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1 ound that Brca1 deficiency activates the Akt oncogenic pathway.
2 nt important downstream effectors of the ALK oncogenic pathway.
3 t of new strategies to target this pervasive oncogenic pathway.
4 d of INPP5D, an inhibitor of the PI3K-driven oncogenic pathway.
5 mutations of the Brca1 gene activate the Akt oncogenic pathway.
6 ase as an essential effector of the HER2/neu oncogenic pathway.
7 apeutic strategies being used to target this oncogenic pathway.
8 to act as either a tumor suppressor or a pro-oncogenic pathway.
9 not identical, signaling elements of the Ras oncogenic pathway.
10 y phosphorylations on BTK and attenuated its oncogenic pathway.
11 HGG through epigenetic regulation of the MYC oncogenic pathway.
12 otent and selective, specifically modulating oncogenic pathways.
13 f DLBCL and have led to the discovery of key oncogenic pathways.
14 ient oncoproteins and shutting down multiple oncogenic pathways.
15 t on carcinogenesis control broad spectra of oncogenic pathways.
16 R in breast cancer and regulates several pro-oncogenic pathways.
17 ructures with basal polarity, and suppressed oncogenic pathways.
18 unrecognized link between the Akt and c-myc oncogenic pathways.
19 atory transcriptome with changes in relevant oncogenic pathways.
20 ts that these malignancies may use different oncogenic pathways.
21 2) is a MAPK that regulates inflammatory and oncogenic pathways.
22 ractions mediate crosstalk between canonical oncogenic pathways.
23 inhibiting the genetic expression of several oncogenic pathways.
24 a central role in the activation of multiple oncogenic pathways.
25 f redundancy and signaling through different oncogenic pathways.
26 thetic lethal relationship between these two oncogenic pathways.
27 which leads to the activation of these same oncogenic pathways.
28 regulatory molecules in tumor-suppressor and oncogenic pathways.
29 oping strategies for optimal intervention of oncogenic pathways.
30 pes are distinct diseases that use different oncogenic pathways.
31 n experimental models that represented other oncogenic pathways.
32 rve as recipients of the Ras- and Myc-driven oncogenic pathways.
33 ns serve as cell cycle recipients of several oncogenic pathways.
34 hat reflect the activation status of several oncogenic pathways.
35 particular D-cyclins responsive to specific oncogenic pathways.
36 gene expression profiles for the analysis of oncogenic pathways.
37 mary epithelial cells by activating multiple oncogenic pathways.
38 e a common denominator of the PI3K and FoxG1 oncogenic pathways.
39 cription factor linking the inflammatory and oncogenic pathways.
40 tumor suppressor miRNA by targeting various oncogenic pathways.
41 thought to be an important player in several oncogenic pathways.
42 duces both DBD-dependent and DBD-independent oncogenic pathways.
43 d enhancer pool to drive distinct downstream oncogenic pathways.
44 such as KLF16 and MEIS3, which are linked to oncogenic pathways.
45 ific vulnerabilities associated with defined oncogenic pathways.
46 ene bodies for transcriptional activation of oncogenic pathways.
47 esults in a combinatorial attack on numerous oncogenic pathways.
48 , plays a pivotal role in regulating various oncogenic pathways.
49 with distinct roles in supporting MYC-driven oncogenic pathways.
50 to compensatory upregulation of alternative oncogenic pathways.
51 s signaling molecules that directly regulate oncogenic pathways.
52 expression of genes involved in CSC-relevant oncogenic pathways.
53 ng this promising intersection point of many oncogenic pathways.
54 igens, antigen presentation, DNA repair, and oncogenic pathways.
55 een innate immune responses and STAT3-driven oncogenic pathways.
56 n utilization, oxidative stress response and oncogenic pathways.
57 (CDK) complexes to be activated by mitogenic/oncogenic pathways.
58 linical biopsies or endogenously deregulated oncogenic pathways.
59 er from the 48 non-redundant genes in the 11 oncogenic pathways.
60 ent kinase 2 phosphorylation orchestrating 2 oncogenic pathways.
61 n-coding RNAs that can have large impacts on oncogenic pathways.
62 d how these genes contribute to dysregulated oncogenic pathways.
63 linical course and by divergent addiction to oncogenic pathways.
64 ules, resulting in the activation of several oncogenic pathways.
