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n3:pmcid
PMC3583298
bibo:doi
10.1038%2Fonc.2011.379
n5:contains
_:vb21909265 _:vb21909291 _:vb21909286 _:vb21909314
Subject Item
_:vb21909265
rdf:type
n5:Section
dc:title
introduction
n5:contains
_:vb21909284 _:vb21909285 _:vb21909282 _:vb21909283 _:vb21909280 _:vb21909281 _:vb21909278 _:vb21909279 _:vb21909276 _:vb21909277 _:vb21909274 _:vb21909275 _:vb21909272 _:vb21909273 _:vb21909270 _:vb21909271 _:vb21909268 _:vb21909269 _:vb21909266 _:vb21909267
Subject Item
_:vb21909266
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n3:Context
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However, the long-term side effects of radiation therapy as well as the potential induction of secondary malignancies have inspired many investigators to find ways to reduce the amount of radiation used (Mueller and Chang >>2009<<).
n3:mentions
n2:19560746
Subject Item
_:vb21909267
rdf:type
n3:Context
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Medulloblastomas bearing evidence of Sonic hedgehog pathway activity, approximately 30% of cases (Northcott et al 2010), are proposed to arise from cerebellar granule neuron precursors (CGNPs) (Eberhart >>2008<<). During cerebellar development, these cells undergo a rapid expansion phase, and their proliferation depends upon activation of the Sonic Hedgehog (Shh) signaling pathway (Dahmane and Ruiz i Altaba 1999, Wallace 1999, Wechsler-Reya and
n3:mentions
n2:18691544
Subject Item
_:vb21909268
rdf:type
n3:Context
rdf:value
During cerebellar development, these cells undergo a rapid expansion phase, and their proliferation depends upon activation of the Sonic Hedgehog (Shh) signaling pathway (Dahmane and Ruiz i Altaba >>1999<<, Wallace 1999, Wechsler-Reya and Scott 1999).
n3:mentions
n2:10375501
Subject Item
_:vb21909269
rdf:type
n3:Context
rdf:value
During cerebellar development, these cells undergo a rapid expansion phase, and their proliferation depends upon activation of the Sonic Hedgehog (Shh) signaling pathway (Dahmane and Ruiz i Altaba 1999, Wallace >>1999<<, Wechsler-Reya and Scott 1999).
n3:mentions
n2:10226030
Subject Item
_:vb21909270
rdf:type
n3:Context
rdf:value
cerebellar development, these cells undergo a rapid expansion phase, and their proliferation depends upon activation of the Sonic Hedgehog (Shh) signaling pathway (Dahmane and Ruiz i Altaba 1999, Wallace 1999, Wechsler-Reya and Scott >>1999<<). Shh, a secreted ligand, signals by binding to the transmembrane protein Patched (Ptc), a tumor suppressor whose function is inhibit the activity of Smoothened, a transmembrane protein resembling a G protein-coupled receptor.
n3:mentions
n2:10027293
Subject Item
_:vb21909271
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n3:Context
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downstream signaling activity, resulting in activation of Gli, N-myc, and E2F1 transcription factors, and stabilization of insulin receptor substrate-1 (IRS1), all of which contribute to proliferation (Bhatia et al 2010, Kenney et al >>2004<<, Oliver et al 2003, Parathath et al 2008, Ruiz i Altaba 1999).
n3:mentions
n2:14660435
Subject Item
_:vb21909272
rdf:type
n3:Context
rdf:value
activity, resulting in activation of Gli, N-myc, and E2F1 transcription factors, and stabilization of insulin receptor substrate-1 (IRS1), all of which contribute to proliferation (Bhatia et al 2010, Kenney et al 2004, Oliver et al >>2003<<, Parathath et al 2008, Ruiz i Altaba 1999).
n3:mentions
n2:12777630
Subject Item
_:vb21909273
rdf:type
n3:Context
rdf:value
in activation of Gli, N-myc, and E2F1 transcription factors, and stabilization of insulin receptor substrate-1 (IRS1), all of which contribute to proliferation (Bhatia et al 2010, Kenney et al 2004, Oliver et al 2003, Parathath et al >>2008<<, Ruiz i Altaba 1999).
