ライフサイエンスコーパス: cell transformation

1 process involved in Cryptosporidium-induced cell transformation.

2 which leads to an epigenetic switch allowing cell transformation.

3 , E6 and E7, which work together to initiate cell transformation.

4 ar link between the normal GC response and B-cell transformation.

5 -Pbx1 to activate target genes and to induce cell transformation.

6 ical feature of cancer and a driver of tumor cell transformation.

7 into the mechanistic basis of Meq-dependent cell transformation.

8 ral replication but also contributes to host cell transformation.

9 scence (OIS), thereby facilitating oncogenic cell transformation.

10 Fer in PDGF-BB-induced STAT3 activation and cell transformation.

11 in MCV DNA replication as well as sT-induced cell transformation.

12 for understanding crucial events leading to cell transformation.

13 y help elucidate crucial events that lead to cell transformation.

14 Pin1 to induce centrosome amplification and cell transformation.

15 it impaired the efficiency of EBV-induced B cell transformation.

16 ta receptor, causing receptor activation and cell transformation.

17 sms for HER2-induced sustained signaling and cell transformation.

18 nvasion in a manner essential for neoplastic cell transformation.

19 n target, and both were reported to regulate cell transformation.

20 IAH2, thus contributing to breast epithelial cell transformation.

21 icted a tumor-suppressor role for RUNX1 in T cell transformation.

22 cancer, and some of them have been linked to cell transformation.

23 tor of IKKepsilon-induced mammary epithelial cell transformation.

24 on for the regulation of gene expression and cell transformation.

25 ced AP-1 activity and anchorage- independent cell transformation.

26 c-Fos, which regulates anchorage-independent cell transformation.

27 utations, indicating that RUNX1 suppresses T-cell transformation.

28 ts contributed to an elevation of IR-induced cell transformation.

29 ngth SHIP significantly reduces Ab-MLV pre-B-cell transformation.

30 Pin1 to induce centrosome amplification and cell transformation.

31 UP98-HOXA9 in transcriptional regulation and cell transformation.

32 otein-1 activity, which is a major driver in cell transformation.

33 d opposes oncogenic tyrosine kinase-mediated cell transformation.

34 ells, ultimately contributing to efficient T cell transformation.

35 g by using mutant H3S28A reduced EGF-induced cell transformation.

36 nscription through Brf1 and TBP and promotes cell transformation.

37 fibroblasts and recapitulates early steps of cell transformation.

38 n of the Musashi2 variant 2 isoform promoted cell transformation.

39 nd pathways perturbed by SV40ST during human cell transformation.

40 PK) pathway plays a major role in neoplastic cell transformation.

41 an important role in EGF-induced neoplastic cell transformation.

42 in genome instability and is associated with cell transformation.

43 d replaced the expression of SV40ST in human cell transformation.

44 EGFR-mediated tumor migration, survival and cell transformation.

45 motility disorders and intestinal epithelial cell transformation.

46 essed in human cancers and is induced during cell transformation.

47 crucial roles in both virus replication and cell transformation.

48 cted efficiently with FOXK1/K2 and inhibited cell transformation.

49 tical role in proliferation, cell cycle, and cell transformation.

50 CYSLTR1 and CYSLTR2) contribute to malignant cell transformation.

51 netic changes that lead to ovarian carcinoma cell transformation.

52 lation within the nucleus, thereby promoting cell transformation.

53 ole in EGF-stimulated cell proliferation and cell transformation.

54 m to induce c-Myc, which may be critical for cell transformation.

55 the essential latent antigens for primary B-cell transformation.

56 e-limiting for expression of an oncogene and cell transformation.

57 with H-RasV12 or c-Myc to promote fibroblast cell transformation.

58 activate endogenous oncogenes, resulting in cell transformation.

59 verall impact of enhanced HER2 signaling and cell transformation.

60 ted in suppressed TPA-induced or EGF-induced cell transformation.

