ライフサイエンスコーパス: oncogene

1 instability associated with the human c-MYC oncogene.

2 ukaryotic initiation factor, eIF4E, a potent oncogene.

3 enhancer that drives expression of the LMO2 oncogene.

4 stablish PRKCI as an ovarian cancer-specific oncogene.

5 thelial cells for transformation by a single oncogene.

6 oding the DNA binding protein HMGA1, a known oncogene.

7 is effect is mediated via effects on the MYC oncogene.

8 of a transduced tetracycline-regulated v-myc oncogene.

9 pathway causing overexpression of the c-MYC oncogene.

10 view the mechanisms of deregulation of these oncogenes.

11 and the association of metabolic states with oncogenes.

12 development of therapeutics targeting mutant oncogenes.

13 d proliferation and upregulation of cellular oncogenes.

14 key tumor suppressor genes or by activating oncogenes.

15 nally validate CSNK1A1 and RLTPR as putative oncogenes.

16 dback on the Nrf2-dependent transcription of oncogenes.

17 ection of clones harboring integrations near oncogenes.

18 l-studied F-box proteins, which often act as oncogenes.

19 bserved in enhancer DNA sequences near known oncogenes.

20 ty, but also involves the regulation of many oncogenes.

21 rtant roles in cell survival, apoptosis, and oncogenes.

22 lated in lung cancer where they may serve as oncogenes.

23 ignals may be equally significant as mutated oncogenes.

24 ities, and the DeltaN isoforms, which act as oncogenes.

25 est induced by stress such as DNA damage and oncogenes.

26 umour suppressor genes and downregulation of oncogenes.

27 ediate early AP-1 member induced by melanoma oncogenes.

28 c effects by regulating expression of target oncogenes.

29 ates at the chromatin and activates multiple oncogenes.

30 ely linked E26 transformation-specific proto-oncogene 1 (ETS1) is overexpressed in these FLI1-deficie

31 of the orphan receptor tyrosine kinase c-ros oncogene 1 (ROS1), which has a kinase domain that is phy

32 ymphoma kinase (ALK)-rearranged or ROS proto-oncogene 1 (ROS1)-rearranged non-small-cell lung cancer

33 ways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).

34 with a 4.5-fold increase in ETS1 (ETS proto-oncogene 1) mRNA, suggesting that ETS1 is involved in re

35 The polyomavirus middle T antigen (PyMT) oncogene activates the cellular nonreceptor tyrosine kin

36 rmined that tsRNA expression is altered upon oncogene activation and during cancer staging.

37 etrovirus vectors have caused cellular proto-oncogene activation and leukemia, necessitating the use

38 ive or "plastic" states may allow stochastic oncogene activation or nonphysiologic cell fate transiti

39 escent by stress, replicative exhaustion, or oncogene activation, mTORC1 is constitutively active and

40 This was due to higher ROS production and/or oncogene activation, such as RAS, MYC, and c-SRC.

41 cause is currently unknown, but may involve oncogene activation.

42 ls to evade proteostasis stress triggered by oncogene activation.

43 paradigm emerging in cancer biology is that oncogenes actively reprogram cellular metabolism to enab

44 ganoids as a novel approach to understanding oncogene activities and guiding the development of targe

45 chanisms that bypass the requirement for Ras oncogene activity and drive leukemia relapse.

46 underlying incomplete tumor cell killing in oncogene-addicted cancer cells, we investigated the role

47 ility, and response to targeted therapies of oncogene-addicted cells.

48 Notably, KIAA1199 silencing in oncogene-addicted tumor cells improved therapeutic respo

49 together, our results show how blunting MYC oncogene addiction can leverage cancer cell sensitivity

50 lly targetable mechanism of escape from NRAS oncogene addiction in AML.

51 tion and survival, a phenomenon described as oncogene addiction.

52 nd driving resistance to therapies targeting oncogene-addiction.Significance: These important finding

53 trinsic role, recent evidence indicates that oncogenes also directly regulate immune responses, leadi

54 emic cells expressing the t(8;21)-associated oncogene AML1-ETO (AE).

55 Oncogene amplification confers a growth advantage to tum

56 (EZH2) has been characterized as a critical oncogene and a promising drug target in human malignant

57 ell cycle regulators and function as a proto-oncogene and a tumor suppressor respectively in human on

58 ammary tumorigenesis harboring the MMTV-HER2 oncogene and mutation of MED1 to evaluate its role in HE

59 udy EGFR inhibitor resistance and review the oncogene and non-oncogene signalling mechanisms that hav

60 r squares to guanine quadruplexes, including oncogene and telomere-associated DNA and RNA sequences.