n3:mentions
n2:18755774
Subject Item
_:vb21909274
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n3:Context
rdf:value
N-myc, and E2F1 transcription factors, and stabilization of insulin receptor substrate-1 (IRS1), all of which contribute to proliferation (Bhatia et al 2010, Kenney et al 2004, Oliver et al 2003, Parathath et al 2008, Ruiz i Altaba >>1999<<). Loss of Patched or activating mutations in Smoothened are found in human medulloblastomas, and can be phenocopied in mice, through mutational inactivation of Ptc or transgenic expression of activating alleles of Smoothened
n3:mentions
n2:10375510
Subject Item
_:vb21909275
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n3:Context
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in Smoothened are found in human medulloblastomas, and can be phenocopied in mice, through mutational inactivation of Ptc or transgenic expression of activating alleles of Smoothened (NeuroD2-SmoA1) in the cerebellum (Goodrich et al >>1997<<, Hatton et al 2008).
n3:mentions
n2:9262482
Subject Item
_:vb21909276
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n3:Context
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found in human medulloblastomas, and can be phenocopied in mice, through mutational inactivation of Ptc or transgenic expression of activating alleles of Smoothened (NeuroD2-SmoA1) in the cerebellum (Goodrich et al 1997, Hatton et al >>2008<<). Recent observations in mouse models have demonstrated the importance of genome surveillance, as loss of DNA damage repair mechanisms can lead to genomic instability in neural progenitor cells, resulting in medulloblastoma, and can also
n3:mentions
n2:18339857
Subject Item
_:vb21909277
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n3:Context
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as loss of DNA damage repair mechanisms can lead to genomic instability in neural progenitor cells, resulting in medulloblastoma, and can also cooperate with Shh signaling to enhance medulloblastoma formation in mice (Frappart et al >>2009<<, Leonard et al 2008, Pazzaglia et al 2006, Tanori et al 2008).
n3:mentions
n2:19164512
Subject Item
_:vb21909278
rdf:type
n3:Context
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repair mechanisms can lead to genomic instability in neural progenitor cells, resulting in medulloblastoma, and can also cooperate with Shh signaling to enhance medulloblastoma formation in mice (Frappart et al 2009, Leonard et al >>2008<<, Pazzaglia et al 2006, Tanori et al 2008).
n3:mentions
n2:18955550
Subject Item
_:vb21909279
rdf:type
n3:Context
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can lead to genomic instability in neural progenitor cells, resulting in medulloblastoma, and can also cooperate with Shh signaling to enhance medulloblastoma formation in mice (Frappart et al 2009, Leonard et al 2008, Pazzaglia et al >>2006<<, Tanori et al 2008).
n3:mentions
n2:16407852
Subject Item
_:vb21909280
rdf:type
n3:Context
rdf:value
instability in neural progenitor cells, resulting in medulloblastoma, and can also cooperate with Shh signaling to enhance medulloblastoma formation in mice (Frappart et al 2009, Leonard et al 2008, Pazzaglia et al 2006, Tanori et al >>2008<<).
n3:mentions
n2:18660545
Subject Item
_:vb21909281
rdf:type
n3:Context
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have oncogenic properties, including the ability to promote epithelial-mesenchymal transition (EMT), suppression of apoptosis, growth factor-independent proliferation, and anchorage-independent growth in soft agar (Overholtzer et al >>2006<<). YAP is involved in the formation of numerous tumors, including glioblastomas, oral squamous-cell carcinomas, and cancers of the pancreas, lung, ovary, and cervix (Fernandez and Kenney 2010, Zeng and Hong 2008, Zhao et al 2008).
n3:mentions
n2:16894141
Subject Item
_:vb21909282
rdf:type
n3:Context
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YAP is involved in the formation of numerous tumors, including glioblastomas, oral squamous-cell carcinomas, and cancers of the pancreas, lung, ovary, and cervix (Fernandez and Kenney 2010, Zeng and Hong >>2008<<, Zhao et al 2008).
