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

1 llular metabolism is an emerging hallmark of neoplastic transformation.

2 nses to growth factors, genotoxic stress and neoplastic transformation.

3 n cells harboring mutations that prime their neoplastic transformation.

4 capable of dysregulating gene expression for neoplastic transformation.

5 UC) allele a sensitive, unbiased reporter of neoplastic transformation.

6 lex subunit 12 mutation, a genetic marker of neoplastic transformation.

7 in dampening AID-dependent autoimmunity and neoplastic transformation.

8 erexpression of BARD1beta was sufficient for neoplastic transformation.

9 ng organogenesis, gastric acid secretion and neoplastic transformation.

10 -regulated kinase (ERK; MEK) MEK1/2 to drive neoplastic transformation.

11 nce, and collaborate with other oncogenes in neoplastic transformation.

12 rt these miRNAs role in suppression of HCSCs neoplastic transformation.

13 ntiated phenotype that transiently resembles neoplastic transformation.

14 Dlc1 knockout allele reproducibly underwent neoplastic transformation.

15 features of anergy and apoptosis instead of neoplastic transformation.

16 can be genetically ablated prior to or after neoplastic transformation.

17 ays, for example, src-STAT3, responsible for neoplastic transformation.

18 uring development and in adult tissue during neoplastic transformation.

19 nomic mutations and metabolic alterations in neoplastic transformation.

20 ormation, an early characteristic of mammary neoplastic transformation.

21 nduction of ODC activity is an early step in neoplastic transformation.

22 e in the mammary epithelium before and after neoplastic transformation.

23 ver tumor cells may normally aid in limiting neoplastic transformation.

24 s, some of which have a significant risk for neoplastic transformation.

25 ndogenous PRR ligands when damaged or during neoplastic transformation.

26 duce polyploidy, which likely contributes to neoplastic transformation.

27 sociated with an increased susceptibility to neoplastic transformation.

28 ptosis as a hallmark feature acquired during neoplastic transformation.

29 ment, response to cellular perturbation, and neoplastic transformation.

30 they produce, have a major role in promoting neoplastic transformation.

31 in the mammary gland may predispose MECs to neoplastic transformation.

32 on in cancer tissues and different models of neoplastic transformation.

33 eplication fidelity, thereby contributing to neoplastic transformation.

34 , suggesting that Thoc1 may be important for neoplastic transformation.

35 nder (P = 0.146) in the GHP patients who had neoplastic transformation.

36 ansduction networks of melanoma cells during neoplastic transformation.

37 nces of aberrant expression of ZNF217 during neoplastic transformation.

38 based model of the early events in cervical neoplastic transformation.

39 rsibly prevent damaged cells from undergoing neoplastic transformation.

40 slocations and aneuploidy, which can promote neoplastic transformation.

41 3 in various tumors, plays a key role during neoplastic transformation.

42 in cellular energetics, stress defense, and neoplastic transformation.

43 ability in the epithelium and, subsequently, neoplastic transformation.

44 evelopment are frequently reactivated during neoplastic transformation.

45 l factor-dependent transcription and promote neoplastic transformation.

46 vents the proliferation of cells at risk for neoplastic transformation.

47 atients, elevation of serum CA19-9 marks the neoplastic transformation.

48 specific genomic events taking place during neoplastic transformation.

49 6 tumor-suppressor gene might be involved in neoplastic transformation.

50 rve to maintain genomic stability and resist neoplastic transformation.

51 ases to stimulate STAT3-signaling to promote neoplastic transformation.

52 ance to programmed cell death, underlie this neoplastic transformation.

53 r can lead to uncontrolled proliferation and neoplastic transformation.

54 n cascades is one of the principal causes of neoplastic transformation.

55 /SNF (hSWI/SNF) complexes may be involved in neoplastic transformation.

56 lar phenotype, the loss of which can lead to neoplastic transformation.

57 an important host defense mechanism against neoplastic transformation.

58 uced apoptosis and inhibition of Ras-induced neoplastic transformation.

59 how that adult stem cells can be targets for neoplastic transformation.

60 ecting essential transcriptional features of neoplastic transformation.

61 been reported to contribute significantly to neoplastic transformation.

