ライフサイエンスコーパス: transformed cell

1 rameters, and the initial state of the first transformed cell.

2 owth, and cell migration and invasion in HPV-transformed cells.

3 n of the HPV genome, a common feature of HPV-transformed cells.

4 bility to induce terminal differentiation of transformed cells.

5 ltaneous prediction of effects on normal and transformed cells.

6 after binding stress ligands on infected or transformed cells.

7 fferentiation and pluripotency in normal and transformed cells.

8 n and diminishes IRF4 phosphorylation in EBV-transformed cells.

9 that recognize and lyse virally infected or transformed cells.

10 tic proteins is critical for the survival of transformed cells.

11 nds leads to impaired NK cell recognition of transformed cells.

12 r its cytotoxic activity against malignantly transformed cells.

13 tions, while only C>T/G>A are major types in transformed cells.

14 une responses against virally or malignantly transformed cells.

15 Epstein-Barr virus LMPs) to favor spread of transformed cells.

16 e first line of defense against infected and transformed cells.

17 us oncogenes led to CAS up-regulation in non-transformed cells.

18 ically inhibited growth and proliferation of transformed cells.

19 protein constitutively accumulated in these transformed cells.

20 response to virally infected or malignantly transformed cells.

21 mitochondrion-STAT3-dependent pathway in Ras-transformed cells.

22 in the localization of activated Ras in CrkI-transformed cells.

23 phenotypic and molecular characteristics of transformed cells.

24 h ROS levels and As(3+)-induced apoptosis in transformed cells.

25 f the surrounding cells toward the extruding transformed cells.

26 single isoleucine at a particular position, transformed cells.

27 significantly increased deformability of the transformed cells.

28 ARPi resistance to AML1-ETO and PML-RARalpha transformed cells.

29 mmune recognition of virally and malignantly transformed cells.

30 inhibitors impacts the metabolic program of transformed cells.

31 Gln may also contribute to redox balance in transformed cells.

32 y regulated erythropoietin expression in the transformed cells.

33 ch p53 prevents the malignant progression of transformed cells.

34 o in orchestrating dissemination of Ras(V12)-transformed cells.

35 presses apical extrusion of the neighbouring transformed cells.

36 pathways necessary for the proliferation of transformed cells.

37 ramatically increased in the cadmium-exposed transformed cells.

38 ys a positive role in the elimination of the transformed cells.

39 olarization and migration in both normal and transformed cells.

40 favourable therapeutic index compared to non-transformed cells.

41 tes increased nucleotide biosynthesis in Myc-transformed cells.

42 tivity in breast cancer cells but not in non-transformed cells.

43 AtABCG14 localizes to the plasma membrane of transformed cells.

44 ability to recognize and kill neoplastically transformed cells.

45 /2) activity via MKP3 in both cancer and non-transformed cells.

46 occurs preferentially in embryonic cells and transformed cells.

47 e of inhibiting the drug resistance of v-Src-transformed cells.

48 ls, an indication of autophagy deficiency of transformed cells.

49 fically at the interface with Src- or RasV12-transformed cells.

50 lex-forming sequence Pu-27 selectively kills transformed cells.

51 une response against infected or malignantly transformed cells.

52 , Nrf2 and p62 are highly expressed in these transformed cells.

53 t viral infections and in the elimination of transformed cells.

54 1 alters levels of these proteins in virally transformed cells.

55 6 oncoprotein, and preferentially killed HPV-transformed cells.

56 as NKp30 are involved in the recognition of transformed cells.

57 dose-dependently increased levels of ATF4 in transformed cells.

58 d prevents repression of Wnt target genes in transformed cells.

59 transcription of the IRF4 target BIC in EBV-transformed cells.

60 gh killing of infected, foreign, stressed or transformed cells.

61 activation of the MAPK pathway in RAS-mutant transformed cells.

62 ation, a phenotype also observed in TGF-beta-transformed cells.

63 nverse RT-PCR and northern blotting of HPV16-transformed cells.

