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Generally speaking, a fully developed cancer can be described as going through two stages: initiation and progression. Here we are going to discuss that changes in "epigenetic modifications" can be associated with both phases. However, before describing specific examples, we will consider the mechanisms by which abnormal histone modification profiles or deregulated activity of related enzymes may actually lead to cancer. Current evidence suggests that this can occur through at least two mechanisms. As one of the best peptide synthesis companies, we consider that histone modifications may affect genome integrity or chromosome segregation by altering gene expression programs, including dysregulation of oncogenes or tumor suppressors, and at a more global level.
It now appears that abnormal common histone modifications profiles are closely related to cancer. Crucially, unlike DNA mutations, cancer-related epigenomic changes may be reversible, opening the possibility that "epigenetic drugs" could have a powerful impact on the treatment regimens of various cancers. In fact, HDAC inhibitors have been found to be particularly effective at inhibiting tumor growth, promoting apoptosis, and inducing differentiation, and at least in part through the reactivation of certain tumor suppressor genes. Additionally, the Food and Drug Administration has recently approved them for the treatment of certain types of cancer, such as T-cell cutaneous lymphoma. Other compounds are currently in Phase II and Phase III clinical trials. Apart from that, a detailed peptide drugs list will be provided by us.
Other enzyme inhibitors of histone modifications such as HMT inhibitors are currently in development. First, we do not fully understand how HDAC inhibitors achieve their efficacy. For example, do they function by modulating the acetylation of histone or non-histone substrates? Second, most HDAC inhibitors are not enzyme specific, that is they inhibit a wide range of different HDAC enzymes. It is unclear whether this would increase their efficacy, or whether developing inhibitors that could target specific HDACs would be therapeutically beneficial. Therefore, when developing new inhibitors such as those targeting HMT, we need to consider whether we should target enzyme-specific inhibitors, enzyme subfamily-specific inhibitors, or pan-inhibitors similar to HDAC inhibitors. Nonetheless, the fact that these drugs are safe and that they do work is very encouraging given the broad target specificity. So the truth is, while there's still a lot to learn about chromatin as a target, "epigenetic" drugs clearly show great promise.
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