ライフサイエンスコーパス: immortalization

1 epithelial cells without previous culture or immortalization.

2 lerance and its abrogation leads to cellular immortalization.

3 maintaining telomere integrity and cellular immortalization.

4 he oncogenic steps required for Tax-mediated immortalization.

5 unction is necessary for MLL fusion-mediated immortalization.

6 nd secondary adaptation due to selection and immortalization.

7 ration can be an essential step for cellular immortalization.

8 rtance of viral integration site in cellular immortalization.

9 HL2 in telomerase activation during cellular immortalization.

10 d pathways that regulate cellular senescence/immortalization.

11 by cellular adaptation, is required for MEC immortalization.

12 ediated extension of host cell life span and immortalization.

13 ing to progeroid phenotypes to those of cell immortalization.

14 downstream induction of telomerase and cell immortalization.

15 le mechanism for telomere maintenance during immortalization.

16 but not sufficient, for spontaneous cellular immortalization.

17 ommon signature characteristic of tumor cell immortalization.

18 1 loss cooperate in pRb inactivation and MEF immortalization.

19 c might be able to substitute for E6 in cell immortalization.

20 nce, and its disruption enhances primary MEF immortalization.

21 molecules, which leads to B-cell growth and immortalization.

22 he p16(INK4a)/Rb pathway is not required for immortalization.

23 is usurped by EBV genes essential for B-cell immortalization.

24 spensable for viral replication and cellular immortalization.

25 t maintains chromosomal telomeres and allows immortalization.

26 pressed in tumor cells and mediates cellular immortalization.

27 Rb, INK4a, and ARF) that are associated with immortalization.

28 uestion in the biology of EBV-induced B-cell immortalization.

29 lomerase function, is implicated in cellular immortalization.

30 ormal human cells rarely undergo spontaneous immortalization.

31 tinue to proliferate and undergo spontaneous immortalization.

32 iated transition through telomere crisis and immortalization.

33 n and correlates with the timing of cellular immortalization.

34 cancers to maintain telomere length for cell immortalization.

35 ction of either gene alone did not result in immortalization.

36 cannot interact with p300 to induce cellular immortalization.

37 gth and is an important determinant for cell immortalization.

38 II genes increases reaching a plateau during immortalization.

39 understanding of the pathways that attenuate immortalization.

40 perone to promote viral latency and cellular immortalization.

41 of oxidative stress in senescence bypass and immortalization.

42 ymphocyte-specific processes and induce cell immortalization.

43 lomeres) directly contributes to cancer cell immortalization.

44 feron-alpha/beta receptor (IFNAR) by in vivo immortalization.

45 , suggesting this as a common aspect of cell immortalization.

46 ting that this regulation is acquired during immortalization.

47 -prone recovery from serum deprivation after immortalization.

48 omere maintenance mechanism (TMM) to support immortalization.

49 from primary culture through senescence and immortalization.

50 ming of pluripotency genes may initiate cell immortalization.

51 lenced p16(INK4a) during telomerase-mediated immortalization.

52 to cells exposed to oxidative stress during immortalization.

53 is essential for genomic stability and cell immortalization.

54 erived from the human embryo without genetic immortalization.

55 vation or alternative mechanisms of cellular immortalization; (6) angiogenic activity; and (7) the ab

56 ate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).

57 e (LFS) patients during spontaneous cellular immortalization, a necessary step in carcinogenesis.

58 Thus, reversible immortalization allows the expansion of human RPTECs, le

59 ucible proteins are associated with cellular immortalization, an important early event in the develop

60 intenance is a requisite feature of cellular immortalization and a hallmark of human cancer.

61 tivation of telomerase occur during cellular immortalization and are maintained in cancer cells.

62 on of several genes previously implicated in immortalization and breast cancer progression.

63 als in somatic cells is critical to cellular immortalization and carcinogenesis.

