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

1 to the epigenetic plasticity that underlies malignant transformation.

2 isseminata with a few of the lesions showing malignant transformation.

3 cesses, such as transcription, to facilitate malignant transformation.

4 otype, and level of ss-catenin activation in malignant transformation.

5 nt in HGPIN, rendering it a new biomarker of malignant transformation.

6 ent roles in regulating epigenetic state and malignant transformation.

7 sion is induced in human chondrocytes during malignant transformation.

8 genetic changes leading to tumorigenesis or malignant transformation.

9 the genetic changes that enable and promote malignant transformation.

10 Epithelial cells are major sites of malignant transformation.

11 mbryonic development, tissue homeostasis and malignant transformation.

12 ssively increases proliferation and leads to malignant transformation.

13 nduces resistance to apoptosis, and promotes malignant transformation.

14 increased cellular proliferation and induced malignant transformation.

15 xpression of the protease suffices to induce malignant transformation.

16 eristic of a metabolic shift observed during malignant transformation.

17 ctivity constitutes a robust barrier against malignant transformation.

18 pports colon epithelial tumour expansion and malignant transformation.

19 ectional imaging should raise a suspicion of malignant transformation.

20 a central role for ETV6 in hematopoiesis and malignant transformation.

21 of Gclm prevents a tumor's ability to drive malignant transformation.

22 causes the cell cycle to go awry, leading to malignant transformation.

23 s principally by influencing early events in malignant transformation.

24 actor in age-related tissue degeneration and malignant transformation.

25 oncogenic metabolites that may contribute to malignant transformation.

26 ripheral blood cytopenias, and potential for malignant transformation.

27 to epithelial-to-mesenchymal transition and malignant transformation.

28 ender carriers susceptible to DNA damage and malignant transformation.

29 nt to induce many features characteristic of malignant transformation.

30 PD, and, with persistent stress, can undergo malignant transformation.

31 of the cytoskeleton, can promote features of malignant transformation.

32 of TRIP13 in non-malignant cells results in malignant transformation.

33 , implicating it as having a central role in malignant transformation.

34 lity, and this contributes to suppression of malignant transformation.

35 viewed as a passive response required for a malignant transformation.

36 s are present in a subset of AA, and predict malignant transformation.

37 risk factors, histopathology, bleeding, and malignant transformation.

38 ubtypes of IPMNs display a relevant risk for malignant transformation.

39 by a long period of dormancy, and then final malignant transformation.

40 enetic events that predispose blood cells to malignant transformation.

41 the pancreas with respect to risk factors of malignant transformation.

42 inoma tissues, supporting a role for CHKA in malignant transformation.

43 ntributes to mitochondrial reprogramming and malignant transformation.

44 to acquire additional mutations required for malignant transformation.

45 s, resulting in organ failure and leading to malignant transformation.

46 ome system (UPS) promotes carcinogenesis and malignant transformation.

47 normal host defense against infection and/or malignant transformation.

48 endent effects of estrogen in the process of malignant transformation.

49 tic biomarkers or candidate causal genes for malignant transformation.

50 tion can sometimes cause chronic disease and malignant transformation.

51 an RNA-mediated regulatory event could drive malignant transformation.

52 iomyomatosis peritonealis disseminata with a malignant transformation.

53 further insight into how these cells undergo malignant transformation.

54 rative responses, paradoxically resulting in malignant transformation.

55 ression of aromatase in MCF-10A cells causes malignant transformation.

56 tes epithelial-to-mesenchymal transition and malignant transformation.

57 iral infection correlated with the extent of malignant transformation.

58 T lymphocytes with NPM-ALK results in their malignant transformation.

59 for normal T cell development while limiting malignant transformation.

60 ng the intricate perturbations that underlie malignant transformation.

61 f lineage stage-dependent genetic changes to malignant transformation.

62 t, homeostasis, activation, and occasionally malignant transformation.

63 rant DNA methylation patterns that can drive malignant transformation.

64 s, which together increase the potential for malignant transformation.

65 ecific pathways develop early or late during malignant transformation.

66 ng cascade is a common critical event during malignant transformation.

67 ammation and when dysregulated contribute to malignant transformation.

68 by mutant BRAF or NRAS is a primary cause of malignant transformation.

69 both selection and active regulation during malignant transformation.

70 maintains genomic integrity, and suppresses malignant transformation.

71 itical role in the innate immune response to malignant transformation.

72 d deletions, can be causal events leading to malignant transformation.

73 h alterations in the presentation of risk of malignant transformation.

