ライフサイエンスコーパス: oncogene

1 ed translation initiation of this well-known oncogene.

2 target gene Notch2 which is well known as an oncogene.

3 (BET) gene BRD4, forming the BRD4-NUT fusion oncogene.

4 rrying the hotspot mutation G12D in the KRAS oncogene.

5 strocytes, supporting AVIL being a bona fide oncogene.

6 dal differentiation, TBXT acts as a putative oncogene.

7 ed in many human cancers and functions as an oncogene.

8 n reported as both a tumor suppressor and an oncogene.

9 actions and shifts p27 from CDK inhibitor to oncogene.

10 uppressors APC and TP53 and gain of the KRAS oncogene.

11 ed by the human papillomavirus 16 (HPV16) E6 oncogene.

12 for pediatric malignancies driven by the MYC oncogene.

13 he viral enhancer induced transactivation of oncogenes.

14 RNA splicing constitute an emerging class of oncogenes.

15 hybrid glycans, especially for KRAS and HER2 oncogenes.

16 ribute to shaping the expression profiles of oncogenes.

17 ection for mutation-independent discovery of oncogenes.

18 cles, leading to high-level amplification of oncogenes.

19 ar senescence overlap with pro-longevity and oncogenes.

20 ng new proteins that cooperate with dominant oncogenes.

21 se Cbeta (PLCbeta) signaling driven by these oncogenes.

22 ndent induction of proinflammatory genes and oncogenes.

23 on chromatin as an epigenetic signature for oncogenes.

24 to an orphan receptor tyrosine kinase, c-ros oncogene 1 (ROS1), and mediates the differentiation of t

25 ion of cancer by mediating overexpression of oncogenes(1-3), and to the development of cancer therapy

26 Discovered as a proto-oncogene 40 years ago, mutations in KRAS exist in ~30% o

27 c variant predicted to cis-activate the TAL1 oncogene, a finding validated in vivo by chromatin immun

28 tumor suppressor genes and activation of one oncogene, accounting for the well-known path to colorect

29 Herein, we pointed that Pdcd4, a suppressor oncogene, acted as an endogenous inhibitor for the trans

30 For years it seemed that HPV oncogenes activated the homologous recombination pathway

31 t clones, the mechanisms behind tolerance to oncogene activation across broader regions of tissue are

32 mic reticulum (ER) stress caused by cellular oncogene activation and a hostile tumor microenvironment

33 Oncogene activation and loss of tumor suppressor functio

34 us stresses, including telomere dysfunction, oncogene activation and persistent DNA damage.

35 Oncogene activation during tumorigenesis generates DNA r

36 We investigated the effect of oncogene activation on this process in normal epithelial

37 tumors often experience genomic instability, oncogene activation, increased protein secretion demands

38 of these interactions demonstrated that: (i) oncogene addiction effects are more robust than oncogene

39 med cell death represents a critical form of oncogene addiction in cancer cells.

40 , these data reveal a novel mechanism of ERG oncogene addiction in prostate cancer, whereby ERG facil

41 HSP27 is highly expressed in, and supports oncogene addiction of, many cancers.

42 d therapeutics for cancer generally exploit "oncogene addiction," a phenomenon in which the growth an

43 sult in silencing of tumor-suppressor genes, oncogene addictions, and enhancement of immune responses

44 Chromothripsis contributes to oncogene amplification and to inactivation of genes such

45 presented here demonstrate that ecDNA-based oncogene amplification is common in cancer, is different

46 Oncogene amplification, a major driver of cancer pathoge

47 whose cancers were not driven by ecDNA-based oncogene amplification.

48 plified ecDNA, and the most common recurrent oncogene amplifications arose on ecDNA.

49 man cancers with acquired drug resistance or oncogene amplifications.

50 s establish roles for PLK1 as a potent proto-oncogene and a CIN gene and provide insights for the dev

51 In addition, Notch can function as an oncogene and a tumour suppressor in different cancers an

52 Therefore, P-Rex1 can act as an oncogene and cooperate with HER2/neu to enhance breast c

53 7BL/6 background, which is driven by the Myc oncogene and expresses an immunodominant CD8 T cell epit

54 In neuroblastoma, amplification of the MYCN oncogene and inactivation of the ATRX tumor-suppressor g

55 tivates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignan

56 1-7 and alamandine, which activate MAS proto-oncogene and MAS-related D receptors, respectively.

57 which indicates that it could be a potential oncogene and target for PDAC.

