ライフサイエンスコーパス: oncogenic

1 ociated epigenomic alterations are primarily oncogenic.

2 intenance, whereas mutant-PDGFRA is potently oncogenic.

3 orylation deficient mutant of cyclin D3, has oncogenic activity are undefined.

4 ACE1 disrupts its role as a regulator of the oncogenic activity of RAC-family GTPases in human and mu

5 poptotic BFL-1 to selectively neutralize its oncogenic activity using a covalent stapled-peptide inhi

6 For maximal oncogenic activity, cellular MYC protein levels need to

7 are a potentially targetable motif of TIMP-1 oncogenic activity.

8 We also discuss how oncogenic alterations in lymphoma cells may affect the c

9 MEK/ERK pathway, providing new insight into oncogenic alterations of glutamine metabolism.

10 in normal cells, hyperactivation of NRF2 is oncogenic, although the detailed molecular mechanisms by

11 They have oncogenic and neuronal functions and are reported in exo

12 These sets of microRNAs include both oncogenic and tumor suppressor microRNAs.

13 ds to APA of many transcripts affecting core oncogenic and tumor suppressors, including cyclin D2 and

14 ough defective gene regulation often affects oncogenic and tumour-suppressor networks, tumour immunog

15 the plasma membrane, we discovered that the oncogenic avian alpharetrovirus Rous sarcoma virus (RSV)

16 MAX also dimerizes with MYC, an oncogenic bHLH transcription factor.

17 alized Barrett's cell, CP-C and CP-A, to the oncogenic bile acid, deoxycholic acid (DCA), for 1 year.

18 dy establishes a framework for rationalizing oncogenic BRAF mutations and provides new avenues for im

19 inical use of targeted therapies against the oncogenic BRAF->MEK->ERK pathway and immune checkpoint i

20 and its co-factor NEMO in the activation of oncogenic c-Jun N-terminal kinase (JNK) signaling, induc

21 Coinfection with CT may potentiate the oncogenic capability of HPV16 and increase the risk of H

22 elop new treatment approaches targeting this oncogenic cascade.

23 s, resulting in significant up-regulation of oncogenic CD44 isoforms (CD44v) and increased CRC cell g

24 egulation and its functional consequences in oncogenic cell extrusion.

25 n toward oncogenic cells and is required for oncogenic cell extrusion.

26 scription in response to protein misfolding, oncogenic cell proliferation, and other environmental st

27 oordinates neighboring cell migration toward oncogenic cells and is required for oncogenic cell extru

28 ion conflicts, DNA damage, and cell death in oncogenic cells.

29 E2A and the oncogenic chimera E2A-PBX1 contain three transactivation

30 nctionally specialized roles for bacteria in oncogenic communities.

31 of ERG-mediated tumorigenesis and subsequent oncogenic dependencies in prostate cancer.

32 uding those targeted to the tumor epithelia (oncogenic, developmental, metabolic, epigenomic) and tum

33 as AID targeting of non-Ig loci can generate oncogenic DNA lesions.

34 More recently, several oncogenic double-stranded DNA viruses have been found to

35 tions that are not aligned with this central oncogenic driver activate divergent pathways and subvert

36 A hotspot mutation is well established as an oncogenic driver event in cancer and its durable and eff

37 RNA-binding protein HuR/ELAVL1 as a central oncogenic driver for malignant peripheral nerve sheath t

38 r increases (genomic amplification) pinpoint oncogenic driver genes and therapeutic targets in cancer

39 ion is associated with RNA expression of the oncogenic driver genes AR, MYC and ERG.

40 ulin receptor super-family that functions as oncogenic driver in a range of human cancers such as neu

41 translation, and is widely recognized as an oncogenic driver in several solid tumors, including colo

42 consequences of a second-site mutation in an oncogenic driver may include not only a mechanism for dr

43 t HTLV-1-infected T-cell clones carrying key oncogenic driver mutations can be detected in cases of A

44 As the catalog of oncogenic driver mutations is expanding, it becomes clea

45 ngs suggest that MITF-A is a transcriptional oncogenic driver of angiomyolipoma tumor development, ac

46 rate that the FHL2-GLI2 fusion is likely the oncogenic driver of SSTs, defining a genotypic-phenotypi

47 ve and sustained inhibition of non-enzymatic oncogenic driver proteins is a major pharmacological cha

48 herapies, none of which directly inhibits an oncogenic driver.

49 es strongly with inhibition of the principal oncogenic driver.

