The study conducted by researchers at the University of New Hampshire is published in the journal
For the study, the researchers focused on the epigenetic (which is the study of how DNA is opened and closed to allow certain genes to be expressed or encoded) regulation of WM cancer cells. Each protein has a specific function like writing, reading, interpreting or erasing the genetic code.
The researchers focused on two epigenetic readers proteins- bromodomain and extraterminal (BET) which are involved in pathological conditions including cancer. By using drugs to target these proteins can block the gene expression that regulates cancer cells by slowing and stopping their growth.
In the lab, WM cancer cells were treated with the BET inhibitors JQ-1 and I-BET-762 which reduced the growth of the WM cells. For both the drugs, dose dependent effect was significant. However, at the highest dose JQ-1 showed the strongest inhibitory effect with 70 percent reduction in cell proliferation.
None of the inhibitors were effective in inducing cell death.
The researchers then added three different drugs, venetoclax, panabinostat, and ibrutinib one at a time in combination with the BET inhibitors (JQ-1 and I-BET-762). Ibrutinib is the only FDA approved therapy specifically for WM patients.
It was found that adding venetoclax or panabinostat to the inhibitors was much more effective than adding ibrutinib. Panobinostat offered the greatest combination therapy. Even though using ibrutinib alone has shown in WM patients, the study suggests that epigenetic targeting is likely to provide a better therapeutic outcome.
WM patients given ibrutinib therapy can benefit from the addition of JQ1 which may enhance the efficacy of ibrutinib.
Source: Medindia