58 MYCN, which is both a functionally important oncogene and transcriptional target of PAX3-FOXO1.

59 e activating mutations in growth-controlling oncogenes and inactivating mutations in tumor-suppressor

60 Some lncRNAs function as oncogenes and some function as tumor suppressors.

61 KRAS, one of the most prevalent oncogenes and sought-after anticancer targets, has elude

62 involves gradual acquisition of mutations in oncogenes and tumor suppressor genes, as well as changes

63 We further curated VIS-involved oncogenes and tumor suppressor genes, virus-host interac

64 ulation of genetic and epigenetic changes in oncogenes and tumor suppressor genes.

65 ng the effects of a combinatorial library of oncogenes and tumor suppressors on cell growth.

66 Only a small number of genes are bona fide oncogenes and tumor suppressors such as Ras, Myc, beta-c

67 Despite harboring mutations in oncogenes and tumor suppressors that promote cancer grow

68 tumorigenesis through altered expression of oncogenes and tumor suppressors.

69 plicing, and mRNA expression levels of proto-oncogenes and tumor suppressors.

70 Unlike some pan-cancer oncogenes and tumour suppressor genes that drive transfo

71 Whereas many of the most frequently mutated oncogenes and tumour-suppressor genes have been studied

72 chmark BETi, JQ-1, showing downregulation of oncogenes and upregulation of tumor suppressors and apop

73 They may act as oncogenes and when overexpressed in tumors become plausi

74 We found repression of MYC proto-oncogene, and up to four-fold reduction in accumulated m

75 translation of the mRNAs of JUND (JunD proto-oncogene AP-1 transcription factor subunit) and HIV-1 ge

76 a tumor-suppressor gene and activation of an oncogene are incompatible.

77 e and tumor tissue harbor a gain of the same oncogene arising in parallel from distinct parental hapl

78 and autoimmunity identified the c-Fos proto-oncogene as a mediator of ER stress responses in epithel

79 nhancer and modulates the activation of GAS6 oncogene as part of a topologically organized region, as

80 cal armamentarium for targeting G(q) protein oncogenes as well as broaden our mechanistic understandi

81 m of KRAS, depletion of RalB (RAS-like proto-oncogene B) and IkappaB kinase-related TANK-binding kina

82 a member of the ErbB (avian erythroblastosis oncogene B) family of receptors that play a role in cell

83 t-characterized PP2A substrates is MYC proto-oncogene basic helix-loop-helix transcription factor (MY

84 imary lymphocytes, and identificed the proto-oncogene BCL2 as a replication stress-induced fragile si

85 A-seq of cancer cells illuminated targetable oncogenes beyond those detected clinically.

86 This activation required MYC proto-oncogene bHLH transcription factor (c-Myc) and depended

87 n-bridge cycles and translocations activated oncogenes (BMI1, MIR17HG, TERT, MYC, and MYCN), generati

88 Hotspot mutations of the oncogenes BRAF and NRas are the most common genetic alte

89 Like most other oncogenes, BRAF(V600E) causes oncogenic stress to normal

90 FRET analyses, we demonstrate that the proto-oncogene c-Fos (c-Fos) activates cytoplasmic lipid synth

91 ntaining protein, SAMD14, promotes SCF/proto-oncogene c-Kit (c-Kit) signaling, erythroid progenitor f

92 rmal growth factor receptor (EGFR) and proto-oncogene c-Met (MET), and shunts their trafficking into

93 at EPHB4 stimulates the AR by inducing proto-oncogene c-Myc (c-Myc) expression.

94 PPP2R2A negatively regulated translation of oncogene c-Myc protein.

95 8G glioma cells, including downregulation of oncogene c-Myc.

96 ncreased the binding of AXL to the Cbl proto-oncogene (c-Cbl); promoted AXL ubiquitination; decreased

97 ined the combined and separate effects of an oncogene (c-MYC) and exposure to interleukin-3 (IL-3), g

98 lopmental transcription factor by a dominant oncogene can promote malignancy, but provide opportuniti

99 rimary mouse mammary epithelial acini, where oncogenes can be switched on in single cells within an o

100 1/S phase transition genes (myelocytomatosis oncogene cellular homolog [Myc], cyclin D1/3, chromatin

101 A repair and replication, as well as MiR-155 oncogene, concomitant with an upregulation of caspase 3

102 can co-occur in liver cancer, but how these oncogenes cooperate in tumorigenesis remains unclear.

103 s predicted to regulate CRKL (CRK-like proto-oncogene, cytoplasmic adaptor) expression.

