Some types of brain tumors are extremely resistant to brain tumors, but researchers may have discovered their "Achilles' heel."
A team of researchers uncovered a "key player" in the ability for brain tumor stem cells to maintain their resiliency, Washington University in St. Louis reported. When this process is disrupted, the spread of the cancer is disrupted as well.
"This discovery may help us attack the root of some of the deadliest brain tumors," said senior author Albert H. Kim, 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."
The researchers focused on glioblastoma, which affects about 18,000 people in the United States every year. The average length of survival after diagnosis is 15 months, and only 30 percent of patients survive me for more than two years; this type of cancer is also particularly resistant to treatment.
"These tumor stem cells are really the kingpins of cancers - the cells that direct and drive much of the harm done by tumors," Kim said.
The team pinpointed the protein SOX2, which was shown to be active in brain tumor stem cell as well as healthy stem cells throughout the body. Humor tumor samples showed patients with glioblastomas that had the highest CDC20 levels also tended to have the shortest survival rates.
They discovered tumor stem cells' ability to make SOX2 could be turned up or down with the help of the protein CDC20. Increasing CDC20 also boosted levels of SOX2, which proved to help tumors grow when transplanted into mice. On the other hand, eliminating CDC20 took away tumor 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.
The lab is now working to block CDC20 in brain tumors, in hopes of creating an effective new therapy for deadly glioblastoma and other treatment-resistant cancers.
The findings were published in a recent edition of the journal Cell Reports.
