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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
73             Recently, we have shown that the oncogenic pathway activated by Galpha(12) involves the r
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
76      Gene expression signatures representing oncogenic pathway activation and tumor biology/microenvi
77                      Signatures representing oncogenic pathway activation and tumor biology/microenvi
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
80 n the pattern of gene expression, as well as oncogenic pathway activation.
81 R or constitutively active mutants, leads to oncogenic pathway activation.
82 enomic taxonomy stratified by tumor type and oncogenic pathway activation.
83  on the use of gene expression signatures of oncogenic pathway activity (n = 52) as a framework to an
84      Importantly, we show that signatures of oncogenic pathway activity provide further dissection of
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
100 hich have distinct biological differences in oncogenic pathways and prognosis.
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
107                                              Oncogenic pathways and tumor-host interactions also were
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
119 targeting AR signaling, DNA repair, multiple oncogenic pathways, and spliceosome regulation.
120 pressors p53 and PTEN, activation of several oncogenic pathways, and the TMPRSS2-ERG fusion.
121                  Therefore, IL6/STAT3 and ER oncogenic pathways are functionally decoupled, highlight
122                                           As oncogenic pathways are highly conserved in vertebrates,
123 eneous group of conditions in which multiple oncogenic pathways are involved.
124 s as a proliferation regulator by inhibiting oncogenic pathways as a transcriptional repressor.
125 oviding a mechanistic link between two major oncogenic pathways, as well as promising therapeutic imp
126 ntensive efforts directed at the analysis of oncogenic pathways associated with human cancer.
127 because of their ability to repress multiple oncogenic pathways at once.
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
131 ach for functional drug target validation in oncogenic pathway contexts.
132 fying an additional mechanism by which these oncogenic pathways cooperate and a critical role for Ras
133                            The activation of oncogenic pathways could be responsible for the clinical
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
141             Our findings imply that multiple oncogenic pathways drive chromosomal instability during
142                               However, SOX11 oncogenic pathways driving MCL tumor progression are poo
143 ansion of the original tumors and identified oncogenic pathways driving progression.
144           The aberrant activation of the ERG oncogenic pathway due to the TMPRSS2-ERG gene fusion is
145 ypes may result from activation of different oncogenic pathways during tumorigenesis and/or from a di
146  signature exhibited activation of different oncogenic pathways (e.g., EGFR, SRC, and MYC).
147 ated alternative exon in a constituent of an oncogenic pathway eliminates tumor suppressor functions
148          Moreover, the activation of several oncogenic pathways failed to alleviate the fitness defec
149                          We describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in
150             These observations ascribe a new oncogenic pathway for T-antigen, and offer an alternativ
151 yanate (BITC) acts by targeting multiple pro-oncogenic pathways/genes, including signal transducer an
152 ors that cause constitutive activity of this oncogenic pathway have been identified.
153                                          Two oncogenic pathways have been hypothesized for multiple m
154                               Several common oncogenic pathways have been implicated in the emergence
155              Androgen receptor (AR)-mediated oncogenic pathways have not been fully elucidated.
156       Anti-cancer drugs targeted to specific oncogenic pathways have shown promising therapeutic resu
157 hput sequencing technologies that can reveal oncogenic pathways have stimulated interest in tailoring
158                                    Targeting oncogenic pathways holds promise for brain tumor treatme
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
165  to Wnt/beta-catenin signaling, itself a key oncogenic pathway in colorectal cancer.
166 regulatory loop is an important, targetable, oncogenic pathway in CTCL.
167 r findings reveal a critical function of the oncogenic pathway in innate immune regulation and unexpe
168 stability, which cooperates with the neu-ras oncogenic pathway in mammary tumorigenesis.
169 s identify MITF-BCL2A1 as a lineage-specific oncogenic pathway in melanoma and underscore its role fo
170           However, STAT3 activation is a key oncogenic pathway in natural killer (NK)-lineage large g
171  OPA tumor cells, indicating a role for this oncogenic pathway in OPA.
172 in signaling can be both a physiological and oncogenic pathway in the liver.
173 onent of the ErbB2/Ras (but not the Wnt/Myc) oncogenic pathway in the mammary epithelium.
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
176 as, and virus infection can induce important oncogenic pathways in colon-cancer cells.
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
179 ate (S1P), a bioactive lipid that stimulates oncogenic pathways in glioblastoma.
180 nd PI3K enzymes, which are members of common oncogenic pathways in haematological malignancies.
181 ribe a protocol for quantitative analysis of oncogenic pathways in HCC biopsies and obtained first in
182                                 To elucidate oncogenic pathways in HNSCC with and without HPV infecti
183 dominant feedback network regulating central oncogenic pathways in human cancer.
184  cancer types and has been shown to modulate oncogenic pathways in in vitro studies.
185 eta-catenin signaling can combine with other oncogenic pathways in lung epithelium to produce a more
186 e ibrutinib resistance by targeting multiple oncogenic pathways in MCL.
187 thereby suppressing epigenetically-activated oncogenic pathways in melanoma.
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
191              Wnt signaling is one of the key oncogenic pathways in multiple cancers, and targeting th
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
194 ability to inhibit protein farnesylation and oncogenic pathways in patients with relapsed MM.
195  signaling, one of the most highly activated oncogenic pathways in PCa.
196 d therapeutic interventions against multiple oncogenic pathways in prostate cancer.
