Unlocking the Molecular Targets in Non-Small-Cell Lung Cancer and a Nanomedicine-Based Remedy

Lung cancer has the second highest occurrence and lowest survival rate among all cancers and incidence rates are increasing. From the tumor milieu, tumors exude chemokines and cytokines that hassle the pulmonary drug administration hinders the success of treatment. A few mutations lead to generation of lungs cancer. It has prominent levels of mutated genes such as TP53, KRAS, MET, and EGFR. Various molecular pathways involved in causing lung cancer such as PTEN/PI3K/AKT pathway, JAK/STAT pathways, RAF-MEK-ERK, PI3K-AKT-mTOR, and RALGDS-RA, PI3K, AKT, and PI3K/AKT/mTOR pathway. Inhibition of such biological pathway through active targeting, using various biological inhibitors, and blockers could help in treating and recurrence of lungs tumor. The conventional therapeutic modalities concomitant with personalized genomic nanomedicine can have potential in improving treatment regimen. This study explored the different genomic changes that occur due to the prime etiological factors, their reported treatment profile, and nanocarrier mediated therapeutic strategy by targeting tumor microenvironment (TME). Nanocarriers confront multiple obstacles in their journey to the TME therapeutic approach as leaky vasculature, large fenestration, and usually carried off from immune system and phagocytosis process. However, formulators designed a bio-functionalized carrier that enable to evade opsonization, escape immune system, modulate TME, identify reticuloendothelial system, and thus facilitates biological interaction, and enhance cellular uptake.