64 RNA of oncogene CDCP1 was found in malignant transformed cells.

65 at selectively impair the fitness of BCR-Abl-transformed cells.

66 eed for glutamine between nontransformed and transformed cells.

67 th of tumor xenografts established from KRAS-transformed cells.

68 und associated with E1B-55K in adenovirus E1-transformed cells.

69 er such regulatory loops operate also in non-transformed cells.

70 c-mediated tyrosine phosphorylation in virus-transformed cells.

71 vels of RNF31 and LMP1 are correlated in EBV-transformed cells.

72 epresents an Achilles' heel in p53-deficient transformed cells.

73 ants, and PTMs in primary, immortalized, and transformed cells.

74 ng to measure changes between normal and iAs-transformed cells.

75 promoting optimal cell cycle progression in transformed cells.

76 HPV-transformed cells actively instruct their microenvironme

77 Transformed cells adapt metabolism to support tumor init

78 ranscriptional effector of the ISR, protects transformed cells against anoikis - a specialized form o

79 ls, whereas these increases are not shown in transformed cells, an indication of autophagy deficiency

80 nsformed cells, calcium wave occurs from the transformed cell and propagates across the surrounding c

81 ell invasion and motility phenotypes seen in transformed cells and also highlight an important role f

82 (NK) cells induce apoptosis in infected and transformed cells and are important producers of immunor

83 -124a, is constitutively activated in HTLV-I-transformed cells and ATL cells, and activating STAT3 mu

84 decreased growth and progression of chemical-transformed cells and bladder cancer cells.

85 was mediated by Rab11 and Drp1 in viral Src-transformed cells and contributed to the biogenesis of p

86 cluding natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed

87 effective and efficient system to select for transformed cells and generate transgenic cotton plants.

88 een isogenic untransformed cells and BCR-Abl-transformed cells and identified several compounds that

89 Formin activation impairs novel aspects of transformed cells and informs the development of anti-GB

90 Reovirus preferentially kills transformed cells and is in clinical trials to assess it

91 ly induces apoptosis of SV40 large T-antigen transformed cells and significantly reduces colony forma

92 c reprogramming that are unattainable in non-transformed cells and that cooperate to maximize tumor g

93 ecognize and actively eliminate neighbouring transformed cells and that filamin is a key mediator in

94 ctor-beta-induced cellular senescence in non-transformed cells and that HPV E6/E7 targets Notch1 for

95 th LMP1 and IRF7 in Epstein-Barr virus (EBV)-transformed cells and that LUBAC stimulates linear ubiqu

96 by the interplay of cytoskeletal changes in transformed cells and the existing tubular geometry.

97 of tumors mediates the interface between the transformed cells and the general microenvironment, incl

98 cancer could be induced by a small number of transformed cells and was not prevented by the presence

99 ome amplification is poorly tolerated by non-transformed cells and, in the absence of selection, extr

100 rus (reovirus) selectively infects and kills transformed cells, and a serotype 3 reovirus is in clini

101 a significant impact on survival of MLL-AF9-transformed cells, and additional Mll1 loss further redu

102 targeting virus-infected cells, malignantly transformed cells, and immature dendritic cells.

103 sential for promoting chemoresistance in the transformed cells, and targeting NF-kappaB or VLA-4/VCAM

104 entous networks in the cytoplasm, whereas in transformed cells, apoptin is present in the nucleus and

105 The high requirement of glutamine for transformed cells applies to the development of neoplast

106 re we demonstrate that ATL-derived or HTLV-1-transformed cells are dependent on continuous Tax expres

107 In the first phase, Elimination, transformed cells are destroyed by a competent immune sy

108 ent studies have shown that certain types of transformed cells are extruded from an epithelial monola

109 bly, we find that although genes specific to transformed cells are highly translated, their translati

110 Interestingly, transformed cells are more prone to adopt this fast migr

111 The vGPCR-transformed cells are sensitive to pharmacologic inhibit

112 Furthermore, NUP98-NSD1-transformed cells are sensitive to small-molecule inhibi

113 We previously reported that while non-transformed cells arrest in the latter portion of G1 upo

114 activation is characteristic of mutant FLT3-transformed cells, as well as observed residual Akt acti

115 T3 and forced expression of PDCD4 in arsenic transformed cells (AsT) also inhibited cell proliferatio

116 shRNA-mediated knockdown of YAP1 or SOX9 in transformed cells attenuates CSC phenotypes in vitro and

117 transformed 208F cells, suggesting that JSRV-transformed cells became dependent on Zfp111.