61 TbetaRIII-mediated epithelial to mesenchymal cell transformation.

62 rongly suppressed TPA-induced or EGF-induced cell transformation.

63 TCL lymph node lesions with or without large cell transformation.

64 -S6K pathway as a critical mediator of glial cell transformation.

65 itor of MEK) on MEK1 activity and neoplastic cell transformation.

66 c-translocated cells, and the incidence of B cell transformation.

67 ID directly contributes to the dynamics of B cell transformation.

68 cell-cell junction was sufficient to promote cell transformation.

69 oding proteins involved in breast epithelial cell transformation.

70 ory atrophy are foci for prostate epithelial cell transformation.

71 genitors as the final target for cancer stem cell transformation.

72 ant negative mutants dramatically suppressed cell transformation.

73 s-aberrant miRNA expression is acquired upon cell transformation.

74 with RUNX3-a protein induced by EBV during B cell transformation.

75 nts of these GTPases is sufficient to induce cell transformation.

76 g myelomagenic mutations that promote plasma cell transformation.

77 nizes ligands whose expression is induced by cell transformation.

78 and represents an ideal model for study of T-cell transformation.

79 iomarkers of early fallopian tube epithelial cell transformation.

80 t genetic and epigenetic etiologies for GC B-cell transformation.

81 t, which became silenced during EBV-driven B-cell transformation.

82 ut is not required for MCV sT-induced rodent cell transformation.

83 uppressor role by interfering with malignant cell transformation.

84 ion and thereby regulates macrophage to foam cell transformation.

85 ted tumor-stage MF,with no evidence of large-cell transformation.

86 Tax and the antisense protein APH-3 promote cell transformation.

87 n in vitro model of human mammary epithelial cell transformation.

88 lying additional GR loss as a consequence of cell transformation.

89 (PTC) and is causally involved in malignant cell transformation.

90 in related states of post-germinal centre B-cell transformation.

91 suppressors by regulating the occurrence of cell transformation.

92 ell-to-cell variability) are able to trigger cell transformation.

93 SRPK1 in mouse embryonic fibroblasts induces cell transformation.

94 inflammatory signal (Src) needed to promote cell transformation.

95 s of STAT3, which is a crucial activator for cell transformation.

96 on of KRAS and was required for KRAS-induced cell transformation.

97 in assembly in FA-mediated transcription and cell transformation.

98 sitive feedback loop linking inflammation to cell transformation.

99 es, we found one squamous cell and two small-cell transformations.

100 e in IFN-gamma-induced inflammation and foam cell transformation, a better understanding of the mecha

101 is stably expressed in Src-Y527F-transformed cells, transformation activities are blocked, indicating

102 could not be phosphorylated antagonized the cell transformation activity of MCV sT.

103 3+, NANOG+ and OCT3/4+ liver progenitor/stem cell transformation, along with inactivation of transfor

104 tance of the NOTCH1-MYC regulatory axis in T cell transformation and as a therapeutic target in T-ALL

105 trigger its nuclear accumulation leading to cell transformation and cancer.

106 accumulation of DNA damage that can lead to cell transformation and carcinogenesis.

107 anistic link between oncogene E6/E7-mediated cell transformation and circadian (BMAL1) disruption.

108 ferase activity, promotes mammary epithelial cell transformation and cooperates with H-RasV12 or c-My

109 at they cooperate to enhance virus-induced B cell transformation and decrease the antigenic load of v

110 sting that other viral proteins are key to T-cell transformation and development of adult T-cell leuk

111 n epigenetically mediated miRNA control in B cell transformation and DLBCL.

112 eal an important role for RUNX3/CBF during B cell transformation and EBV latency that was hitherto un

113 of Kras activation and Pten deletion during cell transformation and epithelial-to-mesenchymal transi

114 oduction of let-7 microRNAs was critical for cell transformation and expansion of prostate CSC.

