Annibali, Daniela
Whitfield, Jonathan R.
Favuzzi, Emilia
Jauset González, Toni
Serrano, Erika
Cuartas, Isabel
Redondo Campos, Sara
Folch, Gerard
Gonzàlez-Juncà, Alba
Sodir, Nicole M.
Massó Vallés, Daniel
Beaulieu, Marie-Eve
Swigart, Lamorna B.
Mc Gee, Margaret M.
Somma, Maria Patrizia
Nasi, Sergio
Seoane Suárez, Joan
Evan, Gerard I.
Soucek, Laura
2014
Gliomas are the most common primary tumours affecting the adult central nervous system and respond poorly to standard therapy. Myc is causally implicated in most human tumours and the majority of glioblastomas have elevated Myc levels. Using the Myc dominant negative Omomyc, we previously showed that Myc inhibition is a promising strategy for cancer therapy. Here, we preclinically validate Myc inhibition as a therapeutic strategy in mouse and human glioma, using a mouse model of spontaneous multifocal invasive astrocytoma and its derived neuroprogenitors, human glioblastoma cell lines, and patient-derived tumours both in vitro and in orthotopic xenografts. Across all these experimental models we find that Myc inhibition reduces proliferation, increases apoptosis and remarkably, elicits the formation of multinucleated cells that then arrest or die by mitotic catastrophe, revealing a new role for Myc in the proficient division of glioma cells. Myc has been implicated in the development of multiple types of cancer. Here, the authors explore the therapeutic potential and mechanism of action of Myc inhibition in mouse and human models of glioblastoma, an aggressive type of tumour that is often resistant to conventional therapy.
English
European Commission 205819
Nature communications ; Vol. 5 (August 2014), art. 4632
open access
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