In glioblastoma multiforme, the most common adult primary brain tumor, the glycolytic enzyme hexokinase 2 facilitates growth and therapeutic resistance.

Gliomas are the most common primary brain tumors in children and adults. We recently identified frequent alterations in chromatin remodelling pathways including recurrent mutations in H3F3A and mutations in ATRX (α-thalassemia/mental-retardation-syndrome-X-linked) in pediatric and young adult glioblastoma (GBM, WHO grade IV astrocytoma). H3F3A mutations were specific to pediatric high-grade gliomas and identified in only 3.4 % of adult GBM. Using sequencing and/or immunohistochemical analyses, we investigated ATRX alterations (mutation/loss of expression) and their association with TP53 and IDH1 or IDH2 mutations in 140 adult WHO grade II, III and IV gliomas, 17 pediatric WHO grade II and III astrocytomas and 34 pilocytic astrocytomas. In adults, ATRX aberrations were detected in 33 % of grade II and 46 % of grade III gliomas, as well as in 80 % of secondary and 7 % of primary GBMs. They were absent in the 17 grade II and III astrocytomas in children, and the 34 pilocytic astrocytomas. ATRX alterations closely overlapped with mutations in IDH1/2 (p < 0.0001) and TP53 (p < 0.0001) in samples across all WHO grades. They were prevalent in astrocytomas and oligoastrocytomas, but were absent in oligodendrogliomas (p < 0.0001). No significant association of ATRX mutation/loss of expression and alternative lengthening of telomeres was identified in our cohort. In summary, our data show that ATRX alterations are frequent in adult diffuse gliomas and are specific to astrocytic tumors carrying IDH1/2 and TP53 mutations. Combined alteration of these genes may contribute to drive the neoplastic growth in a major subset of diffuse astrocytomas in adults.

We present a comprehensive data description for Ks-band measurements of Sgr A*. We characterize the statistical properties of the variability of Sgr A* in the near-infrared, which we find to be consistent with a single-state process forming a power-law distribution of the flux density. We discover a linear rms-flux relation for the flux-density range up to 12 mJy on a timescale of 24 minutes. This and the power-law flux density distribution implies a phenomenological, formally non-linear statistical variability model with which we can simulate the observed variability and extrapolate its behavior to higher flux levels and longer timescales. We present reasons why data with our cadence cannot be used to decide on the question whether the power spectral density of the underlying random process shows more structure at timescales between 25 min and 100 min compared to what is expected from a red noise random process.