115 sion adapter protein paxillin contributes to cell transformation and extends our knowledge of the div

116 We show that GWL overexpression promotes cell transformation and increases invasive capacities of

117 cell transformation, enhances MycWT-induced cell transformation and increases the size of MycWT-indu

118 ta and BMP signals essential for endothelial cell transformation and invasion of cardiac neural crest

119 gly activated mTOR/p70S6K signaling, induced cell transformation and invasion, and remarkably, caused

120 ne KLF5 loss as a critical event in squamous cell transformation and invasion.

121 oncogenic transcription factor MYC induces B-cell transformation and is a driver for B-cell non-Hodgk

122 and apoptosis, which must be overcome during cell transformation and kept at bay throughout all stage

123 FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all

124 regulatory loop that positively influences B cell transformation and lymphoma progression.

125 clude that PRMT5 is critical to EBV-driven B-cell transformation and maintenance of the malignant phe

126 non-Ig sites in the genome, which initiates cell transformation and malignancies.

127 B and T cell leukemias and the mechanisms of cell transformation and malignant progression that are r

128 MP1) is important for EBV contributions to B cell transformation and many EBV-associated malignancies

129 arity are closely associated with epithelial cell transformation and metastatic capacity.

130 nexpected discovery that E1A also suppresses cell transformation and oncogenesis.

131 n-Barr virus, is required for EBV-mediated B cell transformation and plays a significant role in the

132 c for pooled EBV Ags expressed during both B cell transformation and productive viral replication and

133 LK stimulates signaling pathways that induce cell transformation and promote tumor growth.

134 Oncogenic Ras induces cell transformation and promotes an invasive phenotype.

135 operation between JAK1 and JAK3 mutants in T-cell transformation and represent a new mechanism of acq

136 Age at diagnosis, large cell transformation and secondary bacterial infection we

137 rate a novel role for H2B phosphorylation in cell transformation and show that H2BS32 phosphorylation

138 PL2 was found to antagonize oncogene-induced cell transformation and survival through a pathway invol

139 l downstream mediator for Gli-dependent PDAC cell transformation and survival.

140 naling plays an important role in neoplastic cell transformation and that eriodictyol is a novel natu

141 th loss of Pten is enough to promote ovarian cell transformation and that we have developed a model s

142 eals a novel function of CDK2 in EGF-induced cell transformation and the associated signal transducti

143 eveal transcriptional parallels between germ cell transformation and the generation of iPS cells and

144 to identify key molecular changes that drive cell transformation and the likely clonal outgrowth of p

145 Such restraints are compromised during cell transformation and the problem is accentuated by on

146 ite biology and their relationship with host cell transformation and tropism.

147 reases Pol III gene transcription to promote cell transformation and tumor formation in vitro and in

148 sly shown that LOX-PP inhibits breast cancer cell transformation and tumor formation, but mechanisms

149 enic is a carcinogen that is known to induce cell transformation and tumor formation.

150 ge and acts in parallel with p53 to suppress cell transformation and tumor formation.

151 ncrease in translational capacity to promote cell transformation and tumor formation.

152 , WRC disruption also promoted FAK-dependent cell transformation and tumor growth in vivo.

153 ar target genes, which are rate limiting for cell transformation and tumor growth.

154 of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissu

155 biological functions of TIP-1, especially in cell transformation and tumor progression, are still con

156 ar response to hypoxia, which contributes to cell transformation and tumor progression, is a prominen

157 uppressor p53 is a key protein in preventing cell transformation and tumor progression.

158 molybdenum but not silica, similarly induced cell transformation and tumor promotion, suggesting the

159 Here, we show that HSF1 is required for the cell transformation and tumorigenesis induced by the hum

160 th inhibition of PDCD4, and caused malignant cell transformation and tumorigenesis of BEAS-2B cells.

161 itive HTLV-1-infected cells and Tax-mediated cell transformation and tumorigenesis.

162 ur in many cancer types and are critical for cell transformation and tumorigenesis.

163 death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.