65 s been implicated as downstream effectors in oncogenic pathways.
66 ne domains harboring downstream effectors of oncogenic pathways.
67 ons of two to six drugs that target critical oncogenic pathways.
68 n an inhibitor capable of targeting multiple oncogenic pathways.
69 olling a network of interacting partners and oncogenic pathways.
70 lpha functions, and activating AKT-regulated oncogenic pathways.
71 uence cancer susceptibility can identify key oncogenic pathways.
72 As many tumour types rely on overlapping oncogenic pathways, a core set of microRNAs may exist, w
74 Together, these results demonstrate that the oncogenic pathway activated within a tumor is a primary
75 study, we examined the relationship between oncogenic pathway activation and breast cancer subtype b
78 ignificant clusters representing patterns of oncogenic pathway activation and tumor biology/microenvi
79 of patients with NSCLC, subgroups defined by oncogenic pathway activation profiles were associated wi
83 on the use of gene expression signatures of oncogenic pathway activity (n = 52) as a framework to an
85 ctivation of Notch1 synergizes with multiple oncogenic pathways altered in early disease to promote t
86 ges with hormone therapy and progression and oncogenic pathway analysis was used to identify biologic
87 l oxidase, a phenotypic inhibitor of the ras oncogenic pathway and a tumor suppressor, as SLPI-repres
88 cate the GPI anchoring system as a potential oncogenic pathway and therapeutic target in human cancer
89 olve either mutational activation of the Ras oncogenic pathway and/or inactivation of the retinoblast
90 renhancers, PBX1 directly regulates critical oncogenic pathways and a FOXM1-dependent transcriptional
91 tify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatm
92 aset, finding increased curvature in several oncogenic pathways and decreased curvature in tumor supp
93 ations were associated with hyperactivity of oncogenic pathways and hepatic infiltration of inflammat
94 recent study, Dias et al. propose activating oncogenic pathways and inducing replication stress, resu
95 These lead to activation of HIF-dependent oncogenic pathways and inhibition of histone and DNA dem
96 geted tyrosine kinase inhibitor that targets oncogenic pathways and is a more potent inhibitor than i
97 (Akt) signaling pathway is one of the major oncogenic pathways and is activated in many types of hum
98 so revealed that JQ1 can activate additional oncogenic pathways and may affect epithelial-to-mesenchy
99 of NAALADL2 can impact upon a number of pro-oncogenic pathways and processes, making it a useful bio
101 lish TH action as a critical hub of multiple oncogenic pathways and provide functional and mechanisti
102 tment to and action on target genes to drive oncogenic pathways and repress differentiation programs.
103 e paradigm for defining both the function of oncogenic pathways and the clinically relevant subgroups
104 olecular links between tumor-suppressive and oncogenic pathways and the control of protein synthetic
105 We sought to investigate the Src-mediated oncogenic pathways and tumor biology using AZD0530, a no
106 ession signatures reflecting deregulation of oncogenic pathways and tumor microenvironment to highlig
108 pression in leukemias, particularly with the oncogenic pathways and with the IKZF1/Ikaros and MEF2C-p
109 miRNA 5p/3p pairs that coordinately modulate oncogenic pathways and/or cell survival/growth across ca
110 fy progression-associated somatic mutations, oncogenic pathways, and association between the mutation
111 states, lineage plasticity, clonal dynamics, oncogenic pathways, and cellular interactions to their s
112 that coordinates the activation of multiple oncogenic pathways, and demonstrate for the first time t
113 vised applications, including characterizing oncogenic pathways, and identifying rare populations of
114 cific copy number alterations, activation of oncogenic pathways, and is associated with worse outcome
115 is important for the activation of multiple oncogenic pathways, and its deletion suppresses the abil
116 transcriptional changes in developmental and oncogenic pathways, and noted a marked upregulation of E
117 BC xenografts reprograms cistromes, inhibits oncogenic pathways, and promotes cellular elasticity tow
118 he biological activities of cancer genes and oncogenic pathways, and recent studies have poignantly i
125 oviding a mechanistic link between two major oncogenic pathways, as well as promising therapeutic imp
