Histological Transformation to Small Cell Carcinoma of an Adenosquamous Carcinoma of the Lung With Epidermal Growth Factor Receptor Mutation in Exons 20 and 21 After Treatment With Erlotinib: Case Report

L. Fernández-Trujillo, Laura Tapia, Marcela Vallejo, M. Aguirre, J. Lores, L. Sua
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引用次数: 1

Abstract

Lung carcinoma currently represents 1 of the leading causes of death from cancer worldwide and regionally. The molecular identification of sensitive mutations of targeted treatment have changed the strategies of pharmacologic management in non-small cell lung carcinoma. However, mechanisms of resistance have been described, among them the change of histological type to small cell carcinoma. We present the case of a 46-year-old male patient, non-smoker, with a clinical history of a mass in the upper lobe of the right lung and an initial histological diagnosis of adenosquamous carcinoma of the lung, with the presence of mutations for epidermal growth factor receptor (EGFR) in exons 20 (S768I) and 21 (L858R). He received treatment with tyrosine kinase inhibitor (Erlotinib) with good clinical and radiological response. However, 1 year after the start of the medication, he consulted for a progressive onset of constitutional symptoms and respiratory symptoms, with radiographic worsening and new biopsy with a diagnosis of adenosquamous carcinoma with the adenocarcinoma component transformed to small cell carcinoma, with persistence of EGFR mutation. We describe the clinical, radiological, and laboratory characteristics as well as the outcome of this case. To conclude, among the mechanisms of resistance described to the treatment with tyrosine kinase inhibitors in patients with carcinomas with mutated EGFR, the transformation to small cell carcinoma besides being infrequent is particular, requiring a different diagnostic and therapeutic approach.
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厄洛替尼治疗后表皮生长因子受体20和21外显子突变的肺腺鳞癌组织学转化为小细胞癌:病例报告
肺癌目前是全世界和区域癌症死亡的主要原因之一。靶向治疗敏感突变的分子鉴定改变了非小细胞肺癌的药物治疗策略。然而,耐药机制已被描述,其中包括组织学类型向小细胞癌的转变。我们报告一例46岁男性患者,非吸烟者,有右肺上叶肿块的临床病史,最初的组织学诊断为肺腺鳞癌,表皮生长因子受体(EGFR)外显子20 (S768I)和21 (L858R)存在突变。他接受了酪氨酸激酶抑制剂(厄洛替尼)治疗,临床和放射学反应良好。然而,在开始用药1年后,他就诊时发现身体症状和呼吸系统症状进行性发作,影像学恶化,新的活检诊断为腺鳞癌,腺癌成分转化为小细胞癌,并持续存在EGFR突变。我们描述了临床,放射学和实验室的特点,以及这个病例的结果。综上所述,在EGFR突变的癌症患者对酪氨酸激酶抑制剂治疗的耐药机制中,向小细胞癌的转化除了罕见之外是特殊的,需要不同的诊断和治疗方法。
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来源期刊
CiteScore
4.20
自引率
0.00%
发文量
9
审稿时长
8 weeks
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