164 Hotspot mutations of Ras drive cell transformation and tumorigenesis.

165 scence and a stem cell-associated SASP drive cell transformation and tumour initiation in vivo in an

166 established model for tumor promoter-induced cell transformation and was used to study the function o

167 ease in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene ex

168 A significantly inhibits MLL-fusion-mediated cell transformation, and coexpressed PBX3 exhibits a sig

169 ion activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melano

170 of signaling pathways in differentiation and cell transformation, and for assessing the in vivo pheno

171 ested, four (stage IV, age > 60 years, large-cell transformation, and increased lactate dehydrogenase

172 nitiate chromosomal instability, DNA damage, cell transformation, and malignancy.

173 1 is sufficient to promote mmp15 expression, cell transformation, and mesenchymal cell migration and

174 uppressed Tax-mediated signaling activation, cell transformation, and oncogenesis both in vitro and i

175 the actin cytoskeleton, gene transcription, cell transformation, and other processes that are known

176 YC interaction is necessary for C1/M2-driven cell transformation, and the C1/M2 transcriptional signa

177 nd contact-site mutants share a property for cell transformation, and the domains critical for wild-t

178 COP1 expression promoted cell proliferation, cell transformation, and tumor progression, manifesting

179 red for ERBB2 mutant-induced cell signaling, cell transformation, and tumorigenesis.

180 en implicated in KSHV-associated endothelial cell transformation, angiogenesis, and KS-induced malign

181 e molecular genetic mechanisms that underlie cell transformation are less clear.

182 cell migration but more dramatic effects on cell transformation as assessed by growth in soft agar.

183 on, without affecting cell proliferation, or cell transformation as measured by soft agar colony form

184 of gene expression, cell proliferation, and cell transformation, as well as cancer development.

185 nd inhibition of in vitro characteristics of cell transformation, as well as in vivo tumor growth.

186 id, in vitro pull-down and transient tobacco cell transformation assays.

187 herefore define not only new mechanisms of B-cell transformation but also clinically important subgro

188 amma-PP2A can inhibit cell proliferation and cell transformation by an unknown mechanism.

189 Our observations that cell transformation by cooperating oncogenic lesions dep

190 trains that confer high cancer risk mediates cell transformation by deregulating host cellular proces

191 s early region 1A (E1A) oncoprotein mediates cell transformation by deregulating host cellular proces

192 2 transcription factor plays a key role in B cell transformation by EBV and defines the two EBV types

193 t subsets of B-cell neoplasms, which promote cell transformation by elevating the global level of H3K

194 e with ROS production in 32D cells inhibited cell transformation by FLT3 ITD in a DEP-1-dependent man

195 1 oxidation as a novel event contributing to cell transformation by FLT3 ITD.

196 ore, could be essential for inducing oxyphil cell transformation by increasing mtDNA/mitochondrial bi

197 ransmitted to other retroviruses and produce cell transformation by itself.

198 wn of endogenous Zfp111 caused a decrease in cell transformation by JSRV Env, while overexpression of

199 that TCEAL7 may restrict ovarian epithelial cell transformation by limiting Myc activity.

200 ill lacking to show that Pin1 contributes to cell transformation by Rel/NF-kappaB.

201 t that cocoa procyanidins inhibit neoplastic cell transformation by suppressing the kinase activity o

202 y the human c-Rel protein and also increased cell transformation by the potent viral Rel/NF-kappaB on

203 Cell transformation by the v-rel oncogene is mediated by

204 The mechanisms of malignant cell transformation caused by the oncogenic, chimeric nu

205 ion is thought to be an important step for T-cell transformation caused by viral infection.

