ライフサイエンスコーパス: genomic instability

1 e ability to suppress R loops and associated genomic instability.

2 ontribution to defective DNA methylation and genomic instability.

3 d reveal how defects in completion result in genomic instability.

4 re and RUNX3 loss exhibited higher levels of genomic instability.

5 priate DNA repair processes that can lead to genomic instability.

6 plication and transcription, and may lead to genomic instability.

7 tion and suppresses transcription-associated genomic instability.

8 trade-off between the costs and benefits of genomic instability.

9 plication, repair and recombination to avoid genomic instability.

10 atus can cause replication fork collapse and genomic instability.

11 achineries represent a significant source of genomic instability.

12 suppressor p73, have also been implicated in genomic instability.

13 and repair interact functionally to prevent genomic instability.

14 e telomeres can eliminate B cells at risk of genomic instability.

15 and progression, resulting in DNA damage and genomic instability.

16 eletion elicits dramatic hypomethylation and genomic instability.

17 ng agent mitomycin C, and karyotypes feature genomic instability.

18 mulation of DNA strand breaks and results in genomic instability.

19 roperly repaired can result in cell death or genomic instability.

20 nd breaks during replication thus triggering genomic instability.

21 likely tumor evolution, rather than ongoing genomic instability.

22 promotes cell proliferation, metabolism, and genomic instability.

23 ssive single-stranded DNA that could lead to genomic instability.

24 intermediates, they are also associated with genomic instability.

25 DNA replication stress is a source of genomic instability.

26 ed in regulating gene expression and causing genomic instability.

27 s it can lead to insertional mutagenesis and genomic instability.

28 the role of complex genomic architecture in genomic instability.

29 owever, cohesin mutant leukemias do not show genomic instability.

30 e at work in stem cells to protect them from genomic instability.

31 ogen-activated protein kinase signalling and genomic instability.

32 NA damaging agents, defective DNA repair and genomic instability.

33 r, and that SPOP mutation is associated with genomic instability.

34 hat manifests with endocrine dysfunction and genomic instability.

35 which goes along with development of severe genomic instability.

36 toxins cause DNA damage, which can result in genomic instability.

37 ncoding RNAs (ncRNAs) that in turn triggered genomic instability.

38 ion of the immunoglobulin genes and to avoid genomic instability.

39 rnate DNA structures that can be a source of genomic instability.

40 onds to stalled replication forks to prevent genomic instability.

41 ivo as Apc is lost earlier than the onset of genomic instability.

42 ormation of multi-polar mitotic spindles and genomic instability.

43 nd joining (NHEJ) repair systems, leading to genomic instability.

44 the H9 human embryonic stem cell line, and a genomic instability.

45 stically show a high level of aneuploidy and genomic instability.

46 antigen, slowed cell division, and increased genomic instability.

47 tionality leads to reduced cell survival and genomic instability.

48 oxidative stress, chromatin remodeling, and genomic instability.

49 and hypermutation, which are all sources of genomic instability.

50 is and that aneuploidy itself is a nidus for genomic instability.

51 NA (ssDNA), has emerged as a major source of genomic instability.

52 nown to hamper optimal HR and trigger global genomic instability.

53 ave been identified as endogenous sources of genomic instability.

54 esions intensifies, progressively leading to genomic instability.

55 or over fragile sites, regions of increased genomic instability.

56 the versatile role of RPA in suppression of genomic instability.

57 pairing with the template, which can lead to genomic instability.

58 fic transcriptional signature, and increased genomic instability.

59 ta-dependent tumor progression by preventing genomic instability.

60 gical, constituting in this case a source of genomic instability.

61 '-flap specificity and catalysis, preventing genomic instability.

62 enome replication is a significant source of genomic instability.

63 urodegeneration is driven at least partly by genomic instability.

64 ly been considered to reflect cancer somatic genomic instabilities.

65 ) be genotoxic; 3) alter DNA repair or cause genomic instability; 4) induce epigenetic alterations; 5

66 sk for cancer, since short telomeres lead to genomic instability - a hallmark of cancer.

67 most destructive chromosomal lesions driving genomic instability, a core hallmark of cancer.

68 Genomic instability, a major hallmark of cancer cells, i

69 l health; regulatory failure correlates with genomic instability and a number of cancer phenotypes.

70 iciency of UNG and MSH2 or MSH2 alone causes genomic instability and a shorter latency to the develop

71 oss of DNA methylation, which contributes to genomic instability and aberrant gene expression by mech

72 rogeneity, or acquire drug resistance due to genomic instability and acquisition of mutations.

73 helial cells would induce the development of genomic instability and aggressive disease with metastat

74 Hoxb13 regulatory locus synergize to induce genomic instability and aggressive prostate cancer that

75 We conclude that genomic instability and an elevated load of DNA alterati

76 signs of premature aging are associated with genomic instability and an elevated risk of cancer.

77 ve Mendelian disorder display constitutional genomic instability and an elevated risk of important ag

78 ion of ATR triggers premature mitotic entry, genomic instability and apoptosis.