n3:mentions
n2:18328423
Subject Item
_:vb21909283
rdf:type
n3:Context
rdf:value
YAP is involved in the formation of numerous tumors, including glioblastomas, oral squamous-cell carcinomas, and cancers of the pancreas, lung, ovary, and cervix (Fernandez and Kenney 2010, Zeng and Hong 2008, Zhao et al >>2008<<). However, the effects exerted by YAP are highly context-dependent, as it acts as a tumor suppressor in other malignancies, such as some breast cancers (Yuan et al 2008). Similarly, YAP activity can have pro- or anti-apoptotic effects
n3:mentions
n2:18579750
Subject Item
_:vb21909284
rdf:type
n3:Context
rdf:value
However, the effects exerted by YAP are highly context-dependent, as it acts as a tumor suppressor in other malignancies, such as some breast cancers (Yuan et al >>2008<<). Similarly, YAP activity can have pro- or anti-apoptotic effects depending on the tissue and cell context (Bertini et al 2009).
n3:mentions
n2:18617895
Subject Item
_:vb21909285
rdf:type
n3:Context
rdf:value
Similarly, YAP activity can have pro- or anti-apoptotic effects depending on the tissue and cell context (Bertini et al >>2009<<).
n3:mentions
n2:19106601
Subject Item
_:vb21909286
rdf:type
n5:Section
dc:title
materials and methods
n5:contains
_:vb21909287 _:vb21909290 _:vb21909288 _:vb21909289
Subject Item
_:vb21909287
rdf:type
n3:Context
rdf:value
Exon array profiling and data analysis with tumor sub-grouping were performed as published (Northcott et al 2009a).
n3:mentions
n2:19351822
Subject Item
_:vb21909288
rdf:type
n3:Context
rdf:value
CGNP cultures were generated as previously described (Kenney and Rowitch >>2000<<). Cells were plated on individual poly-DL-ornithine (Sigma) pre-coated plates or pre-coated glass coverslips.
n3:mentions
n2:11074003
Subject Item
_:vb21909289
rdf:type
n3:Context
rdf:value
3′ or 5′ end of the coding sequence were designed using the Cold Spring Harbor Laboratory RNAi OligoRetriever database and ligated into pSHAG vector, then transferred to MSCV retroviral vector and produced as described (Nahle et al >>2008<<). A control scrambled shRNA retrovirus was also prepared.
n3:mentions
n2:18308721
Subject Item
_:vb21909290
rdf:type
n3:Context
rdf:value
Protein extracts were prepared as previously described (Kenney and Rowitch, >>2000<<). Protein content was determined by using the Bio-Rad protein assay.
n3:mentions
n2:11074003
Subject Item
_:vb21909291
rdf:type
n5:Section
dc:title
results
n5:contains
_:vb21909312 _:vb21909313 _:vb21909302 _:vb21909303 _:vb21909300 _:vb21909301 _:vb21909298 _:vb21909299 _:vb21909296 _:vb21909297 _:vb21909310 _:vb21909311 _:vb21909308 _:vb21909309 _:vb21909306 _:vb21909307 _:vb21909304 _:vb21909305 _:vb21909294 _:vb21909295 _:vb21909292 _:vb21909293
Subject Item
_:vb21909292
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and mouse medulloblastomas, the YAP locus is highly amplified in 3% of the human medulloblastomas analyzed, and YAP expression is sufficient to drive proliferation of CGNPs in the absence of their obligate mitogen Shh (Fernandez et al >>2009<<). In NeuroD2-SmoA1 mouse medulloblastomas, YAP is most highly expressed in tumor cells surrounding blood vessels, a micro-environment known as the peri-vascular niche (PVN).
n3:mentions
n2:19952108
Subject Item
_:vb21909293
rdf:type
n3:Context
rdf:value
CGNPs are proposed to be the cell-of-origin for medulloblastomas associated with increased Shh pathway activity (Wechsler-Reya and Scott >>1999<<). Consistent with this hypothesis, treatment of CGNPs in culture with exogenous Shh causes expression of many of the same proliferation markers seen in this class of medulloblastomas, including Gli1, N-myc and YAP.