50 ng a broad spectrum of activated RTKs as the oncogenic driver.

51 that molecularly guided treatments targeting oncogenic drivers and the DNA damage response and repair

52 Numerous signaling pathways and oncogenic drivers can cause changes in mRNA transcriptio

53 As more data is generated, oncogenic drivers for specific cancer types are discover

54 arrangements retaining the kinase domain are oncogenic drivers in papillary thyroid cancer, non-small

55 the methylome landscape and characterize the oncogenic drivers of esophageal squamous cell carcinoma

56 MET exon 14 alterations are oncogenic drivers of non-small-cell lung cancers (NSCLCs

57 Its unique genomic landscape shaped by oncogenic drivers promotes immune suppression from the e

58 ell lung cancer (NSCLC) are directed against oncogenic drivers that are more prevalent in patients wi

59 fically targets the E2A gene and produces an oncogenic E2A-PBX1 fusion protein.

60 2 inhibitors targeting either WT SHP2 or its oncogenic E76K variant.

61 However, the underlying cause of the oncogenic effect of Arg882His in DNMT3A is not fully und

62 al DNA viruses are highly suspicious to have oncogenic effects in humans.

63 comparing low- and high-affinity ligands and oncogenic EGFR mutants.

64 We find that oncogenic EpdSCs are serine auxotrophs whose growth and

65 Here, we show that oncogenic ERG repressed PI3K signaling through direct tr

66 helium and particularly in cancers driven by oncogenic ETS fusion genes.

67 Both genetic programs arising from oncogenic events and transcriptional programs and epigen

68 The oncogenic events involved in breast implant-associated a

69 This work provides insight on how initiating oncogenic events may directly influence the selection of

70 a well-known regulator of physiological and oncogenic events, the role of PKI proteins in these path

71 d podosomes, that are directly implicated in oncogenic events.

72 KPyV) infection is recognized as a potential oncogenic factor of urothelial carcinoma (UC) in renal t

73 urothelial cells driven by a set of defined oncogenic factors give rise to a mixture of tumor phenot

74 s acquired in a chronology driven in part by oncogenic fitness, and arise in an allelic configuration

75 In addition, some mutp53 have acquired new oncogenic function (gain of function).

76 Our findings elucidate the potential oncogenic function of intergenic fusions and highlight t

77 These results highlight a previously unknown oncogenic function of Mdm2 during the progression of can

78 Although previous studies have shown the oncogenic functions of E2A-PBX1 in cell and animal model

79 In addition to the oncogenic functions of WBP2, this review discusses the l

80 LL) is characterized by the expression of an oncogenic fusion kinase termed BCR-ABL1.

81 eloid leukemia (APL) is characterized by the oncogenic fusion protein PML-RARalpha, a major etiologic

82 with membranes and would be perturbed in the oncogenic fusion protein.

83 gical framework of a molecular mechanism for oncogenic fusion proteins in cancers.

84 ving the Mll1 (Kmt2a) gene generate powerful oncogenic fusion proteins, predominantly affecting infan

85 erging, filtering, and prioritizing putative oncogenic fusions across large cancer datasets, as demon

86 express mutant p53 (mtp53) and some contain oncogenic gain-of-function (GOF) p53.

87 sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus that causes Kaposi's sarcoma

88 erpesvirus (KSHV; human herpesvirus 8) is an oncogenic gammaherpesvirus that is the causative agent o

89 Here, we therapeutically exploit the oncogenic GOF mechanisms of p53 codon 158 (Arg(158)) mut

90 Additional ablation of the oncogenic GTPase Rac1 partially reduced progression of H

91 l gene expression.IMPORTANCE MDV is a potent oncogenic herpesvirus that induces T-cell lymphoma in in

92 n modes are modulated by accessory subunits, oncogenic histone mutations, and the methylation state o

93 blineage variants of seven vaccine-relevant, oncogenic HPV genotypes by using a large panel of monocl

94 the HPV capsid proteins of vaccine-relevant oncogenic HPV genotypes.

95 nicity of the HPV capsid of vaccine-relevant oncogenic HPV genotypes.IMPORTANCE Human papillomavirus

96 90%) coverage has the potential to eradicate oncogenic HPVs, but such high coverage is hard to achiev

97 onal status, class switch recombination, and oncogenic Ig translocations.

98 builds a strong framework to understand the oncogenic impact of p53 in human tissues.

