ライフサイエンスコーパス: oncogenic

1 lignancies suggests that STAT mutants may be oncogenic.

2 direct link between IDO1 expression and the oncogenic activation of RET in thyroid carcinoma and des

3 rface-associated HA was required for eIF4E's oncogenic activities suggesting that eIF4E potentiates a

4 ild-type p53 together with poorly understood oncogenic activity encoded by missense mutations.

5 asiveness of cancer cell lines and has liver oncogenic activity in mice.

6 PRKACA was unable to fully recapitulate the oncogenic activity of DNAJB1-PRKACA, implying that FL-HC

7 As result, the oncogenic activity of NOTCH1 in T-ALL is strictly depend

8 Mechanistically, we show that the oncogenic activity of PRKCI relates in part to the up-re

9 RA, suggesting a mechanism through which the oncogenic activity of the mutant receptor is tempered by

10 ic strategy due to the potential deleterious oncogenic activity of this miRNA.

11 ion promoted Bmi-1 protein stability and its oncogenic activity.

12 ed in other cancers displaying enhanced BRD4 oncogenic activity.

13 Oncogenic addiction to the Fms-like tyrosine kinase 3 (F

14 croenvironments with uneven distributions of oncogenic alterations and signaling networks.

15 various combinations of TP53, KRAS, and MYC-oncogenic alterations commonly found in non-small cell l

16 anoma that arose from DPN we find additional oncogenic alterations.

17 gene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulatio

18 There is growing understanding of the oncogenic and tumor suppressive functions of JARID1 prot

19 Cell, Sun et al. describe context-dependent oncogenic and tumor-suppressive functions for the mammal

20 oles in different cellular contexts, such as oncogenic and tumor-suppressor functions and hematopoiet

21 of neuropeptide signaling systems with both oncogenic and tumour-suppressing roles for cancer progre

22 , and demonstrated its essential role in the oncogenic AR signaling axis.

23 te cancer, functioning as an enhancer of the oncogenic AR signaling pathway but also as a suppressor

24 SCC, shedding light upon the tumor promoting oncogenic aspect of Notch1 in SCC.

25 ed from transgenic mice inducibly expressing oncogenic beta-catenin and/or PIK3CA(H1047R) to follow s

26 n and probes-based schemes, and targeted the oncogenic BRAF V600E and KRAS G12D mutations.

27 l exon 3' untranslated region, generating an oncogenic, C-terminally modified isoform (PACE4-altCT).

28 esions unleash cellular plasticity and favor oncogenic cellular reprogramming.

29 nt as wild-type Arf(+/+) cells to comparable oncogenic challenge and do not produce tumors.

30 prone owing to genome instability caused by oncogenic challenges.

31 gulatory loops leading to propagation of the oncogenic chromatin complex in BRD4-NUT patient cells.

32 of reductional segregation can contribute to oncogenic chromosome dynamics and that the embryonal the

33 f target genes of the MLL chimeras and their oncogenic cofactor, the super elongation complex.

34 Overall, our results establish the oncogenic contributions of EVI1 in ER- and HER2-negative

35 ultiple tumor types, we constructed a map of oncogenic dependencies associated with cellular pathways

36 ents should be stratified according to their oncogenic dependencies when treated with PI3K and AKT in

37 also increased miR-15a/16-1, shifting their oncogenic dependency from the BCL-2 to the ERK signaling

38 the genome and shares features with reported oncogenic DNA insertions.

39 ent of leukaemia cells harboring a different oncogenic driver (K-562 cell line) did not result in sel

40 modeling to uncover impactful mutations and oncogenic driver alleles with clinical importance in the

41 The Notch1 gene is a major oncogenic driver and therapeutic target in T-cell acute

42 votal breast cancer biomarker and targetable oncogenic driver associated with aggressive breast cance

43 thway occurs frequently in cancers and is an oncogenic driver in many solid tumors.

44 Despite the identification of several oncogenic driver mutations leading to constitutive JAK-S

45 ere predominantly homogenous, independent of oncogenic driver mutations, and similar in benign and ma

46 el, we recently demonstrated that ZEB2 is an oncogenic driver of immature T-cell acute lymphoblastic

47 limitation of this strategy is that not all oncogenic driver proteins are "druggable" enzymes or rec

48 Second, findings that defy the orthodoxy of oncogenic "driver mutations" are now accumulating: the u

49 NBL oncogenesis, to functionally assess NBL oncogenic drivers and to characterize NBL metastasis.

50 Identification and functional validation of oncogenic drivers are essential steps toward advancing c

51 Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC.