61 ors led to the repression of BRD4 downstream oncogenes and abrogation of cellular transformation.

62 romodomain proteins impact the expression of oncogenes and anti-apoptotic proteins.

63 rates that are comparable to those of known oncogenes and are ten-fold higher than those of random g

64 numerous common integration sites near proto-oncogenes and by increased abundance of clones with inte

65 While frequently mutated oncogenes and differentially expressed genes, which we t

66 We have now determined how HPV oncogenes and estrogen treatment affect genome-wide host

67 ase (PI3K) activity is stimulated by diverse oncogenes and growth factor receptors, and elevated PI3K

68 hort-term inflammation to restrain activated oncogenes and to chronic inflammation that associates wi

69 Known oncogenes and tumor suppressor genes, beyond those engin

70 ociated with specific genetic alterations in oncogenes and tumor suppressors are highly context-depen

71 We also discuss how oncogenes and tumour suppressors promote nutrient uptake

72 Many activate known oncogenes, and CRC growth can be mitigated through pharm

73 We discuss here how oncogenes, and in particular MYC, suppress immune survei

74 s its function via regulation of a subset of oncogenes, and knockdown of circCCDC66 inhibited tumor g

75 lities (STAT3 and BCL6) downstream of common oncogenes, and tumor suppressors may provide a potent wa

76 activated T cells 3 (NFATc3) and FosB proto-oncogene, AP-1 transcription factor subunit (FosB) are i

77 nstitutive activation of NRAS and KRAS proto-oncogenes are among the most common in human cancer and

78 Here we show that the ERBB2 oncogene at 17q12 is susceptible to palindromic gene amp

79 Twenty-six patients were tested for a proto-oncogene B-Raf (V600E) (BRAF) mutation (18 had the mutat

80 s disorder leading to over-expression of the oncogene BCL6 and stabilization of hypoxia-induced facto

81 enized a selected region within the leukemic oncogene BCR-ABL1 Using bulk competitions with a deep-se

82 his strategy, we engineered the known fusion oncogenes, BCR-ABL1, EML4-ALK, and ETV6-NTRK3, as well a

83 The viral oncogene blocks p53-mediated adverse effects during vira

84 propagation of an amplification in the BRAF oncogene (BRAF(amp)) in patient-derived tumor xenografts

85 The MYC oncogene broadly promotes transcription mediated by all

86 Therefore, the induction of the viral oncogene by p53 provides a means for the virus to cope w

87 d this problem and identified a CNV-targeted oncogene by performing comparative oncogenomics of human

88 transcriptional repression of 5-LO by proto-oncogene c-Myb and conclude that loss of stromal 5-LO ex

89 Subsequently, upregulation of proto-oncogene c-Myb in TAMs induced a stable transcriptional

90 It also repressed the expression of the oncogene c-Myc and the neural ESC marker CDK2 in vitro,

91 that included Notch pathway components, the oncogene c-Myc, and the mammary stem cell regulator Id4

92 n of the signaling proteins FBJ osteosarcoma oncogene (c-FOS, encoded by Fos) and dual-specificity ph

93 atus and somatic mutation in the B-Raf proto-oncogene (c.1799T>A [V600E]; BRAFV600E) or exon 2 of the

94 KP2 axis forms an oncogene-tumour suppressor-oncogene cascade to control cancer cell growth with FBXW

95 miR-23 target genes, including the oncogenes Ccnd1 as well as Adam19, Plau, and Wsb1 that p

96 secondary DNA structures to modulate two key oncogenes, cellular-myelocytomatosis (MYC) and B-cell ly

97 osomal breakpoint hotspot in the human c-MYC oncogene containing both potential G4-forming and H-DNA-

98 For example, the human KRAS proto-oncogene contains a nuclease-hypersensitive element loca

99 , these data support our hypothesis that HPV oncogenes contribute to the genomic instability observed

100 cted that ecDNA amplification would increase oncogene copy number and intratumoural heterogeneity mor

101 these cells to form glioma-like tumors in an oncogene-driven mouse brain tumor model.

102 Murine-reconstituted, oncogene-driven prostate cancer cells (0.1 x 10(6)) (RM1

103 ing clear causality between the mutation and oncogene dysregulation.

