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000157608 1001_ $$0P:(DE-He78)a56d7a8e916d458441b5ac9484d73c5d$$aKutscher, Lena$$b0$$eFirst author$$udkfz
000157608 245__ $$aFunctional loss of a noncanonical BCOR-PRC1.1 complex accelerates SHH-driven medulloblastoma formation.
000157608 260__ $$aCold Spring Harbor, NY$$bLaboratory Press$$c2020
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000157608 520__ $$aMedulloblastoma is a malignant childhood brain tumor arising from the developing cerebellum. In Sonic Hedgehog (SHH) subgroup medulloblastoma, aberrant activation of SHH signaling causes increased proliferation of granule neuron progenitors (GNPs), and predisposes these cells to tumorigenesis. A second, cooperating genetic hit is often required to push these hyperplastic cells to malignancy and confer mutation-specific characteristics associated with oncogenic signaling. Somatic loss-of-function mutations of the transcriptional corepressor BCOR are recurrent and enriched in SHH medulloblastoma. To investigate BCOR as a putative tumor suppressor, we used a genetically engineered mouse model to delete exons 9/10 of Bcor (BcorΔE9-10 ) in GNPs during development. This mutation leads to reduced expression of C-terminally truncated BCOR (BCORΔE9-10). While BcorΔE9-10 alone did not promote tumorigenesis or affect GNP differentiation, BcorΔE9-10 combined with loss of the SHH receptor gene Ptch1 resulted in fully penetrant medulloblastomas. In Ptch1+/-;BcorΔE9-10 tumors, the growth factor gene Igf2 was aberrantly up-regulated, and ectopic Igf2 overexpression was sufficient to drive tumorigenesis in Ptch1+/- GNPs. BCOR directly regulates Igf2, likely through the PRC1.1 complex; the repressive histone mark H2AK119Ub is decreased at the Igf2 promoter in Ptch1+/-;BcorΔE9-10 tumors. Overall, our data suggests that BCOR-PRC1.1 disruption leads to Igf2 overexpression, which transforms preneoplastic cells to malignant tumors.
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000157608 7001_ $$0P:(DE-He78)34b3639de467b2c700920d7cbc3d2110$$aOkonechnikov, Konstantin$$b1$$eFirst author$$udkfz
000157608 7001_ $$0P:(DE-He78)adcf3efc31d93c73cbcfa044513c2a93$$aBatora, Nadja$$b2$$eFirst author
000157608 7001_ $$0P:(DE-HGF)0$$aClark, Jessica$$b3
000157608 7001_ $$0P:(DE-HGF)0$$aSilva, Patricia B G$$b4
000157608 7001_ $$0P:(DE-He78)7a849fbc18c1307faf2b3a4f84a62500$$aVouri, Mikaella$$b5
000157608 7001_ $$0P:(DE-He78)6f3ac5e773e94ee6127aaba91db70b25$$avan Rijn, Sjoerd$$b6
000157608 7001_ $$0P:(DE-He78)a4101d4d75f0b7d1f24f67ccbe63164b$$aSieber, Laura$$b7$$udkfz
000157608 7001_ $$0P:(DE-He78)5f5223d7faa01a1e1df8a30d85cff5b0$$aStatz, Britta$$b8$$udkfz
000157608 7001_ $$aGearhart, Micah D$$b9
000157608 7001_ $$aShiraishi, Ryo$$b10
000157608 7001_ $$0P:(DE-He78)e73a0a4fab40344d89d693cbe1df3109$$aMack, Norman$$b11$$udkfz
000157608 7001_ $$aOrr, Brent A$$b12
000157608 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b13$$udkfz
000157608 7001_ $$aGudenas, Brian L$$b14
000157608 7001_ $$aSmith, Kyle S$$b15
000157608 7001_ $$aMercier, Audrey L$$b16
000157608 7001_ $$aAyrault, Olivier$$b17
000157608 7001_ $$aHoshino, Mikio$$b18
000157608 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b19$$udkfz
000157608 7001_ $$avon Hoff, Katja$$b20
000157608 7001_ $$aGraf, Norbert$$b21
000157608 7001_ $$aFleishhack, Gudrun$$b22
000157608 7001_ $$0P:(DE-HGF)0$$aBardwell, Vivian J$$b23
000157608 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan M$$b24$$udkfz
000157608 7001_ $$aNorthcott, Paul A$$b25
000157608 7001_ $$0P:(DE-He78)0ac2bd1a9fb1823a351ee4434d80808b$$aKawauchi, Daisuke$$b26$$eLast author$$udkfz
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