52 e 7 (USP7) results in the degradation of the oncogenic E3 ligase MDM2, and leads to re-activation of

53 proliferation, and that efforts to block the oncogenic effect of aerobic glycolysis must target react

54 is likely to significantly contribute to the oncogenic effect of the inactivation of BRCA1 or BRCA2.

55 RG and propose that ERG stabilization is the oncogenic effector of SPOP mutation.

56 ely, our results argue that MYC mediates its oncogenic effects in part by altering mevalonate metabol

57 The oncogenic effects of Gab2 in HepG2 cells were promoted b

58 The oncogenic effects of nutrients were reversed by SIRT3, w

59 on of gene expression, and likely additional oncogenic effects.

60 tion of 5-hmC and preferential enrichment at oncogenic enhancers is a novel regulatory mechanism in h

61 nd stress factors collaborate, they activate oncogenic enhancers that distinguish cancers from wounds

62 Moreover, GRHL2 suppresses the oncogenic epithelial-mesencyhmal transition, thereby act

63 Our study also demonstrates that oncogenic ErbB2 signaling can be activated in SCs but no

64 and TP53 and MYC amplification are frequent oncogenic events in small cell lung cancer (SCLC).

65 subgroups are refined by the presence of key oncogenic events or methylation profiles more closely re

66 active domain 5B (ARID5B) as a collaborating oncogenic factor involved in the transcriptional program

67 We conclude that ZEB1 is a major oncogenic factor required for UM progression and could b

68 In recent years, it has also shown oncogenic features by activating the canonical Wnt/beta-

69 We demonstrate that the expression of the oncogenic forkhead transcription factor FOXM1 is upregul

70 Our results establish an oncogenic function for secretory autophagy in HNSCC stro

71 bour a number of alterations without obvious oncogenic function including BRAF-inactivating mutations

72 all, our study demonstrates the multifaceted oncogenic function of the protein lysine methyltransfera

73 H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in

74 identified mechanism by which mutp53 confers oncogenic functions by promoting cancer cell adaptation

75 al roles during normal development and exert oncogenic functions during tumorigenesis.

76 l roles in germ cell and neural development, oncogenic functions in cancer, and potential as therapeu

77 vering Skp2-mediated Twist stabilization and oncogenic functions in CRPC offers new knowledge on how

78 t Skp2 regulates CRPC through Twist-mediated oncogenic functions including epithelial-mesenchymal tra

79 These oncogenic functions of GRHL2 were counterbalanced by its

80 oMYC discriminates between physiological and oncogenic functions of MYC is unclear.

81 The unexpected pro-oncogenic functions of Rac GTPase-activating proteins al

82 ll GTPase RAB25 can exert both pro- and anti-oncogenic functions.

83 ediatric disease driven by expression of the oncogenic fusion gene PAX3-FOXO1A.

84 nal and functional effects of ETO2-GLIS2, an oncogenic fusion protein frequently encountered in AMKL,

85 chromosomal translocation that results in an oncogenic fusion protein, whereas pleomorphic liposarcom

86 eneic murine AML model driven by the MLL-AF9 oncogenic fusion protein.

87 Driven by EWS/Ets, or rarely variant, oncogenic fusions, Ewing Sarcoma is a biologically and c

88 focus not only on the effects of mutant p53 oncogenic gain of function but also on the mechanisms un

89 Many mutant p53 proteins exert oncogenic gain-of-function (GOF) properties that contrib

90 Many mutant p53 proteins exert oncogenic gain-of-function (GOF) properties that promote

91 Identification of specific oncogenic gene changes has enabled the modern generation

92 CtBP modulates oncogenic gene expression programs and is an emerging dr

93 ften exploit chromatin machinery to activate oncogenic gene expression programs.

94 Here we present a systematic analysis of oncogenic gene fusions among a clinically well-character

95 Oncogenic gene fusions drive many human cancers, but too

96 In summary, we identified several novel oncogenic gene fusions in colorectal cancer that may dri

97 seven activated pathways associated with pro-oncogenic genes at network analysis.

98 following random somatic alterations of key oncogenic genes, which are favoured by a number of risk

99 ntial therapy options for patients harboring oncogenic genomic alterations.

100 plexes has adverse effects on normal but not oncogenic growth.