104 In addition, multiple oncogenes depend on IFITM3 to assemble PIP3-dependent si

105 different levels of signaling potency and/or oncogene dependence.

106 helation as a therapeutic strategy to target oncogene-dependent tumor cell growth and survival by enh

107 er as a contextual tumor suppressor or as an oncogene, depending on the tissue being studied.

108 activation of the T-cell leukemia 1A (TCL1A) oncogene distinguishes the (pre)leukemic cell from regul

109 ugh PKClambda/iota promotes tumorigenesis in oncogene-driven cancer models, emerging evidence demonst

110 Oncogene-driven changes in tumor cell metabolism can imp

111 al. show how oncogene-driven fatty-acid synthesis favors Treg cells o

112 stration of TKIs before chemoradiotherapy in oncogene-driven NSCLC.

113 l tissue repair mechanism usurped to promote oncogene-driven overgrowth.

114 Our results show that SOD1 is essential for oncogene-driven proliferation, but not normal proliferat

115 Moreover, CD8-MP cells infiltrate oncogene-driven prostate tumors and express high densiti

116 Interestingly, in tumor cells with oncogene-driven replication stress, CHK1 can directly ph

117 Rad51ap1-deficient mice were protected from oncogene-driven spontaneous mouse mammary tumor growth a

118 Thus, oncogene-driven translation is not necessarily inherentl

119 The MYC oncogene drives T- and B- lymphoid malignancies, includi

120 ation to prevent the expression of the viral oncogene E5.

121 he impact of altering a well-established HCC oncogene (either MYC or beta-catenin) in combination wit

122 by hydrodynamic tail vein injection of proto-oncogenes, enhanced HCC development.

123 The oncogene epidermal growth factor receptor variant III (E

124 here miR-1300 is normally not expressed, the oncogene Epithelial Cell Transforming 2 (ECT2) was valid

125 genes shared by the two cell types are proto-oncogenes ERK2, a component of the ERK/MAPK pathway, and

126 The proto-oncogene ets1 is highly expressed in the pre-migratory a

127 We also show that cells expressing activated oncogenes experience apoptotic caspase activation, and t

128 Analysis of mouse and human oncogene-expressing wild-type and p53-deficient cells in

129 Altered oncogene expression in cancer cells causes loss of redox

130 d intense tyrosine hydroxylase and RET proto-oncogene expression in nigral neurons in the patient whe

131 Here, we show that oncogene expression leads to either pulsatile or sustain

132 uggest an important role in context-specific oncogene expression regulation.

133 tency under regenerative conditions and upon oncogene expression(3,9-13).

134 nt that promotes persistent inflammation and oncogene expression.

135 utonomous and non-cell autonomous effects of oncogene expression.

136 Indeed, in the RAS family and other oncogene families with two or three members, the most pr

137 revalence of mutations in certain members of oncogene families.

138 ux, a process that required RAB24 member RAS oncogene family (RAB24), a small GTPase that facilitates

139 9 (TCEAL9) has been proposed as a candidate oncogene for human colorectal cancers with microsatellit

140 the E3 ligase HUWE1 in modulating c-MYC, an oncogene frequently dysregulated in MM.

141 ur mechanistic understanding of G(q) protein oncogene function.

142 The B-cell lymphoma 9 (BCL9) oncogene functions as a transcriptional co-activator of

143 (0%-29%), SCLC transformation (2%-15%), and oncogene fusions (1%-10%) as the most common mechanisms

144 ains binding sites for the glioma-associated oncogene (Gli) proteins.

145 n, a GTPase-activating protein for RAS proto-oncogene GTPase (RAS).

146 We find that each oncogene has somewhat different surfaceomes, but the fun

147 sent in the upstream of P1 promoter of c-MYC oncogene has the ability to form an intramolecular paral

148 Whether truncated glioma-associated oncogene homolog 1 (TGLI1), a transcription factor known

149 V-ERB-B avian erythroblastic leukemia viral oncogene homolog 3 (ERBB3) receptor kinase.

150 ivating ErbB2 (erythroblastic leukemia viral oncogene homolog B2), ErbB3, and ErbB4 receptor tyrosine

151 RAF) mutation, and Kirsten rat sarcoma viral oncogene homolog gene (KRAS) mutation.

152 Through the actions of its oncogenes, HPV evades host immune responses to facilitat

153 te, formation of tumors induced by a control oncogene (HRAS/G12V).

