ReviewDiscover oncology2026
Prognostic and therapeutic roles of B7-H3 and B7-H4 in prostate cancer.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Molecular Architecture and Clinical Landscape of Immune Checkpoint Receptors and Ligands.Antibodies (Basel, Switzerland) · 2026Review
- The molecular underpinnings of the immune landscape in prostate cancer: decoding a "cold" tumor.Frontiers in oncology · 2026Review
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
Abstract
Prostate cancer (PCa) remains a leading cause of cancer-related morbidity and mortality in men worldwide, with metastatic castration-resistant prostate cancer (mCRPC) presenting a particularly formidable therapeutic challenge. The limited efficacy of conventional immunotherapies targeting the PD-1/PD-L1 axis in PCa has spurred intensive research into alternative immune checkpoints. Among the B7 family of immunomodulatory proteins, B7-H3 (CD276) and B7-H4 (VTCN1/B7x/B7S1) have emerged as critical regulators of PCa pathogenesis, progression, and therapeutic resistance. This comprehensive review synthesizes current evidence from preclinical and clinical studies to delineate the multifaceted roles of B7-H3 and B7-H4 in PCa. We first detail the expression patterns of these molecules in PCa tissues and their robust correlation with adverse clinicopathological features, including high Gleason score, advanced tumor stage, metastasis, and poor survival outcomes. We then explore the complex molecular mechanisms underlying their pro-tumorigenic functions, encompassing immune suppression (inhibition of T-cell activity, modulation of myeloid-derived suppressor cells [MDSCs] and tumor-associated macrophages [TAMs]) and non-immune effects (regulation of cancer stem cells [CSCs], DNA damage repair [DDR], androgen receptor [AR] signaling, and tumor dormancy). Furthermore, we systematically review the rapidly expanding landscape of therapeutic strategies targeting B7-H3 and B7-H4, including antibody–drug conjugates (ADCs), chimeric antigen receptor (CAR) T-cell therapy, monoclonal antibodies, bispecific agents, and combination therapies with radiotherapy, AR pathway inhibitors (ARPIs), or other immunotherapies. We also discuss emerging directions such as liquid biopsy for B7-H3 detection, B7-H4-targeted immunoPET imaging, racial disparities in B7-H3 expression, and the development of predictive biomarkers for treatment response. Collectively, this review establishes B7-H3 and B7-H4 as pivotal nodes in PCa biology and highlights their promising potential to improve the clinical management of advanced and treatment-resistant PCa through improved prognostic stratification and the development of novel precision therapies.
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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.