101 ivities suggesting that eIF4E potentiates an oncogenic HA program.

102 the YAP:TEAD interaction at the heart of the oncogenic Hippo pathway, and possessing the potency and

103 Here, we show that oncogenic HRas induces ER stress and activation of IRE1a

104 rthermore, tissue aberrancies generated from oncogenic Hras, and even mutation-independent deformatio

105 Oncogenic human papillomaviruses (HPVs) are closely link

106 EGFR, of which half strongly interacted with oncogenic, hyperactive EGFR variants.

107 hat a lack of caveolin-1 expression inhibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescen

108 rimary and metastatic colon cancers and that oncogenic K-RAS activates TGF-beta signaling to promote

109 Lung cancer cells expressing oncogenic K-Ras have bypassed the senescence barrier.

110 hey demonstrate that continued expression of oncogenic K-RAS is required for the survival of primary

111 y complex in cell proliferation signaling by oncogenic K-Ras.

112 Oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)

113 Here we report that oncogenic kinase and growth-factor signaling converge to

114 D stem or progenitor cells in the absence of oncogenic kinase signaling, a phenomenon referred to as

115 2 by miR-194 resulted in derepression of the oncogenic kinases FLT3 and JAK2, leading to enhanced ERK

116 lar targets, are predominantly inhibitors of oncogenic kinases.

117 of metastatic CRC that harbors an inducible oncogenic Kras allele (Kras(mut) ) and conditional null

118 s underlying the transcriptional response to oncogenic KRAS and provide a framework to develop strate

119 ) to combine a transcriptional signature for oncogenic KRAS derived from a murine isogenic cell line

120 state GTP-bound levels or the ability of the oncogenic KRAS G12V mutant to cause morphologic transfor

121 To understand the role of oncogenic KRAS in CRC, we engineered a mouse model of me

122 hat regulate the transcriptional response of oncogenic KRAS in pancreatic cancer and to understand th

123 Our results indicate that oncogenic Kras induces constitutive activation of SOX9 i

124 Our studies reveal that oncogenic Kras induces SOX9 mRNA and protein expression

125 ancer (NSCLC) and is commonly comutated with oncogenic KRAS mutations.

126 In calmodulin (CaM)-rich environments, oncogenic KRAS plays a critical role in adenocarcinomas

127 In this model, stochastic extinction of oncogenic Kras signalling and emergence of Kras-independ

128 rfering RNA or short hairpin RNA specific to oncogenic Kras(G12D), a common mutation in pancreatic ca

129 Inducible expression of oncogenic Kras(V12) in hepatocytes of transgenic zebrafi

130 Oncogenic KRas, HRas, and NRas (K-Ras, H-Ras, and N-Ras)

131 While many attempts have been made to target oncogenic KRAS, no clinically useful therapies currently

132 Despite expression of oncogenic KRAS, premalignant pancreatic intraepithelial

133 iments to identify all-d peptide ligands for oncogenic KRas, providing a useful tool in the search fo

134 igated the mechanistic link between SOX9 and oncogenic Kras, studied biological function of SOX9, and

135 n extensively modeled in mice expressing the oncogenic KrasG12D mutation.

136 uncharacterized, the identification of novel oncogenic lncRNAs is difficult.

137 tochondrial function in melanoma cells after oncogenic MAPK inhibition.

138 that integration may represent an additional oncogenic mechanism through direct effects on cancer-rel

139 The oncogenic mechanisms of overnutrition, a confirmed indep

140 s of regenerating liver (PRL) are infamously oncogenic members of the PTP superfamily.

141 st tumors is linked to increases in putative oncogenic metabolites that may contribute to malignant t

142 Oncogenic microRNAs (miRs) have emerged as diagnostic bi

143 lisers on the relative quantification of the oncogenic miR-1290 was also assessed.

144 Here we show that oncogenic miR-182 is a strong regulator of C/EBPalpha.

145 es mesothelioma that exhibits common key pro-oncogenic molecular events throughout the latency period

146 ed miRNA regulating 719 tumor suppressive or oncogenic mRNA associated with increased proliferation a

147 n translation and protein synthesis, certain oncogenic mRNAs are spared.

148 genetic or pharmacological targeting of the oncogenic MUC1 subunit MUC1-C is sufficient to suppress

149 ree different species and in the SF3B1 K700E oncogenic mutant background.