197 ptomic analysis indicated that iAs activated oncogenic pathways in PrSPCs, including the KEAP1-NRF2 p
198 -205 (miR-205) in inhibition of Src-mediated oncogenic pathways in renal cancer.
199 AKT and up-regulation of COX-2, two critical oncogenic pathways in skin tumorigenesis.
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
203 cal justification for targeting PRMT5-driven oncogenic pathways in this deadly disease.
204       Our data suggest that targeting common oncogenic pathways in tumor epithelia together with bloc
205 ic transformation triggered by activation of oncogenic pathways in vitro, but the relevance of senesc
206 s Hedgehog signaling, a proproliferative and oncogenic pathway, in murine pancreatic islets.
207 fecting the oxidative stress response or the oncogenic pathways included in the model.
208 of therapeutic agents targeting a variety of oncogenic pathways including cancer stem cells.
209 ith an increase in expression of potentially oncogenic pathways including inflammation processes and
210                                     Multiple oncogenic pathways including PI3K/AKT/mTOR converged on
211           This causes activation of multiple oncogenic pathways including Ras, PI3K/Akt, Raf/ERK, Src
212 tumor progression by downregulating multiple oncogenic pathways including Wnt signaling and cyclin D1
213           Furthermore, ZFP90 affects several oncogenic pathways, including BMP4, and promotes carcino
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
216 the most prevalent EWS/ETS fusion, activates oncogenic pathways independent of its DBD.
217 dm2 is activated in response to a variety of oncogenic pathways independent of p53.
218                           Co-targeting these oncogenic pathways induced tumor growth arrest.
219  by genomic alterations that dysregulate key oncogenic pathways influencing cell growth and survival.
220 c strategies with chemotherapeutics or other oncogenic pathway inhibitors.
221 nd malignant progression is dependent on the oncogenic pathway involved.
222 lated FGFR2 signaling is one of the critical oncogenic pathways involved in the initiation and/or mai
223 nesis proceeds through a preferred secondary oncogenic pathway involving Kras2.
224                                        These oncogenic pathways, involving leukocytes and fibroblasts
225 crodomains, and the overall activity of this oncogenic pathway is dependent on raft function.
226 esults suggest that the activated TLR4/NANOG oncogenic pathway is linked to suppression of cytostatic
227           Concomitant inhibition of multiple oncogenic pathways is a desirable goal in cancer therapy
228              Transcriptional deregulation of oncogenic pathways is a hallmark of cancer and can be du
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
231 ve pressure or is inherently orchestrated by oncogenic pathways is unresolved.
232              These results identify multiple oncogenic pathways leading to TPL2 deregulation and high
233                          Disruption of these oncogenic pathways led to growth retardation and apoptot
234         Identifying such metastasis-specific oncogenic pathways may help to manipulate tumor behavior
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
240 ul tool in cancer genomics, our knowledge of oncogenic pathway modules is incomplete.
241   Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitoc
242                                 However, the oncogenic pathway of Notch1-induced transformation is no
243  for the first time to our knowledge, in EMT oncogenic pathways of cancer progression.
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.
256                                  Analysis of oncogenic pathways revealed that older patients had high
257 nses to overcome resistance to inhibitors of oncogenic pathway signaling.
258 provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targete
259                                        Using oncogenic pathway signatures, we show that gene sets bui
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
265 ticularly via FOS family members, activating oncogenic pathways such as MAPK and TNF signaling.
266                   Additionally, NAC1 affects oncogenic pathways such as the CD44-JAK1-STAT3 axis and
267 -ranked cancer cell eccDNAs were enriched in oncogenic pathways such as the Ras and PI3K-Akt signalin
268                     NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase
269 er through deregulation of developmental and oncogenic pathways, such as the Wnt/beta-catenin signali
270 ding repressor activity that blocks multiple oncogenic pathways targeting cyclin D genes.
271   Here we identify a melanoma-cell-intrinsic oncogenic pathway that contributes to a lack of T-cell i
272                      These data delineate an oncogenic pathway that functionally links FGF-2 with EZH
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
275        Wnt/beta-catenin signaling is a known oncogenic pathway that plays a well-defined role in colo
276 reby establishing a functional DEK-DeltaNp63 oncogenic pathway that promotes HNSCC.
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
279            Thus, its inhibition may activate oncogenic pathways that contribute to metastatic castrat
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
288                TBC1D15 activated three novel oncogenic pathways to promote self-renewal, p53 loss, an
289 ndant role in coupling diverse intracellular oncogenic pathways to the tumor microenvironment, furthe
290 ghlighting these genes as drivers of a novel oncogenic pathway underlying ILC development.
291 R transcriptional signature enriched for pro-oncogenic pathways unique to this tumor subclass.
292 ulate the expression of hundreds of genes in oncogenic pathways via a positive feedback loop.
293        Our data also showed that the pSmad3L oncogenic pathway was activated in HBx and HCP-induced I
294    Changes in gene expression and associated oncogenic pathways were attenuated in men on the glucora
295                                              Oncogenic pathways were previously implicated in HDAP su
296                         A common set of five oncogenic pathways were significantly inhibited in diffe
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
299            GSEA was used to identify various oncogenic pathways with MR imaging features.
300 it tumorigenesis induced by the HER2/neu-RAS oncogenic pathway without compromising normal cell divis

 
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