104 -related transcription factor 1, Fli-1 proto-oncogene, E-twenty-six (ETS) transcription factor (frien

105 tral role in cervical carcinogenesis and its oncogene E7 is essential in this process.

106 Compared with the capsid proteins, the oncogenes E7 and E6 had increased substitution rates ind

107 c consequences ranged from strong individual oncogene effects to weak but quantifiable multigene expr

108 Human ALC1 is an oncogene-encoded chromatin-remodeling enzyme required fo

109 rming oncogenic activity of the known fusion oncogenes engineered by our construction strategy, we va

110 21 prevent detrimental hyperproliferation of oncogene expressing SVZ cells by facilitating an antipro

111 Neat1 deficiency enhances transformation in oncogene-expressing fibroblasts and promotes the develop

112 In vivo, nonproliferating oncogene-expressing melanocytes localize to skin-drainin

113 n this aggressive cervical cancer is not HPV oncogene expression but rather the overexpression of Myc

114 th DAXX and, in turn PTEN directly regulates oncogene expression by modulating DAXX-H3.3 association

115 We demonstrate the spatiotemporal control of oncogene expression in live zebrafish, and characterize

116 at allows for the precise optical control of oncogene expression in live zebrafish.

117 , we show that light can be used to activate oncogene expression in selected tissues and single cells

118 HPV oncogene expression in the cervical epithelium elicited

119 bining p53 inactivation with E1A or HRas-V12 oncogene expression, we reproduced a similar up-regulati

120 mediators, extracellular matrix proteins and oncogene expression.

121 ion of v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B, which promotes beta-cell fun

122 g in drug-naive cancer cells harboring these oncogene fusions.

123 mal translocations producing a chimaeric MLL oncogene give rise to a highly aggressive acute leukaemi

124 Uncontrolled hedgehog (HH)/glioma-associated oncogene (GLI) and WNT/beta-catenin signaling are import

125 the 3' untranslated region of mRNAs encoding oncogenes, growth factors, and various cytokines leads m

126 In this issue of Oncogene, Gu et al. present evidence that POT1, like SSB

127 Targeting somatically activated oncogenes has revolutionized the treatment of non-small

128 ing genomic regions that aberrantly activate oncogenes have remained poorly characterized.

129 The HPV oncogenes hinder HR by allowing the process to begin at

130 in p53 (TP53), erythroblastic leukemia viral oncogene homolog (ErbB), and MAPK signaling pathways.

131 v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog (KIT) receptor tyrosine kinase.

132 itionally compared Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations in pancreatic CTC and

133 xamine whether the Kirsten rat sarcoma viral oncogene homolog (KRAS)-variant, a germline mutation in

134 ntly in PSC and that neuroblastoma RAS viral oncogene homolog (NRAS) is activated in PSC cholangiocyt

135 /threonine kinase V-Akt murine thymoma viral oncogene homolog 1 (AKT1), and the protease cathepsin H

136 , show increased levels of glioma-associated oncogene homolog 1 and 2 (GLI1/GLI2) compared with naive

137 Sepsis inhibited the V-Akt thymoma viral oncogene homolog 1 and complex 1 of the mammalian target

138 ion in the kinase v-RAF murine sarcoma viral oncogene homolog B (BRAF(V600E)), oncogenic signaling en

139 K-Ras (Kirsten-rat sarcoma viral oncogene homolog) is a prominent oncogene that has been

140 g in histamine-abelson murine leukemia viral oncogene homology 1 (ABL1)-mediated VE dysfunction and f

141 morph, antimorph or amorph) or activation of oncogenes (hypermorph).

142 family of receptor tyrosine kinases includes oncogenes important in the progression of breast and oth

143 as a tumor suppressor or, conversely, as an oncogene in a context-dependent manner, and it also cont

144 KRAS is the most frequently mutated oncogene in cancer and KRAS mutation is commonly associa

145 c regulatory elements, thus implicating this oncogene in CLL development.

146 to act either as a tumor suppressor or as an oncogene in different human cancers, but direct evidence

147 r results suggest that ADAR2 functions as an oncogene in endometrial carcinogenesis and could be a po

148 tory complex RISC, has been implicated as an oncogene in hepatocellular carcinoma (HCC).

149 anism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogen

150 oma susceptibility gene that functions as an oncogene in high-risk neuroblastoma.

