While the existing HDAC inhibitors did return BRM expression, the effect was short-lived. Once the drugs were taken away, BRM expression decreased.
“The HDAC inhibitors are not the perfect answer, but in principle this tells us we can turn our gene back on. If we can turn the gene back on, it may not be a cure for cancer, but it could slow it down or make it responsive to existing drugs,” Reisman says.
The researchers targeted lung cancer cell lines in particular, although they found similar results in a variety of other cancer cell lines tested. A potential target to treat lung cancer is particularly crucial as the death rate from lung cancer has not changed in 30 years. Newer treatments are much less toxic and extend lives by months, but the same people who died from lung cancer 30 years ago, would still succumb to this disease today.
Targeted therapies have dramatically improved cancer care in recent years, because they thwart the specific genes which drive the development and progress of cancers. They typically have few toxic side effects, unlike traditional chemotherapy, making them more tolerable as a long-term treatment or in combination with other drugs.
“Tumors are not the same from one person to the next, and even the cells within a single tumor are not the same. Giving a single drug or drug combination to 500 people is setting ourselves up for failure, much like a one-size-fits-all clothing store would never succeed,” Reisman says.
“Targeted therapies are now opening the door, because they are ess
Source:University of Michigan Health System