Objective: To analyze the clinical data of a case of lung adenocarcinoma with Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) resistance transforming into sarcoma, and to conduct a literature review to improve the understanding of the resistance mechanism. Histological transformation is a unique form of acquired resistance of EGFR-TKIs in non-small cell lung cancer (NSCLC). Thereinto, the transformation of small cell carcinoma is more common, and the transformation of sarcoma is rarely reported. Methods: Clinicopathological data on the treatment process, pathological features, and clinical outcome of the patient with EGFR-TKIs-resistance lung adenocarcinoma transforming into sarcoma were collected. The literature was reviewed to analyze the pathogenetic mechanism for sarcomatoid carcinoma or sarcoma transformation after drug resistance of adenocarcinoma, as well as the clinical characteristics of the patients and the corresponding therapeutic schemes. Results: We reported a patient with lung adenocarcinoma who developed EGFR-T790M mutation after first-line treatment with icotinib and sarcoma transformation after second-line treatment with almonertinib. Chemotherapy, radioactive particle implantation, antiangiogenic therapy and immunotherapy were followed, but the results were unsatisfactory. There was no report of EGFR-TKIs-resistant lung adenocarcinoma transforming into sarcoma. Among the 14 reports of adenocarcinoma transforming into sarcomatoid carcinoma, 8 cases had EGFR mutation, 3 cases had ALK mutation, 2 cases had ROS1 mutation, and 1 case had no asscoiated sensitive mutation. The median survival of 14 patients with adenocarcinoma transforming to sarcomatoid carcinoma was only 3 months. Conclusions: Sarcoma transformation can be one of the forms of drug resistance in patients with lung adenocarcinoma with EGFR-TKIs. The prognosis of patients with adenocarcinoma after transformation into sarcoma is poor.
目的： 组织学转化是非小细胞肺癌（non-small cell lung cancer，NSCLC）表皮生长因子受体（epidermal growth factor receptor，EGFR）-酪氨酸激酶抑制剂（tyrosine kinase inhibitor，TKI）耐药的一种形式，其中以小细胞癌转化多见，肉瘤转化鲜有报道。本文报道1例肺腺癌EGFR-TKI耐药后转化为肉瘤的临床资料，并复习文献，以提高对该耐药机制的认识。 方法： 收集该例肺腺癌EGFR-TKI耐药后肉瘤转化患者的诊治过程、病理特征、临床转归等资料，并检索文献，对腺癌耐药后肉瘤样癌/肉瘤转化的发生机制、患者的临床特点以及治疗方案等进行分析。 结果： 本例患者接受埃克替尼一线治疗后出现EGFR-T790M突变，二线使用阿美替尼治疗后出现肉瘤转化，随后行化疗、放射性粒子植入、抗血管生成治疗及免疫治疗等，效果均不理想。检索文献未见EGFR-TKI耐药肺腺癌转化为肉瘤的相关报道，14例腺癌转化为肉瘤样癌的相关报道中，8例伴EGFR突变，3例伴ALK突变，2例ROS1突变，1例未见相关敏感突变；14例患者转为肉瘤样癌后中位存活时间仅为3个月。 结论： 肉瘤组织转化可为肺腺癌患者EGFR-TKI治疗后耐药的形式之一，腺癌患者肉瘤样转化后预后较差。.