ӳ��ý

Bead-based profiling of tyrosine kinase phosphorylation identifies SRC as a potential target for glioblastoma therapy.

Du J, Bernasconi P, Clauser KR, et al. Bead-based profiling of tyrosine kinase phosphorylation identifies SRC as a potential target for glioblastoma therapy. Nat Biotechnol. 2009;27(1):77-83. doi:10.1038/nbt.1513

Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domain.

Lee JC, Vivanco I, Beroukhim R, et al. Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domain. PLoS Med. 2006;3(12):e485. doi:10.1371/journal.pmed.0030485

Integrative functional genomics identifies RINT1 as a novel GBM oncogene.

Quayle SN, Chheda MG, Shukla SA, et al. Integrative functional genomics identifies RINT1 as a novel GBM oncogene. Neuro Oncol. 2012;14(11):1325-31. doi:10.1093/neuonc/nos246

An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma.

Rheinbay E, Suvà ML, Gillespie SM, et al. An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma. Cell Rep. 2013;3(5):1567-79. doi:10.1016/j.celrep.2013.04.021

Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas.

Wang P, Dong Q, Zhang C, et al. Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas. Oncogene. 2013;32(25):3091-100. doi:10.1038/onc.2012.315

The somatic genomic landscape of glioblastoma.

Brennan CW, Verhaak RGW, McKenna A, et al. The somatic genomic landscape of glioblastoma. Cell. 2013;155(2):462-77. doi:10.1016/j.cell.2013.09.034

ZFHX4 interacts with the NuRD core member CHD4 and regulates the glioblastoma tumor-initiating cell state.

Chudnovsky Y, Kim D, Zheng S, et al. ZFHX4 interacts with the NuRD core member CHD4 and regulates the glioblastoma tumor-initiating cell state. Cell Rep. 2014;6(2):313-24. doi:10.1016/j.celrep.2013.12.032

Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.

Suvà ML, Rheinbay E, Gillespie SM, et al. Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells. Cell. 2014;157(3):580-94. doi:10.1016/j.cell.2014.02.030

Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1.

Verhaak RGW, Hoadley KA, Purdom E, et al. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. Cancer Cell. 2010;17(1):98-110. doi:10.1016/j.ccr.2009.12.020

Whole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolution.

Kim H, Zheng S, Amini SS, et al. Whole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolution. Genome Res. 2015;25(3):316-27. doi:10.1101/gr.180612.114