64 antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human

65 ion, which renders MEFs prone to spontaneous immortalization and confers an early growth advantage th

66 vation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumor

67 ing HCECs as knockdown of KLG regarding both immortalization and down-regulation of the tumor suppres

68 tified universal genes regulating senescence/immortalization and found that the key regulator genes r

69 antigen 3C (EBNA 3C) is essential for B-cell immortalization and functions as a regulator of viral an

70 PMs contribute to tumorigenesis by promoting immortalization and genomic instability in two phases.

71 protein is important for EBV-mediated B-cell immortalization and is a potent gene-specific coactivato

72 rotein 1 (LMP1), is essential for EBV B-cell immortalization and is sufficient to transform rodent fi

73 An improved understanding of cell immortalization and its manifestation in clinical tumors

74 coplasma-mediated promotional effect in cell immortalization and its potential clinical implications

75 strate that, in the context of hematopoietic immortalization and leukemogenesis, individual HOX prope

76 atent antigen EBNA3C is implicated in B-cell immortalization and linked to several B-cell malignancie

77 in this repression, allowing for the classic immortalization and loss of cell contact inhibition seen

78 e mouse TERT protein is sufficient to confer immortalization and maintenance of telomere length and f

79 (HPV) plays a critical role in inducing cell immortalization and malignancy.

80 T lymphocytes with NPM-ALK results in their immortalization and malignant transformation.

81 promoter is a bystander effect of oncogenic immortalization and not likely causal in GC pathogenesis

82 of telomerase has been associated with cell immortalization and oncogenesis.

83 ndependent primary hMEC strains led to their immortalization and preneoplastic transformation.

84 ffected by human papillomavirus type 16/E6E7 immortalization and proinflammatory cytokine stimulation

85 We report herein that sequential immortalization and ras-transformation of mouse fibrobla

86 A second step coincides with immortalization and results in hundreds of additional DN

87 In contrast, following spontaneous immortalization and the loss of functional p53 signaling

88 early region 1A (E1A) protein promotes cell immortalization and transformation by mediating the acti

89 The role of HPV oncogenes in cellular immortalization and transformation has been extensively

90 osis plays an important role in the cellular immortalization and transformation induced by E6 and E7

91 from high-risk HPV types contributes to the immortalization and transformation of cells by multiple

92 Ectopic T antigen expression results in the immortalization and transformation of many cell types in

93 anisms are used by T antigens to induce cell immortalization and transformation.

94 ish that TERT promoter mutations can promote immortalization and tumorigenesis of incipient cancer ce

95 d keratinocytes is not required for inducing immortalization and, more importantly, that irradiation

96 le are actually late events that may reflect immortalization and, possibly, disease progression.

97 kine that regulates cell proliferation, cell immortalization, and cell death, acting as a key homeost

98 ooperate in promoting pRb inactivation, cell immortalization, and H-ras(V12)/c-myc-induced loss of co

99 inases became required following HPV-induced immortalization, and the requirement for two kinases, SG

100 d chemical compound mediating efficient cell immortalization, and this finding could have wide-rangin

101 to alterations in signaling, proliferation, immortalization, and transformation.

102 ed that it might be involved in cell growth, immortalization, and/or senescence.

103 modulate receptor-mediated effects; 9) cause immortalization; and 10) alter cell proliferation, cell

104 ma pathogenesis, including growth, survival, immortalization, angiogenesis and metastasis.

105 luenced by the genetic lesion that triggered immortalization, as alpha3beta1-dependent fibulin-2 expr

106 e reduced EBV replication was independent of immortalization, as human telomerase-immortalized normal

107 nd immortalization of keratinocytes with E7, immortalization assays were performed using specific mut

108 r a 9-week period using in vitro cell growth/immortalization assays.

109 t majority of genes dysregulated during cell immortalization belongs to gene families that converge i

110 t HBZ was not required for in vitro cellular immortalization, but enhanced infectivity and persistenc

111 s competent for viral replication and B-cell immortalization, but quantitative assays showed that clo

112 d the foundation for the field of senescence/immortalization, but were labor intensive and the result

113 with lenti-MnSOD(K122-R) inhibited in vitro immortalization by an oncogene (Ras), inhibited IR-induc

114 portant for both binding KIX and bone marrow immortalization by E2A-PBX1.

