ライフサイエンスコーパス: oncogenic transformation

1 ive receptors, augmenting PI3K signaling and oncogenic transformation.

2 nses and, when deregulated, can promote cell oncogenic transformation.

3 many genome rearrangements, some leading to oncogenic transformation.

4 erts a central role in protecting cells from oncogenic transformation.

5 during normal development, regeneration and oncogenic transformation.

6 tant functions in cellular proliferation and oncogenic transformation.

7 Induction of these genes is required for oncogenic transformation.

8 th studies showing that AMPK is required for oncogenic transformation.

9 idation of novel pathways that contribute to oncogenic transformation.

10 nfluence each other and cooperate to promote oncogenic transformation.

11 actions with the Arf GTPases and paxillin in oncogenic transformation.

12 lecular insights into cytokine resistance in oncogenic transformation.

13 the high Ran GTPase activity resulting from oncogenic transformation.

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

15 BCR specificity per se did not contribute to oncogenic transformation.

16 -replicative complex proteins have a role in oncogenic transformation.

17 everal histone modifications associated with oncogenic transformation.

18 ocket and are critical for BCR-ABL-dependent oncogenic transformation.

19 iciently promote cell cycle arrest and limit oncogenic transformation.

20 n SMOC-2 that has important consequences for oncogenic transformation.

21 idative phosphorylation and are resistant to oncogenic transformation.

22 lization appears essential for HuR-dependent oncogenic transformation.

23 Moreover, inhibition of Akt suppresses IKBKE oncogenic transformation.

24 T cells are associated with vulnerability to oncogenic transformation.

25 a link between transgenic AR expression and oncogenic transformation.

26 and suggested that paxillin might facilitate oncogenic transformation.

27 nflammation, myeloid cell proliferation, and oncogenic transformation.

28 hancing both HBV replication and pX-mediated oncogenic transformation.

29 1/K2 induced enhanced cell proliferation and oncogenic transformation.

30 ged DNA, resulting in partial polyploidy and oncogenic transformation.

31 cell morphogenesis, osteoclastogenesis, and oncogenic transformation.

32 d microRNAs (miRNAs) that have a role in the oncogenic transformation.

33 rmed cells and human tumors, is required for oncogenic transformation.

34 acinar architecture that are consistent with oncogenic transformation.

35 ifferentiated cells resist reprogramming and oncogenic transformation.

36 a is the sole mediator of p85 mutant-induced oncogenic transformation.

37 Reduction of GSTM4 levels caused a loss of oncogenic transformation.

38 man acute myeloid leukemia, is causative for oncogenic transformation.

39 T cell-mediated immune control that resists oncogenic transformation.

40 Matrigel culture, a trait that is lost upon oncogenic transformation.

41 ults identify Plk1 as crucial in pX-mediated oncogenic transformation.

42 anscriptional consequences and also abrogate oncogenic transformation.

43 ance of long noncoding RNAs (lncRNAs) during oncogenic transformation.

44 ysiological function of progenitor cells and oncogenic transformation.

45 man malignancies and plays a crucial role in oncogenic transformation.

46 or- and anchorage-independent, indicative of oncogenic transformation.

47 icroRNAs that have previously been linked to oncogenic transformation.

48 bypass are associated with susceptibility to oncogenic transformation.

49 ced by pX is not immediately associated with oncogenic transformation.

50 al influences are required for short latency oncogenic transformation.

51 y of YAP to stimulate cell proliferation and oncogenic transformation.

52 pressed c-Myc-dependent apoptosis and led to oncogenic transformation.

53 3 function, enhanced expression of Plk1, and oncogenic transformation.

54 e altered metabolic state that is rewired by oncogenic transformation.

55 lysophosphatidic acid and had a function in oncogenic transformation.

56 ghts into fundamental cellular processes and oncogenic transformation.

57 that is important for viral replication and oncogenic transformation.

58 pathways; increased Srx has been linked with oncogenic transformation.

