A new discovery has been made that the steroid dexamethasone may play a key role in inhibiting the growth of a type of prostate cancer that was previously resistant to medications.
One of the studies senior authors, Dr Elemento at Cornell Medicine, says that prostate cancer is usually linked to mutations and over-expression within a gene known as “ERG” – which is resistant to drugs. Statistically, mutations in ERG are very common in prostate cancer sufferers, and are one of the leading correlations in its incidence. Targeting it with drugs has proven elusive.
“It’s like match-making between drugs and mutations,” says Elemento.
Kaitlyn Gayvert, doctoral candidate and research assistant of Elemento’s, whom Forbes recently recognized on its top list of “30 Under 30”, created the computational method that discovered dexamethasone as a primary candidate for inhibiting cancer activity initiated by mutations in the ERG gene. Whilst dexamethasone is usually interchangeable with prednisone clinically, the computational algorithm developed by Gayvert did not predict prednisone to produce the same therapeutic effect.
Further laboratory experiments within a prostate cancer cell line confirmed the results of the modelling, verifying that dexamethasone inhibited the mutation’s negative effects – notably cell migration and invasion.
Interestingly, upon further examination it was also found that dexamethasone may serve as a preventative against prostate cancer. A study examining incidence of prostate cancer in men found that those who consumed dexamethasone regularly were less likely in the future to develop the genetic mutations in ERG.
Whilst further research is required to confirm these findings, dexamethasone or other drugs that act via a similar mechanism may soon be used in clinical settings to potentially help prevent prostate cancer, or at the very least treat those who have mutations within their ERG genes.
Source: Cornell News