n3:mentions
n2:10027293
Subject Item
_:vb21909294
rdf:type
n3:Context
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As shown in Figure 2A, ectopic YAP expression is associated with increased CGNP proliferation as determined by cyclin D2 levels, and as we have previously reported (Fernandez et al >>2009<<). At 20 hours post-irradiation, YAP-infected CGNPs had reduced levels of cleaved caspase 3 in comparison with GFP-infected CGNPs, and reduced numbers of apoptotic cells as determined by quantification of pyknotic nuclei (GFP: 62.5+/−0.5%
n3:mentions
n2:19952108
Subject Item
_:vb21909295
rdf:type
n3:Context
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We also observed that YAP-transduced Pzp53med cells (Berman et al >>2002<<) showed a similar loss of irradiation-induced foci and increased number of cells with DNA breaks after irradiation (Supplementary Figure 3A, B).
n3:mentions
n2:12202832
Subject Item
_:vb21909296
rdf:type
n3:Context
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During G2, Cdk1 is maintained in an inactive state by phosphorylation on Thr 14 and Tyr 15 (Castedo et al >>2002<<); de-phosphorylation by cdc25 disinhibits Cdk1.
n3:mentions
n2:12145207
Subject Item
_:vb21909297
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Chk2, in turn, phosphorylates cdc25c, resulting in its inactivation and preventing entry into mitosis (Reinhardt and Yaffe >>2009<<). Irradiation resulted in increased levels of phosphorylated ATM and its substrate Chk2 in both GFP- and YAP-infected cells. However, in the presence of ectopic YAP, ATM and Chk2 were more rapidly dephosphorylated (Figure 4B, western blot
n3:mentions
n2:19230643
Subject Item
_:vb21909298
rdf:type
n3:Context
rdf:value
YAP functions in a complex with TEAD to regulate gene expression and proliferation (Zhao et al >>2008<<). To determine which genes may be induced or suppressed by YAP in irradiated CGNPs, we carried out microarray analysis of mRNA prepared from GFP- or YAP-infected control or irradiated CGNPs. Among the genes most highly expressed in
n3:mentions
n2:18579750
Subject Item
_:vb21909299
rdf:type
n3:Context
rdf:value
IGF signaling is required for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al >>2001<<, Corcoran et al 2008, Hahn et al 2000, Hartmann et al 2005, Rao et al 2004, Tanori et al 2010).
n3:mentions
n2:11207641
Subject Item
_:vb21909300
rdf:type
n3:Context
rdf:value
IGF signaling is required for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al 2001, Corcoran et al >>2008<<, Hahn et al 2000, Hartmann et al 2005, Rao et al 2004, Tanori et al 2010).
n3:mentions
n2:18974121
Subject Item
_:vb21909301
rdf:type
n3:Context
rdf:value
IGF signaling is required for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al 2001, Corcoran et al 2008, Hahn et al >>2000<<, Hartmann et al 2005, Rao et al 2004, Tanori et al 2010).
n3:mentions
n2:10884376
Subject Item
_:vb21909302
rdf:type
n3:Context
rdf:value
IGF signaling is required for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al 2001, Corcoran et al 2008, Hahn et al 2000, Hartmann et al >>2005<<, Rao et al 2004, Tanori et al 2010).
n3:mentions
n2:15793295
Subject Item
_:vb21909303
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signaling is required for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al 2001, Corcoran et al 2008, Hahn et al 2000, Hartmann et al 2005, Rao et al >>2004<<, Tanori et al 2010).
n3:mentions
n2:15195141
Subject Item
_:vb21909304
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for survival of CGNPs in vivo and in vitro, and increased activity of the IGF pathway is found in human medulloblastomas (Chrysis et al 2001, Corcoran et al 2008, Hahn et al 2000, Hartmann et al 2005, Rao et al 2004, Tanori et al >>2010<<). Interestingly, when we queried a genetically characterized database of over 100 human medulloblastomas (Northcott et al 2009b) we found that IGF2 was most highly expressed in the subclass of medulloblastomas associated with activation
n3:mentions
n2:20214787
Subject Item
_:vb21909305
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Interestingly, when we queried a genetically characterized database of over 100 human medulloblastomas (Northcott et al 2009b) we found that IGF2 was most highly expressed in the subclass of medulloblastomas associated with activation of the Shh pathway (T test, p=3.553E-14) (Figure 5D).
