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Researchers discover the action mechanism of an antitumor drug to treat glioblastoma

Structure of EGFR.

Structure of EGFR.

Professor Modesto Orozco, from the Department of Biochemistry and Molecular Biomedicine of the Faculty of Chemistry of the UB.

Professor Modesto Orozco, from the Department of Biochemistry and Molecular Biomedicine of the Faculty of Chemistry of the UB.

02/05/2019

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Glioblastoma is a type of brain tumor with no cure, usually associated with mutations in the epidermal growth factor receptor (EGFR). The main EGFR mutation found in this tumor –known as EGFRvlll- is treated with the antibody mAb806, a drug developed by the Ludwig Institute for Cancer Research (United States) about twenty years ago, although its action mechanism was unknown. Now, a new study published in the journal Proceedings of the National Academy of Science (PNAS) reveals for the first time –the action mechanism of this antibody on the mutated EGFR receptor.

 

The results of the study, which open new pathways for the treatment of cancer, suggest the antibody mAb806 could be used in many tumours in which EGFR has mutated and not only in a specific mutation –like researchers believed so far. The study counts on the participation of experts from the University of Barcelona, the Institute for Research in Biomedicine (IRB Barcelona), Stockholm University (Sweden), and the University of California (United States), among other institutions.


Moreover, the scientific team proved that, even if EGFR has not mutated yet, it can be treated to make it sensitive to the protocol with the antibody mAb806. “These findings provide the rational basis to conduct anti-EGFR therapies combined with antibodies and kinase inhibitors, instead of blind testing them, as it has happened so far”, notes Modesto Orozco, professor at the Department of Biochemistry and Molecular Biology at the Faculty of Chemistry of the UB, head of the Molecular Modelling and Bioinformatics Lab at IRB Barcelona and member of the Bioinformatics Barcelona platform (BIB).

 

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