Potential therapeutic molecular targets for better outcomes for patients with lung cancer

Abstract

Lung cancer is the leading cause of death among all types of cancers in the U.S. and worldwide. Although more treatments have continuously been made over the past 30 years, the prognosis remains the same. This is mainly due to the late stage of the cancer at diagnosis and the eventual development of resistance seen in many types of cancer. The introduction of targeted therapies represents a major advancement in the treatment of tumor progression and an avenue to target its mechanisms of resistance. These agents are a novel therapeutic approach targeting specific molecules aberrantly expressed in these cells and through these mechanisms, alter the internal environment of the tumor cells. In this article, we present a critical discussion of the current clinical standards of treating non-small cell lung cancer (NSCLC), signal pathways of how these tumors acquire resistance, potential drug targets for these pathways, and the role heat shock proteins (HSP) play in NSCLC. Targeting HSP, phosphatidylinositol-3-kinase pathway anomalies, multidrug resistance protein 1 overexpression, and using these therapies to examine possible cooperative properties to resensitize tumor cells to chemotherapy or apoptosis are a worthwhile therapeutic direction. This is because some therapies may play a role as an adjuvant, while others may have a direct role in inducing the apoptotic effects. Therefore, combination therapeutics are an ideal direction to take in drug discovery. Comprehensive knowledge on current clinical standards of treating NSCLC, treatment resistance, novel drug targets, and the role HSP will allow for repurposing of current drugs on the market or develop completely new gene targets and therapies with more efficacy or a larger therapeutic index.