150 The specific targeting of oncogenic mutant epidermal growth factor receptor (EGFR)

151 nd all-d-amino acid biotinylated variants of oncogenic mutant KRas(G12V).

152 Disrupting Intu in an oncogenic mutant Smo (SmoM2)-driven BCC mouse model prev

153 Many oncogenic mutants of the tumor suppressor p53 rapidly ag

154 We identified an oncogenic mutation, F247L, whose expression robustly act

155 ian cancer and cell lines harboring specific oncogenic mutations and representing different stages of

156 Recently, oncogenic mutations in NRAS/KRAS, upstream regulators of

157 Despite the high incidence of oncogenic mutations in PIK3CA, the gene encoding the cat

158 now accumulating: the ubiquitous presence of oncogenic mutations in silent premalignancies or the dyn

159 demonstrate that sequential accumulation of oncogenic mutations in Wnt, EGFR, P53, and TGF-beta sign

160 tudied neoplastic tumor model in Drosophila, oncogenic mutations of the proto-oncogene Ras (Ras(V12))

161 By targeting the same oncogenic mutations to discrete skin compartments, we sh

162 9,176 cancer patients across 1,018 recurrent oncogenic mutations.

163 potential of tumor cells lacking one of the oncogenic mutations.

164 Here, we report a deep transcriptional, oncogenic network regulated by miRNAs.

165 aging of the oxidative stress response by an oncogenic noncoding RNA.

166 trate that p53(-/-) synergizes with enhanced oncogenic Nras signaling to transform MEPs and drive AML

167 tress during chronic HCV infection activates oncogenic Nrf2 signaling that promotes hepatocyte surviv

168 tases of regenerating liver (PRLs), the most oncogenic of all protein-tyrosine phosphatases (PTPs), p

169 ell autonomous activities that may be either oncogenic or tumor suppressive.

170 cancer types and has been shown to modulate oncogenic pathways in in vitro studies.

171 ht on how the skin handles the activation of oncogenic pathways in the stem cell compartment and how

172 fecting the oxidative stress response or the oncogenic pathways included in the model.

173 Transcriptional deregulation of oncogenic pathways is a hallmark of cancer and can be du

174 NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase

175 (CDK) complexes to be activated by mitogenic/oncogenic pathways.

176 een innate immune responses and STAT3-driven oncogenic pathways.

177 n utilization, oxidative stress response and oncogenic pathways.

178 critical for conferring and maintaining the oncogenic phenotype in tumors with poor prognoses.

179 elies on ETV4 expression for maintaining its oncogenic phenotype.

180 role of RAB25 in regulating context-specific oncogenic phenotypes.The Ras-family small GTPase RAB25 c

181 PTEN is a PIP3 phosphatase that antagonizes oncogenic PI3-kinase signalling.

182 During infection the bacteria translocate an oncogenic piece of DNA (transferred DNA, T-DNA) into pla

183 lay between these pathways allows cells with oncogenic PIK3CA mutations or PTEN deletion to grow usin

184 In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated dai

185 the anticancer drug dasatinib on Src kinase oncogenic potential in vivo We further show that myristo

186 g to rapidly and effectively interrogate the oncogenic potential of genomic rearrangements identified

187 In this study, we investigated the oncogenic potential of IGF-2 in IGF2-overexpressing CRC

188 ese results provided evidence supporting the oncogenic potential of NFAT3 and suggested that CDK3-med

189 ogenesis of this disease, but its functional oncogenic potential remains uncertain.

190 r-specific chromosomal rearrangements, whose oncogenic potential remains unknown.

191 Consistent with this oncogenic potential, exogenous CtBP2 transformed primary

192 rphan" receptor tyrosine kinases (RTKs) with oncogenic potential.

193 are unknown, and whether SGG influences the oncogenic process or benefits from the tumor-prone envir

194 y alternative downstream mechanisms to drive oncogenic processes in a context-dependent manner.

195 t constitutive NOTCH3 signaling can drive an oncogenic program in a subset of basal breast cancers.

196 F1 expression or mTOR activity abolishes the oncogenic properties of MALAT1, suggesting that SRSF1 in

197 Mutant p53 protein(s) (mutp53) can acquire oncogenic properties that increase metastasis, prolifera

198 dent escaper populations (cells that acquire oncogenic properties) are associated with de-differentia

199 f stem cell active homeobox genes to acquire oncogenic properties.