59 role in Myc-induced genomic instability and oncogenic transformation.

60 ends on a mechanism for intrinsic sensing of oncogenic transformation.

61 gets upon DNA damage, and are predisposed to oncogenic transformation.

62 lobal H3K18 hypoacetylation may be linked to oncogenic transformation.

63 , F-actin organization, or susceptibility to oncogenic transformation.

64 cells with the desired rearrangement before oncogenic transformation.

65 tic exhaustion, bone marrow failure, or even oncogenic transformation.

66 rage-independent growth, a characteristic of oncogenic transformation.

67 d senescence markers, and are permissive for oncogenic transformation.

68 r inhibiting tumour growth and as markers of oncogenic transformation.

69 numerous cell lines and may be a pathway for oncogenic transformation.

70 sion alone in MCF10A cells did not result in oncogenic transformation.

71 merase activation, etc.) that play a role in oncogenic transformation.

72 inases in normal epithelial cells and during oncogenic transformation.

73 ion of PRAK prevents senescence and promotes oncogenic transformation.

74 enescence is not necessarily a precursor for oncogenic transformation.

75 dy documents the central role of PSF-TFE3 in oncogenic transformation.

76 evidence suggesting a novel role of KLF8 in oncogenic transformation.

77 ession in prostate epithelial cells triggers oncogenic transformation.

78 vation in response to RTA/Orf50 and complete oncogenic transformation.

79 at interest as their alterations can lead to oncogenic transformation.

80 uses play key roles in viral replication and oncogenic transformation.

81 f apoptosis by E1B proteins are required for oncogenic transformation.

82 and cells lacking Pokemon are refractory to oncogenic transformation.

83 , survival, and proliferation, as well as in oncogenic transformation.

84 ibit mTOR signaling, cell proliferation, and oncogenic transformation.

85 letal rearrangement, cell-cell adhesion, and oncogenic transformation.

86 ream of TP53, and TGM2 synergized to promote oncogenic transformation.

87 th alterations and reduced susceptibility to oncogenic transformation.

88 s during V(D)J recombination as one cause of oncogenic transformation.

89 g Icmt activity has profound consequences on oncogenic transformation.

90 egulation of histone methylation can lead to oncogenic transformation.

91 as characterizing potential vulnerability to oncogenic transformation.

92 ther Erk's activity per se is sufficient for oncogenic transformation.

93 DNA demethylation mechanism functions during oncogenic transformation.

94 nt barriers in the TP53 pathway that prevent oncogenic transformation.

95 mediated cholangiocellular proliferation and oncogenic transformation.

96 rogram that causes resistance to anoikis and oncogenic transformation.

97 in Drosophila somatic cells coincident with oncogenic transformation.

98 caspase-3 promoted persistent DNA damage and oncogenic transformation.

99 enetic reprogramming associated broadly with oncogenic transformation.

100 intracellular magnesium levels that promote oncogenic transformation.

101 hereby represses several known inhibitors of oncogenic transformation.

102 n be induced in cells of somatic origin upon oncogenic transformation.

103 MMR-defective cells and their propensity for oncogenic transformation.

104 including differentiation, proliferation and oncogenic transformation.

105 ndependent growth is one of the hallmarks of oncogenic transformation.

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

107 ogical differences in the target cell of the oncogenic transformation.

108 of Aurora B to inhibit colony formation and oncogenic transformation.

109 which are critical to viral reactivation and oncogenic transformation.

110 y-induced elevated PI3K/AKT signaling drives oncogenic transformation.

111 a dedifferentiated state that is poised for oncogenic transformation.

112 broad range of physiological settings and in oncogenic transformation [1-3].

113 Using an in vitro model of oncogenic transformation, a down-regulation of Bgn expre

114 vity leads to a selective attenuation of the oncogenic transformation activity of mutant KRAS-express

115 nd RACK1 has no DNA replication licensing or oncogenic transformation activity.

