决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
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CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
CD8 阳性 T 细胞是预测三阴性乳腺癌新辅助化疗疗效的关键免疫细胞
英文原题：CD8-Positive T-Cells Are Key Immune Cells for Predicting the Therapeutic Effect of Neoadjuvant Chemotherapy in Triple-negative Breast Cancer.
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CD8-Positive T-Cells Are Key Immune Cells for Predicting the Therapeutic Effect of Neoadjuvant Chemotherapy in Triple-negative Breast Cancer.
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研究概要
评估原发肿瘤中 CD8 阳性 TIL 的浸润情况，是预测淋巴结阳性 TNBC 患者 pCR 和改善预后的有用生物标志物。
研究思路结论见上方概要
背景
三阴性乳腺癌（TNBC）患者在新辅助化疗后获得病理完全缓解（pCR）者预后改善。淋巴细胞为主型乳腺癌更可能对新辅助化疗产生应答。在此，我们研究了TNBC患者治疗前活检标本中TIL（肿瘤浸润淋巴细胞）（TILs）与新辅助化疗应答之间的相关性。
方法
采用多光谱免疫荧光标记法检测了52例TNBC患者活检标本中表达免疫细胞谱系表面标志物（CD8、CD4、CD19、CD14、CD11c和CD11b）的免疫细胞浸润水平。
结果
CD8阳性TIL水平在pCR患者中显著更高（p=0.045）。Cox比例风险模型证实，淋巴结受累与较差的无病生存期相关（p=0.008）。在淋巴结阳性TNBC患者中，高水平的CD8阳性TIL与显著延长的无病生存期相关（p=0.018）。
展开英文摘要原文
PATIENTS AND METHODS
The level of infiltration by immune cells expressing immune cell lineage surface markers (CD8, CD4, CD19, CD14, CD11c, and CD11b) in biopsy specimens from 52 patients with TNBC was examined using multispectral immunofluorescent labelling.
RESULTS
The level of CD8-positive TILs was significantly higher in patients with a pCR (p=0.045). The Cox proportional hazard model confirmed that lymph node involvement was associated with poorer disease-free survival (p=0.008). A high level of CD8-positive TILs was related to significantly prolonged disease-free survival in patients with node-positive TNBC (p=0.018).
CONCLUSION
Assessing infiltration by CD8-positive TILs in the primary tumor is a useful biomarker to predict pCR and improved outcome in patients with node-positive TNBC.
论文信息
- 作者
- Uenaka N、Sato E、Horimoto Y、Kawai S、Asaoka M、Kaise H、Yamada K、Ishikawa T
- 第一作者单位
- Department of Breast Surgery and Oncology, Tokyo Medical University, Tokyo, Japan.Japan
- 通讯作者单位
- Department of Pathology (Medical Research Center), Institute of Medical Science, Tokyo Medical University, Tokyo, Japan; sato-e@tokyo-med.ac.jp.Japan
- 期刊
- Anticancer research2024 Oct
- 原文标识
- PubMed 39348963 · DOI 10.21873/anticanres.17281