115 rate that degradation of p53 is required for immortalization by E6/E7, while increased telomerase act

116 al role for CD40-CD40L interaction in B-cell immortalization by EBV, indicating that LMP1 does not ad

117 is the EBV oncoprotein essential for B-cell immortalization by EBV.

118 ave indicated that EBNA-LP may contribute to immortalization by enhancing EBNA2-mediated transcriptio

119 Although in vitro immortalization by HTLV-I virus is very efficient, we re

120 ole of Dot1 in hematopoietic progenitor cell immortalization by MLL fusion proteins.

121 ed AF9/ENL interacting site is essential for immortalization by MLL-AF9, indicating that DOT1L intera

122 his suggests that miR-155 contributes to EBV immortalization by modulation of NF-kappaB signaling and

123 of p16 is the primary event associated with immortalization by nickel, a human non-genotoxic carcino

124 Using this model, we show that keratinocyte immortalization by p53-null mutation causes a switch in

125 re potent isoform, we show that mPR promotes immortalization by preventing cellular senescence, imped

126 Forced expression of KDM2B promotes immortalization by silencing these miRNAs through locus-

127 c activity in human primary T cells and that immortalization by Tax is rare.

128 in gene expression, and reversal of cellular immortalization by telomerase.

129 Regardless, cell immortalization by the Myc + E7 genes occurred independe

130 The common factor in cell immortalization by the three gene sets (E6 + E7, Myc + E

131 Immortalization by TPMs requires a gradual up-regulation

132 Some human cancer cells achieve immortalization by using a recombinational mechanism ter

133 In cell cultures, the immortalization capacities of APH-2 mutant viruses were

134 ral gene expression, protein production, and immortalization capacity.

135 showed that the BAC-derived virus was B-cell immortalization competent.

136 the genes and pathways regulating senescence/immortalization could provide novel molecular targets fo

137 Interestingly, an immortalization-defective E6 mutant localized to the hTE

138 An immortalization-defective HPV-18 E6 mutant genome was al

139 B cell immortalization depends on expression of viral latency g

140 Despite the lack of immortalization, E6 was functional in the fibroblasts, m

141 ey events of the viral life cycle, including immortalization, episomal maintenance, late promoter act

142 r essential tumor-specific traits, including immortalization, escape from antimitogenic signaling, ne

143 ponding postnatal cell types, and to require immortalization for clonal isolation and expansion, thes

144 This strategy for immortalization has found special utility in the central

145 antigen 3C (EBNA 3C) is essential for B-cell immortalization, has potent cell cycle deregulation capa

146 e and mutagenesis in cellular senescence and immortalization, here we profiled spontaneous and methyl

147 t are shared with some cancers, most notably immortalization, hyperproliferation, and dissemination.

148 ent infection and the need for selection and immortalization.IMPORTANCE To establish infection and co

149 that transition through telomere crisis and immortalization in breast cancer occurs during progressi

150 a novel mesenchymal stem cell origin for ALT immortalization in cell lines and mesenchymal tissues.

151 ely contribute to HVS-mediated lymphoid cell immortalization in culture and lymphoma induction in pri

152 eplication but is required for lymphoid cell immortalization in culture and lymphoma induction in pri

153 ced Tax expression, hyper-proliferation, and immortalization in culture.

154 This work explores spontaneous immortalization in keratinocytes, derived from two skin

155 on of these same pathways causes spontaneous immortalization in MEFs, and oncogenic transformation by

156 serum-containing medium but does not lead to immortalization in the absence of feeder cells.