116 It is increasingly appreciated that oncogenic transformation alters cellular metabolism to f

117 tions in chromatin play an important role in oncogenic transformation, although the underlying mechan

118 ortance of molecular and cellular context in oncogenic transformation and acquisition of a malignant

119 e in a mouse model of liver cancer, based on oncogenic transformation and adoptive transfer of primar

120 multiple cancers and plays a crucial role in oncogenic transformation and angiogenesis, which are ess

121 plays a dominant positive role in regulating oncogenic transformation and angiogenesis.

122 end-joining events, which commonly underlie oncogenic transformation and can scramble the genome.

123 d has since been implicated as a promoter of oncogenic transformation and cancer progression.

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

125 and, when expressed in cells, they drive the oncogenic transformation and chronic activation of downs

126 cell cycle and also plays a critical role in oncogenic transformation and epithelial to mesenchymal t

127 Here, we show that SCCA1 expression promoted oncogenic transformation and epithelial-mesenchymal tran

128 is of kinases involved in cell signaling and oncogenic transformation and for analyzing the effect of

129 on of the epithelial homeostasis potentiates oncogenic transformation and growth.

130 ecific HDAC member is required for efficient oncogenic transformation and indicate that HDAC6 is an i

131 pel-like factor 8 (KLF8) plays a key role in oncogenic transformation and is highly overexpressed in

132 that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinob

133 However, their overexpression can lead to oncogenic transformation and is responsible for drug res

134 Oncogenic transformation and its reversion can be explai

135 matopoietic progenitor cells, which promotes oncogenic transformation and leukemogenesis.

136 AS GTPase signalling is a critical driver of oncogenic transformation and malignant disease.

137 ly shown that GRIM-19 inhibits v-Src-induced oncogenic transformation and metastatic behavior of cell

138 vities of several proteins implicated in the oncogenic transformation and metastatic progression of c

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

140 such processes as cell growth, development, oncogenic transformation and perhaps even axon pathfindi

141 y important regulatory proteins that support oncogenic transformation and progression.

142 for how sphingolipids may be contributing to oncogenic transformation and provide some of the first e

143 ing of the mechanisms underlying Ras-induced oncogenic transformation and regulation of Dnmt1 express

144 uncovered a translational program induced by oncogenic transformation and revealed a critical role fo

145 t for context-specific molecular etiology of oncogenic transformation and suggest intervention strate

146 iated deacetylase, is required for efficient oncogenic transformation and tumor formation.

147 ent or AMPK-deficient cells are resistant to oncogenic transformation and tumorigenesis, possibly bec

148 ontrol to prevent DNA errors and potentially oncogenic transformation and tumorigenesis.

149 d epigenetic modifications, which facilitate oncogenic transformation and tumorigenic potential.

150 regulation of HAI-1 expression by androgen, oncogenic transformation, and cancer progression.

151 s also required for YAP-induced cell growth, oncogenic transformation, and epithelial-mesenchymal tra

152 ction of apoptosis by developmental signals, oncogenic transformation, and genotoxic stress.

153 y roles in regulation of cell proliferation, oncogenic transformation, and human carcinogenesis.

154 premature cellular senescence, resistance to oncogenic transformation, and hyperactive DNA damage che

155 ypoacetylation of H3K18Ac has been linked to oncogenic transformation, and in patients is associated

156 important mechanisms of surveillance against oncogenic transformation, and its inactivation occurs in

157 PAF stimulates cell growth, oncogenic transformation, and metastasis, but can also l

158 Lastly, Taspase1(-/-) cells are resistant to oncogenic transformation, and Taspase1 is overexpressed

159 MLL-fusion proteins are potent inducers of oncogenic transformation, and their expression is consid

160 n folding in the ER to mechanisms underlying oncogenic transformation, and they make CypB an attracti

161 lated with increased cellular proliferation, oncogenic transformation, and tumor growth.