74 ular ATP to levels that are insufficient for malignant transformation.

75 nk during normal hepatocyte regeneration and malignant transformation.

76 rolonged wound-healing program that promotes malignant transformation.

77 iver disease processes, thereby facilitating malignant transformation.

78 ients showed (18)F-FET uptake at the time of malignant transformation.

79 HCA), particularly associated with a risk of malignant transformation.

80 ver cell proliferation, differentiation, and malignant transformation.

81 slation of specific mRNAs and participate in malignant transformation.

82 nd S45 allele duplication is associated with malignant transformation.

83 eukemic Pre-Meg/E progenitors predisposed to malignant transformation.

84 dromes are linked with genetic disorders and malignant transformation.

85 e bone marrow niche may be key regulators of malignant transformation.

86 s, as well as systemic isotonicity, prevents malignant transformation.

87 rate of aerobic glycolysis is a hallmark of malignant transformation.

88 atal iNKT cells that ultimately led to their malignant transformation.

89 concerning the detection of progression and malignant transformation.

90 ng the need to detect the earliest stages of malignant transformation.

91 ope with centrosomal defects acquired during malignant transformation.

92 enewal, promote differentiation, and prevent malignant transformation.

93 ax was significantly higher in patients with malignant transformation (11/20) than in those without m

94 cells with a gain-of-function that leads to malignant transformation, a function independent of any

95 s of such adhesions has been associated with malignant transformation, a process most often accompani

96 expressed focal adhesion plaque proteins and malignant transformation across multiple types of solid

97 te efforts to identify predictive markers of malignant transformation, alterations driving this progr

98 Our results suggest that malignant transformation alters the pathways through whi

99 all three paralogs can be re-expressed upon malignant transformation and are found in a broad range

100 nd sonic hedgehog activation associated with malignant transformation and bleeding, respectively.

101 ulation of NFAT signaling is associated with malignant transformation and cancer development and prog

102 fferentiation is a fundamental early step in malignant transformation and cancer initiation.

103 lastic characteristics of cells occur during malignant transformation and cancer progression.

104 nd Eed heterozygous mice were susceptible to malignant transformation and developed leukemia in coope

105 g previous observations on its importance in malignant transformation and development of drug resista

106 -associated pathways that occur early during malignant transformation and enable the recognition and

107 B complex, in the early stages of pancreatic malignant transformation and in established PDAC.

108 neous DSB repair and are crucial culprits in malignant transformation and IR-induced cell lethality.

109 Chronic inflammation often precedes malignant transformation and later drives tumor progress

110 ormal breast luminal cells can contribute to malignant transformation and lead to progression of ER+

111 auses human bronchial epithelial cell (HBEC) malignant transformation and lung cancer.

112 umor aggressiveness and widely implicated in malignant transformation and metastasis, is a hallmark o

113 eased sialylation, have been associated with malignant transformation and metastasis.

114 vironment (TME) contributes significantly to malignant transformation and pathogenesis.

115 ansferase blocked T cell progenitor renewal, malignant transformation and peripheral T cell clonal ex

116 Despite a causative role during malignant transformation and progression in hepatocarcin

117 investigation into the cellular mechanics of malignant transformation and progression.

118 the virus escapes immune elimination during malignant transformation and progression.

119 opment, reprogramming normal adult cells and malignant transformation and progression.

120 of EBV in diverting the functions of MYC in malignant transformation and provide a rationale for tar

121 , naked mole-rat cells become susceptible to malignant transformation and readily form tumours in mic

122 melanomas, they are not sufficient to drive malignant transformation and require additional events.

123 is could be helpful in evaluating tumors for malignant transformation and response to treatment.

124 rring in adults, because they rarely undergo malignant transformation and show excellent overall surv

125 ant for sustained tumor growth but preceding malignant transformation and that additional oncogenic e

126 onsible for this differing susceptibility to malignant transformation and that loss of p53 can overco

127 reates an environment that is permissive for malignant transformation and the development of AML.

128 SATB2 induced malignant transformation and these transformed cells gai

129 in a constitutively activated state to drive malignant transformation and tumor growth.

130 he signals of RAS and that drive and sustain malignant transformation and tumor growth.

131 ess induces focal adhesion assembly to drive malignant transformation and tumor metastasis.

132 Malignant transformation and tumor progression to metast

133 wever, JNKs have also been implicated in the malignant transformation and tumorigenesis of cells.

134 Telomere dysfunction is a crucial event in malignant transformation and tumorigenesis.

135 ure experiments; its loss is associated with malignant transformation and tumorigenesis.