99 ranscriptional coactivator YAP is considered oncogenic in many tissues, its roles in intestinal homeo

100 , YAP1-FAM118B, YAP1-TFE3, and YAP1-SS18 are oncogenic in mice.

101 l for tumorigenesis, its combination with an oncogenic insult, illustrated by Pten heterozygosity, el

102 interaction is a tractable approach to block oncogenic K-Ras activity.

103 in lung, breast, and colon cancer driven by oncogenic K-Ras.

104 Here, we addressed whether the oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)

105 Kaposi's sarcoma (KS) caused by oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)

106 In B cell leukaemia, oncogenic kinases phosphorylate IFITM3 at Tyr20, which c

107 xpression was potentiated by the presence of oncogenic Kras (G12D) Knockdown of Smad4 further enhance

108 Here we show that oncogenic KRAS alters the expression of a myriad of cell

109 We observed that oncogenic Kras and CXCR2 signaling alter CAFs, producing

110 hes for uncovering the early consequences of oncogenic KRAS expression.

111 epithelial progenitor (AT2) cells expressing oncogenic KRAS had reduced expression of mature lineage

112 cancers, including colorectal cancers (CRC), oncogenic KRAS has been extremely challenging to target

113 changes occurring early after activation of oncogenic KRAS in epithelial cells remain poorly underst

114 syngeneic mouse models, we demonstrate that oncogenic Kras is associated with secretory CAFs and tha

115 r L-arginine-induced pancreatitis, and in an oncogenic Kras murine model of spontaneous pancreatic du

116 S-mutated CRC, we characterize the impact of oncogenic KRAS on the cell surface of intestinal epithel

117 Oncogenic Kras presents in 90% of human PDAs.

118 We recently reported that oncogenic KRAS promotes a gene expression program of de

119 Oncogenic KRAS, a critical driver of pancreatic cancer,

120 f AGO2(Y393) disrupts both the wild-type and oncogenic KRAS-AGO2 interaction, albeit under different

121 In this study, we demonstrate that the oncogenic Kras-CXCR2 axis regulates the CAFs function in

122 To understand the altered mobility of an oncogenic KRAS4b, we used complementary experimental and

123 forms of aneuploidy represent the initiating oncogenic lesion in patients with B cell acute lymphobla

124 rabasal stiffness gradients are generated as oncogenic lesions progress towards malignancy, which we

125 We have thus unveiled a pro-oncogenic lncRNA that mediates cancer immune evasion, po

126 rity of human cancers and has been linked to oncogenic malignancies.

127 Collectively, our results describe an oncogenic mechanism of action for ACVR1 mutations, and s

128 Here we identify TBC1D15-mediated oncogenic mechanisms and tested the tumorigenic roles of

129 and pathway analysis demonstrates different oncogenic mechanisms in these samples.

130 The oncogenic mechanisms of action of ACVR1 mutations are cu

131 limiting investigations of enhancer-mediated oncogenic mechanisms.

132 We define oncogenic mediators as genes controlling biological proc

133 and SmgGDS-558, facilitate the activation of oncogenic members of the Ras and Rho families of small G

134 ned from sequence to target the precursor to oncogenic microRNA-21 (pre-miR-21) for enzymatic destruc

135 several fragments that bind the precursor to oncogenic microRNA-21 (pre-miR-21).

136 NA-binding protein, as a new target gene for oncogenic miR-106b, which was identified as an induced m

137 The findings explain how oncogenic mutants can counteract inhibitory mechanisms t

138 Other B cell lymphomas have acquired an oncogenic mutation in the myeloid differentiation primar

139 on strategies for the management of multiple oncogenic mutations activating PI3K and RAS signaling.

140 Cancers arise through the acquisition of oncogenic mutations and grow by clonal expansion(1,2).

141 Our findings therefore suggest that oncogenic mutations are propagated in the stem cell nich

142 tive patients with other concurrent acquired oncogenic mutations had a significantly shorter PFS (p =

143 ze fundamental biological processes, but how oncogenic mutations impact these interactions and their

144 Oncogenic mutations in RAS genes, like KRAS(G12D) or NRA

145 nomic landscapes with potentially targetable oncogenic mutations in the JAK/STAT, MAPK, MYC, and chro

146 Oncogenic mutations in the RNA splicing factors SRSF2, S

147 Although oncogenic mutations predispose tissue stem cells to tumo

148 Understanding how oncogenic mutations rewire regulatory-protein networks i

149 Oncogenic mutations were identified in the Ras superfami

150 ence in genetic alterations including common oncogenic mutations, whole genome mutations and copy num

151 ns in cancer represent convergent effects of oncogenic mutations.