162 The striking effects of HSF1 on oncogenic transformation are not limited to mouse system

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

164 ired permanent genetic changes and underwent oncogenic transformation at a higher frequency than cont

165 tant model for transcription-factor-mediated oncogenic transformation because of its reliance on the

166 l cellular context-specific requirements for oncogenic transformation between infant and adult leukem

167 he phosphorylation of eIF4E is essential for oncogenic transformation but is of no significance to no

168 n of SHP2 is necessary for BCR-ABL-dependent oncogenic transformation, but the precise signaling mech

169 e absence of Smad3 protects fibroblasts from oncogenic transformation by (i) augmenting farnesyl tran

170 Our result raises a novel paradigm in oncogenic transformation by a DNA viral oncogene, the E1

171 Oncogenic transformation by adenovirus E1A and E1B-55K r

172 Oncogenic transformation by adenovirus small e1a depends

173 ant to viral and bacterial infections and to oncogenic transformation by BCR-ABL, and highlight USP18

174 Ubp43 deficiency increases the resistance to oncogenic transformation by BCR-ABL.

175 a and beta chains were highly susceptible to oncogenic transformation by expression of BCR-ABL.

176 40 (SV40) large tumor antigen (LT) triggers oncogenic transformation by inhibition of key tumor supp

177 ental disorders and disease, most notably in oncogenic transformation by mutant RTKs or downstream pa

178 lar tumors, offer insight into mechanisms of oncogenic transformation by mutations affecting Gaq fami

179 blasts (MEFs) lacking Mnt were refractory to oncogenic transformation by Myc.

180 ses spontaneous immortalization in MEFs, and oncogenic transformation by Ras requires ablation of one

181 We show that Rat1a fibroblasts undergoing oncogenic transformation by the TATA-binding protein or

182 More generally, our results show a single oncogenic transformation can have differing effects on c

183 translation, mRNA export, proliferation, and oncogenic transformation dependent on this cap-binding a

184 nd epigenetic alterations that is central to oncogenic transformation downstream of the liver kinase

185 Moreover, oncogenic transformation enhances the spontaneous conver

186 o-senescence activity needs to be evaded for oncogenic transformation, even though NPMc+ can concomit

187 functions that mediate viral replication and oncogenic transformation events are regulated in a cell

188 the intestinal epithelium and many underwent oncogenic transformation, forming intestinal neoplasias.

189 lays a central role in the expression of the oncogenic transformation functions of EWS/FLI-1.

190 e findings demonstrate that the induction of oncogenic transformation gives rise to MVs, which unique

191 Oncogenic transformation has been associated with decrea

192 egulation of mitogenic pathways is linked to oncogenic transformation, herein we define the pX region

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

194 tly reduced radiation-induced DNA damage and oncogenic transformation, identifying EndoG as a downstr

195 tion of Plk1 activity suppresses pX-mediated oncogenic transformation, identifying Plk1 as a promisin

196 most frequent mutation, A775insYVMA, lead to oncogenic transformation in a cellular assay.

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

198 nesis in the donor cancer cells and prevents oncogenic transformation in cell culture as well as tumo

199 Constitutively active mutants of Rheb induce oncogenic transformation in cell culture.

200 KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or o

201 HMGA1 induces oncogenic transformation in cultured cells and causes ag

202 Oncogenic transformation in Ewing sarcoma tumors is driv

203 r ROS levels, such as those that result from oncogenic transformation in hematopoietic malignancies,

204 , which confers a common capacity to promote oncogenic transformation in human epithelial cells.

205 onstitutive PI3K activation that can provoke oncogenic transformation in human epithelial cells.

206 Oncogenic transformation in invasive breast cancer was a

207 ents of the MEK signaling cascade can induce oncogenic transformation in many cell systems.

208 ied as the most common pathways that mediate oncogenic transformation in melanoma, and the majority o

209 at Spry2, Dusp6, and Etv5 were essential for oncogenic transformation in mouse models for pre-B acute

210 rfism in humans; somatic mutations can drive oncogenic transformation in multiple myeloma and bladder

211 Although reduced HDAC-activity facilitates oncogenic transformation in normal cells, resulting tumo

212 l population that is an efficient target for oncogenic transformation in prostate cancer.