136 cells markedly inhibited the arsenic induced malignant transformation and tumorigenesis.

137 ith choroidal nevi carry a moderate risk for malignant transformation and visual loss.

138 itiation, premalignant clonal expansion, and malignant transformation, and even some limited informat

139 ytic proteins have long been associated with malignant transformation, and genes encoding membrane tr

140 nization, molecular heterogeneity, time from malignant transformation, and rate of mutation and apopt

141 he Lin28/let-7 axis is a critical barrier to malignant transformation, and they also suggest new stra

142 Numerous metabolic changes are required for malignant transformation, and they render malignant cell

143 Oncogenic KRAS contributes to malignant transformation, antiapoptosis, and metastasis

144 tion of gene expression and understanding of malignant transformation are discussed.

145 Metabolic rearrangements subsequent to malignant transformation are not well characterized in e

146 d progresses, but the miRNAs involved during malignant transformation are unknown.

147 l of miR-155 expression is required to avoid malignant transformation, as evidenced by miR-155 overex

148 sm to prevent oncogene-expressing cells from malignant transformation, as high ITK-Syk oncogene activ

149 nchorage-independent growth, a criterion for malignant transformation, as well as tumorigenicity in m

150 neoplasia (PanIN) formation, which precedes malignant transformation, associates with the expression

151 ne of the tumors were considered at risk for malignant transformation at the time; for example, there

152 This process is tightly connected to malignant transformation because B-lineage acute lymphob

153 B cells are particularly prone to malignant transformation because the machinery used for

154 ing from genetically induced astrogliosis or malignant transformation, both of which render the inhib

155 s numerous biological pathways implicated in malignant transformation, but the contribution of mutant

156 nitor cell population expansion can initiate malignant transformation by enabling cells to evade DNA

157 Malignant transformation by oncogenes requires additiona

158 ology-why are some cells more susceptible to malignant transformation by particular genetic lesions a

159 Stat3 activation and signaling contribute to malignant transformation by promoting cell cycle progres

160 In particular, malignant transformation by Ras oncogenes exploits mitoc

161 chanism whereby oncogenic signaling promotes malignant transformation by regulating transcription of

162 s or loss of tumour suppressor genes opposes malignant transformation by triggering a stable arrest i

163 The p53 tumor suppressor can restrict malignant transformation by triggering cell-autonomous p

164 We previously reported that malignant transformation changes the assortment of relea

165 omatin loops, and use it to demonstrate that malignant transformation compromises the DNA-nuclear mat

166 ropose an additional generalized hallmark of malignant transformation corresponding to the differenti

167 a senescent-like state, but with occasional malignant transformation events.

168 ing Clara cells have the ability to initiate malignant transformation following the introduction of t

169 001), resulting in a high detection rate for malignant transformation (for TBRmax > 2.46: sensitivity

170 ior to dynamic analysis for the detection of malignant transformation (for TTPmin </= 17.5 min: sensi

171 Malignant transformation from hepatocellular adenoma to

172 We examine this malignant transformation from the perspective of the com

173 ind that under conditions of stress, such as malignant transformation fuelled by MYC, the chaperome b

174 After the malignant transformation has been accomplished and auton

175 FINDINGS: Multiple predictive markers of OPL malignant transformation have been identified in retrosp

176 ral human malignancies that directly lead to malignant transformation, have not been identified in CL

177 disrupted lncRNA function can contribute to malignant transformation, highlighting opportunities for

178 tivate MAPK signaling and are sufficient for malignant transformation; however, here we characterized

179 ty alteration of nuclear architecture during malignant transformation in animal models of colon carci

180 ostulated to promote genomic instability and malignant transformation in B cells.

181 s that cyclin E1 dysregulation acts to drive malignant transformation in fallopian tube secretory cel

182 Here, we modeled malignant transformation in human bronchial epithelial c

183 locking hyperactivated STAT3 and suppressing malignant transformation in human cancer cells that depe

184 asis of the intestinal epithelium and during malignant transformation in human cells and mice.

185 preexisting immunity and ICPs on the risk of malignant transformation in human preneoplasia has not b

186 n increased TGFbeta bioactivity and promoted malignant transformation in immunodeficient mice.

187 tion of DPPIV is known to be associated with malignant transformation in melanocytes, SPRIGHTLY-media

188 t splenic ECs are involved in the process of malignant transformation in MF.