206 Malignant cell transformation commonly results in the deregulation

207 ful B cell differentiation and prevention of cell transformation depends on balanced and fine-tuned a

208 However, the specific mechanisms of T cell transformation downstream of TLX1 remain to be eluc

209 regulation during embryonic development and cell transformation during oncogenesis share common sign

210 show that Nol5a is necessary for Myc-induced cell transformation, enhances MycWT-induced cell transfo

211 gnaling pathway is necessary, independent of cell transformation, for herpesvirus pathogenesis and th

212 recent studies have demonstrated the direct cell transformation from chondrocytes into bone cells in

213 Epithelial cell transformation has been demonstrated in numerous an

214 a molecular pathway linking inflammation to cell transformation has been discovered.

215 option for type 1 diabetes, pancreatic islet cell transformation has been hindered by immune system r

216 gnaling pathways essential to Myc-mediated B-cell transformation have not been fully elucidated.

217 Kepsilon substrates necessary for regulating cell transformation have not been identified.

218 talizes primary cells and mediates oncogenic cell transformation in cooperation with other viral or c

219 innate immune responses and can also promote cell transformation in culture.

220 voir in vivo and act as cellular targets for cell transformation in humans.

221 ith the inactivation of DLC1 to give rise to cell transformation in MEFs, and the identified genes ar

222 fibroblast growth factor receptor-dependent cell transformation in NIH3T3 fibroblasts.

223 ic leukemia for 29 and 7 months before large-cell transformation in the eye.

224 nes represent the molecular basis of oxyphil cell transformation in the parathyroids.

225 pression and EGFR overexpression for Schwann cell transformation in vitro (immortalized human Schwann

226 e, and examined the hallmarks of mesothelial cell transformation in vitro and in vivo.

227 y synergistic effect with HOXA9 in promoting cell transformation in vitro and leukemogenesis in vivo.

228 5 significantly inhibits MLL-fusion-mediated cell transformation in vitro and leukemogenesis in vivo.

229 only EBNA3B is completely dispensable for B cell transformation in vitro.

230 rkedly impaired in their ability to induce B cell transformation in vitro.

231 However, the role of Dnmt3a in T-cell transformation in vivo is poorly understood.

232 alized human cells was sufficient to promote cell transformation in vivo.

233 irus 40 large T antigen (TAg) contributes to cell transformation, in part, by targeting two well-char

234 SCD1 is found upregulated upon renal cell transformation indicating that its activity, while

235 sent study explored a potential mechanism of cell transformation induced by arsenic exposure.

236 the stability of histone H2AX and prevented cell transformation induced by EGF.

237 Our data show that cell transformation induced by endomembrane-restricted o

238 etin also dose dependently suppressed JB6 P+ cell transformation induced by epidermal growth factor o

239 CPF or procyanidin B2 suppressed JB6 P+ cell transformation induced by epidermal growth factor o

240 mutant 4E-BP1.S83A partially reverses rodent cell transformation induced by Merkel cell polyomavirus

241 mb proteins, BMI1 and SUZ12 are required for cell transformation induced by organic arsenic exposure.

242 in cells and severely affects chemotaxis and cell transformation induced by PI3Kgamma overexpression.

243 tin assembly represents a novel mechanism of cell transformation induced by the environmental and occ

244 2 plays a critical role in proliferation and cell transformation induced by tumor promoters, such as

245 EBV-mediated B cell transformation involves large changes in gene expre

246 idues serine-17 and tyrosine-416 and mammary cell transformation is driven through a mechanism involv

247 virus-encoded E6 oncoproteins contribute to cell transformation is restricted to human papillomaviru

248 (JSRV) is an oncogene, but its mechanism of cell transformation is still unclear.

249 How this haloacetonitrile promotes malignant cell transformation is unknown.

250 le of cdk3 in cell proliferation, as well as cell transformation, is not yet clearly understood.

251 e diversity and potency of TFs as drivers of cell transformation justifies a continued pursuit of TFs

252 ignaling, with PLA2R1-mediated inhibition of cell transformation largely reverted in JAK2-depleted ce

253 Large cell transformation (LCT) in mycosis fungoides (MF) is g

254 vanced-stage disease (ASD, n = 92) and large cell transformation (LCT, n = 22).

