Abstract
Lung cancer continues to be the most common cause of cancer-related mortality in the United States and other developed countries. The most common subtype is non-small cell lung cancer (NSCLC). Within NSCLC, we are discovering remarkable molecular heterogeneity. Most current actionable mutations have been identified in patients with adenocarcinoma histology, but now new mutations are being discovered in squamous cell histology patients as well. This molecular heterogeneity provides an opportunity for clinical trials to exploit various candidate oncogene-addicted pathways in NSCLC. This article focuses on 2 shifting paradigms in NSCLC management: the recent advances in targeted therapy and maintenance treatment.
MeSH terms
-
Antineoplastic Agents / pharmacology
-
Antineoplastic Agents / therapeutic use*
-
Carcinoma, Non-Small-Cell Lung / drug therapy*
-
Carcinoma, Non-Small-Cell Lung / genetics
-
Carcinoma, Non-Small-Cell Lung / pathology*
-
Carcinoma, Non-Small-Cell Lung / secondary
-
Enzyme Activation / drug effects
-
ErbB Receptors / genetics
-
ErbB Receptors / metabolism
-
Gene Expression Regulation, Neoplastic / drug effects
-
Genes, ras / drug effects
-
Humans
-
Immunotherapy / methods
-
Lung / drug effects
-
Lung / metabolism
-
Lung / pathology*
-
Lung Neoplasms / drug therapy*
-
Lung Neoplasms / genetics
-
Lung Neoplasms / pathology*
-
Lung Neoplasms / secondary
-
Molecular Targeted Therapy / methods*
-
Mutation / drug effects
-
Protein-Tyrosine Kinases / genetics
-
Protein-Tyrosine Kinases / metabolism
-
Proto-Oncogene Proteins / genetics
-
Proto-Oncogene Proteins / metabolism
-
Proto-Oncogene Proteins c-met / genetics
-
Proto-Oncogene Proteins c-met / metabolism
Substances
-
Antineoplastic Agents
-
Proto-Oncogene Proteins
-
ErbB Receptors
-
MET protein, human
-
Protein-Tyrosine Kinases
-
Proto-Oncogene Proteins c-met
-
ROS1 protein, human