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1 nt important downstream effectors of the ALK oncogenic pathway.
2 t of new strategies to target this pervasive oncogenic pathway.
3 d of INPP5D, an inhibitor of the PI3K-driven oncogenic pathway.
4 mutations of the Brca1 gene activate the Akt oncogenic pathway.
5 ase as an essential effector of the HER2/neu oncogenic pathway.
6 to act as either a tumor suppressor or a pro-oncogenic pathway.
7 not identical, signaling elements of the Ras oncogenic pathway.
8 ound that Brca1 deficiency activates the Akt oncogenic pathway.
9 een innate immune responses and STAT3-driven oncogenic pathways.
10  unrecognized link between the Akt and c-myc oncogenic pathways.
11 atory transcriptome with changes in relevant oncogenic pathways.
12 ts that these malignancies may use different oncogenic pathways.
13 2) is a MAPK that regulates inflammatory and oncogenic pathways.
14 ractions mediate crosstalk between canonical oncogenic pathways.
15 er from the 48 non-redundant genes in the 11 oncogenic pathways.
16 a central role in the activation of multiple oncogenic pathways.
17 f redundancy and signaling through different oncogenic pathways.
18 thetic lethal relationship between these two oncogenic pathways.
19  which leads to the activation of these same oncogenic pathways.
20 regulatory molecules in tumor-suppressor and oncogenic pathways.
21 ent kinase 2 phosphorylation orchestrating 2 oncogenic pathways.
22 oping strategies for optimal intervention of oncogenic pathways.
23 pes are distinct diseases that use different oncogenic pathways.
24 n experimental models that represented other oncogenic pathways.
25 rve as recipients of the Ras- and Myc-driven oncogenic pathways.
26 d how these genes contribute to dysregulated oncogenic pathways.
27 ns serve as cell cycle recipients of several oncogenic pathways.
28 hat reflect the activation status of several oncogenic pathways.
29  particular D-cyclins responsive to specific oncogenic pathways.
30 gene expression profiles for the analysis of oncogenic pathways.
31 mary epithelial cells by activating multiple oncogenic pathways.
32 e a common denominator of the PI3K and FoxG1 oncogenic pathways.
33 cription factor linking the inflammatory and oncogenic pathways.
34 thought to be an important player in several oncogenic pathways.
35 duces both DBD-dependent and DBD-independent oncogenic pathways.
36 linical course and by divergent addiction to oncogenic pathways.
37 ules, resulting in the activation of several oncogenic pathways.
38 s been implicated as downstream effectors in oncogenic pathways.
39 ne domains harboring downstream effectors of oncogenic pathways.
40 n utilization, oxidative stress response and oncogenic pathways.
41 ons of two to six drugs that target critical oncogenic pathways.
42 n an inhibitor capable of targeting multiple oncogenic pathways.
43 olling a network of interacting partners and oncogenic pathways.
44 (CDK) complexes to be activated by mitogenic/oncogenic pathways.
45 lpha functions, and activating AKT-regulated oncogenic pathways.
46 uence cancer susceptibility can identify key oncogenic pathways.
47 f DLBCL and have led to the discovery of key oncogenic pathways.
48 ient oncoproteins and shutting down multiple oncogenic pathways.
49 t on carcinogenesis control broad spectra of oncogenic pathways.
50 R in breast cancer and regulates several pro-oncogenic pathways.
51 ructures with basal polarity, and suppressed oncogenic pathways.
52 linical biopsies or endogenously deregulated oncogenic pathways.
53     As many tumour types rely on overlapping oncogenic pathways, a core set of microRNAs may exist, w
54             Recently, we have shown that the oncogenic pathway activated by Galpha(12) involves the r
55 Together, these results demonstrate that the oncogenic pathway activated within a tumor is a primary
56  study, we examined the relationship between oncogenic pathway activation and breast cancer subtype b
57      Gene expression signatures representing oncogenic pathway activation and tumor biology/microenvi
58                      Signatures representing oncogenic pathway activation and tumor biology/microenvi
59 ignificant clusters representing patterns of oncogenic pathway activation and tumor biology/microenvi
60 of patients with NSCLC, subgroups defined by oncogenic pathway activation profiles were associated wi
61 n the pattern of gene expression, as well as oncogenic pathway activation.
62 enomic taxonomy stratified by tumor type and oncogenic pathway activation.
