Doctors and medical professionals will know how hard it is to treat some brain tumours – even if they are surgically removed, zapped by radiation or infiltrated by chemotherapy drugs, they find a way to return. Now a new research that may have found the Achilles’ heel in brain tumour stem cells will prove to be a vital discovery as researchers claim they have been able to disrupt brain tumour stem cells.
According to researchers, the ability of many brain tumors to regenerate can be traced to cancer stem cells that evade treatment and spur the growth of new tumor cells.
Scientists at Washington University School of Medicine claim that there are some brain tumor stem cells that may have an Achilles’ heel. The scientists found that for the cancer tumour to grow, stem cells’ remarkable abilities have to be maintained. They say that they have identified a key player in that maintenance process, which when disrupted, stops the spread of cancer.
“This discovery may help us attack the root of some of the deadliest brain tumors,” said senior author Albert H. Kim, MD, PhD, assistant professor of neurological surgery. “A successful brain cancer treatment will very likely require blocking the tumor stem cells’ ability to survive and replenish themselves.”
Scientists have realized in recent years that some cancer cells in glioblastoma, a deadly form of brain cancer that each year strikes about 18,000 people in the US alone, and other tumors are more resistant to treatment than others. Those same, more defiant cells also are much better at re-establishing cancer after treatment.
“These tumor stem cells are really the kingpins of cancers — the cells that direct and drive much of the harm done by tumors,” said Kim, who treats patients at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.
Kim and his colleagues identified a protein, known as SOX2, that is active in brain tumor stem cells and in healthy stem cells in other parts of the body.
The researchers found that the tumor stem cells’ ability to make SOX2 could be turned up or down via another protein, CDC20. Increasing SOX2 by boosting levels of CDC20 also increased a tumor’s ability to grow once transplanted into mice. Eliminating CDC20, meanwhile, left tumor stem cells unable to make SOX2, reducing the tumor stem cells’ ability to form tumors.
“The rate of growth in some tumors lacking CDC20 dropped by 95 percent compared with tumors with more typical levels of CDC20,” Kim said.
When the scientists analyzed human tumor samples, they found that a subset of patients with glioblastomas that had the highest CDC20 levels also had the shortest periods of survival after diagnosis.
Kim’s lab is exploring methods to block CDC20 in brain tumors, including RNA interference, an approach in which the production of specific proteins is blocked. That general approach is in clinical trials as a therapy for other cancers, viral infections and other illnesses.
The findings are published online in Cell Reports.
