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1  conserved mammalian mutational processes in gliomagenesis.
2 l differentiation and simultaneously lost in gliomagenesis.
3 atase and tensin homolog), in the process of gliomagenesis.
4  the coselection of these alterations during gliomagenesis.
5 PTBP1-specific splicing targets that enhance gliomagenesis.
6 y be involved in cancer stem cell-associated gliomagenesis.
7 on of two separate pathways is necessary for gliomagenesis.
8 were highly susceptible to radiation-induced gliomagenesis.
9  TP53BP1, and BIK) that could have a role in gliomagenesis.
10 and epidermal growth factor receptor-induced gliomagenesis.
11 and do not support a major role for DMBT1 in gliomagenesis.
12 sors and is potentially sufficient to induce gliomagenesis.
13 ing glial cell-fate decision and controlling gliomagenesis.
14 ysregulated epigenetic mechanisms underlying gliomagenesis.
15  uncovered the crucial role of metabolism in gliomagenesis.
16 n otherwise heterogeneous and multifactorial gliomagenesis.
17 s, which is thought to be a driving event in gliomagenesis.
18 bility to dissect developmental processes of gliomagenesis.
19 el enables the analysis of various stages of gliomagenesis.
20 astoma, which constitutes a primary event in gliomagenesis.
21 of how their dysregulation may contribute to gliomagenesis.
22 -like lesions but is not sufficient for full gliomagenesis.
23  principal mediator for COX-2 cascade-driven gliomagenesis.
24 tem cell niche causes a phenotype resembling gliomagenesis.
25 lls, and transcription of genetic drivers of gliomagenesis.
26 neural subtype of glioblastoma and can drive gliomagenesis.
27 luripotent stem cells (hiPSCs) for modelling gliomagenesis.
28 es new tools for functional interrogation of gliomagenesis.
29 n of these pathways plays a critical role in gliomagenesis.
30 ith telomere length implicates telomerase in gliomagenesis.
31 or microenvironment and genomic modifiers in gliomagenesis.
32 lation of INPP5F may lead to contribution to gliomagenesis.
33 r, it is unknown whether TLX is required for gliomagenesis.
34 el of platelet-derived growth factor-induced gliomagenesis.
35 odel, we demonstrated that miR-128 repressed gliomagenesis.
36 tions directly into OPCs consistently led to gliomagenesis.
37  unique mouse model of wild-type EGFR-driven gliomagenesis.
38 of INK4A/ARF and PTEN, is a leading cause of gliomagenesis.
39 t it is unknown how oncohistone type affects gliomagenesis.
40 n cAMP levels account for the pattern of NF1 gliomagenesis.
41 lance from regulated differentiation towards gliomagenesis.
42 ulature pathway at a given specific stage of gliomagenesis.
43 n, thus showing that MIIP is an inhibitor of gliomagenesis.
44  in particular immunoregulatory proteins, in gliomagenesis.
45 hat these are initiating events in childhood gliomagenesis.
46 es to the mechanisms that initiate and drive gliomagenesis(1,2).
47 se (MAPK) and mTOR signaling pathways, drive gliomagenesis, activate neuronal transcriptional program
48 ks were assembled around the myc oncogene in gliomagenesis and around the integrin signaling pathway
49 ce of alternative splicing as a mechanism in gliomagenesis and as an avenue for exploration of drug t
50 P has an important role in the inhibition of gliomagenesis and attenuation of mitotic transition.
51 facilitate better understanding of brainstem gliomagenesis and classification, and guide future studi
52 derstanding of the role of HCMV infection in gliomagenesis and GBM pathogenesis could reveal novel th
53 th different ploidy, thereby modulating both gliomagenesis and GBM recurrence.
54 oplastic cellular compartments contribute to gliomagenesis and glioma growth.
55            IDH mutation is an early event in gliomagenesis and has significant implications for gliom
56  expressed in these tumours, and GPC3 drives gliomagenesis and hyperexcitability.
57 ate a critical role for TLX in NSC-dependent gliomagenesis and implicate TLX as a therapeutic target
58 nical, regarding the possible role of CMV in gliomagenesis and maintenance.
59 tion and identification of genes involved in gliomagenesis and may characterize genetic subgroups of
60 ling pathways that link neural stem cells to gliomagenesis and may lead to new strategies for treatin
61 ence of driver mutations and their impact on gliomagenesis and patient outcomes, we analyzed genomic
62 idate the roles of HDAC class IIa enzymes in gliomagenesis and progression and to optimize therapeuti
63 n glioma stem cells which are key drivers of gliomagenesis and recurrence.
