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

1 llular scaffold, frequently perturbed during oncogenic transformation.

2 anges that accumulate, eventually leading to oncogenic transformation.

3 enetic reprogramming associated broadly with oncogenic transformation.

4 hereby represses several known inhibitors of oncogenic transformation.

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

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

7 including differentiation, proliferation and oncogenic transformation.

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

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

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

11 which are critical to viral reactivation and oncogenic transformation.

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

13 a dedifferentiated state that is poised for oncogenic transformation.

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

15 many genome rearrangements, some leading to oncogenic transformation.

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

17 during normal development, regeneration and oncogenic transformation.

18 tant functions in cellular proliferation and oncogenic transformation.

19 Induction of these genes is required for oncogenic transformation.

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

21 idation of novel pathways that contribute to oncogenic transformation.

22 hanism and rendered NMR cells susceptible to oncogenic transformation.

23 nfluence each other and cooperate to promote oncogenic transformation.

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

25 lecular insights into cytokine resistance in oncogenic transformation.

26 the high Ran GTPase activity resulting from oncogenic transformation.

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

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

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

30 iciently promote cell cycle arrest and limit oncogenic transformation.

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

32 idative phosphorylation and are resistant to oncogenic transformation.

33 Moreover, inhibition of Akt suppresses IKBKE oncogenic transformation.

34 T cells are associated with vulnerability to oncogenic transformation.

35 a link between transgenic AR expression and oncogenic transformation.

36 and suggested that paxillin might facilitate oncogenic transformation.

37 nflammation, myeloid cell proliferation, and oncogenic transformation.

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

39 1/K2 induced enhanced cell proliferation and oncogenic transformation.

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

41 cell morphogenesis, osteoclastogenesis, and oncogenic transformation.

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

43 acinar architecture that are consistent with oncogenic transformation.

44 ifferentiated cells resist reprogramming and oncogenic transformation.

45 d oligomerisation of TFG-RET is required for oncogenic transformation.

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

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

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

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

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

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

52 anscriptional consequences and also abrogate oncogenic transformation.

53 ysiological function of progenitor cells and oncogenic transformation.

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

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

56 icroRNAs that have previously been linked to oncogenic transformation.

57 bypass are associated with susceptibility to oncogenic transformation.

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

59 al influences are required for short latency oncogenic transformation.

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

61 omote liver injury, fibrosis, cirrhosis, and oncogenic transformation.

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

63 3 function, enhanced expression of Plk1, and oncogenic transformation.

64 lysophosphatidic acid and had a function in oncogenic transformation.

65 ghts into fundamental cellular processes and oncogenic transformation.

66 that is important for viral replication and oncogenic transformation.

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

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

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

70 ogression, and their loss has been linked to oncogenic transformation.

71 lobal H3K18 hypoacetylation may be linked to oncogenic transformation.

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

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

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

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

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

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

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

79 inases in normal epithelial cells and during oncogenic transformation.

80 ion of PRAK prevents senescence and promotes oncogenic transformation.

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

82 ol; this function is absolutely required for oncogenic transformation.

83 ontrolling cell growth, differentiation, and oncogenic transformation.

84 eIF4E-dependent RNA export, translation, and oncogenic transformation.

85 hat they might be susceptible to Kras-driven oncogenic transformation.

86 is critical for ES maintenance and supports oncogenic transformation.

87 basal and luminal cells are able to initiate oncogenic transformation.

88 ive receptors, augmenting PI3K signaling and oncogenic transformation.

89 mediated cholangiocellular proliferation and oncogenic transformation.

90 intracellular magnesium levels that promote oncogenic transformation.

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

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

93 everal histone modifications associated with oncogenic transformation.

94 lization appears essential for HuR-dependent oncogenic transformation.

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

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

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

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

99 cells with the desired rearrangement before oncogenic transformation.

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

101 of proinflammatory signals required for full oncogenic transformation.

102 ession in prostate epithelial cells triggers oncogenic transformation.

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

104 egulation of histone methylation can lead to oncogenic transformation.

105 as characterizing potential vulnerability to oncogenic transformation.

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

107 DNA demethylation mechanism functions during oncogenic transformation.

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

109 rogram that causes resistance to anoikis and oncogenic transformation.

110 in Drosophila somatic cells coincident with oncogenic transformation.

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

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

113 normal tissue architecture is a hallmark of oncogenic transformation(1).

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

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

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

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

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

119 Oncogenic transformation alters lipid metabolism to sust

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 g in prostatic p63-expressing cell initiated oncogenic transformation and tumor formation.

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

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

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

151 essing cells possess the ability to initiate oncogenic transformation and, in the presence of androge

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

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

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

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

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

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

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

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

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

166 Related to oncogenic transformation, both HPV16 E7-mediated PTPN14

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

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

171 Oncogenic transformation by adenovirus small e1a depends

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

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

174 process that acts as a final barrier against oncogenic transformation by eliminating pre-cancerous ce

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

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

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

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

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

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

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

184 Oncogenic transformation dramatically increases the wave

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

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

189 hanistic insight into NUP98-fusion-dependent oncogenic transformation has so far precluded the develo

190 on of CCR5 in epithelial cells, induced upon oncogenic transformation, hijacks this migratory phenoty

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

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

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

194 associated with cellular therapy, including oncogenic transformation, immunoreactivity and cost.

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

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

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

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

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

200 Oncogenic transformation in colorectal cancer (CRC) is d

201 HMGA1 induces oncogenic transformation in cultured cells and causes ag

202 Oncogenic transformation in Ewing sarcoma tumors is driv

203 hese families have long been known to induce oncogenic transformation in experimental systems.

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

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

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

207 Oncogenic transformation in invasive breast cancer was a

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 a tumor suppressor and how its loss leads to oncogenic transformation in Schwann cells (SCs).

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

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

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

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

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

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

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

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

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

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

225 Oncogenic transformation increases the expression of tis

226 types of the luminal cell are susceptible to oncogenic transformation induced by loss of function of

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

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

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

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

231 The view that oncogenic transformation is a shift to a lower threshold

232 Oncogenic transformation is associated with profound cha

233 Oncogenic transformation is suppressed in the absence of

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

235 Oncogenic transformation leads to dysregulated cell prol

236 Oncogenic transformation may reprogram tumor metabolism

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

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

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

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

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

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

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

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

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

246 Oncogenic transformation of hematopoietic cells by the B

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

248 uman papillomavirus (HPV) E7 proteins enable oncogenic transformation of HPV-infected cells by inacti

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

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

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

252 Oncogenic transformation of human epithelial cells in cu

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

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

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

256 by the aberrant self-renewal and subsequent oncogenic transformation of immature thymocytes.

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

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

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

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

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

262 The oncogenic transformation of normal cells into malignant,

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

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

265 Oncogenic transformation of pancreatic ducts led to two

266 Oncogenic transformation of postmitotic neurons triggers

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

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

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

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

271 When oncogenic transformation or apoptosis occurs within epit

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

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

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

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

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

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

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

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

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

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

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

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

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

285 Despite oncogenic transformation, this basic mechanism of negati

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

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

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

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

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

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

292 in pulp-like complexes, and are resistant to oncogenic transformation when compared to BM-MSCs.

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

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

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

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

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

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 Fli-1 is linked to oncogenic transformation with up-regulation in radio/TMZ