62 intracellular signaling pathway perturbed in neoplastic transformation.

63 include loss of cellular growth control and neoplastic transformation.

64 ular memory, transcriptional repression, and neoplastic transformation.

65 sm of apoptosis that is peculiarly linked to neoplastic transformation.

66 growth in vitro and in vivo, and suppresses neoplastic transformation.

67 pendent transcription is a good correlate to neoplastic transformation.

68 ute to replicative senescence, apoptosis, or neoplastic transformation.

69 tors of muscle development and implicated in neoplastic transformation.

70 at CIN impairs cellular fitness and prevents neoplastic transformation.

71 ways, cancer cell proliferation and cellular neoplastic transformation.

72 rrounding tissue that in turn promotes their neoplastic transformation.

73 Cdh1 would exhibit a phenotype indicative of neoplastic transformation.

74 rs on cells harboring Kras mutations promote neoplastic transformation.

75 omote genomic instability as a mechanism for neoplastic transformation.

76 s can exert an equally significant effect on neoplastic transformation.

77 ish risk factors that may be associated with neoplastic transformation.

78 providing a molecular basis for its role in neoplastic transformation.

79 stricting proliferation of cells at risk for neoplastic transformation.

80 one of the risk factors for GHPs to undergo neoplastic transformation.

81 em or progenitor cells, appear to facilitate neoplastic transformation.

82 s epithelium, which undergoes a high rate of neoplastic transformation.

83 ing prospectively collected samples prior to neoplastic transformation.

84 expression in melanocytes is sufficient for neoplastic transformation.

85 ession pattern of tissues was modified after neoplastic transformation.

86 talyze the genomic instability necessary for neoplastic transformation.

87 nsity was observed at the earliest stages of neoplastic transformation.

88 d to protect against genomic instability and neoplastic transformation.

89 rom human embryonic stem cells, resulting in neoplastic transformation.

90 TPase Rac has been implicated in Ras-induced neoplastic transformation.

91 e delay in normal cells to protect them from neoplastic transformation.

92 ng recent larger DNAm data to predict future neoplastic transformations.

93 NAm patterns which are associated with later neoplastic transformations.

94 MTM, but not control particle PMCON, induced neoplastic transformation, accelerated cell proliferatio

95 y normal HPV- samples that (i) predispose to neoplastic transformations after HPV infection and (ii)

96 enotypic plasticity that predisposes them to neoplastic transformation and acquisition of stem cell c

97 ectopic HMGA2 expression is associated with neoplastic transformation and anchorage-independent cell

98 the mechanisms by which CaSm contributes to neoplastic transformation and cellular proliferation are

99 ze and texture of cell nuclei as a result of neoplastic transformation and chemopreventive action are

100 stent activation of Stat5 are sufficient for neoplastic transformation and development of multi-linea

101 functions of claudin-2 that are relevant to neoplastic transformation and growth.

102 c impact of biguanides during the process of neoplastic transformation and in CSCs is unknown.

103 ellular stresses, many of which occur during neoplastic transformation and in the tumor microenvironm

104 and human endogenous retrovirus, accompanies neoplastic transformation and infection with viruses suc

105 cause anoikis deficiency is a key feature of neoplastic transformation and invasive growth of epithel

106 , autoimmune disorders, transplantation, and neoplastic transformation and metastasis.

107 s process is necessary and/or sufficient for neoplastic transformation and metastasis.

108 of both HOXA5 and RARbeta expression during neoplastic transformation and progression in the breast

109 xpression is related to endocrine and acinar neoplastic transformation and progression of malignancy,

110 ical roles played by some protein kinases in neoplastic transformation and progression provide a rati

111 ould contribute to genome instability during neoplastic transformation and progression.

112 e genomic instability that can contribute to neoplastic transformation and progression.

113 is study, 7,3',4'-THIF prevented EGF-induced neoplastic transformation and proliferation of JB6 P+ mo

114 expression of HMGA1 proteins in vivo induces neoplastic transformation and promotes a highly metastat

115 ransgenic HMGA1 proteins in cells results in neoplastic transformation and promotes progression to ma

116 ential role of cellular reprogramming during neoplastic transformation and the major players involved

117 2 was suggested to play an important role in neoplastic transformation and tumor development.