152 e expression of key oncogenes, including the oncogenic MYC pathway.

153 The undruggable nature of oncogenic Myc transcription factors poses a therapeutic

154 ide a rationale for therapeutic targeting of oncogenic MYC via AURKB inhibition.

155 or locally advanced solid tumours harbouring oncogenic NTRK1, NTRK2, and NTRK3 gene fusions treated i

156 Of these 9 mutations, 4 were oncogenic (NTRK2A203T, NTRK2R458G, NTRK3E176D, and NTRK3

157 S-mutant type NSCLC have been conducted, new oncogenic or tumor suppressive genes need to be detected

158 c strategies with chemotherapeutics or other oncogenic pathway inhibitors.

159 mogenesis unless they converge on one single oncogenic pathway that is characteristic of the differen

160 s downstream effector STAT3 constitute a key oncogenic pathway, which has been thought to be function

161 HGG through epigenetic regulation of the MYC oncogenic pathway.

162 so revealed that JQ1 can activate additional oncogenic pathways and may affect epithelial-to-mesenchy

163 Therefore, IL6/STAT3 and ER oncogenic pathways are functionally decoupled, highlight

164 o simultaneously regulate multiple essential oncogenic pathways in MPNST cells, including the Wnt/bet

165 , non-cell-autonomous activation of specific oncogenic pathways might also offer opportunities that c

166 Cs and SCCs that likely impact the divergent oncogenic pathways, paving the way for targeted drug dis

167 shock protein 90 inhibitor, blocks multiple oncogenic pathways, resulting in antitumor activity.

168 n-coding RNAs that can have large impacts on oncogenic pathways.

169 otent and selective, specifically modulating oncogenic pathways.

170 a key SFMBT1 target gene contributing to its oncogenic phenotype.

171 fication of target substrates to promote pro-oncogenic phenotypes.

172 rst-in-class small molecule inhibitor of the oncogenic phosphatase protein tyrosine phosphatase 4A3 b

173 e phosphomimetic IFITM3(Y20E) mutant induced oncogenic PI3K signalling and initiated the transformati

174 Oncogenic PIK3CA results in an increase in arachidonic a

175 ces of mouse origin, the actual incidence of oncogenic polymorphisms arising in naive pluripotent ste

176 sm for drug resistance, but changes in tumor oncogenic potential and differential activation of signa

177 ude MNT's ability to fortify or weaken MYC's oncogenic potential depending on cell type and biologica

178 ome loss could create a cellular crisis with oncogenic potential in prostate epithelial cells.

179 ysteine (Cys-462), suggesting that CYP24A1's oncogenic potential is independent of its catalytic acti

180 NCE Epstein-Barr virus (EBV) has significant oncogenic potential that is linked to its latent infecti

181 tructured bacterial communities may increase oncogenic potential, and consortia of P. gingivalis and

182 significant new insight into EBV biology and oncogenic potential.

183 ion of a latent HHV-8 infection endowed with oncogenic potentialities and, in turn, the onset of KS.

184 although these mutations tended to be weakly oncogenic, probably explaining why they did not give ris

185 stic of field cancerization, the presence of oncogenic processes adjacent to cancer cells.

186 Oncogenic processes exert their greatest effect by targe

187 ased nutrient demands and regulates numerous oncogenic processes in tumors, leading to tumor malignan

188 FBP2 is upregulated and promotes several key oncogenic processes, such as epithelial-to-mesenchymal t

189 ated by growth factors or by mutation, drive oncogenic processes.

190 e-expression program and turning off STAT3's oncogenic program.

191 te PTEN provides a biochemical basis for its oncogenic propensity.

192 Despite its oncogenic properties however, the regulation of FOXA1 ex

193 y be a mechanism that contributes to the pro-oncogenic properties of TMPRSS13 in breast cancer.

194 Depletion of Axl suppressed cell intrinsic oncogenic properties, decreased tumor growth, reduced th

195 the SHH pathway results in reversal of these oncogenic properties, indicating its role in the pathoge

196 riched in OSCC, and they possess a number of oncogenic properties.

197 d protein kinase pathway leading to enhanced oncogenic properties.

198 This renders the oncogenic protein SKP2 a promising therapeutic target.Se

199 ave been shown to engender dependence on the oncogenic protein Skp2 for survival of transformed cells

200 ion processing pathway that modifies several oncogenic proteins, including RAS.