n3:mentions
n2:19270706
Subject Item
_:vb21909306
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This class of tumors also expresses high levels of N-myc, Gli1, and miR17/92 (Kool et al >>2008<<, Northcott et al 2009b, Pomeroy et al 2002).
n3:mentions
n2:18769486
Subject Item
_:vb21909307
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This class of tumors also expresses high levels of N-myc, Gli1, and miR17/92 (Kool et al 2008, Northcott et al 2009b, Pomeroy et al 2002).
n3:mentions
n2:19270706
Subject Item
_:vb21909308
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This class of tumors also expresses high levels of N-myc, Gli1, and miR17/92 (Kool et al 2008, Northcott et al 2009b, Pomeroy et al >>2002<<). The increased level of IGF2 protein in YAP-expressing tumors was conserved in YAP-SmoA1 medulloblastomas, as determined by western blot and immunohistochemical analysis (Figure 5E, F). As we observed in CGNPs, IGF2 levels are increased
n3:mentions
n2:11807556
Subject Item
_:vb21909309
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We have previously shown that Akt cooperates with Shh signaling to promote proliferation through stabilization of N-myc (Kenney et al >>2004<<). Akt activity has been linked to abrogation of the G2/M checkpoint after irradiation, through inactivation of ATM/Chk2 (Hirose et al 2005, Kandel et al 2002). Consistent with increased IGF1 receptor activity in response to IGF2
n3:mentions
n2:14660435
Subject Item
_:vb21909310
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Akt activity has been linked to abrogation of the G2/M checkpoint after irradiation, through inactivation of ATM/Chk2 (Hirose et al >>2005<<, Kandel et al 2002).
n3:mentions
n2:15930307
Subject Item
_:vb21909311
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Akt activity has been linked to abrogation of the G2/M checkpoint after irradiation, through inactivation of ATM/Chk2 (Hirose et al 2005, Kandel et al >>2002<<). Consistent with increased IGF1 receptor activity in response to IGF2 secretion, YAP-Smo-driven medulloblastomas exhibit higher levels of activated Akt (S473-phosphorylated), most notably in cells surrounding the vasculature (Figure 5G);
n3:mentions
n2:12391152
Subject Item
_:vb21909312
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most notably in cells surrounding the vasculature (Figure 5G); interestingly, these cells also express the highest levels of YAP and they have been proposed to function as tumor repopulating cells after irradiation (Fernandez et al >>2009<<, Hambardzumyan et al 2008).
n3:mentions
n2:19952108
Subject Item
_:vb21909313
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the vasculature (Figure 5G); interestingly, these cells also express the highest levels of YAP and they have been proposed to function as tumor repopulating cells after irradiation (Fernandez et al 2009, Hambardzumyan et al >>2008<<). Taken together these observations raise the possibility that YAP-mediated IGF2 induction not only promotes survival and proliferation through Akt activation but may also affect the phosphorylation of ATM/Chk2, resulting in disruption of
n3:mentions
n2:18281460
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discussion
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_:vb21909330 _:vb21909331 _:vb21909328 _:vb21909329 _:vb21909334 _:vb21909335 _:vb21909332 _:vb21909333 _:vb21909338 _:vb21909336 _:vb21909337 _:vb21909315 _:vb21909318 _:vb21909319 _:vb21909316 _:vb21909317 _:vb21909322 _:vb21909323 _:vb21909320 _:vb21909321 _:vb21909326 _:vb21909327 _:vb21909324 _:vb21909325
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signaling that promotes proliferation and inhibits apoptosis of cerebellar granule cell precursors and we showed that YAP is over-expressed and amplified in the Sonic hedgehog-associated class of medulloblastomas (Fernandez et al >>2009<<). Here, we report a new role for YAP in promoting IGF2/Akt-dependent radio-resistance and ongoing proliferation in the presence of unrepaired DNA, illustrating a novel link between Shh signaling, YAP, and the Akt pathway.