64 sights into the genetic determinants of EGFR gliomagenesis and sensitivity to TKIs and provide a robu
65 s provide insight into PDGFRalpha-stimulated gliomagenesis and suggest that phosphorylated Dock180(Y1
66  and epitranscriptomic machinery to initiate gliomagenesis and suggests potential treatment strategie
67 els, we show that PPM1D mutations potentiate gliomagenesis and that PPM1D phosphatase activity is req
68 d knowledge of early driving events in their gliomagenesis and the lack of effective therapies availa
69  Over the past 4 years, our understanding of gliomagenesis and the practice of neuro-oncology have be
70 on has been found to be an inciting event in gliomagenesis and to have a profound effect on the molec
71 bility to dissect developmental processes of gliomagenesis and to provide new avenues for therapeutic
72 ine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a nove
73 portunity to investigate the role of LGI1 in gliomagenesis and, since LGI1 is predicted to be a membr
74 , including those proposed to be involved in gliomagenesis, and has been shown to induce tumors in ma
75 e Nf1 mouse strain are sufficient to promote gliomagenesis, and justify the implementation of cAMP-ba
76 tumor surveillance, advance understanding of gliomagenesis, and potentially identify novel therapeuti
77           The mechanisms of IDH mutations in gliomagenesis, and their value as diagnostic, prognostic
78                    Furthermore, EGFR-induced gliomagenesis appears to require additional mutations in
79       Molecular functions of these miRNAs in gliomagenesis are mainly unknown.
80             The selective forces that govern gliomagenesis are strong, shaping the composition of tum
81 ction of a distinct genetic landscape during gliomagenesis, are associated with patient prognosis.
82 , genes and pathways already associated with gliomagenesis, as well as a set of general cancer genes,
83  the molecular and cellular underpinnings of gliomagenesis, attention deficit, and learning problems
84 tends earlier evidence of a role for cAMP in gliomagenesis based on results in a genetically engineer
85 n most lower grade glioma and not only drive gliomagenesis but are also associated with longer patien
86 ession of EGFRvIII alone is insufficient for gliomagenesis but rather contributes to glioma progressi
87         Epigenetic regulators have a role in gliomagenesis, but a broad, functional investigation of
88  We propose that p53 mutations contribute to gliomagenesis by both allowing the overexpression of c-M
89 indings show that the COX-2 pathway promotes gliomagenesis by directly supporting systemic developmen
90 ur study suggests that IDH mutations promote gliomagenesis by disrupting chromosomal topology and all
91 rovide evidence that p190RhoGAP may suppress gliomagenesis by inducing a differentiated glial phenoty
92 othesized that COX-2 blockade would suppress gliomagenesis by inhibiting MDSC development and accumul
93  with double markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1 mutations
94                           p21 contributes to gliomagenesis by stabilizing cyclin D1-cdk4 kinase compl
95 the functions of PDGF autocrine signaling in gliomagenesis by transferring the overexpression of PDGF
96      Mechanistically, axonal injury promotes gliomagenesis by triggering Wallerian degeneration, a ta
97 We evaluated the role of each Akt isoform in gliomagenesis by using a model system driven by common g
98 gical manipulation of key signaling nodes in gliomagenesis complemented with shotgun lipidomics, we s
99 tion in both normal cortical development and gliomagenesis, controlling Neurog2-Ascl1 expression and
100 e view that one role of loss of Ink4a-Arf in gliomagenesis could be to sensitize astrocytes to transf
101                                  MMRD-driven gliomagenesis defines the role of nonrandom mutagenesis
102                       Moreover, EGFR-induced gliomagenesis does not occur in conjunction with p53 def
103 ediated activation of EGFR was necessary for gliomagenesis, functionally substantiating the clinical
104       The role of PPM1D mutations in de novo gliomagenesis has not been systematically explored.
105 f key functions and pathways associated with gliomagenesis in a set of 50 human gliomas of various hi
106 egion NSC heterogeneity in the patterning of gliomagenesis in children and adults.