157 s engineered to express Ndy1 or Ndy2 undergo immortalization in the absence of replicative senescence

158 progenitor cells is relevant to the role of immortalization in the initiation and progression of can

159 myeloid progenitors in vitro, causing their immortalization in the presence of stem cell factor and

160 EBNA-3B has no significant impact on B-cell immortalization in tissue culture, this finding suggeste

161 ient for MLL-AF6 mediated myeloid progenitor immortalization in vitro and short latency leukemogenesi

162 of 707 transcriptional changes accompanying immortalization including reduced p16(INK4A) mRNA.

163 or signaling in primary fibroblasts, whereas immortalization induced by SV40 large T antigen supporte

164 n-Barr virus (EBV) in vitro results in their immortalization into lymphoblastoid cell lines (LCLs); t

165 With ionizing radiation, immortalization is invariably accompanied by efficient b

166 The up-regulation of survivin during immortalization likely contributes to the vulnerability

167 Need for selection and immortalization made it impossible to distinguish betwee

168 pes of human cancer and associates with cell immortalization, malignant transformation, and chemoresi

169 genetic changes that occur during senescence/immortalization may help elucidate crucial events that l

170 lly expressed to construct an ACOO-specific 'immortalization network' comprised of 40 genes, one of w

171 the oncogenic agents alone in the absence of immortalization, nor by expression of exogenously introd

172 rather, pRb loss leads to the expansion and immortalization of an immature progenitor pool character

173 nerated by means of ex vivo immunization and immortalization of antigen-specific human B cells for th

174 eping Beauty transposons in NSCs induced the immortalization of astroglial-like cells, which were the

175 BNA2 and is important for Epstein-Barr virus immortalization of B cells.

176 (EBNA2) is a key latency gene essential for immortalization of B lymphocytes and transactivation of

177 signaling pathways and is essential for EBV immortalization of B lymphocytes.

178 nsion of telomeres is a critical step in the immortalization of cancer cells.

179 T-antigen immortalization of cells allowed cell growth.

180 lomeres, appears to provide a barrier to the immortalization of cells and development of cancer.

181 ular events leading to transformation and/or immortalization of cells have an impact on their relativ

182 Here we apply this strategy during Ras(V12) immortalization of Drosophila embryonic cells, a phenome

183 may be a critical factor facilitating hTERT immortalization of epithelial cells.

184 lting in extensive ex vivo proliferation and immortalization of erythroid progenitors.

185 er in human old versus young fibroblasts and immortalization of fibroblasts with telomerase resulted

186 Our model is based on (i) immortalization of FTSECs isolated from primary samples

187 st that KLB is an important regulator in the immortalization of HCECs by facilitating FGF19 growth fa

188 omerase reverse transcriptase (hTERT) in the immortalization of HCECs.

189 sis can also identify genes that promote the immortalization of hematopoietic cells, which normally h

190 rs in the MLL fusion protein MLL-AF9 blocked immortalization of hematopoietic progenitors.

191 Here we show that immortalization of HFK with HPV-16 or 18 causes down-reg

192 viral genes essential for the infection and immortalization of human B cells by the cancer-associate

193 way induces B cell proliferation in vivo and immortalization of human B cells in vitro.

194 n 3C (EBNA-3C) is essential for EBV-mediated immortalization of human B lymphocytes and regulates bot

195 Immortalization of human epithelial cells involves both

196 The role of this pathway in immortalization of human epithelial cells is not clear.

197 quired for the conditional reprogramming and immortalization of human epithelial cells.

198 are proposed to contribute to the efficient immortalization of human epithelial cells: the degradati

199 r, it cannot substitute the T antigen in the immortalization of human fibroblasts, indicating that it

200 e E7 protein, is essential for the efficient immortalization of human foreskin keratinocytes (HFKs).

201 ng-defective HPV16 E6 mutations that induced immortalization of human mammary epithelial cells.

202 shows that up-regulation of survivin during immortalization of human myofibroblasts is an indirect c

203 Here, we show the immortalization of human prostate epithelial cells (HPrE

204 hat results in successful transformation and immortalization of infected cells.

