Antineoplastic drug resistance refers to the phenomenon when cancer cells adapt and become less responsive or resistant to the effects of antineoplastic drugs, also known as chemotherapy drugs, which are designed to destroy or inhibit the growth of cancer cells. It is a significant challenge in cancer treatment, as it reduces the effectiveness of these drugs, leading to treatment failure and disease progression.
The development of drug resistance in cancer cells can be attributed to various mechanisms. One common mechanism is the overexpression or amplification of drug-efflux transporters, such as P-glycoprotein, which actively pump the drugs out of the cancer cells, reducing their intracellular concentration. Another mechanism involves alterations in drug targets, such as genetic mutations or modifications in the targeted proteins, making them less susceptible to the effects of the drugs.
Drug resistance can also arise due to changes in cellular signaling pathways, DNA repair mechanisms, or the activation of survival pathways, which collectively contribute to the survival and proliferation of cancer cells despite the presence of the antineoplastic drugs.
Antineoplastic drug resistance poses a significant obstacle in cancer treatment and limits the effectiveness of chemotherapy. Overcoming this resistance requires the development of innovative treatment strategies, such as combination therapies, targeted therapies, immunotherapies, or the use of drug-sensitizing agents to restore drug sensitivity in resistant cancer cells. Understanding the mechanisms underlying antineoplastic drug resistance is crucial for the design of effective therapeutic approaches to combat cancer and improve patient outcomes.