255 dratase-deficient cells, plays a key role in cell transformation, making it a bona fide oncometabolit

256 These results indicate that 4-OH-E2-induced cell transformation may be mediated, in part, through re

257 The mechanisms of malignant cell transformation mediated by the oncogenic anaplastic

258 reases epidermal growth factor (EGF)-induced cell transformation mediated through the downregulation

259 d tested their oncogenic potential in rodent cell transformation models.

260 tor (EGFR, ErbB1) signaling is implicated in cell transformation, motility, and invasion in a variety

261 r ability to cooperate with oncogenic Ras in cell transformation, NASP expression reduced the transac

262 Oxyphil cell transformation of epithelial cells due to the accum

263 on of Cdk3 resulted in anchorage-independent cell transformation of JB6 Cl41 cells induced by EGF and

264 Foam cell transformation of lipid-laden THP-1 macrophages was

265 points to the fundamental role in malignant cell transformation of potent oncogenes expressed in the

266 for epidermal growth factor (EGF)-stimulated cell transformation of the HaCaT immortalized skin cell

267 Large cell transformation often hallmarks cases with a more ag

268 egulates a number of critical events such as cell transformation, polarization, development, stress r

269 exhibited suppressed growth and EGF-induced cell transformation, possibly because of decreased activ

270 rget site exhibits an enhanced signaling and cell transformation potential.

271 sphorylate a variety of cellular proteins in cell transformation process including altered cell adhes

272 rotein kinases play crucial roles in several cell transformation processes and are validated drug tar

273 otypic cellular change (inhibit LEF-1-driven cell transformation) provided two lead compounds: lefmyc

274 SUMOylation of p53 is required for efficient cell transformation, provides evidence for the idea that

275 olled by specific PP2A complexes involved in cell transformation remain incompletely understood.

276 dren to T-ALL, yet how LMO2 contributes to T cell transformation remains unclear.

277 ing recombinant EBVs, we show that optimal B-cell transformation requires a minimum of 5 W repeats (5

278 These data suggest that efficient cell transformation requires Ras proteins to interact wi

279 Malignant cell transformation requires the cooperation of a few on

280 tress-induced self-molecules associated with cell transformation serves as a mode of cell recognition

281 hese results support a model in which cancer cell transformation shares key genetic components with n

282 the stimulatory effects of NEK6 on STAT3 and cell transformation suggest that this family of serine/t

283 The demonstration that miR-21 promotes cell transformation supports the concept that mir-21 fun

284 have established epigenetic etiologies for B cell transformation that are being exploited in novel th

285 MSK1 is required for tumor promoter-induced cell transformation through its phosphorylation of histo

286 an be generated either prior to or following cell transformation through mutations.

287 demonstrated that pseudogenes contribute to cell transformation through several mechanisms.

288 n in vitro model of human mammary epithelial cell transformation to assess how malignancy-associated

289 ved in the progression from HPV infection to cell transformation to cancer.

290 models of Epstein-Barr virus (EBV)-induced B-cell transformation to document the relevance of protein

291 Here, we show that cell transformation triggers a tissue-resident lymphocyt

292 nsic environmental factors promote malignant cell transformation, tumor growth, and metastasis.

293 forme and has been to shown to contribute to cell transformation, tumor initiation, progression, and

294 In cancer, RSKs modulate cell transformation, tumorigenesis, and metastasis.

295 Cell transformation was assessed by soft agar assay.

296 Thus, arsenic-induced cell transformation was blocked by inhibition of PcG fun

297 Indeed, the mutant EGFR-mediated cell transformation was inhibited by Src- as well as EGF

298 To study how ITAM signaling affects mammary cell transformation, we utilized mammary cell lines expr

299 ed by telomerase (HTCE cells) and SV-40 (HCE cells) transformation were suppressed and enhanced by CT

300 little evidence exists for human epithelial cell transformation without previous immortalization via