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

1 ecular switch between normal development and malignant transformation.

2 ance, has been associated with cholangiocyte malignant transformation.

3 to the epigenetic plasticity that underlies malignant transformation.

4 iver disease processes, thereby facilitating malignant transformation.

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

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

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

8 oncogenic metabolites that may contribute to malignant transformation.

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

10 d as a B cell receptor (BCR) mimic promoting malignant transformation.

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

12 iomyomatosis peritonealis disseminata with a malignant transformation.

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

14 ically activated, the PI3K pathway can drive malignant transformation.

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

16 both selection and active regulation during malignant transformation.

17 maintains genomic integrity, and suppresses malignant transformation.

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

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

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

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

22 nk during normal hepatocyte regeneration and malignant transformation.

23 rolonged wound-healing program that promotes malignant transformation.

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

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

26 ver cell proliferation, differentiation, and malignant transformation.

27 slation of specific mRNAs and participate in malignant transformation.

28 nd S45 allele duplication is associated with malignant transformation.

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

30 dromes are linked with genetic disorders and malignant transformation.

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

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

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

34 concerning the detection of progression and malignant transformation.

35 w many somatic mutations (sM) must occur for malignant transformation.

36 s through VEGFA to promote oligodendroglioma malignant transformation.

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

38 ope with centrosomal defects acquired during malignant transformation.

39 enewal, promote differentiation, and prevent malignant transformation.

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

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

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

43 ent roles in regulating epigenetic state and malignant transformation.

44 sion is induced in human chondrocytes during malignant transformation.

45 genetic changes leading to tumorigenesis or malignant transformation.

46 the genetic changes that enable and promote malignant transformation.

47 Epithelial cells are major sites of malignant transformation.

48 mbryonic development, tissue homeostasis and malignant transformation.

49 ssively increases proliferation and leads to malignant transformation.

50 nduces resistance to apoptosis, and promotes malignant transformation.

51 c studies of distal TE susceptibility to the malignant transformation.

52 increased cellular proliferation and induced malignant transformation.

53 xpression of the protease suffices to induce malignant transformation.

54 eristic of a metabolic shift observed during malignant transformation.

55 ctivity constitutes a robust barrier against malignant transformation.

56 pports colon epithelial tumour expansion and malignant transformation.

57 ectional imaging should raise a suspicion of malignant transformation.

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

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

60 monstrating that metastasis can occur before malignant transformation.

61 s principally by influencing early events in malignant transformation.

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

63 ripheral blood cytopenias, and potential for malignant transformation.

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

65 ender carriers susceptible to DNA damage and malignant transformation.

66 nt to induce many features characteristic of malignant transformation.

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

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

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

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

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

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

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

74 esis to promote oligodendroglioma growth and malignant transformation.

75 elta activity in B and T cells that leads to malignant transformation.

76 Disruption of these pathways can result in malignant transformation.

77 atic dissemination is not contingent on full malignant transformation.

78 zes and reactivates p53 and thereby inhibits malignant transformation.

79 t drive normal stem cell differentiation and malignant transformation.

80 of de novo infection may reduce the risk of malignant transformation.

81 ard a stem-like state susceptible to further malignant transformation.

82 Growing DNA damage accompanied this malignant transformation.

83 ells in the bone marrow niche that regulates malignant transformation.

84 ecur after treatment and an elevated rate of malignant transformation.

85 esis to promote oligodendroglioma growth and malignant transformation.

86 erexpression and may represent a hallmark of malignant transformation.

87 le was employed as a validated biomarker for malignant transformation.

88 s, successful tissue repair, and in opposing malignant transformation.

89 ng complexes and amplify PI3K signalling for malignant transformation.

90 with the genomic rearrangements that support malignant transformation.

91 ours treated with the technique, the risk of malignant transformation.

92 cellular cues that promote cell survival and malignant transformation.

93 the viral latent reservoir and the target of malignant transformation.

94 NPM-ALK results in their immortalization and malignant transformation.

95 ressed in the OSE, but it is turned on after malignant transformation.

96 matopoietic stem cell integrity and prevents malignant transformation.

97 sion to chronic liver disease and subsequent malignant transformation.

98 ance, has been associated with cholangiocyte malignant transformation.

99 ort, dysfunctional telomeres, and preventing malignant transformation.

100 promotes oncogenic NRAS-mediated melanocyte malignant transformation.

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

102 In 3 patients, MGUS underwent malignant transformation 24 to 144 months after diagnosi

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

104 00 000 patient-years (95% CI 1.15-22.71) for malignant transformation and 2.26 per 100 000 patient-ye

105 ls, reflecting rapid drift after the initial malignant transformation and a greater proliferative his

106 weat gland differentiation and potential for malignant transformation and aggressive behaviour.

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

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

109 ccur in epithelial stem cells, contribute to malignant transformation and cancer development(1-3).

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

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

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

113 uum of its development, inextricably linking malignant transformation and disease progression with in

114 The subversion of endocytic routes leads to malignant transformation and has been implicated in huma

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

116 ular alterations occurring during urothelial malignant transformation and indicates TAZ as a possible

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

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

119 sis during which HCC precursor cells undergo malignant transformation and lead to cancer initiation.

120 vely blocks oncogenic NRAS-driven melanocyte malignant transformation and melanoma growth in vitro an

121 tudies elucidating the relationships between malignant transformation and metastasis and cellular adh

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

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

124 asis, and their disruption can contribute to malignant transformation and metastasis.

125 benign tumours were diagnosed with suspected malignant transformation and one (0.0002%) of 4905 patie

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

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

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

129 Malignant transformation and progression of cancer are d

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

131 namic m(6)A modification in chemical-induced malignant transformation and provide insight into critic

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

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

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

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

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

137 SATB2 induced malignant transformation and these transformed cells gai

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

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

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

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

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

143 s to direct signalling that is essential for malignant transformation and tumour maintenance.

