Abstract
Lung adenocarcinoma is the most common subtype of lung cancer today. With the discovery of epidermal growth factor receptor (EGFR) mutations, anaplastic lymphoma kinase (ALK) rearrangements, and effective targeted therapy, personalized medicine has become a reality for patients with lung adenocarcinoma. Here, we review potential additional targets and novel therapies of interest in lung adenocarcinoma including targets within the cell surface (receptor tyrosine kinases EGFR, human epidermal growth factor receptor 2, RET, ROS1, mesenchymal–epidermal transition, TRK), targets in intracellular signal transduction (ALK, RAS–RAF–MEK, PI3K–AKT–PTEN, WNT), nuclear targets such as poly-ADP ribose polymerase, heat shock protein 90, and histone deacetylase, and selected pathways in the tumor environment. With the evolving ability to identify specific molecular aberrations in patient tumors in routine practice, our ability to further personalize therapy in lung adenocarcinoma is rapidly expanding.
Highlights
In recent years, we have witnessed a transformation of the treatment paradigm for advanced non-small cell lung cancer (NSCLC)
Clinical trials of targeted therapy have demonstrated major improvements in response, quality of life, and progression-free survival compared to chemotherapy, using epidermal growth factor receptor (EGFR) TKI in EGFR mutant NSCLC and crizotinib in anaplastic lymphoma kinase (ALK ) rearranged NSCLC [2, 3]
Activating mutations are significantly associated with response to EGFR TKIs, with erlotinib, gefitinib, and afatinib established as initial standard therapy
Summary
Division of Medical Oncology, Princess Margaret Cancer Centre, University of Toronto, Toronto, ON, Canada. With the discovery of epidermal growth factor receptor (EGFR) mutations, anaplastic lymphoma kinase (ALK ) rearrangements, and effective targeted therapy, personalized medicine has become a reality for patients with lung adenocarcinoma. We review potential additional targets and novel therapies of interest in lung adenocarcinoma including targets within the cell surface (receptor tyrosine kinases EGFR, human epidermal growth factor receptor 2, RET, ROS1, mesenchymal–epidermal transition, TRK), targets in intracellular signal transduction (ALK, RAS–RAF–MEK, PI3K–AKT –PTEN, WNT), nuclear targets such as poly-ADP ribose polymerase, heat shock protein 90, and histone deacetylase, and selected pathways in the tumor environment. With the evolving ability to identify specific molecular aberrations in patient tumors in routine practice, our ability to further personalize therapy in lung adenocarcinoma is rapidly expanding
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