Commentary on "Targeting B7-H3 inhibition-induced activation of fatty acid synthesis boosts anti-B7-H3 immunotherapy in triple-negative breast cancer".
사설/논평
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
환자: TNBC; however, resistance remains a major barrier
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Dual inhibition of B7-H3 and fatty acid synthase synergistically enhances tumor cell apoptosis, suppresses proliferation and migration, and promotes CD8 T-cell infiltration in vitro and in vivo. These findings reveal a novel immune-metabolic resistance mechanism in TNBC and provide a compelling rationale for combinatorial strategies targeting both immune checkpoints and metabolic pathways.
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by limited treatment options and poor prognosis.
APA
Kotaich N, Potteaux S (2026). Commentary on "Targeting B7-H3 inhibition-induced activation of fatty acid synthesis boosts anti-B7-H3 immunotherapy in triple-negative breast cancer".. Journal for immunotherapy of cancer, 14(2). https://doi.org/10.1136/jitc-2025-013210
MLA
Kotaich N, et al.. "Commentary on "Targeting B7-H3 inhibition-induced activation of fatty acid synthesis boosts anti-B7-H3 immunotherapy in triple-negative breast cancer".." Journal for immunotherapy of cancer, vol. 14, no. 2, 2026.
PMID
41741135 ↗
Abstract 한글 요약
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by limited treatment options and poor prognosis. Immune checkpoint blockade, particularly via programmed cell death protein-1/programmed death-ligand 1 inhibition, has improved outcomes in selected patients with TNBC; however, resistance remains a major barrier. Recent studies have identified B7-H3 (CD276) as a key immune-suppressive molecule overexpressed in TNBC, correlating with poor prognosis and immune exclusion. Jiang demonstrate that B7-H3 inhibition triggers a compensatory metabolic adaptation in TNBC cells, marked by upregulation of fatty acid synthesis and β-oxidation, particularly via the AKT-SREBP1-FASN signaling axis. This metabolic reprogramming promotes survival and immune evasion, limiting the efficacy of B7-H3-targeted therapies. Dual inhibition of B7-H3 and fatty acid synthase synergistically enhances tumor cell apoptosis, suppresses proliferation and migration, and promotes CD8 T-cell infiltration in vitro and in vivo. These findings reveal a novel immune-metabolic resistance mechanism in TNBC and provide a compelling rationale for combinatorial strategies targeting both immune checkpoints and metabolic pathways.
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
📖 전문 본문 읽기 PMC JATS · ~13 KB · 영문
Conclusions
Conclusions
Three key areas warrant further investigation. First, post-treatment biopsies from patients with TNBC receiving B7-H3-targeted therapies are needed to confirm metabolic adaptations and assess risk of recurrence. The long-term safety of sustained FASN inhibition also warrants thorough evaluation, given fatty acid oxidation’s essential role in CD8+ memory T cells, regulatory T cells, and M2 macrophages. Second, the impact of dual inhibition on the broader TME remains to be elucidated. The interplay between FASN inhibition, γδ T cells, and CD8+ T-cell function requires further investigation. Does B7-H3 inhibition promote antitumor CD8+ T-cell response by facilitating T-cell recruitment and recovery of effector function, as reported in non-small cell lung cancer by Yonesaka et al?11 In addition, given B7-H3’s expression in multiple stromal and immune cell types, its blockade may affect angiogenesis, fibroblast activation, and cytokine signaling, particularly transforming growth factor beta (TGF-β) and VEGF pathways (figure 1). Finally, although this study focuses on TNBC, similar compensatory metabolic responses may occur in other tumor types. Broadening these investigations could unlock the full therapeutic potential of immune-metabolic combination strategies.
Three key areas warrant further investigation. First, post-treatment biopsies from patients with TNBC receiving B7-H3-targeted therapies are needed to confirm metabolic adaptations and assess risk of recurrence. The long-term safety of sustained FASN inhibition also warrants thorough evaluation, given fatty acid oxidation’s essential role in CD8+ memory T cells, regulatory T cells, and M2 macrophages. Second, the impact of dual inhibition on the broader TME remains to be elucidated. The interplay between FASN inhibition, γδ T cells, and CD8+ T-cell function requires further investigation. Does B7-H3 inhibition promote antitumor CD8+ T-cell response by facilitating T-cell recruitment and recovery of effector function, as reported in non-small cell lung cancer by Yonesaka et al?11 In addition, given B7-H3’s expression in multiple stromal and immune cell types, its blockade may affect angiogenesis, fibroblast activation, and cytokine signaling, particularly transforming growth factor beta (TGF-β) and VEGF pathways (figure 1). Finally, although this study focuses on TNBC, similar compensatory metabolic responses may occur in other tumor types. Broadening these investigations could unlock the full therapeutic potential of immune-metabolic combination strategies.
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🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반
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