128 tics has uncovered many tumor-suppressor and oncogenic pathways, but few alterations have revealed me
129 ctor receptors rank among the most important oncogenic pathways, but pharmacologic inhibitors often d
130 dence for proliferation, disruption of other oncogenic pathways can unmask cooperative antiproliferat
132 fying an additional mechanism by which these oncogenic pathways cooperate and a critical role for Ras
134 ning the signaling output of cilia-localized oncogenic pathways could identify specific targets for c
135 erapy response signatures with signatures of oncogenic pathway deregulation to identify new therapeut
136 ient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development
137 to chemotherapy, coupled with prediction of oncogenic pathway deregulation, as a method to direct th
138 and TbetaRI, resulting in the inhibition of oncogenic pathways downstream of both proteins, subseque
139 e next took a candidate approach to identify oncogenic pathways downstream of Notch, focusing on Myc
140 eptibility to develop neuroblastoma, but the oncogenic pathways downstream of the LMO1 transcriptiona
145 ypes may result from activation of different oncogenic pathways during tumorigenesis and/or from a di
147 ated alternative exon in a constituent of an oncogenic pathway eliminates tumor suppressor functions
151 yanate (BITC) acts by targeting multiple pro-oncogenic pathways/genes, including signal transducer an
157 hput sequencing technologies that can reveal oncogenic pathways have stimulated interest in tailoring
159 n tumor promotion and progression downstream oncogenic pathways; however, the molecular mechanisms un
160 pathways that build on current knowledge of oncogenic pathways; however, we need to address major ba
161 The Ras/Raf/MEK/ERK signal transduction, an oncogenic pathway implicated in a variety of human cance
162 Ras/Raf/MEK/ERK signal transduction is a key oncogenic pathway implicated in a variety of human cance
163 n of the cognate transcripts, including many oncogenic pathways implicated in pancreatic neoplasia, s
164 onstrate that ZNF304 promotes multiple proto-oncogenic pathways important for cell survival, migratio
167 r findings reveal a critical function of the oncogenic pathway in innate immune regulation and unexpe
169 s identify MITF-BCL2A1 as a lineage-specific oncogenic pathway in melanoma and underscore its role fo
174 y and suggest that PGE(2) may act with major oncogenic pathways in a synergistic fashion to activate
175 ryonic hematopoiesis have been implicated in oncogenic pathways in adults, an understanding of blood
177 e cooperative interaction between 2 critical oncogenic pathways in colorectal tumorigenesis and highl
178 triggers necrosis by activating pre-existing oncogenic pathways in cystine-addicted TNBC with promine
181 ribe a protocol for quantitative analysis of oncogenic pathways in HCC biopsies and obtained first in
185 eta-catenin signaling can combine with other oncogenic pathways in lung epithelium to produce a more
188 e likely based on the activation of multiple oncogenic pathways in melanomas in addition to the mitog
189 n AXL kinase inhibitor, influences redundant oncogenic pathways in metastatic lung cancer cells.
190 o simultaneously regulate multiple essential oncogenic pathways in MPNST cells, including the Wnt/bet
192 0 is unique in simultaneously inhibiting key oncogenic pathways in multiple myeloma and supports furt
193 f Sp TFs by RNAi also inhibits two major pro-oncogenic pathways in pancreatic cancer cells, namely ma
197 ptomic analysis indicated that iAs activated oncogenic pathways in PrSPCs, including the KEAP1-NRF2 p
200 imens revealed heterogeneity among activated oncogenic pathways in T-IC (e.g., 80% Gli1, 45% Stat3, 1
201 utic strategies that target overlapping core oncogenic pathways in the context of the 10 hallmarks of
202 ht on how the skin handles the activation of oncogenic pathways in the stem cell compartment and how
205 ic transformation triggered by activation of oncogenic pathways in vitro, but the relevance of senesc
209 ith an increase in expression of potentially oncogenic pathways including inflammation processes and
212 tumor progression by downregulating multiple oncogenic pathways including Wnt signaling and cyclin D1
214 ppressed cell proliferation and targeted key oncogenic pathways, including cell cycle, apoptosis, Akt
215 led that PTEN/p53-loss induced activation of oncogenic pathways, including HIPPO-YAP and PI3K signali
219 by genomic alterations that dysregulate key oncogenic pathways influencing cell growth and survival.