63  on the use of gene expression signatures of oncogenic pathway activity (n = 52) as a framework to an
64      Importantly, we show that signatures of oncogenic pathway activity provide further dissection of
65 ctivation of Notch1 synergizes with multiple oncogenic pathways altered in early disease to promote t
66 ges with hormone therapy and progression and oncogenic pathway analysis was used to identify biologic
67 l oxidase, a phenotypic inhibitor of the ras oncogenic pathway and a tumor suppressor, as SLPI-repres
68 cate the GPI anchoring system as a potential oncogenic pathway and therapeutic target in human cancer
69 olve either mutational activation of the Ras oncogenic pathway and/or inactivation of the retinoblast
70 tify miR-135b as a key downsteam effector of oncogenic pathways and a potential target for CRC treatm
71 ations were associated with hyperactivity of oncogenic pathways and hepatic infiltration of inflammat
72    These lead to activation of HIF-dependent oncogenic pathways and inhibition of histone and DNA dem
73 geted tyrosine kinase inhibitor that targets oncogenic pathways and is a more potent inhibitor than i
74  (Akt) signaling pathway is one of the major oncogenic pathways and is activated in many types of hum
75  of NAALADL2 can impact upon a number of pro-oncogenic pathways and processes, making it a useful bio
76 lish TH action as a critical hub of multiple oncogenic pathways and provide functional and mechanisti
77 e paradigm for defining both the function of oncogenic pathways and the clinically relevant subgroups
78 olecular links between tumor-suppressive and oncogenic pathways and the control of protein synthetic
79    We sought to investigate the Src-mediated oncogenic pathways and tumor biology using AZD0530, a no
80 ession signatures reflecting deregulation of oncogenic pathways and tumor microenvironment to highlig
81                                              Oncogenic pathways and tumor-host interactions also were
82 pression in leukemias, particularly with the oncogenic pathways and with the IKZF1/Ikaros and MEF2C-p
83  that coordinates the activation of multiple oncogenic pathways, and demonstrate for the first time t
84 cific copy number alterations, activation of oncogenic pathways, and is associated with worse outcome
85  is important for the activation of multiple oncogenic pathways, and its deletion suppresses the abil
86 transcriptional changes in developmental and oncogenic pathways, and noted a marked upregulation of E
87 he biological activities of cancer genes and oncogenic pathways, and recent studies have poignantly i
88 pressors p53 and PTEN, activation of several oncogenic pathways, and the TMPRSS2-ERG fusion.
89 eneous group of conditions in which multiple oncogenic pathways are involved.
90 s as a proliferation regulator by inhibiting oncogenic pathways as a transcriptional repressor.
91 oviding a mechanistic link between two major oncogenic pathways, as well as promising therapeutic imp
92 ntensive efforts directed at the analysis of oncogenic pathways associated with human cancer.
93 because of their ability to repress multiple oncogenic pathways at once.
94 dence for proliferation, disruption of other oncogenic pathways can unmask cooperative antiproliferat
95 ach for functional drug target validation in oncogenic pathway contexts.
96 fying an additional mechanism by which these oncogenic pathways cooperate and a critical role for Ras
97                            The activation of oncogenic pathways could be responsible for the clinical
98 erapy response signatures with signatures of oncogenic pathway deregulation to identify new therapeut
99 ient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development
100  to chemotherapy, coupled with prediction of oncogenic pathway deregulation, as a method to direct th
101 e next took a candidate approach to identify oncogenic pathways downstream of Notch, focusing on Myc
102             Our findings imply that multiple oncogenic pathways drive chromosomal instability during
103                               However, SOX11 oncogenic pathways driving MCL tumor progression are poo
104 ansion of the original tumors and identified oncogenic pathways driving progression.
105 ypes may result from activation of different oncogenic pathways during tumorigenesis and/or from a di
106  signature exhibited activation of different oncogenic pathways (e.g., EGFR, SRC, and MYC).
107 ated alternative exon in a constituent of an oncogenic pathway eliminates tumor suppressor functions
108          Moreover, the activation of several oncogenic pathways failed to alleviate the fitness defec
109                          We describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in
110             These observations ascribe a new oncogenic pathway for T-antigen, and offer an alternativ
111 yanate (BITC) acts by targeting multiple pro-oncogenic pathways/genes, including signal transducer an
112 ors that cause constitutive activity of this oncogenic pathway have been identified.
113                                          Two oncogenic pathways have been hypothesized for multiple m
114                               Several common oncogenic pathways have been implicated in the emergence
115              Androgen receptor (AR)-mediated oncogenic pathways have not been fully elucidated.
116       Anti-cancer drugs targeted to specific oncogenic pathways have shown promising therapeutic resu
117 hput sequencing technologies that can reveal oncogenic pathways have stimulated interest in tailoring
118 n tumor promotion and progression downstream oncogenic pathways; however, the molecular mechanisms un
119  pathways that build on current knowledge of oncogenic pathways; however, we need to address major ba
120  The Ras/Raf/MEK/ERK signal transduction, an oncogenic pathway implicated in a variety of human cance
121 Ras/Raf/MEK/ERK signal transduction is a key oncogenic pathway implicated in a variety of human cance
122 n of the cognate transcripts, including many oncogenic pathways implicated in pancreatic neoplasia, s
123 onstrate that ZNF304 promotes multiple proto-oncogenic pathways important for cell survival, migratio
124  to Wnt/beta-catenin signaling, itself a key oncogenic pathway in colorectal cancer.
