Recurrent MET fusion genes represent a drug target in pediatric glioblastoma

  title={Recurrent MET fusion genes represent a drug target in pediatric glioblastoma},
  author={Sebastian Bender and Jan Gronych and Hans-J{\"o}rg Warnatz and Barbara Hutter and Susanne N. Groebner and Marina Ryzhova and Elke Pfaff and Volker Hovestadt and Florian Weinberg and Sebastian Halbach and M. T. N. Kool and Paul A. Northcott and Dominik Sturm and Lynn Margaret Bjerke and Thomas Zichner and Adrian M. St{\"u}tz and Kathrin Schramm and Bingding Huang and Ivo Buchhalter and Michael Heinold and Thomas Risch and Barbara C. Worst and Cornelis M. van Tilburg and Ursula D. Weber and Marc Zapatka and Benjamin Raeder and David Milford and Sabine Heiland and Christof von Kalle and Christopher Previti and Chris Lawerenz and Andreas E Kulozik and Andreas Unterberg and Olaf Witt and Andreas von Deimling and David S. Capper and Nathal{\`e}ne Truffaux and J Grill and Nada Jabado and Astrid Marie Sehested and David Sumerauer and Dorra H’mida-Ben Brahim and Saoussen Trabelsi and Ho Keung Ng and David Zagzag and Jeffrey C. Allen and Matthias A. Karajannis and Nicholas G. Gottardo and Chris V. Jones and Jan O. Korbel and Sabine S. Schmidt and Stephan Wolf and Guido Reifenberger and J{\"o}rg Pd Dr. Felsberg and Benedikt Brors and Christel Herold-Mende and Hans R. Lehrach and Tilman Brummer and Andrey Korshunov and Roland Eils and Marie-Laure Yaspo and Stefan M. Pfister and Peter Lichter and David T. W. Jones},
  journal={Nature Medicine},
Pediatric glioblastoma is one of the most common and most deadly brain tumors in childhood. Using an integrative genetic analysis of 53 pediatric glioblastomas and five in vitro model systems, we identified previously unidentified gene fusions involving the MET oncogene in ∼10% of cases. These MET fusions activated mitogen-activated protein kinase (MAPK) signaling and, in cooperation with lesions compromising cell cycle regulation, induced aggressive glial tumors in vivo. MET inhibitors… CONTINUE READING

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