151 KRAS is the most frequently mutated oncogene in human cancer and plays a central, although p

152 rotein 1 (MTA1), one of the most upregulated oncogene in human cancer, has an important role in gene

153 typical protein kinase Ciota (PKCiota) is an oncogene in lung and ovarian cancer.

154 e expression of Meq gene, the most important oncogene in MDV.

155 This set of data supports PAK4 as an oncogene in myeloma and provide the rationale for the cl

156 xpressing the characteristic SS18-SSX fusion oncogene in myogenic factor 5-expressing (Myf5-expressin

157 y, we report a strategy to suppress the KRAS oncogene in pancreatic cancer cells by means of small mo

158 direct evidence that Cyp24a1 functions as an oncogene in PTC, where its overexpression activates mult

159 However, ETS2 can act as an oncogene in some cellular backgrounds, and as a tumor su

160 Activating mutations of NOTCH1 (a well-known oncogene in T-cell acute lymphoblastic leukemia) are pre

161 insertion region-1 protein (BMI1) acts as an oncogene in various cancers, including breast cancer.

162 Previous efforts have identified chimeric oncogenes in a substantial number of non-DS-AMKL cases,

163 point mutations in the BRAF, KRAS and PIK3CA oncogenes in archival colorectal cancer samples to preci

164 Furthermore, continued interrogation of oncogenes in benign developmental disorders could provid

165 KRAS is one of the most frequently mutated oncogenes in cancer, being a potent initiator of tumorig

166 We engineered the inducible activation of oncogenes in immortalized bronchial epithelial cells.

167 , sT and tLT, but the role of these putative oncogenes in MCC development, and this tumor's cell of o

168 screens identify RUNX genes as collaborating oncogenes in MYC-driven leukemia mouse models.

169 5s) are crucial effectors of tyrosine kinase oncogenes in myeloid leukemias.

170 teins that have been recognized as important oncogenes in various types of cancer.

171 a majority of the recognized protein kinase oncogenes, including 30 receptor tyrosine kinases and 15

172 Mutations were detected in known oncogenes, including BRAF, NRAS, NF1, EGFR, ALK, TERT, a

173 Our findings demonstrate that Ras oncogene-independent activation of RALB signaling is a t

174 so controls metabolic processes and promotes oncogene-induced cell proliferation and survival.

175 tal models, growth factor stimulation and/or oncogene-induced ERK2 activation suppressed EpCAM expres

176 r data suggest that lung cancer cells escape oncogene-induced premature senescence through down-regul

177 MRE11 serves an important role in countering oncogene-induced replication stress.

178 aptive response to endogenous DNA damage and oncogene-induced replication stress.

179 Oncogene-induced senescence (OIS) is considered a powerf

180 ntigen 3A (EBNA3A) and EBNA3C (which inhibit oncogene-induced senescence and apoptosis).

181 view builds upon the canonical hypothesis of oncogene-induced senescence in growth arrest and tumor s

182 RAS-induced DNA damage and thereby reinforce oncogene-induced senescence.

183 activates p53 in part via Arf (that is, the oncogene-induced stress pathway) but not via the DNA dam

184 The concept that EGFR oncogene inhibitor drugs could be used as targeted treat

185 ene senescence to addiction for a single key oncogene involved in lung cancer initiation.

186 The Myc oncogene is a transcription factor with a powerful grip

187 Overexpression of the EVI1 oncogene is associated typically with aggressive myeloid

188 sion of the MECOM (also known as EVI1) proto-oncogene is deregulated by chromosomal translocations in

189 ot express mutant Kras but rather the mutant oncogene is expressed in CNS interstitial cells, includi

190 between embryo and adult, and the impact of oncogenes is cell-context dependent, we hypothesized tha

191 tumor suppressors (TGFBR1 and CHEK2) and two oncogenes (KDR and ERBB2).

192 Unexpectedly, viral oncogene knockdown had no effect on the growth of the ce

193 The oncogene KRAS and tumour suppressor STK11, which encodes

194 Activating mutations in the proto-oncogene KRAS are a hallmark of pancreatic ductal adenoc

195 The two oncogenes KRas and Myc cooperate to drive tumorigenesis,

196 00E]; BRAFV600E) or exon 2 of the KRAS proto-oncogene (KRAS) in the primary tumor with SAR in patient

197 TEN, APC, BRCA1, and BRCA2) and activate one oncogene (KRAS), achieved by delivering Cre recombinase

198 y or constitutively activate a typical human oncogene, kRASG12V, in zebrafish embryos and investigate

199 ons in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band 10q11.21.