118 es; earlier during oncogenesis it suppresses neoplastic transformation and tumor growth, but later it

119 (Pdcd4) is a tumor suppressor that inhibits neoplastic transformation and tumor invasion.

120 d the role of Hsp72 in Her2 oncogene-induced neoplastic transformation and tumorigenesis.

121 on of genetic information and helps suppress neoplastic transformation and tumorigenesis.

122 tic transformations, (ii, iii) cases showing neoplastic transformations and (iv) cases with confirmed

123 nd Undaria pinnatifida on the proliferation, neoplastic transformation, and colony formation of mouse

124 ERK8 promoted neoplastic transformation, and knockdown of ERK8 in HCT1

125 Mutant cells undergo neoplastic transformation, and mice develop a highly pen

126 t its expression might be a prerequisite for neoplastic transformation, and prompts a search for the

127 trated for the first time a role for CIB1 in neoplastic transformation, and revealed a novel mechanis

128 d MYC-mediated transcription, proliferation, neoplastic transformation, and tumor development.

129 ll growth and differentiation, pluripotency, neoplastic transformation, apoptosis, DNA repair, and ma

130 IBD and its associated neoplastic transformation appear inevitable, which may s

131 sm by which its loss of function can lead to neoplastic transformation are poorly understood.

132 tumors affect cell identity, cell state and neoplastic transformation, as well as addressing the pot

133 thway components is likely to be crucial for neoplastic transformation, but little is known about how

134 astic polyps (GHPs) have a potential risk of neoplastic transformation, but the responsible mechanism

135 arcinogenesis and influence initial steps in neoplastic transformation by altering genome stability a

136 tion exacerbates pancreatic inflammation and neoplastic transformation by augmenting the DC-Th2 axis.

137 1 function is required for efficient de novo neoplastic transformation by beta-catenin in RK3E cells.

138 oinsufficient tumor suppressor that inhibits neoplastic transformation by competing with myeloid ecot

139 hat the aberrant cytoskeleton contributes to neoplastic transformation by conferring resistance to an

140 hese results suggest that ZNF217 may promote neoplastic transformation by increasing cell survival du

141 Programmed cell death 4 (Pdcd4) suppresses neoplastic transformation by inhibiting the activation o

142 We conclude that MSH6 protects B cells from neoplastic transformation by preserving genomic stabilit

143 t melanocyte-specific factors present before neoplastic transformation can have a pivotal role in gov

144 +) MEFs to anti-BPDE (0.1 micromol/L) caused neoplastic transformation characterized by colony format

145 WT.BRCA1 also inhibits OPN-mediated neoplastic transformation characterized by morphology ch

146 Spontaneous neoplastic transformation develops within days in the NI

147 reast duct seem to be the primary target for neoplastic transformation events that eventually produce

148 tionarily conserved and defines one class of neoplastic transformation events, regardless of etiology

149 sal defense and, conversely, as a target for neoplastic transformation events.

150 esis and prime the microenvironment prior to neoplastic transformation for accelerated breast oncogen

151 ing sequence, can also be a driving force in neoplastic transformation, for selected genes, and in sp

152 n mammary epithelial MCF-10A cells underwent neoplastic transformation, formed foci in culture and tu

153 tein in the initiation and/or maintenance of neoplastic transformation has not been studied in detail

154 ever, the mechanism of their deregulation in neoplastic transformation has only begun to be understoo

155 uniquely susceptible to immune control upon neoplastic transformation, has not been fully investigat

156 n adjacent keratinocytes and their efficient neoplastic transformation; however, effects of tumor pro

157 27M) and Trp53 loss alone are sufficient for neoplastic transformation if introduced in utero.

158 cytologically normal, but will later develop neoplastic transformations, (ii, iii) cases showing neop

159 Neoplastic transformation in a Drosophila genetic model

160 JB6 cells resulted in tumor-promoter-induced neoplastic transformation in a manner similar to that in

161 ation, increased cell division, and promoted neoplastic transformation in an eIF4E-dependent manner.

