Progression of EGFR Mutant Lung Adenocarcinoma
Objective: Despite recent advances in targeted therapy of epidermal growth factor receptor (EGFR)-mutant lung cancer, narrow therapeutic indices and frequent acquired resistance limit their overall success rate. We reasoned that inhibition of immunologic pathways that support tumor growth and maintenance could represent an alternative treatment approach to provide long-lived tumor destruction in this disease.
Methods: We utilized a genetically engineered bi-transgenic mice mouse model of EGFR mutant lung adenocarcinoma in which mice express a lung-specific mutant human EGFR gene governed by a tetracycline operator (TetO) promoter that is activated by doxycycline administration.
Conclusions: AM play a critical role in the growth and survival EGFR mutant NSCLC and therapeutic strategies targeting AM in have potential to mitigate progression and survival in this disease. There may be an important role for combining immunotherapy-based inactivation of AM with targeted therapy to improve cancer survival.