Feb 27, 2018 3:00 PM


L. Eric Huang, MD, PhD
L. Eric Huang, MD, PhD

In a study published in Acta Neuropathologica, L. Eric Huang, MD, PhD, Huntsman Cancer Institute researcher and associate professor of neurosurgery at the University of Utah, and colleagues report on new findings in the function of an enzyme, IDH1, in the development of gliomas. Gliomas are life-threatening tumors of brain or spinal cord tissue, and this type of tumor affects approximately 25,000 people each year. As changes in IDH1 are found in the vast majority of gliomas, understanding the impact of IDH1 enzyme function is critical to advancing research in this disease. 

Two copies of every gene are present in our cells, one from each parent. The study team, led by Huang, showed that the most common change in the IDH1 gene, appears to suppress tumor-forming activity—but only when it is present in one copy. The study also showed that the second copy of the gene must be normal (wild-type) for the mutant IDH1 copy to suppress cancer-like growth. “This study is the first to demonstrate that IDH1 mutation, the most common form of genetic changes in brain tumor, is counterintuitively inhibitory to tumor growth and therefore beneficial to patients,” says Huang.

According to Huang, the findings support the clinical observation that brain tumor patients with IDH1 mutations generally live longer than those without. However, they may still have poor outcomes because subsequent, additional changes to either copy of the IDH1 gene appear to abolish the suppressive activity and promote tumor growth. Huang believes the next step is to prevent such changes for therapeutic intervention of brain tumors.

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