154 Druggable driver oncogenes, identified by molecular analyses, are present

155 he tumor suppressor CDKN2A gene and the NRAS oncogene in 62.5% and 75%, respectively of the samples t

156 lx5 homeobox gene was first implicated as an oncogene in a T-ALL mouse model expressing myristoylated

157 Estrogen receptor alpha (ER) is a key oncogene in endometrial cancer.

158 lpha isoform, is the most frequently mutated oncogene in estrogen receptor (ER)-positive breast cance

159 PIK3CA is the most commonly altered oncogene in head and neck squamous cell carcinoma (HNSCC

160 RET receptor tyrosine kinase is a driver oncogene in human cancer.

161 f evidence that ATOH1 is a lineage-dependent oncogene in MCC.

162 ATOH1 can be regarded as a lineage-dependent oncogene in MCC.

163 Mutational activation of the BRAF proto-oncogene in melanocytes reliably produces benign nevi (p

164 Amplification and overexpression of the MYC oncogene in tumor cells, including ovarian cancer cells,

165 argets such as TACC3, a prognosis-associated oncogene in various cancers.

166 mation, and the expression of CD47 and other oncogenes in arterial smooth muscle cells.

167 of recurrent somatic mutations or activated oncogenes in pediatric cancers poses a major challenge t

168 he ectopic expression of homeodomain-related oncogenes in T cell acute lymphoblastic leukemia.

169 ped cells, an insignificant role for classic oncogenes in tumor development, the release of bioactive

170 d Ras are two of the most commonly activated oncogenes in tumorigenesis.

171 njecting human NC cells carrying NB relevant oncogenes in utero into gastrulating mouse embryos.

172 lts identify a key role for Ldb1, a nonproto-oncogene, in T-ALL and support a model in which Lmo2-ind

173 Candidate oncogenes include the prolactin receptor PRLR activated

174 l programs to activate the expression of key oncogenes, including MYC, to provide a proliferation sig

175 iption of a subset of SE-associated leukemic oncogenes, including MYC.

176 landscapes that drive the expression of key oncogenes, including the oncogenic MYC pathway.

177 y of six of the most prominent proliferative oncogenes, including the receptor tyrosine kinases, EGFR

178 hibition is expected to decrease function of oncogenes, increase tumor suppressor function, and enhan

179 Transforming fibroblasts with the Ras oncogene induced mitochondrial biogenesis, which further

180 We found massive oncogene-induced changes to the glycoproteome and differ

181 c screening, we provide direct evidence that oncogene-induced loss of progenitor self-renewal is driv

182 Oncogene-induced metabolic reprogramming is a hallmark o

183 entering replicative senescence (RS) or upon oncogene-induced senescence (OIS).

184 Precursor lesions with AGO2 ablation undergo oncogene-induced senescence with altered microRNA expres

185 attributed to a cell-autonomous process of 'oncogene-induced senescence'.

186 upporting cancer cell growth and suppressing oncogene-induced senescence.

187 bitor that blocks MAPK signaling brings each oncogene-induced surfaceome back to a common state refle

188 ssion, hematopoietic cell proliferation, and oncogene-induced transformation through degradation of c

189 ion, TMPRSS13 was genetically ablated in the oncogene-induced transgenic MMTV-PymT tumor model.

190 ormal tissues, than to any cell-autonomous, 'oncogene-induced' program of senescence.

191 breast cancer cells experiencing stress from oncogene inhibition up-regulated the expression of Polka

192 e GRK2-DN transgene dramatically accelerates oncogene-initiated prostate tumorigenesis by increasing

193 ows all expected features of the long-sought oncogene interacting locus.

194 ed to the preferential loss of expression of oncogenes involved in PDGF, EGFR, VEGF, insulin/IGF/MAPK

195 The switch of p53 from tumor suppressor to oncogene is location-dependent and is impacted by microb

196 The c-MYC oncogene is overexpressed in a wide variety of cancers a

197 te the direct allosteric activation of proto-oncogene kinase Src by GPCR-betaarr complexes in vitro a

198 itions move towards a stem-like state, while oncogene knockdowns show an opposing trend.

199 The oncogene KRAS controlled the storage and utilization of

200 ction with oncogenic activation of the proto-oncogene Kras.

201 al expansions of cells carrying an activated oncogene, less than a month after carcinogen exposure.