213 androgen signaling in beta-catenin-initiated oncogenic transformation in prostate tumorigenesis.

214 sion of KIT/CDK4 is a potential mechanism of oncogenic transformation in some BRAF/NRAS wild-type mel

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

216 -null mice have increased susceptibility for oncogenic transformation in the prostate.

217 studies suggest that an important pathway of oncogenic transformation in the stomach is through suppr

218 t the minimal essential contribution to full oncogenic transformation in this context, we evaluated t

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

220 expression is induced as a direct result of oncogenic transformation in vivo.

221 hanisms exist in complex metazoans to resist oncogenic transformation, including a variety of tumor-

222 Oncogenic transformation increases the expression of tis

223 ferentiate into adipocytes, and resistant to oncogenic transformation induced by a variety of oncogen

224 T-4, and WNT-3, also occurred in NSCs during oncogenic transformation induced by noncontact co-cultur

225 Furthermore, overexpression of SnoN inhibits oncogenic transformation induced by Ras and Myc in vitro

226 that PI3K/AKT signaling is critical for the oncogenic transformations induced by gastrin-releasing p

227 Here we show how oncogenic transformation influences the biogenesis and f

228 Oncogenic transformation is suppressed in the absence of

229 Growth factor stimulation and oncogenic transformation lead to increased glucose metab

230 Oncogenic transformation leads to dysregulated cell prol

231 Oncogenic transformation may reprogram tumor metabolism

232 There is increasing evidence that oncogenic transformation modifies the metabolic program

233 e, this compound interferes with Myc-induced oncogenic transformation, Myc-dependent cell growth, and

234 unexpected mechanisms that contribute to the oncogenic transformation of ATM-deficient T lineage cell

235 on factors regulate apoptosis in response to oncogenic transformation of B cells.

236 naling activities that are essential for the oncogenic transformation of cells.

237 Overexpression of the Ski oncogene induces oncogenic transformation of chicken embryo fibroblasts (

238 of function: they induce rapamycin-sensitive oncogenic transformation of chicken embryo fibroblasts,

239 PDGFbeta receptor (PDGFbetaR), resulting in oncogenic transformation of cultured fibroblasts.

240 se that TP63 may contribute to TP53-mediated oncogenic transformation of epithelial cells and shed li

241 rovides a permissive ovarian environment for oncogenic transformation of epithelial cells, presenting

242 ncing of SOCS1 and SOCS3 genes might promote oncogenic transformation of epithelial tissues.

243 Oncogenic transformation of hematopoietic cells by the B

244 haustion and myeloid-lineage skewing promote oncogenic transformation of hematopoietic progenitor cel

245 us consideration as reversible co-factors in oncogenic transformation of HPV16-infected tissues to ca

246 ion, proliferation, survival, senescence and oncogenic transformation of HSCs and relates these new f

247 t membrane protein 1 (LMP1), is required for oncogenic transformation of human B cells by EBV.

248 Oncogenic transformation of human epithelial cells in cu

249 s common in human epithelial cancers, causes oncogenic transformation of human mammary epithelial cel

250 ction debilitated TP53 signaling and enabled oncogenic transformation of human mammary epithelial cel

251 c response and allow continued expansion and oncogenic transformation of hyperplastic neuroblasts, th

252 REST, CDYL, and G9a, but not CoREST, induced oncogenic transformation of immortalized primary human c

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

254 Kruppel-like factor 8 (KLF8) participates in oncogenic transformation of mouse fibroblasts and is hig

255 expression of the IL-3 receptor would allow oncogenic transformation of NIH 3T3 fibroblasts known to

256 es the IL-3 receptor/Jak2/Stat5 pathways for oncogenic transformation of NIH 3T3 fibroblasts.