205 6 are required to allow bypass of crisis and immortalization of keratinocytes with E7, immortalizatio

206 olecule can substitute for E6 in cooperative immortalization of keratinocytes with E7.

207 ) E6 and E7 oncoproteins are critical to the immortalization of keratinocytes.

208 se promoter, potentially contributing to the immortalization of KSHV-infected cells.

209 is by their nature could also be involved in immortalization of leukemic stem cells, and thus represe

210 eration of primary MECs and results in rapid immortalization of MECs in vitro relative to wild-type c

211 n either premature senescence or spontaneous immortalization of MEF cells.

212 Loss of Rassf5 also resulted in spontaneous immortalization of MEFs at earlier passages than the con

213 nduces premature senescence, and counteracts immortalization of MEFs driven by KDM2B.

214 Resveratrol results in immortalization of mixed progenitor cells with mutant p5

215 Telomerase is essential for immortalization of most human cancer cells.

216 Transduction with mutant Setbp1 led to the immortalization of mouse myeloid progenitors that showed

217 reduction by shRNA impairs AML1/ETO-induced immortalization of murine progenitors.

218 Prior studies reported conditional immortalization of myeloid progenitors using retroviral

219 As SIPS/OIS bypass is a prerequisite for the immortalization of normal diploid human epithelial cells

220 Interestingly, immortalization of postselection cells using various met

221 EBNA-2 is essential for EBV-mediated immortalization of primary B lymphocytes.

222 o p53 inactivation during transformation and immortalization of primary cells.

223 al ribosomal protein S18-2 (MRPS18-2) led to immortalization of primary fibroblasts, accompanied by i

224 Telomerase activation is critical for the immortalization of primary human keratinocytes by the hi

225 ace expression and to the efficient in vitro immortalization of primary human T cells to interleukin-

226 contributed to high-risk HPV E6/E7-mediated immortalization of primary keratinocytes and HPV(+) but

227 ation causes constitutive PKA activation and immortalization of primary mouse embryonic fibroblasts (

228 loyed strategy is based on carcinogen-driven immortalization of primary mouse embryonic fibroblasts a

229 in foamy viral vectors caused extremely low immortalization of primary mouse hematopoietic stem/prog

230 Tax-1 PBM in HTLV-induced proliferation and immortalization of primary T cells in vitro and viral su

231 d the contribution of HBZ to HTLV-1-mediated immortalization of primary T lymphocytes in vitro and HT

232 ctional role of APH-2 in the HTLV-2-mediated immortalization of primary T lymphocytes in vitro and in

233 -interacting protein (Tip), required for the immortalization of primary T lymphocytes, targets cellul

234 Similarly, spontaneous immortalization of progerin-expressing cultured keratino

235 rrent expression of RB and S18-2 resulted in immortalization of Rb1 (-/-) primary mouse embryonic fib

236 in LCLs.IMPORTANCE Epstein-Barr virus (EBV) immortalization of resting B lymphocytes (RBLs) is a use

237 frequent event during transformation and/or immortalization of rodent cells.

238 Thus, telomerase expression and consequent immortalization of skin fibroblasts do not alter nucleot

239 Although we focus here on telomerase immortalization of spinal neural progenitors, this is a

240 ctivities, a subset of which likely leads to immortalization of T cells.

241 data with the annotated genome sequence; (3) immortalization of the genome; (4) ability to generate t

242 The immortalization of these cell lines with the expression

243 isolated from a myasthenia gravis patient by immortalization of thymic B cells using Epstein-Barr vir

244 eral miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced, and tumo

245 ints is essential in the process of cellular immortalization, one of the components of the transforma

246 read, which typically does not result in the immortalization or enhanced growth of infected epithelia

247 higher level distribution is not altered by immortalization or long-term culture.

248 odologies to produce hmAbs, including B-cell immortalization or phage display, can be used to isolate

249 tability, which in turn leads to spontaneous immortalization or premature senescence of Dnmt3b-defici

250 induced by HPV or indirectly by the need for immortalization or selection.