222 lated FGFR2 signaling is one of the critical oncogenic pathways involved in the initiation and/or mai
226 esults suggest that the activated TLR4/NANOG oncogenic pathway is linked to suppression of cytostatic
229 gene expression signatures characteristic of oncogenic pathways is an important step toward molecular
230 A combinatory strategy targeting multiple oncogenic pathways is critical to enhance the efficacy o
235 n tumors have poor survival, suggesting that oncogenic pathways may inhibit or change PDCD4 function.
236 tion, an important control point of multiple oncogenic pathways, may be an effective anticancer strat
237 e-scale transcriptional profiling identifies oncogenic pathways mediating PRMT5-driven disease progre
238 y components and suggest that this important oncogenic pathway might usefully be targeted upstream of
239 , non-cell-autonomous activation of specific oncogenic pathways might also offer opportunities that c
241 Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitoc
244 ng cyclin D1 remain fully sensitive to other oncogenic pathways of the mammary epithelium, such as th
245 n cancer development the impact of any given oncogenic pathway on the individual cancer pathology is
246 here that BRCA1 deficiency activates the AKT oncogenic pathway, one of the most common alterations as
247 such as the activation or gene dependency of oncogenic pathways or sensitivity to a drug treatment.
248 Cs and SCCs that likely impact the divergent oncogenic pathways, paving the way for targeted drug dis
249 epletion disrupts two commonly dysregulated, oncogenic pathways-PI3K/AKT and Ras/MEK/ERK, resulting i
250 acteria promote activation of an established oncogenic pathway previously implicated in carcinogenesi
251 2 as a central component in an unappreciated oncogenic pathway promoting intestinal transformation.
252 We also identify genes in DNA repair and oncogenic pathways recurrently subject to MSI and uncove
253 plication in the assessment of activation of oncogenic pathways related to glycogenesis and the detec
254 ging evidence suggests that dysregulation of oncogenic pathways requires precise tuning in order for
255 shock protein 90 inhibitor, blocks multiple oncogenic pathways, resulting in antitumor activity.
258 provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targete
260 mice to UV skin carcinogenesis and activated oncogenic pathways similar to those reported in FVB/N mi
261 ss of cancer gene cassettes that engage many oncogenic pathways simultaneously and that such oncogeni
262 CL6 target gene, our results define a second oncogenic pathway, STAT3 activation, which operates in A
263 e for different molecules targeting the same oncogenic pathway substantiates a rational clinical path
264 inducing genetic instability and activating oncogenic pathways such as AKT and its downstream signal
267 -ranked cancer cell eccDNAs were enriched in oncogenic pathways such as the Ras and PI3K-Akt signalin
269 er through deregulation of developmental and oncogenic pathways, such as the Wnt/beta-catenin signali
271 Here we identify a melanoma-cell-intrinsic oncogenic pathway that contributes to a lack of T-cell i
273 mogenesis unless they converge on one single oncogenic pathway that is characteristic of the differen
274 These results link E2a-Pbx1 with Bmi-1 on an oncogenic pathway that is likely to play a role in the p
277 derived from exploiting our knowledge of the oncogenic pathways that are frequently deregulated in ca
278 arch in this area is beginning to define the oncogenic pathways that can interfere with this process
280 t molecular signature for HSTL and highlight oncogenic pathways that offer rationale for exploring ne
281 directly linked with the deregulation of key oncogenic pathways that provide crucial stimulus for tum
282 nalyzed and robust molecular classifiers and oncogenic pathways that reflect the pathobiology of tumo
283 tools to study potential target proteins and oncogenic pathways that were hitherto regarded as poorly
284 the downstream signaling output of two major oncogenic pathways, the PI3 kinase/AKT and the Rat sarco
285 ukemia, but instead of accessing alternative oncogenic pathways, the tumor cells acquired Notch1 muta
286 ession, both blocking and promoting specific oncogenic pathways through its effects on mTORC1 inhibit
287 hat increased glucose uptake activates known oncogenic pathways to induce malignant phenotype, and pr
289 ndant role in coupling diverse intracellular oncogenic pathways to the tumor microenvironment, furthe
294 Changes in gene expression and associated oncogenic pathways were attenuated in men on the glucora
297 s downstream effector STAT3 constitute a key oncogenic pathway, which has been thought to be function
298 en innate immune signaling and activation of oncogenic pathways, which may be targeted to prevent or
300 it tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell divis