200 The three RAS oncogenes make up the most frequently mutated gene famil

201 lop LCH-like neoplasms, suggesting that each oncogene may initiate pulmonary LCH by transforming diff

202 The impairment of HR by HPV oncogenes may be targeted for treatment of HPV(+) malign

203 her, this attenuation of repair suggests HPV oncogenes may contribute to tumorigenesis by promoting t

204 FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis

205 reprogrammed metabolism, which is driven by oncogene-mediated cell-autonomous pathways, the unique p

206 noma, low expression of the lineage survival oncogene microphthalmia-associated transcription factor

207 ctivation of the melanocyte-lineage survival oncogene MITF, highlighting a new role for PARP1 in mela

208 INT1 can affect the activity of the melanoma oncogene MITF.

209 Enhancer regions revealed putative oncogenes, molecular targets and pathways; inhibition of

210 le T antigen (MT) is the murine polyomavirus oncogene most responsible for tumor formation.

211 Alternative splicing of the oncogene murine double minute 2 (MDM2) is induced in res

212 include the signaling gene TGFBR1, the proto-oncogene MYB as well as many immune-related genes such a

213 ARID5B also activates the expression of the oncogene MYC Importantly, ARID5B is required for the sur

214 Tumour suppressor p53 or proto-oncogene MYC is frequently altered in squamous carcinoma

215 Given the critical role the oncogene MYC plays in tumor initiation and maintenance,

216 , thereby coordinating the expression of the oncogene MYC.

217 cancer, which is closely associated with the oncogene MYC.

218 stigated the relationship between FAM83H and oncogene MYC.

219 d cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and p

220 retinoblastoma (RB) and amplification of the oncogene MYCN.

221 ucing NetSig candidates in 242 patients with oncogene-negative lung adenocarcinomas, we find that two

222 TG-dependent focal adhesion kinase/Src proto-oncogene non-receptor tyrosine kinase signaling.

223 The proto-oncogenes NTRK1/2/3 encode the tropomyosin receptor kina

224 ed, and for some of these, including several oncogenes of the Ras and Src families, palmitoylation is

225 pectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that can genetically modify proliferatio

226 Using transfected (retroviral oncogene or fluorescent reporter construct) rat 208 F ce

227 aused by germline mutations of the RET proto-oncogene or occurs as a sporadic form.

228 dence of preferential integration near known oncogenes or clonal outgrowth.

229 tiated by genetic events that activate proto-oncogenes or inactivate tumor-suppressor genes.

230 Expression of many oncogenes or loss of tumor suppressors induces the expre

231 lymphocyte fate and to conditionally express oncogenes or silence tumour suppressor genes in vivo.

232 rature we excluded those predicted to target oncogenes or tumor suppressor gene.

233 independent of other genetically engineered oncogenes or tumor suppressor loss.

234 egulation of gene expression that can act as oncogenes or tumor suppressors.

235 ons in v-maf musculoaponeurotic fibrosarcoma oncogene ortholog B (MAFB), matrix metalloproteinase (MM

236 es but also identical breakpoints leading to oncogene overexpression.

237 e, Cav3.2 inhibition decreased expression of oncogenes (PDGFA, PDGFB, and TGFB1) and increased expres

238 re, we identify the protein kinase and proto-oncogene PIM3 as being repressed downstream of mTORC1 si

239 be found in both tumor suppressor genes and oncogenes, produce proteins with entirely different func

240 Our studies demonstrate that high-risk HPV oncogenes profoundly reprogram the tumor microenvironmen

241 d its receptor, the product of the MET proto-oncogene, promote invasion and metastasis of tumor cells

242 G-quadruplexes (G4) within oncogene promoters are considered to be promising antica

243 l molecule and a disordered peptide from the oncogene protein c-Myc, we describe a "specific-diffuse"

244 The proto-oncogene PTTG and its binding partner PBF have been wide

245 Drosophila, oncogenic mutations of the proto-oncogene Ras (Ras(V12)) maintain tumorous cells in an 'u

246 ces the prognostic significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet-der

247 1-regulated genes, including the MYB and MYC oncogenes, respectively.

248 te target for therapy, here we identified an oncogene, ROS1, as an important driver for oral squamous

249 Squamous cell carcinoma-related oncogene (SCCRO)/DCUN1D1, a component of the neddylation

250 genetic abnormalities may prime for changing oncogene senescence to addiction for a single key oncoge

251 n of the murine K-Ras locus with H-Ras(G12V) oncogene sequences.

