The paper presents an overview of molecular seminar proceedings held at the Divas United States. Researchers are trying to use chemical genetics to find new pathways and explanations for redundant networks. The aim is to use intermolecular inhibitors to change the protein function and examine the roles of the target protein. It is a search for new medicine by identifying druggable targets. This approach is crucial since it will create a platform for testing of different types of molecular modeling. This study is particularly important because it provides an explanation why cancer is resistant to various kinds of treatment. It looks into elements that enhance drug resistance such as drug target alteration. At the initial stage of the disease, a patient‘s body is receptive to the treatment. However, research shows that with time cancer becomes resistant.DNA mutation along with other metabolic changes are some of the ways that cancerous tumors grow immune. Besides resistance can also result from a decline in drug activation. There is evidence that even the slightest form of alteration in the apoptosis proteins can cause drug resistance. Some detoxifying enzymes meant to prevent the damage of the cellular macromolecules from harmful compounds influences the drug activation process. These enzymes can promote drug resistance by inhibiting the mitogen-activated protein kinase (MAPK) pathway. It is also responsible for direct detoxification of the drugs.
Another area to look out for is anything that can trigger adverse modification at the site of the enzyme expression levels. The proposal is to use multiple therapies approaches as the treatment for cancer patients. It is because the various methods have higher chances of counteracting the increased cases of drug resistance. It is also important that other studies concentrate on finding treatment for eliminating progenitor cells that are the leading cause of cancer relapse.
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