202 ests a novel paradigm whereby critically low oncogene levels, caused by loss of a driver tumor suppre

203 provides mechanistic insights into the novel oncogene-like functions of UBR5 in regulating the OC-TME

204 rolonged or enhanced expression of the proto-oncogene Lmo2 is associated with a severe form of T-cell

205 des an overview of the diverse ways that HPV oncogenes manipulate homologous recombination and ideas

206 angiotensin II receptor (AT(2)R), the proto-oncogene Mas receptor and the Mas-related G protein-coup

207 s harbor thousands of mutations, and a given oncogene may be mutated at hundreds of sites, yet only a

208 0 was deleted in 80% of the cohort while the oncogene MDM4 was amplified.

209 oma, downregulation of the lineage addiction oncogene microphthalmia-associated transcription factor

210 Here, using the melanoma lineage survival oncogene MITF as a model, we show that low-affinity bind

211 As potent proto-oncogenes, models of MYC family function have been large

212 ole has been linked to its function as a MYC oncogene modulator, but little is known about its regula

213 Overexpression of the oncogene MYBL2 (B-Myb) is associated with increased cell

214 en implicated in the repression of the proto-oncogene Myc, but the mechanism has remained unclear.

215 e refractory to the mitogenic effects of the oncogene Myc.

216 rsus diploid cases, and so were gains of the oncogenes MYC and ZNF217.

217 late endosomes allows delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasm

218 ch as the four-nucleotide duplication in the oncogene nucleophosmin (NPM1c), which creates a neoepito

219 Amplification of the MYCN oncogene occurs in ~25% of primary neuroblastomas and is

220 The small GTPase RABL3 is an oncogene of unknown physiological function.

221 Distinguishing passenger genes, oncogenes (OGs) and tumor-suppressor genes (TSGs) for ea

222 tate reflecting the strong dependence of the oncogene on the MAPK pathway to propagate signaling.

223 -state enrichment of metabolites between Myc(oncogene)-On and Myc-Off Tet21N human neuroblastoma cell

224 ect of the circadian clock on this important oncogene/oncoprotein and tumorigenesis.

225 whether DDX3X functions as a medulloblastoma oncogene or tumor suppressor gene is not known.

226 ble information about their combined role as oncogenes or tumor suppressor genes.

227 lity leading to deletion or amplification of oncogenes or tumor suppressors.

228 genes controlled by the circadian clock are oncogenes or tumor suppressors.

229 The order in which oncogenes or tumour suppressor genes are functionally se

230 ved in tumour development and progression as oncogenes or tumour suppressors.

231 ng to their molecular structure (undruggable oncogenes) or because they result in functional loss (tu

232 gene editing by CRISPR-Cas9 to knock out the oncogene p53 in dog oviductal epithelia cultured in a dy

233 pe arising from a driver mutation in the p53 oncogene (p53R175H) presented by HLA-A2.

234 reduced chromatin accessibility for the MYC oncogene pathway correlated with downregulation of perti

235 were performed employing both telomeric and oncogene promoter G-quadruplex-forming sequences.

236 cal DNA structures enriched at telomeres and oncogenes' promoters.

237 ed adenocarcinoma, it is unknown how the ERG oncogene promotes a cancerous phenotype and maintains do

238 The BRCA1-IRIS oncogene promotes breast cancer aggressiveness by recrui

239 DCBLD1 behaved like an oncogene, promoting tumor growth by influencing cell cyc

240 osphatase (PTP) SHP2 is encoded by the proto-oncogene PTPN11 and is a ubiquitously expressed key regu

241 (-/-) mice crossed onto the polyoma middle T oncogene (PyMT) background.

242 The oncogene RAS is one of the most widely studied proteins

243 ant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/beta-cat

244 sistance to approved inhibitors of KIT proto-oncogene, receptor tyrosine kinase (KIT), and platelet-d

245 ogene addiction effects are more robust than oncogene-related synthetic lethal effects; and (ii) robu

246 ad systems-level view of how specific driver oncogenes remodel the surfaceome and the glycoproteome i

247 , MCPyV encodes early T antigen genes, viral oncogenes required for MCC tumor growth.

248 family receptor alpha like (GFRAL)-Ret proto-oncogene (RET) signaling complex in brainstem neurons th

249 r an alternatively spliced exon in the proto-oncogene RON and determine the functional units that con

250 The proto-oncogene ROS1 encodes a receptor tyrosine kinase with an

251 ed interaction of the RAS ITD with Raf proto-oncogene Ser/Thr kinase (RAF), leading to increased phos

252 esence of inhibitors targeting the RAF proto-oncogene Ser/Thr protein kinase (RAF) and MAPK/ERK kinas

253 Class 3 mutations in B-Raf proto-oncogene, Ser/Thr kinase (BRAF), that result in kinase-i

254 Ras-binding domain (RBD) of the C-Raf proto-oncogene, Ser/Thr kinase (CRAF).

255 imerizing with and activating WT C-Raf proto-oncogene, Ser/Thr kinase (CRAF).

