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000127641 0247_ $$2doi$$a10.1016/j.ccr.2014.02.004
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000127641 0247_ $$2pmc$$apmc:PMC4493053
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000127641 0247_ $$2ISSN$$a1878-3686
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000127641 1001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b0$$eFirst author$$udkfz
000127641 245__ $$aGenome sequencing of SHH medulloblastoma predicts genotype-related response to smoothened inhibition.
000127641 260__ $$aCambridge, Mass.$$bCell Press$$c2014
000127641 3367_ $$2DRIVER$$aarticle
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000127641 520__ $$aSmoothened (SMO) inhibitors recently entered clinical trials for sonic-hedgehog-driven medulloblastoma (SHH-MB). Clinical response is highly variable. To understand the mechanism(s) of primary resistance and identify pathways cooperating with aberrant SHH signaling, we sequenced and profiled a large cohort of SHH-MBs (n = 133). SHH pathway mutations involved PTCH1 (across all age groups), SUFU (infants, including germline), and SMO (adults). Children >3 years old harbored an excess of downstream MYCN and GLI2 amplifications and frequent TP53 mutations, often in the germline, all of which were rare in infants and adults. Functional assays in different SHH-MB xenograft models demonstrated that SHH-MBs harboring a PTCH1 mutation were responsive to SMO inhibition, whereas tumors harboring an SUFU mutation or MYCN amplification were primarily resistant.
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000127641 650_7 $$2NLM Chemicals$$aBiphenyl Compounds
000127641 650_7 $$2NLM Chemicals$$aGLI2 protein, human
000127641 650_7 $$2NLM Chemicals$$aHedgehog Proteins
000127641 650_7 $$2NLM Chemicals$$aKruppel-Like Transcription Factors
000127641 650_7 $$2NLM Chemicals$$aLDE225
000127641 650_7 $$2NLM Chemicals$$aMYCN protein, human
000127641 650_7 $$2NLM Chemicals$$aN-Myc Proto-Oncogene Protein
000127641 650_7 $$2NLM Chemicals$$aNuclear Proteins
000127641 650_7 $$2NLM Chemicals$$aOncogene Proteins
000127641 650_7 $$2NLM Chemicals$$aPTCH protein, human
000127641 650_7 $$2NLM Chemicals$$aPatched Receptors
000127641 650_7 $$2NLM Chemicals$$aPatched-1 Receptor
000127641 650_7 $$2NLM Chemicals$$aPtch1 protein, mouse
000127641 650_7 $$2NLM Chemicals$$aPyridines
000127641 650_7 $$2NLM Chemicals$$aReceptors, Cell Surface
000127641 650_7 $$2NLM Chemicals$$aReceptors, G-Protein-Coupled
000127641 650_7 $$2NLM Chemicals$$aRepressor Proteins
000127641 650_7 $$2NLM Chemicals$$aSHH protein, human
000127641 650_7 $$2NLM Chemicals$$aSMO protein, human
000127641 650_7 $$2NLM Chemicals$$aSUFU protein, human
000127641 650_7 $$2NLM Chemicals$$aSmoothened Receptor
000127641 650_7 $$2NLM Chemicals$$aTP53 protein, human
000127641 650_7 $$2NLM Chemicals$$aTumor Suppressor Protein p53
000127641 650_7 $$0EC 2.7.1.-$$2NLM Chemicals$$aPhosphatidylinositol 3-Kinases
000127641 650_7 $$0EC 2.7.11.1$$2NLM Chemicals$$aProto-Oncogene Proteins c-akt
000127641 650_7 $$0EC 2.7.7.49$$2NLM Chemicals$$aTERT protein, human
000127641 650_7 $$0EC 2.7.7.49$$2NLM Chemicals$$aTelomerase
000127641 650_7 $$0EC 3.6.1.-$$2NLM Chemicals$$aDDX3X protein, human
000127641 650_7 $$0EC 3.6.4.13$$2NLM Chemicals$$aDEAD-box RNA Helicases
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000127641 7001_ $$aCollins, V Peter$$b63
000127641 7001_ $$aKieran, Mark W$$b64
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000127641 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b74$$eLast author$$udkfz
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