一种用于克服非小细胞肺癌治疗中抗原异质性的多靶向 CAR-T 细胞平台
A Multi-Targeting Chimeric Antigen Receptor-T Cell Platform to Overcome Antigen Heterogeneity in the Treatment of Non-Small Cell Lung Cancer.
这些发现支持采用多靶点CAR-T 策略来应对NSCLC及可能其他实体瘤中的抗原异质性。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Subtyping of advanced lung cancer based on PD-L1 expression, tumor histopathology and mutation burden (EGFR and KRAS): a study from North India.
Subtyping of advanced lung cancer based on PD-L1 expression, tumor histopathology and mutation burden (EGFR and KRAS): a study from North India.
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。
免疫检查点抑制剂(PD-L1)治疗晚期非小细胞肺癌(NSCLC)的疗效存在差异。基于PD-L1表达、组织病理学和突变负荷的肿瘤亚型分型对于患者分层和治疗指南的制定是必要的。对VPCI病理科(2018-2021年)诊断的肺癌(n=57)进行了回顾性分析。肿瘤细胞表达的PD-L1(SP263)[低(<1%)、中(1-49%)、高(≥50%)]与组织病理学、微环境、EGFR、KRAS表达进行相关性分析。根据以下因素将患者分为高风险和低风险:i)性别:男性(n=47,30-89岁),女性(n=10,45-80岁);ii)吸烟史:男性26/47(45.61%),女性1/10(10%);iii)肿瘤亚型分型:鳞状细胞癌15/57(26.32%),腺癌6/57(17.54%),NSCLC-未分化24/57(42.10%),腺鳞癌5/57(8.77%),癌肉瘤4/57(7.02%),小细胞癌1/57(1.75%);iv)炎性肿瘤微环境/TILs 44/57(77.1%);iv)PD-L1阳性31/57(54.3%);v)合并EGFR/KRAS阳性。
PD-L1阳性病例显示鳞状/未分化组织病理学,合并EGFR+(9/20,45%)和KRAS+(8/15,53.3%),吸烟+(21/31,67.74%)。PD-L1阴性病例(26/57,45.6%),为EGFR+(2/14,14.28%)和KRAS+(6/19,31.5%)。高风险肺癌亚型显示鳞状/未分化组织病理学、炎性微环境、男性优势、吸烟史、较高的合并PD-L1、KRAS和EGFR阳性率。肺癌亚型分型可在启动PD-L1抑制剂治疗前预测患者的临床缓解/耐药,并可用于指导治疗。
Immune checkpoint inhibitor (PD-L1) therapy of advanced non-small-cell lung cancer (NSCLC) has variable outcomes. Tumor subtypes based on PD-L1 expression, histopathology, mutation burden is required for patient stratification and formulation of treatment guidelines. Lung cancers (n=57) diagnosed at Pathology department, VPCI (2018-2021) were retrospectively analyzed. PD-L1(SP263) expressed by tumor cells [low (<1%), medium (1-49%), high (≥50%)] was correlated with histopathology, microenvironment, EGFR, KRAS expression. Patients were categorized into high and low risk based on their: i) gender: males (n=47, 30-89 years), females (n=10, 45-80 years); ii) smoking history: males 26/47 (45. 61%), females 1/10 (10%); iii) tumor subtyping: squamous cell carcinoma 15/57 (26. 32%), adenocarcinoma 6/57 (17. 54%), NSCLC-undifferentiated 24/57 (42.
10%), adenosquamous carcinoma 5/57 (8. 77 %), carcinosarcoma 4/57 (7. 02%), small cell carcinoma 1/57 (1. 75%); iv) inflammatory tumor microenvironment/TILs 44/57 (77. 1%); iv) PD-L1 positivity-31/57 (54. 3%); v) concomitant EGFR/KRAS positivity. PD-L1positive cases showed squamous/undifferentiated histopathology, concomitant EGFR+ (9/20, 45%) and KRAS+ (8/15, 53. 3%), smoking+ (21/31,67. 74%). PD-L1 negative cases (26/57, 45.
6%), were EGFR+ (2/14, 14. 28%) and KRAS+ (6/19, 31. 5%). The high-risk lung cancer subtypes show squamous/undifferentiated histopathology, inflammatory microenvironment, male preponderance, smoking history, higher concomitant PD-L1, KRAS and EGFR positivity. Lung cancer subtyping can predict clinical response/resistance of patients prior to initiation of PD-L1 inhibitor therapies and can be used to guide therapy.
MEMBER ACCOUNT
登录成功会直接打开下一页。