162 tibody formation in autoimmunity and undergo neoplastic transformation in angioimmunoblastic T-cell l

163 Our data indicate that neoplastic transformation in astrocytes is associated wi

164 The mechanisms by which AME induces a neoplastic transformation in bone marrow cells are unkno

165 strate GSTA4 activation during 4-HNE-induced neoplastic transformation in colorectal carcinogenesis.

166 hTERT cells also failed to show evidence of neoplastic transformation in functional assays of tumori

167 Furthermore, SEPT9_v1 markedly enhanced neoplastic transformation in Hs578T cells, a BCC with no

168 induce ROS generation, mtDNA deletions, and neoplastic transformation in human keratinocytes.

169 ility, which greatly increases the threat of neoplastic transformation in humans.

170 C3G also blocked TPA-induced neoplastic transformation in JB6 cells.

171 cing enhanced, respectively, the TPA-induced neoplastic transformation in JB6-Cl.41 preneoplastic mod

172 Neoplastic transformation in kidneys was not detected at

173 viously identified as expression markers for neoplastic transformation in multiple human cancers.

174 ation of CpG sites that indicate the risk of neoplastic transformation in stages prior to neoplasia.

175 e cancers, the molecular events that lead to neoplastic transformation in the uterus are poorly under

176 Neoplastic transformation in this model increased the na

177 e system, plays a critical role in promoting neoplastic transformation in this setting (see the relat

178 have recently shown that Caspase-8 sustains neoplastic transformation in vitro in human GBM cell lin

179 of MCPyV sTAg alone is sufficient for rapid neoplastic transformation in vivo, implicating sTAg as a

180 y genetic pathways in normal development and neoplastic transformation in vivo.

181 hat elevated levels of CIB1 resulted in full neoplastic transformation, in a manner dependent on SK1.

182 mian virus 40 large T antigen contributes to neoplastic transformation, in part, by targeting the Rb

183 cription and processing of genes involved in neoplastic transformation, including CCND1 (the cyclin D

184 B has an essential role in anti-BPDE-induced neoplastic transformation, including regulation of cell

185 knockdown of either NOX1 or AKT1 blocked the neoplastic transformation induced by XPC silencing.

186 Furthermore, neoplastic transformation involves senescence evasion, a

187 Notably, stepwise neoplastic transformation is accompanied by a gradual in

188 Neoplastic transformation is caused by accumulation of g

189 The function of beta-cat in neoplastic transformation is dependent on T-cell factor

190 Neoplastic transformation is driven by oncogenic lesions

191 teins, including tropomyosin-1 (TM1), during neoplastic transformation is hypothesized to contribute

192 f the most highly upregulated enzymes during neoplastic transformation is MTHFD2, a mitochondrial met

193 Neoplastic transformation is often related to abnormal a

194 ole of TGF-beta deficiency in BWS-associated neoplastic transformation is unexplored.

195 of mesenchymal cells in inflammation and/or neoplastic transformation is well recognized, but their

196 Whereas EphA2 immunoreactivity related to neoplastic transformation, it did not correlate with oth

197 though oncogenic ras plays a pivotal role in neoplastic transformation, it triggers an anti-oncogenic

198 In this context, chemokine switch upon neoplastic transformation might represent a novel mechan

199 ion of this pathway during proliferation and neoplastic transformation, more recent studies have exam

200 at invasive capacity was altered even before neoplastic transformation occurred, as triggered by miR-

201 as a risk factor for GHPs which demonstrated neoplastic transformation (odds ratio [OR], 3.729; 95% c

202 This tumor derives from the neoplastic transformation of aberrant intraepithelial T

203 tatic balance between sustained function and neoplastic transformation of aging stem cells.

204 on autoimmune disease, viral infection, and neoplastic transformation of B lineage cells, in which C

205 BPDE, can promote growth, proliferation and neoplastic transformation of breast epithelial cells.

206 Our findings suggest that neoplastic transformation of DCs does not by default ind

207 a model by which to explore the mechanism of neoplastic transformation of endothelial cells.

208 gene expression of hypergastrinemia-induced neoplastic transformation of enterochromaffin-like (ECL)

209 ay function as a tumor suppressor during the neoplastic transformation of epidermal cells.