252 entification of clients, such as Raf-1 proto-oncogene, Ser/Thr kinase (RAF1), that are particularly d

253 these studies identify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic

254 r resistance and review the oncogene and non-oncogene signalling mechanisms that have thus far been u

255 Oncogene-specific changes in cellular signaling have bee

256 mechanism that allows cancer cells to evade oncogene-specific inhibitors, providing a rationale to c

257 roliferation and transformation, and suggest oncogene-specific roles for DUSP5 in controlling ERK sig

258 een shown to predict response and changes in oncogene status via treatment with small-molecule inhibi

259 The c-myc oncogene stimulates ribosomal biogenesis and protein syn

260 override allows premalignant cells to evade oncogene stress barriers, providing a causal link to onc

261 cytometry, or indirectly, by the presence of oncogenes such as BCR-ABL1.

262 rapeutic strategies targeting translation of oncogenes such as c-Myc.

263 ly induced apoptosis in cells overexpressing oncogenes, suggesting MRE11 serves an important role in

264 mic analysis identified MYST3 as a potential oncogene target that is frequently amplified in breast c

265 driving EGFR upregulation and resistance to oncogene- targeted therapies.

266 Cancer cells acquiring resistance to MET oncogene-targeted drugs invariably underwent NRP2 loss,

267 composed of immune checkpoint inhibitors and oncogene-targeted drugs might improve cancer management,

268 r MYC, suppress immune surveillance, and how oncogene-targeted therapies may restore the immune respo

269 of ALK or ROS1(+) lung cancer patients with oncogene-targeted therapy ultimately enables the emergen

270 es, including mutations that likely activate oncogenes TERT and PIK3CA, and alter chromatin-associate

271 ining protein 1 (ADHFE1), is a breast cancer oncogene that decreases patient survival.

272 rcoma viral oncogene homolog) is a prominent oncogene that has been proven to drive tumorigenesis.

273 arcinogen susceptibility, including the BRAF oncogene that has the highest mutation frequency in mela

274 e in vivo validation of LMO1 as an important oncogene that promotes neuroblastoma initiation, progres

275 ta demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in

276 sks, such as the unintentional activation of oncogenes that can result in cancer.

277 n landscape, and present novel candidate FLC oncogenes that merit further investigation.

278 EBV expresses viral oncogenes that promote cell growth and inhibit the apopt

279 CRISPR screen of DLBCL cell lines to define oncogenes that promote cell growth.

280 eals a class of tumor cell-intrinsic "immuno-oncogenes" that modulate the immune microenvironment of

281 sure to continuously express the viral E6/E7 oncogenes, that their intracellular p53 levels are recon

282 the first report that p53 activates a viral oncogene; therefore, the discovery would be interesting

283 or-alpha, progesterone receptor, or the HER2 oncogene; therefore, TNBC lacks targets for molecularly-

284 tages of cancer, for example, functioning as oncogenes, this makes these small molecules suitable tar

285 hepatocellular carcinoma and acts as a proto-oncogene through Wnt pathway activation and induction of

286 Mechanistically, FOSL1 links the KRAS oncogene to components of the mitotic machinery, a pathw

287 FOS is one of the earliest viral oncogenes to be characterized, and normal cellular FOS f

288 here can be broadly applied to a variety of oncogenes to predict patient mutations and evaluate resi

289 Although originally identified as an oncogene, Tropomyosin-related kinase A (TrkA) is linked

290 that the beta-TrCP-FBXW2-SKP2 axis forms an oncogene-tumour suppressor-oncogene cascade to control c

291 models are generated by expressing mammalian oncogenes under tissue-specific promoters, here we descr

292 revisiting the prevailing single-gene driver-oncogene view and links clinical outcomes to co-occurrin

293 ABL1 is a proto-oncogene well known as part of the fusion gene BCR-ABL1

294 Driver oncogenes were amplified most commonly in ecDNA, thereby

295 Ras-oncogenes were discovered over three decades ago, but th

296 edge, this is the first time that both viral oncogenes were shown to disrupt this DSB repair pathway.

297 A few cultures were transformed by ras oncogenes when transfected with DNA from neoplastic cell

298 is cleaved and interacts with the JUN proto-oncogene, which forms part of the activator protein 1 (A

299 marked differences in the association of RAS oncogenes with tumor type.

300 tion, and were established early on as proto-oncogenes, with aberrant expression linked to tumor prog