107                    Importantly, PDGFA-driven gliomagenesis in mice was disrupted when autophagy was i
108  Ptprd cooperates with p16 deletion to drive gliomagenesis in mice.
109                                              Gliomagenesis in NF1 results in a heterogeneous spectrum
110 died the impact of modulating CSF1 levels on gliomagenesis in the context of the GFAP-V12Ha-ras-IRESL
111 nistic information as to how CMV may promote gliomagenesis in the setting of tumor suppressor dysfunc
112 e show mutant EGFR is sufficient to initiate gliomagenesis in vivo, both in the brain and spinal cord
113 on of the Pdgfra insulator and Cdkn2a drives gliomagenesis in vivo.
114 ions to drive OPC proliferation in vitro and gliomagenesis in vivo.
115 on in NG2+ cells is not sufficient for optic gliomagenesis in vivo.
116          Thus, while IDH1 mutation initiates gliomagenesis, in some patients mutant IDH1 and 2HG are
117 tudies are identifying unexpected drivers of gliomagenesis, including mutations in isocitrate dehydro
118       The significance of CD133(+) cells for gliomagenesis is controversial because of conflicting su
119       However, the role of INK4a-ARF loss in gliomagenesis is unclear.
120 e molecular basis for this unique pattern of gliomagenesis is unknown.
121                  The significance of MIIP in gliomagenesis is unknown.
122 d) in alternative splicing are infrequent in gliomagenesis (< 3% of interrogated RefSeq entries).
123 ults suggest that MBD2 overexpression during gliomagenesis may drive tumor growth by suppressing the
124 -Cre transgenic strain that drives Nf1 optic gliomagenesis, NG2-expressing cells also give rise to al
125 eneric oncogenic role for the BMP pathway in gliomagenesis of pDMG and pave the way for specific targ
126  to PTEN/p53-loss-induced transformation and gliomagenesis, pointing to subtype-specific treatment st
127 itrate dehydrogenase 1 mutations drive human gliomagenesis, probably through neomorphic enzyme activi
128 3.1K27M promote tumor initiation, accelerate gliomagenesis, promote a mesenchymal profile partly due
129 mTOR-dependent glial cell growth control and gliomagenesis relevant to the design of therapies for in
130 er, the cooperative partners of EGFR driving gliomagenesis remain poorly understood.
131 However, how this signaling axis operates in gliomagenesis remains underestimated.
132 um (sporadic PA) raises the possibility that gliomagenesis requires more than biallelic inactivation
133 e optic glioma, and support a model in which gliomagenesis requires Nf1 loss in specific neuroglial p
134 nts validate an important role of miR-10b in gliomagenesis, reveal a novel mechanism of miR-10b-media
135 x-specific role for cAMP regulation in human gliomagenesis, specifically identifying ADCY8 as a modif
136 Our study provides a functional landscape of gliomagenesis suppressors in vivo.
137 ically engineered mouse model of EGFR-driven gliomagenesis that uses a somatic conditional overexpres
138 cate that CSF1 signaling is oncogenic during gliomagenesis through a mechanism distinct from modulati
139  Compromised PTEN function may contribute to gliomagenesis through disrupted regulation of proliferat
140      Epigenetic dysregulation contributes to gliomagenesis, tumor progression, and responses to immun
141 ve investigated the role of EGFR mutation in gliomagenesis, using avian retroviral vectors to transfe
142 ell as the role of TLX-dependent NSCs during gliomagenesis, using mouse models.
143  of CDK4 amplification and INK4a-ARF loss in gliomagenesis, we compared the behavior of astrocytes la
144              To define the role of f-BRAF in gliomagenesis, we demonstrate that f-BRAF regulates neur
145 of the INK4A/ARF locus and Pten deletions in gliomagenesis, we generated Pten(-/-)Ink4a/Arf(-/-) mous
146 regulatory pathways that could contribute to gliomagenesis, we have conducted a systematic study of R
147              To clarify the role of DMBT1 in gliomagenesis, we investigated three reported deletion h
148 Using PDGF- and KRAS-driven murine models of gliomagenesis, we show that high Id1 expression (Id1(hig
149                               To model human gliomagenesis, we used a GFAP-HRas(V12) mouse model cros
150 d spatial dynamics of TAM composition during gliomagenesis, we used genetically engineered and GL261-
151          Here, to explore the early steps in gliomagenesis, we utilized conditional gene deletion and
152 overs a Pivotal Determinant of Cell Fate and Gliomagenesis" (Weng et al., 2019) is presented here.
153  tumor suppressor p53 is a frequent event in gliomagenesis, whether or how it affects quiescent NSCs

 
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