n3:mentions
n2:19952108
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Many studies have implicated PI-3 kinase and Akt in cell survival, through its effects on FKHR proteins and Bcl2 family members (Brunet et al >>2001<<, Burgering and Kops 2002, Duronio 2008), and Akt is essential for CGNP survival (Dudek et al 1997).
n3:mentions
n2:11399427
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Many studies have implicated PI-3 kinase and Akt in cell survival, through its effects on FKHR proteins and Bcl2 family members (Brunet et al 2001, Burgering and Kops >>2002<<, Duronio 2008), and Akt is essential for CGNP survival (Dudek et al 1997).
n3:mentions
n2:12114024
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Many studies have implicated PI-3 kinase and Akt in cell survival, through its effects on FKHR proteins and Bcl2 family members (Brunet et al 2001, Burgering and Kops 2002, Duronio >>2008<<), and Akt is essential for CGNP survival (Dudek et al 1997).
n3:mentions
n2:18842113
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studies have implicated PI-3 kinase and Akt in cell survival, through its effects on FKHR proteins and Bcl2 family members (Brunet et al 2001, Burgering and Kops 2002, Duronio 2008), and Akt is essential for CGNP survival (Dudek et al >>1997<<). Transcriptional profiling of human medulloblastomas has shown increased expression of IGF2 (Pomeroy et al 2002), and our report clearly links high levels of IGF2 expression with the Sonic hedgehog-associated subclass of medulloblastomas.
n3:mentions
n2:9005851
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Transcriptional profiling of human medulloblastomas has shown increased expression of IGF2 (Pomeroy et al >>2002<<), and our report clearly links high levels of IGF2 expression with the Sonic hedgehog-associated subclass of medulloblastomas.
n3:mentions
n2:11807556
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IGF2 has been shown to be indispensable for the formation and progression of Shh-driven murine medulloblastomas (Corcoran et al >>2008<<, Hahn et al 2000) and to synergize with Sonic Hedgehog in the induction of tumor formation (Rao et al 2004).
n3:mentions
n2:18974121
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IGF2 has been shown to be indispensable for the formation and progression of Shh-driven murine medulloblastomas (Corcoran et al 2008, Hahn et al >>2000<<) and to synergize with Sonic Hedgehog in the induction of tumor formation (Rao et al 2004).
n3:mentions
n2:10884376
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IGF2 has been shown to be indispensable for the formation and progression of Shh-driven murine medulloblastomas (Corcoran et al 2008, Hahn et al 2000) and to synergize with Sonic Hedgehog in the induction of tumor formation (Rao et al >>2004<<). IGF2 has previously been shown to promote proliferation of medulloblastoma cells and cerebellar neural cell precursors through the activation of Akt (Hartmann et al 2005).
n3:mentions
n2:15195141
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IGF2 has previously been shown to promote proliferation of medulloblastoma cells and cerebellar neural cell precursors through the activation of Akt (Hartmann et al >>2005<<).
n3:mentions
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This has particularly important implications for medulloblastomas; due to their radiosensitivity, radiation therapy is a standard in children older than 3 years of age (Mueller and Chang >>2009<<). We show here that 3 hours after radiation, YAP-driven SmoA1 medulloblastomas feature higher levels of proliferation markers and reduced apoptosis. In vitro, we found a similar effect when we irradiated GFP- or YAP-over-expressing CGNPs.
n3:mentions
n2:19560746
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Activation of Akt suppresses the checkpoint by inhibiting the DNA damage response pathways, either ATM/Chk2 or ATR/Chk1, depending on the cellular context (Hirose et al >>2005<<, Kandel et al 2002, Shtivelman et al 2002, Xu et al 2010).
n3:mentions
n2:15930307
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Activation of Akt suppresses the checkpoint by inhibiting the DNA damage response pathways, either ATM/Chk2 or ATR/Chk1, depending on the cellular context (Hirose et al 2005, Kandel et al >>2002<<, Shtivelman et al 2002, Xu et al 2010).
