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upstart writes:

Researchers discover novel way to inhibit key cancer driver, other mutated genes:

CU Boulder researchers have discovered a new way to inhibit the most commonly mutated gene underlying human tumor growth, opening the door to new therapeutic strategies for cancer and a host of other diseases.

The discovery, published April 5 in the journal Cell Reports, marks an important step forward in the decades-long quest to target transcription factors (TFs), a notoriously hard-to-block class of proteins which, when mutated or dysregulated, can disrupt cell function and drive illness.

"This class of proteins represents one of the most high-impact therapeutic targets in biomedicine," said senior author and biochemistry Professor Dylan Taatjes. "We provide a completely new strategy for blocking transcription factor function that could have broad applications to many diseases, including and beyond cancer."

[...] "A decades-long goal has been to target drug transcription factors directly," said Taatjes. "Here we have found a way to get the functional equivalent without actually targeting the transcription factor but Mediator instead. And, importantly, this does not negatively affect other transcription factors in the cell."

Taatjes stressed that the work is a proof-of-concept study, and that much more research must be done before such a strategy could become implemented in the clinic.

Ultimately, he said the approach could be applied to many other TFs that have been implicated in disease, opening the door to new treatment strategies for everything from heart disease to neurological disorders.

Journal Reference:
Benjamin L. Allen et al, Suppression of p53 response by targeting p53-Mediator binding with a stapled peptide, Cell Reports (2022). (DOI: 10.1016/j.celrep.2022.110630)

Original Submission