257 ld-type Galpha12 (Galpha12WT) results in the oncogenic transformation of NIH3T3 cells (Galpha12WT-NIH

258 weaker compared with ErbB2 in promoting the oncogenic transformation of nontumorigenic human mammary

259 ere using c-Src overexpression) can initiate oncogenic transformation of nontumorigenic human MECs an

260 The oncogenic transformation of normal cells into malignant,

261 upregulation of PAX7, which in turn promotes oncogenic transformation of NSCs and instates 'aggressiv

262 eta-catenin is not similarly associated with oncogenic transformation of other tissues, including T c

263 Oncogenic transformation of postmitotic neurons triggers

264 e regulatory subunit p85beta of PI3K induces oncogenic transformation of primary avian fibroblasts.

265 ion upon t(4;14)-negative cells and promotes oncogenic transformation of primary cells in an H3K36me2

266 the contribution of cellular immortality and oncogenic transformation of primary human cells to epige

267 l regulatory roles in HTLV-1 replication and oncogenic transformation of T lymphocytes.

268 P98 oncoproteins predispose myeloid cells to oncogenic transformation or malignant progression by pro

269 ional estrogen-responsive gene implicated in oncogenic transformation, particularly that of the breas

270 yploid cells to investigate their growth and oncogenic transformation potential over the course of 70

271 owever, pathologic pathway activation during oncogenic transformation produces a tumor that is intrin

272 der conditions of cellular stress, including oncogenic transformation, proteostasis components mainta

273 o efficiently induces fibroblasts to undergo oncogenic transformation, rendering them highly tumorige

274 Moreover, PI3K/AKT-dependent oncogenic transformations require N-myc, an extensively

275 ein modulation of cell cycle progression and oncogenic transformation revealed that these proteins in

276 es requires cell division and is enhanced by oncogenic transformation, some parvoviruses may have pot

277 sis, and increased pX-induced polyploidy and oncogenic transformation, suggesting ZNF198 and SUZ12 ha

278 phenomenon by demonstrating that Ras-induced oncogenic transformation surprisingly depends on functio

279 proto-oncogene IGF2BP1/IMP-1 led to far more oncogenic transformation than did expression of the full

280 During inflammation, differentiation, or oncogenic transformation, the life span of monocytes is

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

282 Despite oncogenic transformation, this basic mechanism of negati

283 e adenovirus E1A C-terminal region restrains oncogenic transformation through interaction with three

284 l region may suppress cell proliferation and oncogenic transformation through interaction with three

285 promotes both normal cell proliferation and oncogenic transformation through the activation and repr

286 dian clock and provide a molecular link from oncogenic transformation to suppression of circadian rhy

287 uggests that PAF plays a significant role in oncogenic transformation, tumor growth, angiogenesis, an

288 The shared mechanisms provide insights into oncogenic transformation, tumor heterogeneity, and cance

289 ctors, which may result in clonal expansion, oncogenic transformation, variegated transgene expressio

290 Our study revealed that RAS(V12)-mediated oncogenic transformation was accompanied by a concomitan

291 to the mechanism of senescence bypass during oncogenic transformation, we dissected the activities of

292 ed in breast carcinomas and shown to promote oncogenic transformation when introduced into cells.

293 oacinar cells are surprisingly refractory to oncogenic transformation, whereas acinar cells readily f

294 n addition, MLL-AF9 cells required Dot1l for oncogenic transformation, whereas cells with other leuke

295 caused an increase in cell proliferation and oncogenic transformation, whereas depletion of Brf1 impe

296 mediates growth factor signaling and causes oncogenic transformation, which includes dramatic change

297 xogenous Gadd153 interferes with Ras-induced oncogenic transformation, which suggests that downregula

298 lammation-associated gastric epithelial cell oncogenic transformation, which they show is mediated by

299 mples of cooperation between Akt and cRaf in oncogenic transformation, which was accompanied by eleva

300 embryo fibroblasts, all three mutants induce oncogenic transformation with high efficiency.