118 HDAC6 inhibitor blocks growth of normal and transformed cells but does not induce death of normal ce

119 sed in proliferative tissues like testis and transformed cells, but scarcely in differentiated tissue

120 to those seen when pRB is depleted from non-transformed cells, but that the presence of wild-type p5

121 the nuclear genome occurs in neoplastically transformed cells, but we do not exclude the possibility

122 on and colony formation in soft agar of KSHV-transformed cells by attenuating mTORC1 activation.

123 lular surface for recognition of infected or transformed cells by CD8(+) cytotoxic T lymphocytes.

124 They transformed cells by forming a stable complex with the p

125 or suppressor that prevents the emergence of transformed cells by inducing apoptosis or senescence, a

126 ny growth is significantly attenuated in the transformed cells by siRNA transfection specific for Nrf

127 os, that prior to apical extrusion of RasV12-transformed cells, calcium wave occurs from the transfor

128 Ras-transformed cells can grow in amino acid-poor environmen

129 Spontaneous regeneration of transformed cells can produce natural transformants carr

130 different human tissue types, including non-transformed cells (cardiomyocytes and lung fibroblasts)

131 In non-transformed cells, centrosome amplification triggers PID

132 anticancer agents since they readily infect transformed cells compared to normal cells, the former a

133 against FLT3 in proliferation assays of FLT3-transformed cells compared with KIT-transformed cells, s

134 phosphotyrosine in cellular proteins in RSV-transformed cells confirmed that v-Src is a tyrosine kin

135 ls, we found that MVs isolated from onco-Dbl-transformed cells contain a unique signaling protein, th

136 broblast and lymphoblast) revealed that only transformed cells contained some unmethylated 12S rRNA t

137 yte differentiation and that loss of TIG3 in transformed cells contributes to the malignant phenotype

138 posi's sarcoma-associated herpesvirus (KSHV)-transformed cells depend on glutamine rather than glucos

139 posi's sarcoma-associated herpesvirus (KSHV)-transformed cells depend on glutamine rather than glucos

140 phological changes in TGF-beta-mesenchymally transformed cells despite their elevated Rac1 activity.

141 encompassing the inherent plasticity of the transformed cells, development of tumor stroma crosstalk

142 ancer progression but inhibiting Tet1 in non-transformed cells did not initiate cellular transformati

143 Despite its importance, how transformed cells disseminate from an intact tissue and

144 events occurring over the course of Ras(V12)-transformed cell dissemination.

145 transformed cells form tumors while isolated transformed cells do not.

146 ail-safe mechanism is eventually bypassed by transformed cells, due to ill-defined epistatic interact

147 ficient elimination of surplus, damaged, and transformed cells during metazoan embryonic development

148 To facilitate selection of transformed cells during RNP delivery, a plasmid carryin

149 In transformed cells, enforced expression of SOCS3 or inter

150 We conclude that transformed cells engage surrounding normal cells as act

151 ncy, whereas depletion of Fzd8 in H-Ras(V12)-transformed cells enhances their tumor initiating capaci

152 air leukemia-initiating activity of PML/RARA-transformed cells ex vivo or in vivo.

