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The natural world has been a rich source of medicinal drugs for many years, from digoxin (found in foxgloves) used to treat cardiac arrythmia to antibiotics such as penicillin (secreted by moulds). For over 40 years, scientists have been asking if bacteria too might synthesize substances of therapeutic value.
Over recent years, histone deacetylase inhibitors (HDACi) – compounds that specifically inhibit a group of enzymes with crucial roles in control of gene function in humans, and have been found to slow the growth of leukaemia cells – have begun to realize the promise as anti-cancer drugs that first drew them to scientists’ attention. The US Food and Drug Administration (FDA) has approved two for clinical use.
However, in a series of clinical trials their effectiveness has been patchy, with not many types of cancer being generally susceptible, and with wide variation from one patient to another. We need to know more about how cells respond to HDACi.
In this regard, it has been a long-standing puzzle that, despite a mountain of evidence that HDACi cause global histone hyperacetylation and extensive disruption of certain aspects of our epigenetic control systems, human cells survive these potential toxins very well, both in the laboratory and in the real world.
A paper published in Epigenetics and Chromatin, provides a possible answer by demonstrating, for the first time, that normal human cells exposed to therapeutic concentrations of two different HDACi, mount a transcription-based survival response.
Read full, original post: Epigenetic survival response suppresses cancer drug toxicity