Drug resistance is a significant challenge in cancer therapy with cancer cells developing mechanisms to evade the effects of anticancer drugs. In primary resistance cancer cells are inherently insensitive to a particular drug before treatment, whilst acquired resistance occurs when cancer cells initially respond to treatment, but eventually become resistant with treatment time. Genetic alterations, such as oncogenic mutations or amplifications in specific genes, can lead to drug resistance. Epigenetic changes, which affect gene expression without altering the DNA sequence, can also contribute to drug resistance by modifying the activity of genes involved in drug metabolism or response. Drug resistance can occur through multiple mechanisms. Cancer cells can modify the drug target molecules, such as receptors or enzymes, to reduce the drug's binding affinity or effectiveness. Cancer cells acquire genetic mutations that may directly affect these drug targets, or drug transporters, or the DNA repair mechanisms that repair drug damage, rendering the drugs ineffective. In targeted cancer therapies, cancer cells may also evade drug action by activating alternative signalling pathways that bypass the drug's intended target pathway. By utilizing alternative pathways, cancer cells can continue to grow and survive despite the presence of the drug. A major mechanism of drug resistance in cancer involves efflux pumps, proteins located on the cell membrane that actively remove drugs from the inside of cancer cells, thereby reducing drug concentration within cells. Overexpression of efflux pumps, such as such as ATP-binding cassette (ABC) transporters or P-glycoprotein, can result in decreased drug accumulation and resistance. For drugs that lead to DNA damage, cancer cells can upregulate DNA repair mechanisms, enabling them to repair drug-induced DNA damage more efficiently. This repair capacity reduces the effectiveness of DNA-damaging chemotherapy drugs. The tumour microenvironment, consisting of various cell types, blood vessels, and signalling molecules, may also contribute to drug resistance. Factors such as hypoxia (low oxygen levels), nutrient deprivation, and the presence of immune cells can promote drug resistance by creating a protective environment for cancer cells. It is now recognised that tumours can exhibit considerable genetic and phenotypic heterogeneity, meaning that different cancer cells within a tumour can have distinct genetic profiles and drug sensitivities. This heterogeneity can allow some cancer cells to survive and proliferate despite the effects of therapy, leading to drug resistance. Cancer stem cells are also thought to play a role in drug resistance as well as tumour initiation and maintenance. These cells can resist chemotherapy and targeted therapies, potentially leading to disease recurrence. We offer a comprehensive product range of research reagents for investigating drug resistance, including Topoisomerase II alpha antibodies, Topoisomerase II alpha+Topoisomerase II beta antibodies, MRP1 antibodies, MVP antibodies, and MRP2 antibodies. Explore our full drug resistance product range below and discover more, for less. Alternatively, you can explore our MRP Related Proteins, Topoisomerases, and P Glycoproteins product ranges.