153 Many transformed cells exhibit altered glucose metabolism and

154 At all times, the transformed cells exhibited complete dependency on hemat

155 Transformed cells exhibited lower rare mutation frequenc

156 rapy-induced senescence in multiple types of transformed cells exposed to either DNA damaging agents

157 Additionally, although transformed cells express a proneural signature, untrans

158 (TRAIL) which induces selective apoptosis in transformed cells expressing its cognate death receptors

159 broad utility of using matched parental and transformed cells for small molecule inhibitor studies b

160 d by us finding that small local clusters of transformed cells form tumors while isolated transformed

161 Notably, Ras(V12)-transformed cells formed the Actin- and Cortactin-rich i

162 iate malignant cell transformation and these transformed cells formed tumors in vivo.

163 drive the segregation and elimination of the transformed cell from the tissue.

164 Stat1 also protects Ras-transformed cells from the genotoxic effects of doxorubi

165 2 induced malignant transformation and these transformed cells gained the characteristics of CSCs by

166 TERT expression promotes oncogene-transformed cell growth by reducing the inhibitory effec

167 DNA (rDNA) and activates rDNA transcription, transformed cell growth, and tumor formation.

168 Adenovirus transformed cells have a dedifferentiated phenotype.

169 gether, this study demonstrates that cadmium-transformed cells have acquired autophagy deficiency, le

170 In neuronal and transformed cells HMGB4 regulated the expression of an o

171 In Ras-transformed cells, however, mTORC1 activity and lysosome

172 ecreased the tumorigenic properties of HBEGF-transformed cells; however, only EGFR was able to rescue

173 ole of key defense mechanisms in maintaining transformed cells in a dormant state.

174 rin-IGF1 receptor (IGF1R) cross-talk) in non-transformed cells in anchorage-dependent conditions.

175 ive oxygen species (ROS) is extremely low in transformed cells in correlation with elevated expressio

176 equired for the proliferation of Hoxa9/Meis1-transformed cells in culture and that loss of C/EBPalpha

177 However, the use of transformed cells in culture does not provide the same e

178 with a reduction in the proliferation of the transformed cells in culture, suggesting that, at least

179 n the oncogenic protein Skp2 for survival of transformed cells in mouse models, we sought to examine

180 ted mTurquoise2 marker to precisely identify transformed cells in order to distinguish true negatives

181 y is the selective replication of viruses in transformed cells in which tumor suppressor function may

182 rporate the cytoskeletal changes observed in transformed cells, indicated that the diameter of the so

183 etabolic switch and dampens the viability of transformed cells indicating that the MnSOD/AMPK axis is

184 protegerin enabled early growth of SS18-SSX2-transformed cells, indicating a paracrine link between t

185 Conversion of antigens from pathogens or transformed cells into MHC-I- and MHC-II-bound peptides

186 Dissemination of transformed cells is a key process in metastasis.

187 ral progression of epigenetic alterations in transformed cells is largely unclear.

188 ent, KIF2A in untransformed and mutant K-Ras-transformed cells is regulated by ERK1/2.

189 While its role in transformed cells is well established, little is known a

190 privation causes G1 cell cycle arrest in non-transformed cells, its impact on the cancer cell cycle i

191 ogression, whereby STAG2 inactivation in non-transformed cells leads to replication fork stalling and

192 1 by transfection of miR-21 mimics into LMP1-transformed cells led to phosphorylase-mediated activati

193 nd by antigen presentation using a Theileria-transformed cell line and autologous T cells from Theile

194 In 2001, a transformed cell line RGC-5 was developed from the rat r

195 In a K-ras transformed cell line we experimentally assessed glutami

196 ere obtained for both blood (N = 24) and EBV-transformed cell-line (N = 36) DNA samples from men aged

197 Transformed cell lines and animal models have been widel

198 d development is that they rely primarily on transformed cell lines and animal models that substantia

199 iruses because HRV growth is limited in most transformed cell lines and animal models.

200 sine triphosphate (GTP) in untransformed and transformed cell lines and determine this phenomenon dep

201 i in seven diverse cell lines, including six transformed cell lines and human induced pluripotent ste

202 (HDACis) on HIV reactivation in established transformed cell lines and primary CD4(+) T cells.

