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1 luripotent stem cells (hiPSCs) for modelling gliomagenesis.
2 n of these pathways plays a critical role in gliomagenesis.
3 ith telomere length implicates telomerase in gliomagenesis.
4 or microenvironment and genomic modifiers in gliomagenesis.
5 lation of INPP5F may lead to contribution to gliomagenesis.
6 principal mediator for COX-2 cascade-driven gliomagenesis.
7 r, it is unknown whether TLX is required for gliomagenesis.
8 el of platelet-derived growth factor-induced gliomagenesis.
9 odel, we demonstrated that miR-128 repressed gliomagenesis.
10 tem cell niche causes a phenotype resembling gliomagenesis.
11 tions directly into OPCs consistently led to gliomagenesis.
12 unique mouse model of wild-type EGFR-driven gliomagenesis.
13 of INK4A/ARF and PTEN, is a leading cause of gliomagenesis.
14 n cAMP levels account for the pattern of NF1 gliomagenesis.
15 lance from regulated differentiation towards gliomagenesis.
16 ulature pathway at a given specific stage of gliomagenesis.
17 n, thus showing that MIIP is an inhibitor of gliomagenesis.
18 in particular immunoregulatory proteins, in gliomagenesis.
19 hat these are initiating events in childhood gliomagenesis.
20 atase and tensin homolog), in the process of gliomagenesis.
21 the coselection of these alterations during gliomagenesis.
22 PTBP1-specific splicing targets that enhance gliomagenesis.
23 y be involved in cancer stem cell-associated gliomagenesis.
24 on of two separate pathways is necessary for gliomagenesis.
25 TP53BP1, and BIK) that could have a role in gliomagenesis.
26 neural subtype of glioblastoma and can drive gliomagenesis.
27 and epidermal growth factor receptor-induced gliomagenesis.
28 and do not support a major role for DMBT1 in gliomagenesis.
29 sors and is potentially sufficient to induce gliomagenesis.
30 ks were assembled around the myc oncogene in gliomagenesis and around the integrin signaling pathway
31 P has an important role in the inhibition of gliomagenesis and attenuation of mitotic transition.
32 derstanding of the role of HCMV infection in gliomagenesis and GBM pathogenesis could reveal novel th
35 ate a critical role for TLX in NSC-dependent gliomagenesis and implicate TLX as a therapeutic target
37 tion and identification of genes involved in gliomagenesis and may characterize genetic subgroups of
38 ling pathways that link neural stem cells to gliomagenesis and may lead to new strategies for treatin
39 sights into the genetic determinants of EGFR gliomagenesis and sensitivity to TKIs and provide a robu
40 s provide insight into PDGFRalpha-stimulated gliomagenesis and suggest that phosphorylated Dock180(Y1
41 Over the past 4 years, our understanding of gliomagenesis and the practice of neuro-oncology have be
42 on has been found to be an inciting event in gliomagenesis and to have a profound effect on the molec
43 ine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a nove
44 portunity to investigate the role of LGI1 in gliomagenesis and, since LGI1 is predicted to be a membr
45 , including those proposed to be involved in gliomagenesis, and has been shown to induce tumors in ma
46 e Nf1 mouse strain are sufficient to promote gliomagenesis, and justify the implementation of cAMP-ba
47 tumor surveillance, advance understanding of gliomagenesis, and potentially identify novel therapeuti
51 ction of a distinct genetic landscape during gliomagenesis, are associated with patient prognosis.
52 , genes and pathways already associated with gliomagenesis, as well as a set of general cancer genes,
53 the molecular and cellular underpinnings of gliomagenesis, attention deficit, and learning problems
54 tends earlier evidence of a role for cAMP in gliomagenesis based on results in a genetically engineer
55 n most lower grade glioma and not only drive gliomagenesis but are also associated with longer patien
56 ession of EGFRvIII alone is insufficient for gliomagenesis but rather contributes to glioma progressi
57 We propose that p53 mutations contribute to gliomagenesis by both allowing the overexpression of c-M
58 indings show that the COX-2 pathway promotes gliomagenesis by directly supporting systemic developmen
59 ur study suggests that IDH mutations promote gliomagenesis by disrupting chromosomal topology and all
60 rovide evidence that p190RhoGAP may suppress gliomagenesis by inducing a differentiated glial phenoty
61 othesized that COX-2 blockade would suppress gliomagenesis by inhibiting MDSC development and accumul
62 with double markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1 mutations
64 the functions of PDGF autocrine signaling in gliomagenesis by transferring the overexpression of PDGF
65 We evaluated the role of each Akt isoform in gliomagenesis by using a model system driven by common g
66 tion in both normal cortical development and gliomagenesis, controlling Neurog2-Ascl1 expression and
67 e view that one role of loss of Ink4a-Arf in gliomagenesis could be to sensitize astrocytes to transf
69 ediated activation of EGFR was necessary for gliomagenesis, functionally substantiating the clinical
70 f key functions and pathways associated with gliomagenesis in a set of 50 human gliomas of various hi
73 died the impact of modulating CSF1 levels on gliomagenesis in the context of the GFAP-V12Ha-ras-IRESL
74 nistic information as to how CMV may promote gliomagenesis in the setting of tumor suppressor dysfunc
77 tudies are identifying unexpected drivers of gliomagenesis, including mutations in isocitrate dehydro
82 d) in alternative splicing are infrequent in gliomagenesis (< 3% of interrogated RefSeq entries).
83 ults suggest that MBD2 overexpression during gliomagenesis may drive tumor growth by suppressing the
84 -Cre transgenic strain that drives Nf1 optic gliomagenesis, NG2-expressing cells also give rise to al
85 itrate dehydrogenase 1 mutations drive human gliomagenesis, probably through neomorphic enzyme activi
86 mTOR-dependent glial cell growth control and gliomagenesis relevant to the design of therapies for in
87 um (sporadic PA) raises the possibility that gliomagenesis requires more than biallelic inactivation
88 e optic glioma, and support a model in which gliomagenesis requires Nf1 loss in specific neuroglial p
89 nts validate an important role of miR-10b in gliomagenesis, reveal a novel mechanism of miR-10b-media
90 x-specific role for cAMP regulation in human gliomagenesis, specifically identifying ADCY8 as a modif
92 ically engineered mouse model of EGFR-driven gliomagenesis that uses a somatic conditional overexpres
93 cate that CSF1 signaling is oncogenic during gliomagenesis through a mechanism distinct from modulati
94 Compromised PTEN function may contribute to gliomagenesis through disrupted regulation of proliferat
95 ve investigated the role of EGFR mutation in gliomagenesis, using avian retroviral vectors to transfe
97 of CDK4 amplification and INK4a-ARF loss in gliomagenesis, we compared the behavior of astrocytes la
99 of the INK4A/ARF locus and Pten deletions in gliomagenesis, we generated Pten(-/-)Ink4a/Arf(-/-) mous
100 regulatory pathways that could contribute to gliomagenesis, we have conducted a systematic study of R
102 Using PDGF- and KRAS-driven murine models of gliomagenesis, we show that high Id1 expression (Id1(hig
104 d spatial dynamics of TAM composition during gliomagenesis, we used genetically engineered and GL261-
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