200 es have suggested that overexpression of the oncogenic protein epithelial membrane protein-2 (EMP2) c

201 ug discovery efforts made in targeting these oncogenic PTPs as compelling candidates for cancer thera

202 Here, we show that oncogenic RAS and BRAF induce perinuclear relocalization

203 Oncogenic Ras causes proliferation followed by premature

204 Oncogenic Ras cooperates with Egfr, which cannot be expl

205 How oncogenic Ras elicits and integrates Egfr and Hedgehog s

206 Oncogenic Ras induces the expression of Egfr ligands.

207 In addition, we target the 3UTR of oncogenic Ras mRNA and suppress Pan-Ras expression, whic

208 Oncogenic RAS mutations are present in 15-30% of thyroid

209 uestion of the difference between normal and oncogenic RAS pathway signaling, this study shows that o

210 more effectively with the stress elicited by oncogenic Ras protein.

211 We report that oncogenic RAS signaling can upregulate tumor cell PD-L1

212 d, in part, by the PI3K/AKT effector axis of oncogenic RAS signalling.

213 RAS pathway signaling, this study shows that oncogenic RAS specifically triggers constitutive endocyt

214 Expression of ATXN7 mutants cooperated with oncogenic RAS to induce thyroid cell proliferation, poin

215 s, suggesting organ-specific contribution of oncogenic RAS to LCH pathogenesis.

216 our model, we show that Egfr cooperates with oncogenic Ras via Arf6, which functions as a novel regul

217 ibited neoplastic growth of cells induced by oncogenic Ras, suggesting an important pro-tumorigenic r

218 nducible SOX2, which is broadly expressed in oncogenic RAS-associated cancers, we show that despite w

219 in the context of cancer and illustrates how oncogenic RAS-mediated degradation of FOXOs, via post-tr

220 ed by Casein Kinase 1 alpha (CK1alpha) in an oncogenic RAS-specific manner, but whether this mode of

221 t lines uncover synthetic lethal partners of oncogenic Ras.

222 ained PSC formation is a critical feature of oncogenic RAS/BRAF signaling in cancer cells that contro

223 F-1alpha co-activating RNA); we describe its oncogenic role as a HIF-1alpha co-activator that regulat

224 However, FOXM1 may also play an oncogenic role by interacting with other proteins, such

225 Our work establishes an oncogenic role for SND1 in promoting TIC formation and h

226 These results support a driver oncogenic role for VAV1 signaling in the pathogenesis of

227 O, as an m(6)A demethylase, plays a critical oncogenic role in acute myeloid leukemia (AML).

228 rams and is an emerging drug target, but its oncogenic role is unclear.

229 Although the oncogenic role of CUL4A has been well established, speci

230 In conclusion, we present an oncogenic role of FAM83H in liver cancer, which is close

231 We verified the oncogenic role of the cytokine tissue inhibitor of matri

232 The oncogenic role of the spliced somatostatin receptor sst5

233 itoneal dissemination was used to assess the oncogenic role of the target miRNA.

234 t its regulation of Lef1 was crucial for its oncogenic role.

235 ic and pharmacologic evidence that RUNX1 has oncogenic roles and reveal RUNX1 as a novel therapeutic

236 the question whether new members might play oncogenic roles as well.

237 Our data support unappreciated and dominant oncogenic roles for MYF5 and MYOD convergence on common

238 has context-dependent tumor-suppressive and oncogenic roles in cancer.

239 ne demethylase PHF8 is upregulated and plays oncogenic roles in various cancers; however, the mechani

240 Dysregulated oncogenic serine/threonine kinases play a pathological r

241 zontal transfer of mtDNA from EVs acts as an oncogenic signal promoting an exit from dormancy of ther

242 this review, we describe connections between oncogenic signaling and cancer cell metabolism and how t

243 Cross-talk among oncogenic signaling and metabolic pathways may create op

244 Therefore, collateral inhibition of oncogenic signaling and mitochondrial respiration may he

245 Energy homeostasis and oncogenic signaling are critical determinants of the gro

246 arly Ras phenotype that is dependent on both oncogenic signaling as well as stress signals imparted b

247 Oncogenic signaling by NOTCH is elevated in brain tumor-

248 coma viral oncogene homolog B (BRAF(V600E)), oncogenic signaling enhances glucose-dependent metabolis

249 -stage clinical development and might impede oncogenic signaling from mutant RAC1.

250 -associated-fibroblasts (CAF) that stimulate oncogenic signaling in TEC.

