Assuntos
Acrospiroma/genética , Acrospiroma/patologia , Neoplasias da Mama/genética , Proteínas de Ligação a DNA/genética , Rearranjo Gênico/genética , Predisposição Genética para Doença , Proteínas Nucleares/genética , Fatores de Transcrição/genética , Acrospiroma/diagnóstico , Feminino , Humanos , Pessoa de Meia-Idade , TransativadoresRESUMO
We report two cases of lung cancer with histologic transformation from adenocarcinoma to squamous cell carcinoma after gefitinib treatment. Both cases involved advanced lung cancers, initially confirmed as adenocarcinomas with sensitive epidermal growth factor gene mutations. After gefitinib treatment, the second pathologic examination in each case revealed squamous cell carcinoma retaining identical mutations without newly acquired resistance mutations. The underlying mechanism may have been pluripotent tumor cells with divergent differentiation or mixed lung cancer including both adenocarcinomatous and squamous cell carcinomatous components. This report widens the spectrum of histologic evolution as a mechanism underlying the acquisition of drug resistance.
Assuntos
Adenocarcinoma/tratamento farmacológico , Adenocarcinoma/patologia , Antineoplásicos/efeitos adversos , Carcinoma de Células Escamosas/induzido quimicamente , Carcinoma de Células Escamosas/patologia , Transformação Celular Neoplásica/induzido quimicamente , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/patologia , Quinazolinas/efeitos adversos , Antineoplásicos/uso terapêutico , Feminino , Gefitinibe , Humanos , Neoplasias Pulmonares/tratamento farmacológico , Pessoa de Meia-Idade , Quinazolinas/uso terapêuticoRESUMO
Lung cancers presenting two different histologic types are relatively rare. This paper presents a case report of mixed lung cancer comprising mucoepidermoid carcinoma and conventional adenocarcinoma, a combination that has not been reported previously. These two carcinomas showed distinct morphologic and immunohistochemical features. However, gene analysis revealed identical mutations in each component, which indicates they possess a monoclonal origin. Specifically, we identified the same mutation in exon 19 of the epidermal growth factor receptor gene. Molecular analysis further substantiated a monoclonal origin with divergent differentiation, as opposed to the collision of discrete tumors.