γδ T Cells in Cancer Immunotherapy, 2000-2025: A Bibliometric Analysis and Clinical-Trial Evidence Map

γδ T cells are promising cancer-immunotherapy effectors because they recognize tumors without major histocompatibility complex (MHC) restriction and carry low graft-versus-host-disease risk in allogeneic settings, yet few bibliometric studies have integrated immunotherapy-specific research trends with clinical-trial mapping and translational-gap analysis. We characterized the global research output, intellectual foundations, emerging frontiers, and clinical translation of γδ T cells in cancer immunotherapy (2000-2025) by combining bibliometric analysis of 3,273 Web of Science publications (bibliometrix, VOSviewer, CiteSpace), a Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR)-guided evidence map of 26 interventional cancer trials (ClinicalTrials.gov, World Health Organization International Clinical Trials Registry Platform [WHO ICTRP], regional registries), and an integrative step linking bibliometric hotspots to the pipeline. Annual output grew from 18 (2000) to 418 (2024) publications (compound annual growth rate [CAGR], 14.0%) across three phases; China (33.1%) and the United States (27.3%) led production. Co-citation analysis identified five intellectual pillars: phosphoantigen recognition, subset heterogeneity, clinical adoptive transfer, tumor-microenvironment suppression, and engineered γδ T therapy. Chimeric antigen receptor-engineered γδ T cells (CAR-γδ T cells), allogeneic platforms, and single-cell RNA sequencing were the leading 2022-2025 frontier terms. Trials shifted toward allogeneic cell sources; early-phase studies consistently met safety and feasibility endpoints, but monotherapy efficacy was modest. The LAVA-051 and LAVA-1207 programs were discontinued for disclosed business or internal-benchmark reasons, whereas allogeneic CAR-Vδ1 therapy (ADI-001) produced the most encouraging early signals before oncology reprioritization in 2024. Three persistent translational gaps-single-cell/T-cell receptor (TCR) profiling, metabolic reprogramming, and γδT17 biology-frame a proposed roadmap to convert bibliometric hotspots into mechanism-guided γδ T-cell cancer immunotherapy.