Brain Tumor Cure: Brain Cancer 'Achilles Heel' Disrupted With Protein In Glioblastomas

First Posted: Jun 15, 2015 06:08 PM EDT

Researchers at the Washington University School of Medicine in St. Louis have discovered that brain tumors may be disrupted by destroying their stem cell growth.

When it comes to these types of tumors, health officials oftentimes surgically remove the tumor, including healthy material surrounding the tissues. However, this may result in loss of brain function, and can make surgery particularly dangerous.

New findings reveal just how essential brain tumor stem cells are to the reproduction of cancer and how interrupting them may potentially reduce the spread of cancerous cells.

For the study, researchers zeroed in on glioblastoma, which is estimated to affect around 18,000 people in the United States every year. However, survival rates are rather short at just 15 months long. Only an estimated 30 percent of patients survive for more than two years, making this type of cancer 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," Albert H. Kim, assistant professor of neurological surgery at the Washington University School of Medicine in St. Louis, said in a news release.

Furthermore, stem cells found in glioblastomas and other cancers are highly resistant to cancer treatments including chemotherapy, radiation and surgery.

However, researchers pinpointed the protein SOX2, which they discovered was active in brain tumor stem cells and healthy stem cells throughout the body, too. Human tumor samples of patients with glioblastomas also held the highest CDC20 levels with the shortest survival rates. However, taking CDC20 away lowered the 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 concluded.

More information regarding the findings can be seen via the journal Cell Reports.

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