189 malian homologs of lin-28, are implicated in malignant transformation in part because of their abilit

190 on, we show that Salmonella enterica induces malignant transformation in predisposed mice, murine gal

191 that DAXX overexpression is associated with malignant transformation in several human cancers, inclu

192 ause its inappropriate up-regulation induces malignant transformation in solid and hematopoietic canc

193 ), short TTPmin was associated with an early malignant transformation in the further disease course.

194 that is thought to be the primary target of malignant transformation in virus-driven lymphomagenesis

195 atoma cells decreased cell proliferation and malignant transformation in vitro and in vivo.

196 ransfer of WT LGL cultured with IL-15 led to malignant transformation in vivo.

197 earrangements confer phenotypic hallmarks of malignant transformation, including unrestricted prolife

198 Considering that malignant transformation involves cellular metabolic cha

199 stration of the molecular changes underlying malignant transformation is a relevant model to study th

200 and tumour-derived cells that progression to malignant transformation is associated with increase in

201 gs demonstrate that in Slp65-deficient mice, malignant transformation is largely limited to particula

202 the molecular mechanism by which they induce malignant transformation is not well understood.

203 Malignant transformation is often accompanied by signifi

204 development, yet the role of this process in malignant transformation is undefined.

205 nclude infection, pneumothorax, bleeding and malignant transformation, justify surgery.

206 chanistic explanation for the aneuploidy and malignant transformation known to occur after disruption

207 that susceptibility of transitional zones to malignant transformation may be explained by the presenc

208 cosystems whose different vulnerabilities to malignant transformation may be partially explained by h

209 ons, including solid tumors; it is linked to malignant transformation, metastatic progression, and tr

210 Hence, (18)F-FET uptake indicating malignant transformation might influence the patient man

211 lly, mutated KRAS is a documented driver for malignant transformation, occurring early during the pat

212 f genetic alterations that contribute to the malignant transformation of a B cell into a DLBCL is hel

213 and differentiation, play a central role in malignant transformation of B cells.

214 ) is a devastating liver tumour arising from malignant transformation of bile duct epithelial cells.

215 rity of previous reports have focused on the malignant transformation of CBM described in only 1 pati

216 stream the effects of mutant IDH, leading to malignant transformation of cells.

217 s oncogenic because of its ability to induce malignant transformation of cells.

218 ding P53, MDM2, and AKT, that may govern the malignant transformation of colon epithelial cells in a

219 molecular mechanisms by which SATB2 induced malignant transformation of colorectal epithelial cells.

220 hile restraining LEF-1 expression to prevent malignant transformation of developing thymocytes.

221 -terminal kinase (JNK) plays a vital role in malignant transformation of different cancers, and JNK i

222 F-kappaB signalling additionally facilitates malignant transformation of differentiated cells.

223 catastrophes have a significant role in the malignant transformation of EAC.

224 subpopulation that can specifically restrict malignant transformation of EBV-infected B cells.

225 S) cells, but the genetic drivers underlying malignant transformation of ECs are unknown.

226 erstanding the mechanisms that might lead to malignant transformation of endometriosis so as to help

227 rsification while simultaneously attenuating malignant transformation of GC B cells.

228 ntly hijacked by cancers that arise from the malignant transformation of germinal center (GC) B cells

229 growth factor (EGF) plays a critical role in malignant transformation of hepatocytes and tumor progre

230 BID suppresses p38 activity and facilitates malignant transformation of hepatocytes.

231 d HIF-1alpha protein translation, as well as malignant transformation of human bronchial epithelial c

232 anslation upregulation, in turn resulting in malignant transformation of human bronchial epithelial c

233 ereby relieving YAP inhibition and promoting malignant transformation of human mammary epithelial cel

234 Studying mechanisms of malignant transformation of human pre-B cells, we found

235 The malignant transformation of human prostatic epithelium i

236 PC biosynthetic capacity that contributes to malignant transformation of intestinal epithelial cells

237 vide evidence that the improved survival and malignant transformation of LMP1/CD40-expressing B cells

238 Malignant transformation of LPD is an extremely rare occ

239 ssive hematological tumor resulting from the malignant transformation of lymphoid progenitors.

240 ctivity drives several pathways that support malignant transformation of lymphoma cells.

241 ass) is a critical rate-limiting step in the malignant transformation of mammalian somatic cells.

242 identified regulatory loop that may underlie malignant transformation of mammary cells.

243 impairs luminal gene expression and promotes malignant transformation of mammary tumors.

