ReviewFrontiers in oncology2018
B7H3 As a Promoter of Metastasis and Promising Therapeutic Target.
Review in Frontiers in oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
What it found
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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
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Immune-related pan-cancer gene expression signatures of patient survival revealed by NanoString-based analyses.PloS one · 2023Pooled it
- A whole-body imaging technique for tumor-specific diagnostics and screening of B7H3-targeted therapies.The Journal of clinical investigation · 2025Trial
- Integrative in silico transcriptomic and pharmacogenomic analysis of CD276 as a candidate prognostic biomarker and therapeutic target in bladder cancer.Discover oncology · 2026Article
- B7-H3 (CD276) and CD47 Expression Are Associated with Immune Evasion and Survival Outcomes in Pediatric Medulloblastoma.Diagnostics (Basel, Switzerland) · 2026Article
- Computational Discovery of Dual-Target LDHA/BRD4 Inhibitors Targeting the Lactate-Kla-B7-H3 Immunosuppressive Axis Through AI-Driven Virtual Screening.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Immunoinformatics-driven multi-epitope vaccine design targeting PSMA, STEAP1, and B7H3 for prostate cancer.Frontiers in medicine · 2026Article
- B7-H3-mediated immune regulation in cancer: biological functions and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Advancing breast cancer treatment through dual targeting CAR T cell therapy.Discover oncology · 2025Review
- The role of immune checkpoints in modulating cancer stem cells anti-tumor immune responses: implications and perspectives in cancer therapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Advances in Nanobody-Based Platforms for Precision Cancer Diagnosis and Therapy.Polymer science & technology (Washington, D.C.) · 2025Review
- Prognostic and Predictive Significance of B7-H3 and CD155 Expression in Gastric Cancer Patients.Diagnostics (Basel, Switzerland) · 2025Article
- IDeate-Lung02: a Phase 3 study of second-line ifinatamab deruxtecan in patients with relapsed small cell lung cancer.Future oncology (London, England) · 2025Article
- A Phase I, Open-Label, Dose Escalation Study of Enoblituzumab in Children and Young Adults with B7-H3-Expressing Relapsed or Refractory Solid Tumors.Cancer research communications · 2025Article
- The B7 family molecules in oral squamous cell carcinoma: a systematic review. Part II: B7-1, B7-2, B7-H2, B7-H3, B7-H4, B7-H5 (VISTA), B7-H6 and B7-H7.Postepy dermatologii i alergologii · 2025Review
- Shifting Shapes: The Endothelial-to-Mesenchymal Transition as a Driver for Cancer Progression.International journal of molecular sciences · 2025Review
- m276-SL-PBD eradicates tumors and instigates long-lasting tumor-free survival in Merkel cell carcinoma preclinical models.iScience · 2025Article
- Chimeric antigen receptor NK-92 cell function is modulated by HLA class I expression of target cells.iScience · 2025Article
- Unveiling transcriptional mechanisms of B7-H3 in breast cancer stem cells through proteomic approaches.iScience · 2025Article
- Identification of the B7-H3 Interaction Partners Using a Proximity Labeling Strategy.International journal of molecular sciences · 2025Article
- Tumor Immunotherapy Targeting B7-H3: From Mechanisms to Clinical Applications.ImmunoTargets and therapy · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B7H3 (also known as CD276, an immune checkpoint molecule) is aberrantly overexpressed in many types of cancer, and such upregulation is generally associated with a poor clinical prognosis. Recent discoveries indicate a crucial role for B7H3 in promoting carcinogenesis and metastasis. This review will focus on the latest developments relating specifically to the oncogenic activity of B7H3 and will describe the upstream regulators and downstream effectors of B7H3 in cancer. Finally, we discuss the emerging roles of microRNAs (miRNAs) in inhibiting B7H3-mediated tumor promotion. Excellent recent studies have shed new light on the functions of B7H3 in cancer and identified B7H3 as a critical promoter of tumor cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, cancer stemness, drug resistance, and the Warburg effect. Numerous miRNAs are reported to regulate the expression of B7H3. Our meta-analysis of miRNA database revealed that 17 common miRNAs potentially interact with B7H3 mRNA. The analysis of the TCGA ovarian cancer dataset indicated that low miR-187 and miR-489 expression was associated with poor prognosis. Future studies aimed at delineating the precise cellular and molecular mechanisms underpinning B7H3-mediated tumor promotion will provide further insights into the cell biology of tumor development. In addition, inhibition of B7H3 signaling, to be used alone or in combination with other treatments, will contribute to improvements in clinical practice and benefit cancer patients.
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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.