Published Paper Details:

Cancer is still a deadly disease around the world. Right now, conventional cancer treatments and modern immunotherapies are not specifically designed to target tumors. They struggle to tell the difference between cancer cells and healthy cells, which results in many unwanted side effects. Recent developments in nanotechnology, along with our improved understanding of cancer biology and Nano-bio interactions, have led to the creation of various Nano carriers. These Nano carriers aim to boost the effectiveness of cancer drugs while lowering the side effects by targeting tumor tissue, cells, or organelles specifically. However, most Nano carriers lack hierarchical targeting ability. Their effectiveness is often reduced due to poor tumor accumulation, ineffective cellular uptake, or incorrect subcellular localization. This review discusses current and future strategies for designing cancer Nano medicines that target tumor tissue, cells, and organelles. It also highlights recent progress in hierarchical targeting technologies that can combine these three targeting stages to improve treatment results. Finally, we touch on the challenges and future possibilities for bringing cancer Nano medicines into clinical use. The major modalities of antitumor drug resistance may be grouped into at least five categories: decreased drug influx, increased drug efflux predominantly via ATP-driven extrusion pumps frequently of the ATP-binding cassette (ABC) superfamily, activation of DNA repair, metabolic modification and detoxification as well as inactivation of apoptosis pathways with parallel activation of anti-apoptotic cellular defense modalities (2009). Members of the ABC superfamily including P-glycoprotein (P-gp/ABCB1), multidrug resistance proteins (MRPs/ABCC) and breast cancer resistance protein (BCRP/ABCG2) function as ATP- driven drug efflux transporters, which form a unique defense against chemotherapeutics and numerous endo- and exotoxins. These pumps significantly decrease the intracellular concentration of a multitude of endogenous and exogenous cytotoxic agents which are structurally and mechanistically distinct, thereby result-ing in MDR.