201 In vivo oncogenic Ras exists in isoform-distinct nanoclusters.

202 (Ras-like) GTPases are directly activated by oncogenic Ras GTPases.

203 clusters reduces the number of the clustered oncogenic Ras molecules, thus suppressing Raf-1 activati

204 Oncogenic RAS mutations pose substantial challenges for

205 ery similar to Ras, was observed to suppress oncogenic Ras phenotype, reverting its transformation.

206 sistant to transcriptomic changes induced by oncogenic Ras than mouse, blind mole-rat, and human cell

207 ency causes acinar atrophy but combines with oncogenic Ras to produce pancreatic tumors.

208 We found that short-term induction of oncogenic Ras(V12) activates downstream mitogen-activate

209 (2020) reveal that oncogenic Ras(V12)-mediated cell rounding and cortical s

210 te a critical role for MYC as an effector of oncogenic RAS, strategies to target MYC activity in RAS-

211 l for developing PKCe-targeted therapies for oncogenic RAS-driven malignancies.

212 transcriptomes and epigenome profiles during oncogenic RAS-induced senescence and validating central

213 Here, we use Hi-C to show that oncogenic RAS-induced senescence in human diploid fibrob

214 tution in SHP2 is unique in that it exhibits oncogenic Ras-like transforming activity.

215 n untransformed cells, and stably expressing oncogenic RasV12 in untransformed cells is sufficient to

216 However, targeting oncogenic regulators of Warburg effect has always been c

217 e of somatic rearrangements, contributing to oncogenic remodeling through chimeric circularization an

218 These data demonstrate a novel oncogenic role for PAK4 in rhabdomyosarcoma and show tha

219 These data reveal a novel unexplored oncogenic role for RUNX genes in kidney cancer and indic

220 er, our results indicate a multi-dimensional oncogenic role for SEMA4C in metastatic osteosarcoma and

221 hese findings indicate that GALC may play an oncogenic role in melanoma by modulating the levels of i

222 EpCAM gain relevance and mediate miR-30e-3p oncogenic role in nonfunctional TP53 backgrounds.

223 These studies reveal an oncogenic role of HIF-1alpha in ccRCC initiation and sug

224 )-methyladenosine (m(6)A) demethylase, plays oncogenic roles in various cancers, presenting an opport

225 cause it can play both tumor suppressive and oncogenic roles.

226 Crosstalk between the oncogenic RTK hepatocyte growth factor receptor (MET), e

227 d-biased repair processes, quantification of oncogenic selection and fine mapping of sister-chromatid

228 t small-molecule inhibitors targeting either oncogenic signal transduction or epigenetic regulation c

229 essive actions of PP2A, thereby potentiating oncogenic signaling and reducing drug sensitivity of RAS

230 r iron to DNA repair, genomic integrity, and oncogenic signaling as well as the discovery of ferropto

231 CDK4/6 inhibitors that target KRAS-directed oncogenic signaling can suppress PDAC proliferation thro

232 All oncogenic signaling could be extinguished by the novel G

233 In turn, oncogenic signaling downstream of RTKs can reciprocally

234 secondary concomitant alterations to promote oncogenic signaling during tumor evolution.

235 Oncogenic signaling elevates lipid ROS production in man

236 f the receptor tyrosine kinase AXL to induce oncogenic signaling in ovarian cancer.

237 of therapies targeting a single node of the oncogenic signaling network.

238 clones and serum autoantibodies reactive to oncogenic signaling pathway proteins.

239 ll as treatment of activated host immune and oncogenic signaling pathways in CRC.

240 Thus, inhibition of hidden oncogenic signaling pathways in DIPG such as TbetaRI tha

241 of both CDC42:ERK1/2 and NF-kappaB:AP-1 pro-oncogenic signaling pathways in nonmalignant versus mali

242 overexpression and coordinated activation of oncogenic signaling pathways, including E2Fs, Wnt, Myc,

243 suppressor by negatively regulating multiple oncogenic signaling pathways.

244 gnosis in neuroblastoma, but TERT-associated oncogenic signaling remains unclear.

245 der to investigate mechanisms underlying Alk oncogenic signaling, we conducted a genetic suppressor s

246 ) (encoded by GNA13) as potent activators of oncogenic signaling.

247 ion-specific characteristics associated with oncogenic signaling.

