Patients with glioma are given a better prognosis when their tumor expresses a mutation in a gene called isocitrate dehydrogenase 1 (IDH1). In this international collaborative study led by the Instituto de Salud Carlos III-UFIEC in Madrid, Spain, those IDHI mutations stimulated the expression of TAU.
Then, the presence of TAU acted as a brake for the formation of new blood vessels, which are necessary for the aggressive behavior of the tumors.
"We report that the levels of microtubule-associated protein TAU, which have been associated with neurodegenerative diseases, are epigenetically controlled by the balance between normal and mutant IDH1/2 in mouse and human gliomas," says co-author Maria G. Castro, Ph.D., a professor of neurosurgery and cell and developmental biology at Michigan Medicine.
"In IDH1/2 mutant tumors, we found that expression levels of TAU decreased with tumor progression."
That means levels of TAU could be used as a biomarker for tumor progression in mutant IDH1/2 gliomas, Castro says.
Her team, funded by the National Institutes of Health, collaborated with lead and senior study authors at the Centro de Biología Molecular "Severo Ochoa" and the Instituto de Salud Carlos III-UFIEC, both in Madrid. Those researchers are funded by the Spanish Ministry of Economy and Competitiveness (MINECO) and the Spanish Association Against Cancer (AECC).