n3:mentions
n2:12391152
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Activation of Akt suppresses the checkpoint by inhibiting the DNA damage response pathways, either ATM/Chk2 or ATR/Chk1, depending on the cellular context (Hirose et al 2005, Kandel et al 2002, Shtivelman et al >>2002<<, Xu et al 2010).
n3:mentions
n2:12062056
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Activation of Akt suppresses the checkpoint by inhibiting the DNA damage response pathways, either ATM/Chk2 or ATR/Chk1, depending on the cellular context (Hirose et al 2005, Kandel et al 2002, Shtivelman et al 2002, Xu et al >>2010<<). In agreement with these studies, we observed a decrease in phosphorylated ATM and Chk2 in irradiated YAP-over-expressing CGNPs and medulloblastoma cells, compared to GFP-expressing cells, and YAP-transduced cells showed fewer DNA
n3:mentions
n2:20679434
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Interestingly, a previous study has shown that aberrant activation of the Shh pathway through Ptc loss-of-function impairs the function of ATR/Chk1, a separate signaling cascade (Leonard et al >>2008<<). We did not detect effects of YAP on this cascade (data not shown); however the impact we report of YAP on ATM/Chk2 may synergize with an already defective DNA damage response due to Smoothened-mediated Chk1 impairment.
n3:mentions
n2:18955550
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High-throughput sequencing studies suggest that mutations in DNA repair genes do not account for the presence of genomic instability in many sporadic cancers (Negrini et al >>2010<<). Alternatively, activation of oncogenes, and more generally of growth signaling pathways, has been shown to induce genomic instability in mammalian cells cultured in vitro and in mouse models (Hernando et al 2004, Negrini et al 2010).
n3:mentions
n2:20177397
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Alternatively, activation of oncogenes, and more generally of growth signaling pathways, has been shown to induce genomic instability in mammalian cells cultured in vitro and in mouse models (Hernando et al >>2004<<, Negrini et al 2010).
n3:mentions
n2:15306814
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Alternatively, activation of oncogenes, and more generally of growth signaling pathways, has been shown to induce genomic instability in mammalian cells cultured in vitro and in mouse models (Hernando et al 2004, Negrini et al >>2010<<). Hyperactive Shh pathway activity has been shown to induce genomic instability and the development of spontaneous and ionizing radiation (IR)-induced tumors (Leonard et al 2008). Now we show that high levels of YAP expression further
n3:mentions
n2:20177397
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Hyperactive Shh pathway activity has been shown to induce genomic instability and the development of spontaneous and ionizing radiation (IR)-induced tumors (Leonard et al >>2008<<). Now we show that high levels of YAP expression further contribute to generation of genomic instability since irradiated YAP-expressing cells present a higher number of chromosomal alterations. The role of genomic instability has
n3:mentions
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Although it is still unclear if it is necessary for tumorigenesis to occur, genomic instability certainly provides the tumor with an advantage in terms of faster progression through the many stages of tumorigenesis (Sieber et al >>2003<<). Indeed, we show that ectopic expression of YAP accelerates medulloblastoma onset and produces tumors that are highly aggressive and rapidly lethal.
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We have previously shown that 48 hours after radiation, the YAP positive population starts to expand (Fernandez et al >>2009<<). Hambardzumyan et al. (Hambardzumyan et al 2008) elegantly demonstrated that the PI3K-Akt pathway regulates survival of these tumor-repopulating cells residing in the PVN. These results point to the importance of YAP regulating survival
n3:mentions
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Hambardzumyan et al. (Hambardzumyan et al >>2008<<) elegantly demonstrated that the PI3K-Akt pathway regulates survival of these tumor-repopulating cells residing in the PVN.
n3:mentions
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instability is solely a consequence of the Akt-mediated cell cycle checkpoint suppression, or whether Akt lying downstream of YAP-induced IGF2 could also inhibit the DNA repair machinery, as previous studies have suggested (Plo et al >>2008<<) (Figure 7).
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