79 hortening and replicative senescence prevent genomic instability and cancer by limiting the number of

80 leading strand maturation and prevention of genomic instability and cancer development.

81 r specimens and have been suggested to cause genomic instability and cancer predisposition.

82 Errors in this DNA repair pathway lead to genomic instability and cancer predisposition.

83 l explanation for how H3K36me3 loss leads to genomic instability and cancer.

84 ired DNA lesion blocking replication promote genomic instability and cancer.

85 nd fragile telomeres, which in turn promotes genomic instability and cancer.

86 DNA repair systems protect cells from genomic instability and carcinogenesis.

87 pon PARP inhibition, ACLY silencing promotes genomic instability and cell death.

88 f MCL-1 but not its isoform MCL-1S increases genomic instability and cell sensitivity to ionizing rad

89 cells to DNA damage, resulting in endogenous genomic instability and cellular transformation, as well

90 ession might be impeded, adding to increased genomic instability and contributing to disease.

91 del to determine how RecQ4 mutations lead to genomic instability and disease.

92 pression of ILF2 in MM promotes tolerance of genomic instability and drives resistance to DNA-damagin

93 r to the cell lacking LKB1 display increased genomic instability and ectopic expression of BRCA1 resc

94 Nussenzweig and colleagues evaluate genomic instability and germinal center derived lymphoma

95 Notably, dNTP pool alterations lead to genomic instability and have been linked to multiple hum

96 hed light on mechanisms by which HPV induces genomic instability and have therapeutic implications.

97 Genomic instability and high mutation rates cause cancer

98 ody of knowledge on transcription-associated genomic instability and highlight recent discoveries in

99 l mechanism by which E2 stimulation leads to genomic instability and highlights how transcriptional p

100 light on the mechanisms by which HPV induces genomic instability and hold promise for the identificat

101 Oxidative stress promotes genomic instability and human diseases.

102 nd mouse tissues results in defective cNHEJ, genomic instability and hypersensitivity to ionizing rad

103 e step of strand cleavage, leading to severe genomic instability and hypersensitivity to Topo-isomera

104 Genomic instability and immune evasion are hallmarks of

105 lls harboring mutations in BRCA1 suffer from genomic instability and increased DNA lesions.

106 apies can in part be due to the induction of genomic instability and increased passenger load.

107 H3-G34R mutants exhibit genomic instability and increased replication stress, in

108 r data demonstrate MCPH1 deficiency promotes genomic instability and increases cancer susceptibility.

109 Increased PKR promotes genomic instability and is associated with inferior outc

110 Deficiency in repair of damaged DNA leads to genomic instability and is closely associated with tumor

111 This response is thought to protect against genomic instability and is important for the effects of

112 The underlying mechanisms that drive initial genomic instability and its continued progression are la

113 g the molecular basis of DNA damage-mediated genomic instability and its role in tumorigenesis is cri

114 lls and its overexpression leads to enhanced genomic instability and lymphoma formation.

115 such, Xlf(-/-)Paxx(-/-) mice display severe genomic instability and neuronal apoptosis, which eventu

116 the effects of deregulated fork resection on genomic instability and on the unscheduled activation of

117 essential, facilitative role in Myc-induced genomic instability and oncogenic transformation.

118 ed from patients with SPRTN mutations elicit genomic instability and people afflicted with this syndr

119 BRCA2 protein, thereby predisposing them to genomic instability and perhaps to cancer.

120 his study, we report a novel linkage between genomic instability and phagocytosis evasion that is coo

121 hare many features including TP53 mutations, genomic instability and poor prognosis.

122 exonuclease is mutated in Werner syndrome of genomic instability and premature aging.

123 ed carcinogenesis as the result of increased genomic instability and promotion of a protumorigenic mi

124 on carriers (BRCA1(mut/+)) exhibit increased genomic instability and rapid telomere erosion in the ab

125 ed, indicating that they might predispose to genomic instability and rearrangement.

126 2 nuclear basket proteins show AID-dependent genomic instability and replication defects that were su

127 Defects in HR trigger genomic instability and result in cancer predisposition.

128 eplication stress, which, in turn, generates genomic instability and selects for escape from apoptosi

129 ES values correlate with increased levels of genomic instability and several specific adverse tumour

130 uadruplex (G4), which has been implicated in genomic instability and some human diseases.

131 n RNase H2 activity are associated with both genomic instability and the human autoimmune/inflammator

132 ghts a potential role of metabolic stress in genomic instability and therapeutic response in cancer.

133 , our murine Rb-deficient tumors demonstrate genomic instability and they show activation of beta-cat

134 t intracellular signaling by p17 may lead to genomic instability and transformation.

135 dm2 overexpression and p73 loss cooperate in genomic instability and tumor development, indicating th

136 Defects in these functions cause genomic instability and tumorigenesis but also generate

137 deficiency in timely DSB repair, leading to genomic instability and tumorigenesis.

138 ely compromises DNA replication, accumulates genomic instability and ultimately leads to cell death.

139 nt of various pathologies that are linked to genomic instability and/or inflammation.

