RESEARCH Chromosome 7 gain and D

with a gain of chromosome 7, and additional epigenetic alterations as key mechanisms triggering a coordinated, but inappropriate, HOX transcriptional program in glioblastoma. Kurscheid et al. Genome Biology (2015) 16:16 DOI 10.1186/s13059-015-0583-7homogenously treated in a clinical trial with combinedSwitzerland Full list of author information is available at the end of the articleBackground Glioblastoma (GBM) is an aggressive brain tumor with a median survival of only 15 months. Despite remarkable efforts targeting prominent pathogenetic biological fea-tures of GBM, efficacy of novel drugs has been disap-pointing and significant gains in overall survival have not been made since the introduction of combined radio-chemotherapy comprising TMZ [1]. GBM are no-torious for their treatment resistance. This has been attributed to the deregulation of major tumor suppress-ing and oncogenic pathways [2], tumor heterogeneity [3], and exhibition of stem cell-like properties by so called tumor stem cells, or glioma initiating cells (GICs) [4]. GICs represent a subpopulation(s) of tumor cells and are believed to, first, give rise to tumor progeny due to their self-renewing capacities, and second, resist radio- and chemotherapy [5,6]. In line with the notion of GICs ’ contribution to treatment resistance, we earlier reported a self-renewal-related, HOX-dominated gene expression signature in GBM as-sociated with significantly worse outcome in patient