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000119945 0247_ $$2doi$$a10.1016/j.devcel.2014.08.010
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000119945 041__ $$aeng
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000119945 1001_ $$aMille, Frédéric$$b0
000119945 245__ $$aThe Shh receptor Boc promotes progression of early medulloblastoma to advanced tumors.
000119945 260__ $$aCambridge, Mass.$$bCell Press$$c2014
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000119945 520__ $$aDuring cerebellar development, Sonic hedgehog (Shh) signaling drives the proliferation of granule cell precursors (GCPs). Aberrant activation of Shh signaling causes overproliferation of GCPs, leading to medulloblastoma. Although the Shh-binding protein Boc associates with the Shh receptor Ptch1 to mediate Shh signaling, whether Boc plays a role in medulloblastoma is unknown. Here, we show that BOC is upregulated in medulloblastomas and induces GCP proliferation. Conversely, Boc inactivation reduces proliferation and progression of early medulloblastomas to advanced tumors. Mechanistically, we find that Boc, through elevated Shh signaling, promotes high levels of DNA damage, an effect mediated by CyclinD1. High DNA damage in the presence of Boc increases the incidence of Ptch1 loss of heterozygosity, an important event in the progression from early to advanced medulloblastoma. Together, our results indicate that DNA damage promoted by Boc leads to the demise of its own coreceptor, Ptch1, and consequently medulloblastoma progression.
000119945 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
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000119945 650_7 $$2NLM Chemicals$$aBoc protein, mouse
000119945 650_7 $$2NLM Chemicals$$aHedgehog Proteins
000119945 650_7 $$2NLM Chemicals$$aImmunoglobulin G
000119945 650_7 $$2NLM Chemicals$$aPTCH protein, human
000119945 650_7 $$2NLM Chemicals$$aPatched Receptors
000119945 650_7 $$2NLM Chemicals$$aPatched-1 Receptor
000119945 650_7 $$2NLM Chemicals$$aPtch1 protein, mouse
000119945 650_7 $$2NLM Chemicals$$aReceptors, Cell Surface
000119945 650_7 $$2NLM Chemicals$$aShh protein, mouse
000119945 650_7 $$0136601-57-5$$2NLM Chemicals$$aCyclin D1
000119945 7001_ $$aTamayo-Orrego, Lukas$$b1
000119945 7001_ $$aLévesque, Martin$$b2
000119945 7001_ $$aRemke, Marc$$b3
000119945 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b4$$udkfz
000119945 7001_ $$aCardin, Julie$$b5
000119945 7001_ $$aBouchard, Nicolas$$b6
000119945 7001_ $$aIzzi, Luisa$$b7
000119945 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b8$$udkfz
000119945 7001_ $$0P:(DE-HGF)0$$aNorthcott, Paul A$$b9
000119945 7001_ $$aTaylor, Michael D$$b10
000119945 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b11$$udkfz
000119945 7001_ $$aCharron, Frédéric$$b12
000119945 773__ $$0PERI:(DE-600)2053870-4$$a10.1016/j.devcel.2014.08.010$$gVol. 31, no. 1, p. 34 - 47$$n1$$p34 - 47$$tDevelopmental cell$$v31$$x1534-5807$$y2014
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