From mechanism to clinical: research evolution and hotspot analysis of CD276/B7-H3 in cancer immunotherapy.

[BACKGROUND] CD276 (B7-H3) is a pivotal immune checkpoint molecule with dual roles in T-cell regulation and tumor immune evasion, representing a promising therapeutic target across multiple cancers. However, a comprehensive analysis of the research landscape, evolutionary pathways, and knowledge structure in this field remains lacking.

[METHODS] Publications related to CD276/B7-H3 in cancer research were systematically retrieved from the Web of Science Core Collection (WoS, n = 688) and Scopus (n = 759) spanning from January 2001 to August 2025. After merging and de-duplication, a final corpus of 830 publications was analyzed using Bibliometrix, VOSviewer, CiteSpace, and Pajek to evaluate publication trends, influential authors and institutions, collaboration networks, core journals, co-citation patterns, and keyword evolution.

[RESULTS] The field exhibited exponential growth with an annual publication increase of 21.77%. China and the United States were the dominant contributing countries. Journal for Immunotherapy of Cancer was the most productive journal, while Clinical Cancer Research produced the most impactful publications. Co-citation analysis highlighted foundational studies on B7-H3's prognostic significance and recent breakthroughs in CAR T-cell therapy targeting B7-H3. Keyword evolution revealed a clear transition from early themes such as "expression" and "prognosis" to contemporary focuses including "immunotherapy," "tumor microenvironment," and "chimeric antigen receptor".

[CONCLUSION] This study provides the first integrated bibliometric overview of CD276/B7-H3 research in cancer, illustrating a rapid transition from mechanistic exploration to clinical application. The findings underscore B7-H3's importance as a pan-cancer antigen and immunotherapeutic target, offering valuable insights for guiding future research directions.