Subject(s)
Acrospiroma/genetics , Acrospiroma/pathology , Breast Neoplasms/genetics , DNA-Binding Proteins/genetics , Gene Rearrangement/genetics , Genetic Predisposition to Disease , Nuclear Proteins/genetics , Transcription Factors/genetics , Acrospiroma/diagnosis , Female , Humans , Middle Aged , Trans-ActivatorsABSTRACT
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.
Subject(s)
Adenocarcinoma/drug therapy , Adenocarcinoma/pathology , Antineoplastic Agents/adverse effects , Carcinoma, Squamous Cell/chemically induced , Carcinoma, Squamous Cell/pathology , Cell Transformation, Neoplastic/chemically induced , Lung Neoplasms/chemically induced , Lung Neoplasms/pathology , Quinazolines/adverse effects , Antineoplastic Agents/therapeutic use , Female , Gefitinib , Humans , Lung Neoplasms/drug therapy , Middle Aged , Quinazolines/therapeutic useABSTRACT
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.