144 f the tumour microenvironment, can result in malignant transformation and tumour progression.

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

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

147 gnals are observed during tumor progression, malignant transformation, and metastasis.

148 ighting the complex clonal dynamics prior to malignant transformation, and providing opportunities fo

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

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

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

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

153 mor initiation, factors contributing to this malignant transformation are poorly known.

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

155 ocumented growth itself, is pathognomonic of malignant transformation as defined by class 2 gene expr

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

157 ctor 2 (FGF2) from adipose tissue stimulates malignant transformation, as measured by growth in soft

158 D genome governs immune cell development and malignant transformation, as well as how underlying (epi

159 However, mechanisms for preferential malignant transformation at the junction areas remain in

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

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

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

163 tein interaction networks are at the core of malignant transformation but have yet to be translated i

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

165 Thus, EZH2 mutation fosters malignant transformation by epigenetically reprograming

166 ugh exposure to environmental carcinogens or malignant transformation by human papillomavirus (HPV).

167 as a previously unrecognized requirement of malignant transformation by oncogenic MLL fusions and id

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

169 In particular, malignant transformation by Ras oncogenes exploits mitoc

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

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

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

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

174 2 included 30 patients with PL who developed malignant transformation during follow-up.

175 nter B cells are thought to be the target of malignant transformation during gammaherpesvirus-driven

176 ir anagen onset are hijacked to promote McSC malignant transformation during melanoma induction.

177 Malignant transformation entails important changes in th

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

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

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

181 Malignant transformation from hepatocellular adenoma to

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

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

184 The ability of CysLTR2-L129Q to cause malignant transformation has been hypothesized to result

185 eukemia (AML); however, the cells leading to malignant transformation have not been directly elucidat

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

187 enomic instability (GI) predisposes cells to malignant transformation, however the molecular mechanis

188 ly to ward off pathogens but also to prevent malignant transformation ("immune surveillance").

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

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

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

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

193 uggest that ATAD2 overexpression may enhance malignant transformation in humans by misregulating cent

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

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

196 YAP1-MAMLD1 fusions are sufficient to drive malignant transformation in mice, and the resulting tumo

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

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

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

200 icrobes and immune and epithelial cells; and malignant transformation in the intestine and liver.

201 cell phenotype, triggering events related to malignant transformation in these cells, and can thus be

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

203 g (APC mutation) alters BA profiles to drive malignant transformations in Lgr5-expressing (Lgr5(+)) c

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

205 accompanied by decreasing susceptibility to malignant transformation, indicating a glioblastoma cell

206 Considering that malignant transformation involves cellular metabolic cha

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

208 ineage identity and differentiation state to malignant transformation is controversial.

209 Malignant transformation is often accompanied by signifi

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

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

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

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

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

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

216 ssociated intracranial malignancy, including malignant transformation of a benign lesion or developme

217 k of an intracranial secondary malignancy or malignant transformation of a benign tumour in patients

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

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

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

221 s may contribute to pro-tumor events such as malignant transformation of cells adjacent to the tumor

222 Malignant transformation of cells depends on accumulatio

223 Malignant transformation of cells typically involves sev

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

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

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

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

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

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

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

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

232 from pancreatic cancer cells could initiate malignant transformation of healthy cells.

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

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

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

236 e genes (ORP3, GJB3, and RXFP1) enhances the malignant transformation of human fibroblasts in culture

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

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

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

240 Malignant transformation of LPD is an extremely rare occ

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

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

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

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

245 We propose that TEVs promote malignant transformation of predisposed cells by inhibit

246 These data reveal a dual mechanism governing malignant transformation of progenitors that is predicat

247 sue-specific Wnt activator that promotes the malignant transformation of prostate cancer.

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

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

250 ng plays a pivotal role during infection and malignant transformation of the gastric epithelium.

251 in and delineating an unforeseen pathway for malignant transformation of the immune system.

252 Mesothelioma is caused by malignant transformation of the mesothelium, is incurabl

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

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

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

256 ffect with chemical carcinogens in promoting malignant transformation of uroepithelial cells and blad

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

258 ation, yet can potentially be reactivated by malignant transformation or epigenetic therapies.

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

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

261 SC depletion and dysfunction and the risk of malignant transformation over time.

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

263 Considering the potential for malignant transformation, periodical surveillance imagin

264 ppressor and show that mutations in H1 drive malignant transformation primarily through three-dimensi

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

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

267 clonal hematopoiesis is not deterministic of malignant transformation, rational surveillance strategi

268 determining an individual patient's risk of malignant transformation remain poorly defined.

269 -order folding of chromatin structure during malignant transformation remains largely unknown.

270 ng of how FGFR3 activation drives urothelial malignant transformation remains limited.

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

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

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

274 Malignant transformation results in increased levels of

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

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

277 and exhibited a significantly higher rate of malignant transformation than mTert (+/+) cells.

278 ular elimination may have increased risk for malignant transformation that is due to subversion of tu

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 ong infection is thought to also precipitate malignant transformation, through a mechanism that remai

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

285 of B cells is important to fully understand malignant transformation to MCL.

286 pact essentially all progressive steps, from malignant transformation to metastases formation.

287 ulated WNT signaling has been shown to favor malignant transformation, tumor progression, and resista

288 Malignant transformations, tumor progression, the onset

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

290 of the benign nodules was 98.6%, although no malignant transformation was observed.

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

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

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

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

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

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

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

298 ristic in early carcinogenesis to facilitate malignant transformation, which may improve cancer diagn

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

300 ogenesis, sEV treatment induced hallmarks of malignant transformation, with deregulated cell death an