210 in different cell types and readily induces neoplastic transformation of fibroblast cell lines.

211 um, we hypothesized that the serum-dependent neoplastic transformation of Galpha12WT-NIH3T3 cells was

212 To investigate the process of neoplastic transformation of GCPs, we generated a new me

213 ) result in constitutive kinase activity and neoplastic transformation of gut pacemaker cells (inters

214 Increased expression of IR-A during neoplastic transformation of hepatocytes could mediate s

215 Here we report that IQGAP1 contributes to neoplastic transformation of human breast epithelial cel

216 tenance mechanism, is equivalent to hTERT in neoplastic transformation of human cells by oncogenes.

217 iral oncogene expression is insufficient for neoplastic transformation of human cells, so human papil

218 origins, and overexpression of Plk1 promotes neoplastic transformation of human cells.

219 ow that targeted disruption of PTEN leads to neoplastic transformation of human neural stem cells (NS

220 thal pathology by 3-months of age, caused by neoplastic transformation of immature T cells in the thy

221 mation drives gene mutations, which leads to neoplastic transformation of intestinal epithelium in th

222 y important in the inhibition of EGF-induced neoplastic transformation of JB6 Cl41 cells.

223 ced or epidermal growth factor (EGF)-induced neoplastic transformation of JB6 Cl41 cells.

224 etradecanoylphorbol-13-acetate (TPA)-induced neoplastic transformation of JB6 P+ cells in a dose-depe

225 Equol dose-dependently inhibited neoplastic transformation of JB6 P+ cells induced by epi

226 etradecanoylphorbol-13-acetate (TPA)-induced neoplastic transformation of JB6 P+ mouse epidermal (JB6

227 etradecanoylphorbol-13-acetate (TPA)-induced neoplastic transformation of JB6 P+ mouse epidermal cell

228 mutations in AIS/MIA/ADC than AAH suggesting neoplastic transformation of lung preneoplasia is predom

229 transcriptional domain is also implicated in neoplastic transformation of mammary epithelium, but res

230 ent may be pathologically reactivated in the neoplastic transformation of mature B cells.

231 metabotropic glutamate receptor 1 (GRM1) in neoplastic transformation of melanocytes in vitro and sp

232 ative role of disruption of cell polarity in neoplastic transformation of neuroepithelial cells.

233 t of PDGFRalpha attenuated Galpha12-mediated neoplastic transformation of NIH 3T3 cells.

234 Galpha(12) stimulates cell proliferation and neoplastic transformation of NIH3T3 cells by attenuating

235 extracellular vesicles (TEVs) results in the neoplastic transformation of nonmalignant human SV-HUC u

236 lso demonstrated that Uro-AR facilitates the neoplastic transformation of normal urothelial cells to

237 ation with other oncogenic elements, induces neoplastic transformation of primary human fibroblasts.

238 Abnormal signaling events may lead to neoplastic transformation of progenitor B cells.

239 active HIF2alpha is not sufficient to cause neoplastic transformation of proximal tubules, arguing a

240 beta-Catenin-dependent neoplastic transformation of RK3E cells was enhanced by

241 the definition of the properties leading to neoplastic transformation of SVZ cells are still elusive

242 Moreover, neoplastic transformation of the antral gastric mucosa d

243 Furthermore, FGF9 could promote neoplastic transformation of the E1A-immortalized RK3E e

244 d tumorigenesis, inducing rapid and complete neoplastic transformation of the entire exocrine pancrea

245 constitutive Wnt activation, which leads to neoplastic transformation of the epithelial hair matrix.

246 -EGF), are sufficient for rapid and complete neoplastic transformation of the exocrine pancreas.

247 ronic Helicobacter pylori infection triggers neoplastic transformation of the gastric mucosa in a sma

248 own until we showed that it induces complete neoplastic transformation of the human breast epithelial

249 of its expression is closely associated with neoplastic transformation of the ovarian surface epithel

250 lated transcription factor ETV1 can initiate neoplastic transformation of the prostate.