203 Here, using both transformed cell lines and primary neurons, we investiga

204 In addition to altered physiology, transformed cell lines are composed of a single cell typ

205 EBV(+) lymphomas and transformed cell lines exhibited abundant expression of

206 Oncogenically-transformed cell lines lack localization-resets and inst

207 nd effects of TFIIB knockdown in primary and transformed cell lines on cellular functionality and glo

208 ncogenic Ras up-regulates autophagy, and Ras-transformed cell lines require autophagy for mitochondri

209 Comparison to analogous data from transformed cell lines revealed respiratory-specific pro

210 Several earlier studies in transformed cell lines suggested that normoxic stabiliza

211 infection, researchers have frequently used transformed cell lines that can have limited translation

212 o move away from the often nonphysiological, transformed cell lines that have been used for decades i

213 In T cells and transformed cell lines used as model systems, HIV-1 asse

214 HRVs, as they generally replicate poorly in transformed cell lines, and host range restriction preve

215 Compared with other transformed cell lines, cultured iCSCL-10A cells exhibit

216 In these cells and transformed cell lines, depletion of Hili increased leve

217 alpha and reduces hypoxic gene expression in transformed cell lines.

218 They are also expressed in many transformed cell lines.

219 ems with the facile in vitro manipulation of transformed cell lines.

220 ments to localize to virological synapses in transformed cell lines.

221 3rd passage as well as the primary and virus-transformed cell lines.

222 ociated with telomere length in DNA from EBV-transformed cell-lines.

223 ls (cardiomyocytes and lung fibroblasts) and transformed cells (LNCaP and MCF-7 cancer cells), as wel

224 Because transformed cells may override anoikis and survive after

225 stablishes an in vivo model for studying how transformed cells migrate out from a complex tissue and

226 also observed after loss of PKCvarepsilon in transformed cell models.

227 r cells suppressed tumor growth but rendered transformed cells more motile and invasive in a manner d

228 ds expressed by stressed, virus-infected, or transformed cells, most inhibitory receptors engage MHC

229 Infected or transformed cells must present peptides derived from end

230 also found in discrete subpopulations of non-transformed cells neighbouring these pre-neoplastic lesi

231 ector cytokines and kill virally infected or transformed cells, NK cells also exhibit adaptive charac

232 In these transformed cells, no synergy is observed between JAK2 a

233 Transformed cells not only possessed several oncogenic p

234 PRMT5 expression was limited to EBV-transformed cells, not resting or activated B lymphocyte

235 istinct open chromatin loci that reflect the transformed cell of origin and suggest that open chromat

236 istones and their differential expression in transformed cells of the nervous system altered the post

237 In contrast, results using transformed cells or altered growth conditions suggested

238 llowing introduction of mutant IDH1 into Ras-transformed cells or established glioma cells.

239 gs), or host-derived pAgs that accumulate in transformed cells or in cells exposed to aminobisphospho

240 In prostatic cancer cells, but not in non-transformed cells or in prostate stem cells, we found th

241 ress aberrant cellular growth of potentially transformed cells or is simply a result of IR-induced lo

242 During tumorigenesis, transformed cells overproliferate and epithelial archite

243 Consequently, Ras-transformed cells override a131-induced growth arrest an

244 the heterogeneity and the plasticity of the transformed cell population are enhanced by exposure to

245 nancies that share in common the presence of transformed cells producing osteoid matrix, even if thes

246 erent 2A(pro) were measured comparatively in transformed cells programed with fluorescent reporter sy

247 The transformed cells proliferate at an increased rate compa

248 cells, also competing processes of partially transformed cell proliferation and differentiation/apopt

249 RD4 and the effects of BET inhibitors in non-transformed cells remain mostly unclear.

250 For example, the transformed cells remodel their metabolic processes to s

251 ying agents that inhibit the growth of FOXC2-transformed cells represents an attractive approach to i

252 port the growth of nontransformed cells, but transformed cells require much larger concentrations to

253 pathway was activated constitutively in KSHV-transformed cells, resulting in chronic induction of IL6

