Kirsi J. Granberg

TL;DR: It is demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and generates an oncogenic protein that promotes tumorigenesis in glioblastoma.

TL;DR: Akt3 is identified as the dominant Akt isoform that robustly stimulates glioma progression and key roles for Akt3 in activating DNA repair pathways are discovered, which led to enhanced survival of human glioblastoma cells following radiation or temozolomide treatment.

TL;DR: This study integrated over 8,000 transcriptomes and 2,000 samples with multilevel genomics of hematological cancers to investigate how immunological features are linked to cancer subtypes, genetic and epigenetic alterations, and patient survival, and validated key findings experimentally.

TL;DR: Small-RNA sequencing of samples from GBM patients demonstrated that both mature products of MIR-491 (miR-491-5p and -3p) are downregulated in tumors compared with the normal brain, and these products are a tumor suppressor gene that coordinately controls the key cancer hallmarks: proliferation, invasion and stem cell propagation.

TL;DR: Evidence is presented that both exogenous IGF BP2 treatment and cellular IGFBP2 overexpression lead to aberrant activation of epidermal growth factor receptor (EGFR), which subsequently activates signal transducer and activator of transcription factor 3 (STAT3) signaling and facilitates EGFR accumulation in the nucleus, thereby deregulating EGFR signaling by two distinct mechanisms.