Akitake Mukasa

TL;DR: The recent confluence of advances in stem cell biology, cell signaling, genome and computational science and genetic model systems have revolutionized understanding of the mechanisms underlying the genetics, biology and clinical behavior of glioblastoma.

TL;DR: Exome sequencing of exomes of 23 initial low-grade gliomas and recurrent tumors resected from the same patients suggests that recurrent tumors are often seeded by cells derived from the initial tumor at a very early stage of their evolution.

TL;DR: It is demonstrated that a paracrine mechanism driven by DeltaEGFR is the primary means for recruiting wtEGFR-expressing cells into accelerated proliferation in vivo, and support the view that a minor tumor cell population can potently drive accelerated growth of the entire tumor mass, and thereby actively maintain tumor cell heterogeneity within a tumor mass.

TL;DR: The results suggest that the clinical use of c-Met kinase inhibitors in combination with either EGFR inhibitors or standard chemotherapeutics might represent a previously undescribed therapeutic approach to overcome the observed chemoresistance in patients with GBMs expressing EGFRvIII.

TL;DR: The findings suggest that a combination of IDH, TERT, and MGMT refines the classification of grade II-IV diffuse gliomas, and patients with TERT mutant-MGMT unmethylated GBM have the poorest prognosis.