248 f cancer: growth factor independence through oncogenic signalling and metabolic reprogramming to supp

249 undance of sterol-and in particular, whether oncogenic signalling has a role-is unclear.

250 ar mechanism involving PDGFRB and associated oncogenic signalling pathways (PI3K-AKT/ERK), which may

251 nown hallmark of cancer progression, yet the oncogenic signals that promote metabolic adaptations to

252 that NRARP is not sufficient to block NOTCH oncogenic signals.

253 Here we report a mechanism regulated by the oncogenic SOX2-GLI1 transcriptional complex driving mela

254 The oncogenic spacer region is alpha-helical, which contrast

255 liceosome) is altered in tumours, leading to oncogenic splicing events associated with tumour progres

256 o-protein analyses reveal the segregation of oncogenic STAT5 and ERK activation to competing clones.

257 r findings shed new lights on regulations of oncogenic stress signaling and may be informative for de

258 le-strand break repair mechanisms induced by oncogenic stress, the highly mutagenic theta-mediated en

259 ing list of genomically driven therapies for oncogenic subsets of NSCLC.

260 of EBV-positive cells and is associated with oncogenic super-enhancers involving long-range regulator

261 Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression

262 t Chinese hamster ovary cells expressing the oncogenic target epithelial cell adhesion molecule and i

263 selective substrates, such as its well-known oncogenic target, c-Myc.

264 rdoma cells promotes epigenetic silencing of oncogenic TBXT, alters gene networks critical to surviva

265 nd amplifies the effect of MYC, a well-known oncogenic TF.

266 Agrobacteria require an oncogenic Ti or Ri plasmid to transfer genes into plants

267 ding NOTCH1-3 in the epidermis and SCCIS and oncogenic TP53 mutations in SCCIS.

268 MYC is a highly validated oncogenic transcription factor and cancer target.

269 The modulation of GLI2, an oncogenic transcription factor commonly upregulated in c

270 ther the tumor suppressor protein p53 or the oncogenic transcription factor TAZ.

271 lls and may inform approaches targeting this oncogenic transcription factor to manage malignancies.

272 s a negative-feedback regulator for multiple oncogenic transcription factors, provides insights into

273 ivation mechanism of HIF-1 and several other oncogenic transcription factors.

274 hibit enhancer activities and are induced by oncogenic transcription factors.

275 tion of CTCF boundary can alter TAL1 TAD and oncogenic transcription networks in leukemogenesis.

276 rived FGF1 as a novel paracrine regulator of oncogenic transcription.

277 s), whose aberrant usage could contribute to oncogenic transcriptional circuits.

278 ATS kinases and phosphorylation of the proto-oncogenic transcriptional co-activator YAP.

279 In several tumour types, diverse oncogenic, transcriptional and metabolic abnormalities c

280 Oncogenic transformation alters lipid metabolism to sust

281 further uncovered that HGF induces prostatic oncogenic transformation and cell growth.

282 s and mouse cells are equally susceptible to oncogenic transformation by SV40LT and H-RasV12.

283 ncluding breast, and are sufficient to drive oncogenic transformation in vitro and in vivo.

284 Moreover, Galpha(13) Arg-200 mutants induced oncogenic transformation in vitro as determined by focus

285 te that transition to naive pluripotency and oncogenic transformation share common epigenetic traject

286 We observed an early onset oncogenic transformation, accelerated tumor cell growth,

287 -related proteins and their diverse roles in oncogenic transformation, proliferation, and metastasis.

288 of proinflammatory signals required for full oncogenic transformation.

289 anges that accumulate, eventually leading to oncogenic transformation.

290 llular scaffold, frequently perturbed during oncogenic transformation.

291 val and proliferation, setting the stage for oncogenic transformation.

292 e show how our annotation allows us to place oncogenic transformations in the context of a broad cell

293 Immunoglobulin (Ig) gene rearrangements and oncogenic translocations are routinely assessed during t

294 al simulation studies, we observe that these oncogenic variants of the p53 not only suffer a loss in

295 (2020) describe studies that establish oncogenic versus tumor-suppressive functions of two BRD4

296 er hand, EBV represents the first identified oncogenic virus, capable of causing >=7 different types

297 In particular, certain oncogenic viruses activate expression of repetitive gene

298 udy investigates the presence of potentially oncogenic viruses such as SV40, JCV, BKV and EBV in pati

299 Group B adenoviruses are weakly oncogenic, whereas most of the remaining human adenoviru

300 this effect led to subsequent activation of oncogenic YAP.