254 microbial pathogens as well as oncogenically transformed cells, resulting in significant immunosuppre

255 microbial pathogens as well as oncogenically transformed cells, resulting in significant immunosuppre

256 extracellular proteins was shown to reduce a transformed cell's dependence on extracellular glutamine

257 of FLT3-transformed cells compared with KIT-transformed cells, shows no toxicity towards normal huma

258 In transformed cells, SIRT5 regulates glutamine metabolism

259 cy factors resulting from these EBV+, B cell-transformed cell states, we performed parallel genome-wi

260 associated with HPV-positive cervical cancer transformed cells such as rapid growth and invasion and

261 ducible nitric oxide synthase (iNOS) in KSHV-transformed cells suppresses growth proliferation, aboli

262 abolic changes, which may in turn render the transformed cells susceptible to specific assaults in a

263 chromosomal aberrations and the formation of transformed cells that exhibited decreased H4K20me3 and

264 Transformed cells that grow to predominate in a culture

265 tion and mitochondrial ROS regulation in Ras-transformed cells that is governed by mitochondrial STAT

266 We find that in U2AF35(S34F)-transformed cells the autophagy-related factor 7 (Atg7)

267 cycle arrest response, whereas, in p53-null transformed cells, the absence of arrest enables the los

268 the activity of leukemogenic kinases to kill transformed cells, this approach selectively eliminates

269 is known for its action to selectively kill transformed cells through mechanisms that include increa

270 targeted post-translationally in infected or transformed cells to avoid immune recognition.

271 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that my

272 and when expressed alone, E4orf4 sensitized transformed cells to drug-induced toxicity.

273 y, E4orf4 inhibits DNA repair and sensitizes transformed cells to killing by DNA-damaging drugs.

274 pletion of eEF-2K reduced the ability of the transformed cells to proliferate and enhanced the sensit

275 ntercellular communication sets the pace for transformed cells to survive and to thrive.

276 e-wide siRNA screen in arrest-competent, non-transformed cells, to identify genes essential for this

277 In non-transformed cells, transient activation of the IL6 infla

278 ly, ectopic expression of TRIM37 renders non-transformed cells tumorigenic.

279 to be associated with p53 expression in EBV-transformed cells under physiological and DNA damaging c

280 Here we show that Ras-transformed cells use macropinocytosis to transport extr

281 nate between healthy and virally infected or transformed cells using diverse surface receptors that a

282 This mutation transformed cells via cysteine-mediated intermolecular d

283 ural killer (NK) cells kill virally infected/transformed cells via degranulation of lysosome-related

284 resses localized Ras pathway activity in Crk-transformed cells via recruitment and/or activation of R

285 Constitutive activation of this loop in transformed cells was dependent on proteolytic degradati

286 to the final state of differentiation in the transformed cells, we compared the relative tumorigenici

287 ough OGG1 depletion is well tolerated in non-transformed cells, we report here that OGG1 depletion ob

288 y passage Burkitt's lymphoma (BL) tumors and transformed cells, we show that compared with B lymphobl

289 genic clones in colorectal cancer and in non-transformed cells, we show that near-tetraploid clones e

290 Both HPV-16- and HPV-18-transformed cells were found to be responsive to targete

291 e expression differed between the native and transformed cells were primarily implicated in cell cycl

292 ession of IL7R which enables the survival of transformed cells when IL7 was added together with the k

293 With stably transformed cells which mimic the glyoxylate metabolic p

294 tion in soft agar, and NO generation of KSHV-transformed cells, which also depends on inducible nitri

295 n has been demonstrated to specifically kill transformed cells while leaving normal cells unharmed in

296 ted formation of tumors induced by RET/C634Y-transformed cells, while it weakened, but did not abroga

297 Our experiments revealed that miR-K10a alone transformed cells with an efficiency similar to that whe

298 that model the progression of a fraction of transformed cells within a tissue.

299 ty and invasive phenotypes characteristic of transformed cells without activation of Src.

300 op the cumulative growth and survival of the transformed cells without reducing the growth rate of th