125 stability, which cooperates with the neu-ras oncogenic pathway in mammary tumorigenesis.
126 s identify MITF-BCL2A1 as a lineage-specific oncogenic pathway in melanoma and underscore its role fo
127           However, STAT3 activation is a key oncogenic pathway in natural killer (NK)-lineage large g
128 in signaling can be both a physiological and oncogenic pathway in the liver.
129 onent of the ErbB2/Ras (but not the Wnt/Myc) oncogenic pathway in the mammary epithelium.
130 y and suggest that PGE(2) may act with major oncogenic pathways in a synergistic fashion to activate
131 ryonic hematopoiesis have been implicated in oncogenic pathways in adults, an understanding of blood
132 as, and virus infection can induce important oncogenic pathways in colon-cancer cells.
133 e cooperative interaction between 2 critical oncogenic pathways in colorectal tumorigenesis and highl
134 triggers necrosis by activating pre-existing oncogenic pathways in cystine-addicted TNBC with promine
135 nd PI3K enzymes, which are members of common oncogenic pathways in haematological malignancies.
136 ribe a protocol for quantitative analysis of oncogenic pathways in HCC biopsies and obtained first in
137                                 To elucidate oncogenic pathways in HNSCC with and without HPV infecti
138 dominant feedback network regulating central oncogenic pathways in human cancer.
139  cancer types and has been shown to modulate oncogenic pathways in in vitro studies.
140 eta-catenin signaling can combine with other oncogenic pathways in lung epithelium to produce a more
141 e ibrutinib resistance by targeting multiple oncogenic pathways in MCL.
142 e likely based on the activation of multiple oncogenic pathways in melanomas in addition to the mitog
143              Wnt signaling is one of the key oncogenic pathways in multiple cancers, and targeting th
144 0 is unique in simultaneously inhibiting key oncogenic pathways in multiple myeloma and supports furt
145 f Sp TFs by RNAi also inhibits two major pro-oncogenic pathways in pancreatic cancer cells, namely ma
146 ability to inhibit protein farnesylation and oncogenic pathways in patients with relapsed MM.
147 d therapeutic interventions against multiple oncogenic pathways in prostate cancer.
148 -205 (miR-205) in inhibition of Src-mediated oncogenic pathways in renal cancer.
149 AKT and up-regulation of COX-2, two critical oncogenic pathways in skin tumorigenesis.
150 imens revealed heterogeneity among activated oncogenic pathways in T-IC (e.g., 80% Gli1, 45% Stat3, 1
151 utic strategies that target overlapping core oncogenic pathways in the context of the 10 hallmarks of
152 ht on how the skin handles the activation of oncogenic pathways in the stem cell compartment and how
153 cal justification for targeting PRMT5-driven oncogenic pathways in this deadly disease.
154       Our data suggest that targeting common oncogenic pathways in tumor epithelia together with bloc
155 ic transformation triggered by activation of oncogenic pathways in vitro, but the relevance of senesc
156 s Hedgehog signaling, a proproliferative and oncogenic pathway, in murine pancreatic islets.
157 fecting the oxidative stress response or the oncogenic pathways included in the model.
158 of therapeutic agents targeting a variety of oncogenic pathways including cancer stem cells.
159                                     Multiple oncogenic pathways including PI3K/AKT/mTOR converged on
160           This causes activation of multiple oncogenic pathways including Ras, PI3K/Akt, Raf/ERK, Src
161 tumor progression by downregulating multiple oncogenic pathways including Wnt signaling and cyclin D1
162 ppressed cell proliferation and targeted key oncogenic pathways, including cell cycle, apoptosis, Akt
163 the most prevalent EWS/ETS fusion, activates oncogenic pathways independent of its DBD.
164 dm2 is activated in response to a variety of oncogenic pathways independent of p53.
165  by genomic alterations that dysregulate key oncogenic pathways influencing cell growth and survival.
166 nd malignant progression is dependent on the oncogenic pathway involved.
167 lated FGFR2 signaling is one of the critical oncogenic pathways involved in the initiation and/or mai
168 nesis proceeds through a preferred secondary oncogenic pathway involving Kras2.
169                                        These oncogenic pathways, involving leukocytes and fibroblasts
170 crodomains, and the overall activity of this oncogenic pathway is dependent on raft function.
171 esults suggest that the activated TLR4/NANOG oncogenic pathway is linked to suppression of cytostatic
172           Concomitant inhibition of multiple oncogenic pathways is a desirable goal in cancer therapy
173              Transcriptional deregulation of oncogenic pathways is a hallmark of cancer and can be du
174 gene expression signatures characteristic of oncogenic pathways is an important step toward molecular
175    A combinatory strategy targeting multiple oncogenic pathways is critical to enhance the efficacy o
176 ve pressure or is inherently orchestrated by oncogenic pathways is unresolved.