251 eton and plays a part in several potentially oncogenic signaling networks.

252 1 (NDRG1) has been shown to inhibit numerous oncogenic signaling pathways in cancer cells.

253 OSPECT (Profiling of Resistance patterns and Oncogenic Signaling Pathways in Evaluation of Cancers of

254 at RNF157 serves as a novel node integrating oncogenic signaling pathways with the cell cycle machine

255 Sustained activation of pro-oncogenic signaling pathways, increased proliferation, a

256 is well documented, but its relationship to oncogenic signaling remains unknown.

257 Our data present a novel oncogenic signaling role of PSMA that can be exploited f

258 by drug-treated CAFs exhibited a decrease in oncogenic signaling, as manifested by downregulation of

259 Driven by oncogenic signaling, glutamine addiction exhibited by ca

260 mmary epithelial cell (MEC) populations, and oncogenic signaling, MMTV-ErbB2 transgenic mice were adm

261 onse pathways that are permissive for strong oncogenic signaling.

262 indings that SK1 is a downstream mediator of oncogenic signalling by Ras, we found that targeting CIB

263 nstream of promiscuously used-and frequently oncogenic-signalling pathways, via a novel combination o

264 in suppressing transformation in response to oncogenic signals.

265 Oncogenic SS18-SSX family fusion genes are known to alte

266 cells of the subventricular zone (SVZ) upon oncogenic stress, whereas their expression in human glio

267 primary HCC may contribute to activation of oncogenic TGF-beta signaling and subsequent tumor progre

268 Our data indicate that KLF4 suppresses oncogenic TGF-beta signaling by activation of Smad7 tran

269 increase in MAPK signalling that results in oncogenic toxicity; this effect can be abolished by phar

270 chromatin remodeling complex is required for oncogenic transcription and tumor growth in non-small-ce

271 The oncogenic transcription factor FoxM1 plays a vital role

272 The oncogenic transcription factor MYC and its binding partn

273 ficient DLBCLs through downregulation of the oncogenic transcription factor MYC.

274 Etv4, an ETS family oncogenic transcription factor, was strongly expressed a

275 ntenance of cancer cell identity and promote oncogenic transcription to which cancer cells become hig

276 ata establish the landscape of SE-associated oncogenic transcriptional network in NPC, which can be e

277 iting reduced levels of beta-catenin and its oncogenic transcriptional target, cyclin D1.

278 PP1R1A resulted in a significant decrease in oncogenic transformation and cell migration in vitro as

279 ss can be triggered by apoptotic signalling, oncogenic transformation and overcrowding of cells.

280 eventing self-renewing brain stem cells from oncogenic transformation are poorly defined.

281 l line, an important cell model for studying oncogenic transformation in breast tissues.

282 h that ATM activity poses a major barrier to oncogenic transformation in the pancreas via maintaining

283 em and progenitor cells and also potentiated oncogenic transformation in vitro.

284 either CASP3 or ENDOG prevented Myc-induced oncogenic transformation of MCF10A cells.

285 intracellular magnesium levels that promote oncogenic transformation.

286 e of genomic stability and the prevention of oncogenic transformation.

287 d site-specific glycosylation is involved in oncogenic transformation.

288 mediated cholangiocellular proliferation and oncogenic transformation.

289 ive receptors, augmenting PI3K signaling and oncogenic transformation.

290 in two highly proliferative tissues prone to oncogenic transformation: the hematopoietic lineage and

291 , is implicated in genomic rearrangement and oncogenic transformation; however, its contribution to r

292 cleavage as a broad DNA damage mechanism in oncogenic translocations as well as a functional role of

293 that a large proportion of genes involved in oncogenic translocations overall contain TOP2A CCRs.

294 s implied ceRNA interaction performs crucial oncogenic/tumor suppressive functions in glioblastoma mu

295 f infection of multiple HPV types, including oncogenic types, by treatment with IFN-gamma, an antivir

296 Genetic mutations leading to oncogenic variants of receptor tyrosine kinases (RTKs) a

297 Immunodeficiency and (chronic/oncogenic) viral infections together constitute a major

298 nancy that is closely associated with one of oncogenic viruses infection, Kaposi's sarcoma-associated

299 ins, such as beta-catenin or SMAD3 to induce oncogenic WNT and TGFbeta signaling pathways, respective

300 ich drives proliferation; however, they lack oncogenic Wnt pathway mutations, suggesting activation b