未经证实:非小细胞肺癌(NSCLC)是世界上最常见的恶性肿瘤之一。Osimertinib是第三代表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI),可有效靶向敏感的表皮生长因子受体突变和外显子20T790M。尽管最初取得了令人印象深刻的结果,获得性抗性(AR)发展迅速,通常在9-13个月内,和抵抗的机制还没有完全理解。在过去的几年里,EGFR-TKI和程序性细胞死亡配体1(PD-L1)抑制剂已被广泛用于治疗晚期肺腺癌患者。
UASSIGNED:在此,我们报告了一名中年女性,根据病理诊断患有肺腺癌。通过下一代测序(NGS)检测到表皮生长因子受体外显子19的缺失。在患者接受了一系列治疗后,包括奥希替尼,鉴定了BTN2A1-BRAF融合。在通过免疫组织化学(IHC)评估PD-L1表达后,患者改用duvalizumab,PD-L1抑制剂,但没有观察到显著的改善。进行NGS和IHC测定以分析在治疗期间获得的活检和血液样品。
未经批准:该病例证实,获得BTN2A1-BRAF融合可能是NSCLC中AR与奥希替尼的一种机制。与IHC中肿瘤组织中PD-L1表达的程度无关,具有敏感表皮生长因子受体突变的患者从PD-L1抑制剂获得的益处最小。我们的病例为治疗该患者人群提供了新的思路。
UNASSIGNED: Non-small cell lung cancer (NSCLC) is one of the most common malignancies in the world. Osimertinib is a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) indicated for NSCLC that effectively targets sensitive epidermal growth factor receptor mutation and exon20 T790M. Despite initially impressive outcomes, acquired resistance (AR) develops rapidly, typically within 9-13 months, and the mechanisms of resistance are not fully understood. Over the past years, EGFR-TKI and programmed cell death-ligand 1 (PD-L1) inhibitors have been widely used to treat for patients with advanced lung adenocarcinoma.
UNASSIGNED: Herein we report a middle-aged female who suffered from lung adenocarcinoma based on the pathological diagnosis. Epidermal growth factor receptor exon 19 deletion was detected by next-generation sequencing (NGS). After the patient underwent a series of treatments, including osimertinib, BTN2A1-BRAF fusion was identified. After assessing PD-L1 expression by immunohistochemistry (IHC), the patient was switched to duvalizumab, a PD-L1 inhibitor, but no significant improvements were observed. NGS and IHC assays were conducted to analyze the biopsy and blood samples obtained during treatment.
UNASSIGNED: This
case substantiates that the acquisition of BTN2A1-BRAF fusion potentially serves as a mechanism of AR to osimertinib in NSCLC. Patients with sensitive epidermal growth factor receptor mutation derive minimal benefit from PD-L1 inhibitors irrespective of the degree of PD-L1 expression in the tumor tissue in IHC. Our
case provides a new train of thought for treating this patient population.