256 ytokine signaling 2/3 (Socs2/3); Pim-1 proto-oncogene, Ser/Thr kinase (Pim1); and Fms-related tyrosin

257 and methylator phenotype (CIMP), B-Raf proto-oncogene serine/threonine kinase (BRAF) mutation, and Ki

258 hylesterase 1 (PME-1), and SET nuclear proto-oncogene (SET) that often are deregulated in cancers.

259 RASER thus provides a new strategy for oncogene-specific cancer detection and treatment.

260 -cell signaling pathway, including LCK proto-oncogene SRC family tyrosine kinase (LCK), LYN proto-onc

261 SRC family tyrosine kinase (LCK), LYN proto-oncogene SRC family tyrosine kinase (LYN), zeta chain of

262 JunD (Jund proto-oncogene subunit), a member of the AP-1 (activator prote

263 of hepatocellular carcinoma-associated proto-oncogenes such as c-Jun and associated transcription fac

264 n part by increasing the expression of proto-oncogenes such as MYC and cyclins.

265 As with expression of other oncogenes, such as adenovirus E1A or MYC, HPV16 E7-expre

266 iting dTAG molecules to degrade recalcitrant oncogenes, supports combination degrader studies and fac

267 daptive survival in tumor cells treated with oncogene targeted therapies, providing a rationale for c

268 Oncogene-targeted and immune checkpoint therapies have r

269 However, the efficacy of oncogene-targeted therapies varies substantially.

270 ing to directly kill cancer cells, including oncogene-targeted therapy and immune-checkpoint therapy

271 icing upon NF-kappaB activation by the viral oncogene Tax of HTLV-1.

272 Mice expressing the HTLV-1 oncogene Tax, driven by the human granzyme B promoter (T

273 BGRDs at oncogenes tend to be conserved across normal cell types.

274 Region-Abelson kinase (BCR-Abl) is a driver oncogene that causes chronic myeloid leukemia and a subs

275 ample of a G protein-coupled receptor driver oncogene that encodes a highly biased constitutively act

276 We propose that SNHG7 is a lncRNA oncogene that is controlled by growth factor signaling i

277 Mutant KRAS is a driver oncogene that is well-known for its ability to regulate

278 monstrate that the translation efficiency of oncogenes that are preferentially mutated in tumor sampl

279 GH-secreting) pituitary tumors are driven by oncogenes that induce cAMP signaling.

280 Oncogenes that induce the development of leukaemia and l

281 targeted therapies directed against a driver oncogene, the clinical response is almost always tempora

282 amplifications resulted in higher levels of oncogene transcription compared to copy number-matched l

283 that translocates into the nucleus, causing oncogene transcription.

284 the MMTV-Delta16HER2 transgenic mouse model, oncogene transformation resulted in a timely abrogation

285 ions containing gene partners that are known oncogenes, tumor suppressor genes, COSMIC genes, and/or

286 s influence cancer development, occurring in oncogenes, tumor suppressors, and dual role genes.

287 Universal expression of HPV E6*1 and E7 oncogenes was a sine qua non of HPV-positive OSCCs.

288 A set of glioma proto-oncogenes was enriched among the transcriptomic correlat

289 In the virus-driven cSCCs the MmuPV1-E6/E7 oncogenes were abundantly expressed, and transcriptional

290 Oncogenes were highly enriched on amplified ecDNA, and t

291 Most known oncogenes were identified by gain-of-function mutations

292 One regulator of p53 is the Mdm2 oncogene, which is correlated with high-grade, metastati

293 hree of the lesions identified a ROS1 fusion oncogene with identical genomic breakpoints, indicating

294 ndicate that ERBB2DeltaEx16 is a lung cancer oncogene with potential clinical importance for a propor

295 Here, we report that Epsin 3 (EPN3) is an oncogene with prognostic and therapeutic relevance in br

296 s suggests that IDH2(R140Q) is an incoherent oncogene, with both positive and negative impacts on leu

297 The oncogene YAP has been shown previously to promote tumor

298 The oncogene yes-associated protein (YAP) controls liver tum

299 our discrete clusters that all expressed the oncogene Yes-associated protein 1 (YAP1).

300 Matriptase 1 (ST14) is commonly known as an oncogene, yet it also plays an understudied role in supp