177              These results identify multiple oncogenic pathways leading to TPL2 deregulation and high
178                          Disruption of these oncogenic pathways led to growth retardation and apoptot
179         Identifying such metastasis-specific oncogenic pathways may help to manipulate tumor behavior
180 n tumors have poor survival, suggesting that oncogenic pathways may inhibit or change PDCD4 function.
181 tion, an important control point of multiple oncogenic pathways, may be an effective anticancer strat
182 y components and suggest that this important oncogenic pathway might usefully be targeted upstream of
183 ul tool in cancer genomics, our knowledge of oncogenic pathway modules is incomplete.
184   Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitoc
185                                 However, the oncogenic pathway of Notch1-induced transformation is no
186  for the first time to our knowledge, in EMT oncogenic pathways of cancer progression.
187 ng cyclin D1 remain fully sensitive to other oncogenic pathways of the mammary epithelium, such as th
188 n cancer development the impact of any given oncogenic pathway on the individual cancer pathology is
189 here that BRCA1 deficiency activates the AKT oncogenic pathway, one of the most common alterations as
190 such as the activation or gene dependency of oncogenic pathways or sensitivity to a drug treatment.
191 epletion disrupts two commonly dysregulated, oncogenic pathways-PI3K/AKT and Ras/MEK/ERK, resulting i
192 acteria promote activation of an established oncogenic pathway previously implicated in carcinogenesi
193 2 as a central component in an unappreciated oncogenic pathway promoting intestinal transformation.
194     We also identify genes in DNA repair and oncogenic pathways recurrently subject to MSI and uncove
195 plication in the assessment of activation of oncogenic pathways related to glycogenesis and the detec
196                                  Analysis of oncogenic pathways revealed that older patients had high
197 provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targete
198                                        Using oncogenic pathway signatures, we show that gene sets bui
199 mice to UV skin carcinogenesis and activated oncogenic pathways similar to those reported in FVB/N mi
200 ss of cancer gene cassettes that engage many oncogenic pathways simultaneously and that such oncogeni
201 CL6 target gene, our results define a second oncogenic pathway, STAT3 activation, which operates in A
202 e for different molecules targeting the same oncogenic pathway substantiates a rational clinical path
203  inducing genetic instability and activating oncogenic pathways such as AKT and its downstream signal
204                     NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase
205 er through deregulation of developmental and oncogenic pathways, such as the Wnt/beta-catenin signali
206 ding repressor activity that blocks multiple oncogenic pathways targeting cyclin D genes.
207   Here we identify a melanoma-cell-intrinsic oncogenic pathway that contributes to a lack of T-cell i
208                      These data delineate an oncogenic pathway that functionally links FGF-2 with EZH
209 These results link E2a-Pbx1 with Bmi-1 on an oncogenic pathway that is likely to play a role in the p
210        Wnt/beta-catenin signaling is a known oncogenic pathway that plays a well-defined role in colo
211 reby establishing a functional DEK-DeltaNp63 oncogenic pathway that promotes HNSCC.
212 derived from exploiting our knowledge of the oncogenic pathways that are frequently deregulated in ca
213 arch in this area is beginning to define the oncogenic pathways that can interfere with this process
214            Thus, its inhibition may activate oncogenic pathways that contribute to metastatic castrat
215 t molecular signature for HSTL and highlight oncogenic pathways that offer rationale for exploring ne
216 directly linked with the deregulation of key oncogenic pathways that provide crucial stimulus for tum
217 nalyzed and robust molecular classifiers and oncogenic pathways that reflect the pathobiology of tumo
218 tools to study potential target proteins and oncogenic pathways that were hitherto regarded as poorly
219 the downstream signaling output of two major oncogenic pathways, the PI3 kinase/AKT and the Rat sarco
220 ukemia, but instead of accessing alternative oncogenic pathways, the tumor cells acquired Notch1 muta
221 ession, both blocking and promoting specific oncogenic pathways through its effects on mTORC1 inhibit
222 hat increased glucose uptake activates known oncogenic pathways to induce malignant phenotype, and pr
223 ndant role in coupling diverse intracellular oncogenic pathways to the tumor microenvironment, furthe
224 ghlighting these genes as drivers of a novel oncogenic pathway underlying ILC development.
225        Our data also showed that the pSmad3L oncogenic pathway was activated in HBx and HCP-induced I
226                                              Oncogenic pathways were previously implicated in HDAP su
227 en innate immune signaling and activation of oncogenic pathways, which may be targeted to prevent or
228            GSEA was used to identify various oncogenic pathways with MR imaging features.
229 it tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell divis

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