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In cancer cells, where normal regulation of gene expression breaks down, the oncogenes are activated via hypomethylation and tumor suppressors are silenced via hypermethylation. Similarly, in drug resistance development, it has been suggested that epigenetic modifications can result in the activation and overexpression of pro-drug resistance genes.
This protein stimulates the growth of cancer cells which are drug-resistant. [12] MicroRNAs have also been shown to affect acquired drug resistance in cancer cells and this can be used for therapeutic purposes. [13] Malaria in 2012 has become a resurgent threat in South East Asia and sub-Saharan Africa, and drug-resistant strains of Plasmodium ...
When tackling endocrine resistance in breast cancer, the current strategies are focused around combining hormonal agents with drugs targeting several escape pathways, as outlined in the mechanisms of endocrine resistance section. The aim is to block all the tumor survival escapes.
Multidrug resistance in cancer cells is thought to be the primary reason for the poor efficacy of cancer chemotherapy. Drug resistance is due to expression of the gene MDR-1. These gene codes for membrane-bound proteins called ABC transporters. One example of an ABC transporter is P-glycoprotein (P-gp).
In the cancer disease state, the interaction of PD-L1 on the tumor cells with PD-1 on a T-cell reduces T-cell function signals to prevent the immune system from attacking the tumor cells. [9] Use of an inhibitor that blocks the interaction of PD-L1 with the PD-1 receptor can prevent the cancer from evading the immune system in this way. [9]
Drug resistance, such as antimicrobial resistance or antineoplastic resistance, may make the first-line drug ineffective, especially in case of multidrug-resistant pathogens and tumors. Such an alternative may be outside of extant regulatory requirements or medical best practices, in which case it may be viewed as salvage therapy .
Another remaining question surrounding CDK inhibitors as a therapy is if certain cancers will evade or be resistant to treatment. One study showed that 20% of the patients being treated for metastatic ER+ HER2-breast cancer did not respond at all to treatment with a CDK4/6 inhibitor due to preexisting mutations allowing the cancer cells to continue proliferating despite treatment with the drug ...
Polymer-drug conjugates are drug molecules held in polymer molecules, which act as the delivery system for the drug. Polymer drugs have passed multidrug resistance (MDR) testing and hence may become a viable treatment for endocrine-related cancers. A cocktail of pendant drugs could be delivered by water-soluble polymer platforms.