基于 DNA 超分子水凝胶的保护性 NK 细胞储库用于增强三阴性乳腺癌治疗
Protective NK Cell Reservoir Based on DNA Supramolecular Hydrogel for Enhanced Triple-Negative Breast Cancer Therapy.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Evaluating the Tumor Burden, Histological Changes, and Immune Landscape of Breast Cancer Post-neoadjuvant Chemotherapy: Insights From 50 Cases.
Evaluating the Tumor Burden, Histological Changes, and Immune Landscape of Breast Cancer Post-neoadjuvant Chemotherapy: Insights From 50 Cases.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
乳腺癌是一种异质性疾病,对新辅助化疗(NACT)的反应各异。评估NACT后乳腺癌标本的组织病理学和免疫变化对于理解治疗反应和指导进一步管理至关重要。
本研究旨在利用残余肿瘤负荷(RCB)指数评估肿瘤负荷,检查组织学改变,通过TIL(肿瘤浸润淋巴细胞)(TILs)评估免疫活性,并通过Ki-67表达分析NACT后乳腺癌标本中的增殖能力。对50例NACT后改良根治术(MRM)标本进行了横断面研究。组织病理学分析包括肿瘤消退变化、间质和细胞改变以及淋巴结受累。通过量化TILs评估免疫反应,并使用Ki-67指数测量增殖。对临床病理参数、TILs和Ki-67表达之间进行了统计相关性分析。39例(78%)检测到残留病灶,11例(22%)无残留病灶。在39例有残留病灶的病例中,大多数被分类为RCB II(22例,56%),16例(41%)被分类为RCB III,1例(3%)被分类为RCB I。NACT后常见的组织学变化包括31例(62%)纤维化、19例(38%)坏死和16例(32%)泡沫状组织细胞浸润。
与良性细胞相比,恶性上皮细胞更常表现出泡沫状细胞质(16例(41%)vs. 2例(5%);p=0.0003)、深染细胞核(26例(67%)vs. 6例(15%);p=0.0001)和显著核仁(26例(67%)vs. 4例(10%);p=0.0001)。在39例残留病灶病例中,20例(51%)观察到低TIL和高Ki-67表达,而12例(32%)显示高TIL和低Ki-67。高TIL和高Ki-67的残留肿瘤(4例,10%)以及低TIL和低Ki-67(3例,8%)较少见。TIL水平与Ki-67表达之间存在显著的负相关关系(p=0.0002),因为低TIL的肿瘤更可能具有高Ki-67表达(20例,51%),而高TIL的肿瘤更常表现为低Ki-67表达(12例,32%)。NACT后对肿瘤负荷、免疫景观和增殖的评估提供了有价值的预后见解。将RCB、TILs和Ki-67整合到常规病理评估中可能有助于患者分层并指导个性化治疗策略。需要进一步的大规模研究来验证这些发现并改善乳腺癌管理中的治疗决策。
Breast cancer is a heterogeneous disease with variable responses to neoadjuvant chemotherapy (NACT). Evaluating the histopathological and immune changes in post-NACT breast cancer specimens is crucial for understanding treatment response and guiding further management.
This study aims to assess tumor burden using the Residual Cancer Burden (RCB) index, examine histological alterations, evaluate immune activity through tumor-infiltrating lymphocytes (TILs), and analyze proliferative capacity via Ki-67 expression in post-NACT breast cancer specimens. A cross-sectional study of 50 modified radical mastectomy (MRM) specimens post-NACT was conducted. The histopathological analysis included tumor regression changes, stromal and cellular alterations, and nodal involvement. Immune response was assessed by quantifying TILs, and proliferation was measured using the Ki-67 index. Statistical correlations were made between clinicopathological parameters, TILs, and Ki-67 expression. Residual disease was detected in 39 cases (78%), and 11 cases (22%) had no residual disease. Among the 39 cases with residual disease, the majority were classified as RCB II (22 cases, 56%), 16 cases (41%) were classified as RCB III, and one case (3%) was classified as RCB I. Common histological changes post-NACT included fibrosis in 31 cases (62%), necrosis in 19 cases (38%), and infiltration by foamy histiocytes in 16 cases (32%).
Malignant epithelial cells more frequently exhibited foamy cytoplasm (16 cases (41%) vs. two cases (5%); p=0. 0003), hyperchromatic nucleus (26 cases (67%) vs. six cases (15%); p=0. 0001), and prominent nucleoli (26 cases (67%) vs. four cases (10%); p=0. 0001) compared to benign cells. Among the 39 cases with residual disease, low TIL and high Ki-67 expression were observed in 20 cases (51%), while 12 cases (32%) showed high TIL and low Ki-67. Residual tumors with high TIL and high Ki-67 (four cases, 10%) and low TIL and low Ki-67 (three cases, 8%) were less common.
A significant inverse relationship was found between TIL levels and Ki-67 expression (p=0. 0002), as tumors with low TIL were more likely to have high Ki-67 expression (20 cases, 51%), whereas those with high TIL more frequently exhibited low Ki-67 expression (12 cases, 32%). Post-NACT evaluation of tumor burden, immune landscape, and proliferation provides valuable prognostic insights. Integrating RCB, TILs, and Ki-67 into routine pathological assessment may aid patient stratification and guide personalized treatment strategies.
Further large-scale studies are needed to validate these findings and improve therapeutic decision-making in breast cancer management.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。