251 ectopic MSX2 expression was found to promote neoplastic transformation of the rodent RK3E model epith

252 ne was derived from the spontaneous in vitro neoplastic transformation of the same parent BDE1 cell l

253 to study RA action, without the influence of neoplastic transformation or artificial RAR over-express

254 to study T3 action, without the influence of neoplastic transformation or artificial TR over-expressi

255 t may render astroglial cells susceptible to neoplastic transformation or malignant progression.

256 not all types of colitis seem to have equal neoplastic transformation potential.

257 dings contribute to our understanding of the neoplastic transformation process, with implications for

258 ification of pathogenetic events driving the neoplastic transformation process.

259 isms that impede differentiation and promote neoplastic transformation remain unclear.

260 target genes responsible for Notch1-induced neoplastic transformation remain undefined.

261 y networks whose perturbation contributes to neoplastic transformation remains a fundamental challeng

262 ion and promotion of KS, the mechanism of KS neoplastic transformation remains unclear.

263 Neoplastic transformation requires changes in cellular i

264 Neoplastic transformation requires the elimination of ke

265 lls by staphylococcal superantigens prior to neoplastic transformation, resulting in a relative incre

266 In some cases, the pagetic tissue undergoes neoplastic transformation, resulting in osteosarcoma and

267 These epigenetic events occur before neoplastic transformation, resulting in what may be a ph

268 Neoplastic transformation results in a wide variety of c

269 Neoplastic transformation sensitizes many cells to apopt

270 mic levels as a result of viral infection or neoplastic transformation share significant overlap.

271 e potential contributions of ductal cells to neoplastic transformation, specifically in pancreatic du

272 s of von Hippel-Lindau is not sufficient for neoplastic transformation, suggesting that hypoxia-induc

273 infiltration by 3 weeks of age before overt neoplastic transformation, suggesting that these cellula

274 matrix, and mechanical cues that can promote neoplastic transformation, support tumor growth and inva

275 ncreased synthesis of rRNAs is a hallmark of neoplastic transformation, the ability of PTEN to contro

276 cell-cycle dysregulation is a core event in neoplastic transformation, the role for SOX10 in maintai

277 Upon neoplastic transformation, the role of PDX1 changes from

278 tal subpopulation may still prove capable of neoplastic transformation, these findings refocus attent

279 en renders the thyroid highly susceptible to neoplastic transformation through mechanisms that includ

280 inhibits the dedifferentiation that precedes neoplastic transformation, thus attenuating tumor initia

281 e, network biomarkers predicting the risk of neoplastic transformation to be identified.

282 al factors responsible for driving steatotic-neoplastic transformation to frank carcinoma, through ge

283 arcinoma (HCC) and are highly susceptible to neoplastic transformation triggered by activation of Erb

284 ular senescence has been theorized to oppose neoplastic transformation triggered by activation of onc

285 e-induced cell proliferation cannot initiate neoplastic transformation unless cellular programs that

286 Malignant neoplastic transformation was achieved after infection o

287 t, toxicity was determined by MTT assay, and neoplastic transformation was assessed by measuring colo

288 n the early stages of Kras-driven pancreatic neoplastic transformation was associated with decreased

289 -10F cell line on the in vitro expression of neoplastic transformation was evaluated.

290 range physio-pathological conditions beside neoplastic transformation, we expect that the ERalpha os

291 ithelial cells (HMEC) at different stages of neoplastic transformation, we found that OSM signaling s

292 To determine how HMGA1 leads to neoplastic transformation, we looked for genes regulated

293 ctional role of AMF/PGI on cell motility and neoplastic transformation, we stably transfected AMF/PGI

294 rmine the cellular origins and mechanisms of neoplastic transformation, we studied highly fractionate

295 he promotion-sensitive JB6 P+ cells initiate neoplastic transformation, whereas the promotion-resista

296 ed regulation of ion channels is part of the neoplastic transformation, which suggests that ion chann

297 ng pathway contributes to the suppression of neoplastic transformation, while leading to compromised

298 , Hif1alpha, and p21(waf1/cip1)) involved in neoplastic transformation, whose altered expression corr

299 We compared 16 patients who had GHPs showing neoplastic transformation with 39 patients who had non-n

300 se developmental abnormalities evolve toward neoplastic transformation with complete penetrance.