence and fitness considerations. This review synthesizes the mechanistic insights, engineering strategies, clinical evidence, and emerging platforms, including
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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 Socratic graph.