251 However, upon immortalization or tumorigenic transformation of mouse f

252 samples varying for telomerase activity and immortalization parameters.

253 al DNA methylation changes regardless of the immortalization pathway.

254 Ink4a/Arf locus and contributing to the Ndy1 immortalization phenotype.

255 Elevated T-SCE was associated with greater immortalization potential and resultant tumors maintaine

256 iated transcriptional up-regulation and cell immortalization potential in vivo.

257 o MLL-ENL blocks the hematopoietic stem cell immortalization potential of the fusion protein in seria

258 BHLF1 (-) viruses exhibited variably reduced immortalization potential relative to the wild-type viru

259 up differences are due to differences in the immortalization procedures used for each group or reflec

260 and TD skin fibroblasts, and (in contrast to immortalization procedures using viral oncogenes) did no

261 f viral and cellular genes important for the immortalization process.

262 ne demonstrated viral replication and B-cell immortalization properties comparable to those of the na

263 ction, the details of its activity on T cell immortalization remain elusive.

264 n, the rate-limiting processes for stem cell immortalization remain unknown.

265 n-Barr virus (EBV) EBNA-LP protein to B-cell immortalization remains an enigma.

266 plication and drive T-cell proliferation and immortalization remains poorly understood.

267 Self-renewal after immortalization requires continuous Setbp1 expression.

268 wth whereas abrogation of senescence through immortalization results in loss of such tumor promoting

269 Immortalization (senescence bypass) is a critical rate-l

270 A predominant feature of this immortalization signature (ImmSig) was the significant o

271 essential, it is not sufficient for cellular immortalization, suggesting that additional alterations

272 Immortalization, the acquisition of the ability to proli

273 To attempt immortalization, the cells were exposed to retroviral hu

274 Immortalization through oncogenic gene expression, but n

275 s and/or epigenetic alterations required for immortalization to occur.

276 an significantly promote, MLL fusion-induced immortalization/transformation of normal mouse bone marr

277 pendently influences the preferential T cell immortalization tropism irrespective of the envelope cou

278 HTLV-1/SU2 shifted the CD4(+) T cell immortalization tropism of wild-type HTLV-1 (wtHTLV-1) t

279 .195) resulted in a shift to a CD8(+) T cell immortalization tropism preference.

280 s involved in determining this CD4(+) T cell immortalization tropism.

281 domains that are involved in determining the immortalization tropism.

282 somal ends, and its crucial role in cellular immortalization, tumorigenesis, and the progression of c

283 egulates PGM, mutation of p53 can facilitate immortalization via effects on PGM levels and glycolysis

284 thelial cell transformation without previous immortalization via genetic influences such as SV40 T-an

285 etween genes that function during astroglial immortalization vs. later stages of tumor development.

286 Immortalization was accompanied by activation of the JAK

287 The transition to cellular immortalization was accompanied by markedly increased ex

288 nhibitor exhibited an extended lifespan, and immortalization was facilitated following transduction t

289 tial role EBNA-LP has in EBV-mediated B-cell immortalization, we asked whether it is a global or gene

290 proposed to be necessary for epithelial cell immortalization, we sought to further characterize the r

291 d/continuous telomerase activity may promote immortalization when differentiation and/or senescent pa

292 l promoters for genes that are necessary for immortalization when it is bound to a cluster of 20 cogn

293 d from tumors or cultured cells selected for immortalization which may have missing or mutated modula

294 -harboring cell lines requires selection and immortalization, which makes it impossible to distinguis

295 n is up-regulated during telomerase-mediated immortalization, which occurs at a relatively early stag

296 s proliferate faster and undergo spontaneous immortalization while retaining both Arf and p53.

297 cking alternative epigenetic routes for cell immortalization will be paramount for understanding cruc

298 e have already observed high-efficiency cell immortalization with the hTERT + E7 or E6 mutant (p53 de

299 iferative capacity and resulted in efficient immortalization without detectable cell crisis.

300 To test whether cellular immortalization would reverse these observations, we exp