244 basis for a detailed functional analysis of malignant transformation of mature T cells and improved

245 on of the signalling pathways sufficient for malignant transformation of mouse fibroblasts fails to t

246 ole of oncogenic ROS1 fusion proteins in the malignant transformation of multiple cancers, including

247 tiple prosurvival BCL2 family genes promotes malignant transformation of myeloid progenitors into BC

248 However, the factors underlying the malignant transformation of plasmocytes in MM are not fu

249 S223 phosphorylation abrogates PAK1-mediated malignant transformation of prostate epithelial cells.

250 cell morphology and motility and to promote malignant transformation of prostate epithelial cells.

251 us T cell lymphoma (CTCL) resulting from the malignant transformation of skin-homing central memory C

252 mmation from indolent infections, leading to malignant transformation of T cells that are anaplastic

253 escribe how sympathetic neuropathy can drive malignant transformation of the hematopoietic stem cell

254 t T-cell receptor engagement is critical for malignant transformation of the T lymphocytes and that p

255 The stiffened collagenous stroma fosters malignant transformation of the tissue by increasing tum

256 hat Wnt pathway activation is sufficient for malignant transformation of these unique liver progenito

257 Malignant transformation of tissue stem cells (SC) may b

258 mal transition (EMT), a critical process for malignant transformation of tumor, via the transactivati

259 Overall, 18 of 31 patients experienced malignant transformation; of these, 16 of 17 (94%) evalu

260 iated carbohydrate antigens (TACA) caused by malignant transformation offers promising targets to dev

261 but it is not clear whether they result from malignant transformation or have a causative role.

262 e of epithelial cells at different stages of malignant transformation, our study reveals how pro-apop

263 horter progression-free survival and time to malignant transformation (P < 0.001).

264 detection rate of both tumor progression and malignant transformation, partly before further signs of

265 ears to be an acquired trait associated with malignant transformation, potentially allowing the use o

266 During the malignant transformation process we observed that 4-OH-E

267 tly up-regulated during the 4-OH-E2-mediated malignant transformation process.

268 cinoma (HCC) tumors that participates in the malignant transformation process.

269 hock, accumulation of misfolded proteins, or malignant transformation promotes the activation and nuc

270 data support a key role for primary cilia in malignant transformation, provide a plausible mechanism

271 omas, the key molecular pathways involved in malignant transformation remain to be determined, as doe

272 ssic model of tumor suppression implies that malignant transformation requires full "two-hit" inactiv

273 s began to expand in neonatal mice and, upon malignant transformation, resulted in mortality between

274 nescence (OIS) is thought to be a barrier to malignant transformation resulting from the strong activ

275 Malignant transformation results in increased levels of

276 ODC-overexpressing prostate cells underwent malignant transformation, revealing that ODC is sufficie

277 al analog RKI-11 is effective at suppressing malignant transformation suggests that inhibition of ROC

278 es on a very different mechanism to suppress malignant transformation than it does to modulate normal

279 he tissues did not significantly change upon malignant transformation, the relative proportion of NK

280 ha5beta1 integrin promotes tension-dependent malignant transformation through engagement of the syner

281 Its expression fosters malignant transformation through the mitigation of criti

282 c and extranodal tissues, eventually driving malignant transformation through triggering NF-kappaB an

283 d that preventing apoptosis would accelerate malignant transformation to acute myeloid leukemia (AML)

284 It is often overcome in malignant transformation to confer a survival advantage.

285 y of these genes are down-regulated, linking malignant transformation to dedifferentiation.

286 to-medium congenital nevi have a low risk of malignant transformation, total excision may not be nece

287 w Orai-STIM-controlled Ca(2+) signals affect malignant transformation, tumour growth and invasion is

288 free survival, overall survival, and time to malignant transformation was investigated.

289 lear localization of beta-catenin, a sign of malignant transformation, was found only in HCC and HB.

290 o understand more about the roles of Ebf1 in malignant transformation, we investigated the impact of

291 r active NF-kappaB inherently contributes to malignant transformation, we isolated a set of NF-kappaB

292 lncRNA transcription can provide signals of malignant transformation, we now understand that lncRNAs

293 ontribute to changes in cell fate, including malignant transformation, we performed genome-wide mappi

294 To address the role of TrkB signaling in malignant transformation, we removed two immunoglobulin-

295 No adverse effects or malignant transformations were seen.

296 ased cell differentiation and also decreased malignant transformation when transfected with the oncog

297 the ovary and which can subsequently undergo malignant transformation, whereas many type II carcinoma

298 tal development, with features suggestive of malignant transformation, whereas overexpression of SIM2

299 mas are common NF1 tumors carrying a risk of malignant transformation, which is typically fatal.

300 bidity of pancreatectomy against the risk of malignant transformation while under continuous surveill