140 minent dermatologic features, constitutional genomic instability, and an elevated risk of cancer.

141 natures have been widely used as markers for genomic instability, and both SCNAs and PMs could be tho

142 E2 also has links to genomic instability, and elevated E2 levels are tied to

143 s associated with chromosomal abnormalities, genomic instability, and HSC aging and might promote hem

144 xcessive recombination between non-homologs, genomic instability, and impaired cell growth, indicatin

145 rives prostate tumorigenesis in part through genomic instability, and indicate that mutant SPOP may i

146 manifest in immunodeficiency, autoimmunity, genomic instability, and lymphoid and other cancers.

147 PCNSLs and PTLs frequently exhibit genomic instability, and near-uniform, often biallelic,

148 Skp2, resulting in polyploid cell division, genomic instability, and oncogenesis.

149 , reprogramming energy metabolism, acquiring genomic instability, and remodeling the tumor microenvir

150 mutation also impairs DNA repair, increases genomic instability, and renders mice hypersensitive to

151 reduced survival, increased tumor formation, genomic instability, and the development of transplantab

152 relationship among centrosome amplification, genomic instability, and tumor development.

153 sms contributing to transcription-associated genomic instability are both complex and incompletely un

154 Recurrent mutations and genomic instability are early events in the disease.

155 d proliferation and keratinocytes displaying genomic instability are maintained within the proliferat

156 ssibility is that tumors with high levels of genomic instability are more immunogenic than other canc

157 ntially deleterious UNG activity and general genomic instability are opposed by the protective influe

158 ed proliferation, escape from apoptosis, and genomic instability are the most pervasive.

159 lular transformation and the accumulation of genomic instability are the two key events required for

160 abolism alterations could vice versa promote genomic instability as a mechanism for neoplastic transf

161 verexpression and p73 loss exhibit increased genomic instability as compared with either alteration a

162 RNA:DNA hybrid structures contribute to the genomic instability associated with cancer.

163 ession in class-switched B cells to suppress genomic instability associated with CSR.

164 These findings identify the genomic instability associated with V(D)J recombination

165 ed genomic instability checkpoint, expressed genomic instability-associated genes at distinct phases

166 nation and, in the absence of p53, increased genomic instability at V(D)J sites.

167 ncreased in GEP70 high risk, consistent with genomic instability being a key feature of high risk.

168 ly during lifespan could provide support for genomic instability being at least partly responsible fo

169 nduced hepatosplenomegaly with signatures of genomic instability, blebbishield emergency program, and

170 way is specific to the intestinal tumors, as genomic instability but not activation of beta-catenin w

171 duces tumor suppressor activity and promotes genomic instability, but how this pleiotropic biomarker

172 tes the G1 cell cycle checkpoint and induces genomic instability, but the mechanism is not fully unde

173 FBXW7 inactivation causes genomic instability, but the mechanism remains elusive.

174 ich somatic mutations in SIRT2 contribute to genomic instability by impairing its deacetylase activit

175 t activity, AID has a much broader effect on genomic instability by initiating oncogenic chromosomal

176 romoted macrophage polyploidy and suppressed genomic instability by regulating Myc and ATR.

177 Hence, transcription-associated genomic instability can be considered as a major driver

178 On the other hand, genomic instability can have catastrophic consequences f

179 Such genomic instability can lead to the activation of specif

180 Migration-induced genomic instability can thus associate with heritable ch

181 d to prevent the replication defects and the genomic instability caused by p21 depletion.

182 (WS) is an accelerated ageing disorder with genomic instability caused by WRN protein deficiency.

183 display embryonic lethality associated with genomic instability, cell death in the central nervous s

184 Analysis of tissue morphology, genomic instability, cell proliferation and apoptosis re

185 leads to DNA damage that, in turn, promotes genomic instability, cellular transformation, and tumori

186 s can arise as a consequence of or result in genomic instability, characterized by the accumulation o

187 Blebbishield emergency program evaded genomic instability checkpoint, expressed genomic instab

188 ia mutated (ATM) defects are associated with genomic instability, clonal evolution, and chemoresistan

189 tated (ATM) aberrations, are associated with genomic instability, clonal evolution, and chemoresistan

190 How directly various forms of genomic instability contribute to lifespan in different

191 Cancer genomic instability contributes to the phenomenon of int

192 rein, we explore the possibility that a high genomic instability could be the basis for a tumor's sen

193 This genomic instability, denoted as the CDK12 TD-plus phenot

194 Our findings indicate that genomic instability derived during the IL6-mediated live

195 In most cases, rates of genomic instability did not consistently increase in you

196 e clinical outcome, strongly suggesting that genomic instability drives prognosis of the disease.

197 growth conditions on lifespan indicates that genomic instability due to changes in recombination rate

198 utation and epigenomic features that promote genomic instability during cancer evolution.

199 yclin E-mediated replication stress promotes genomic instability during carcinogenesis.

200 Our results define a higher-order genomic instability element that has shaped the structur

201 cquire their hallmark characteristics, while genomic instability enables cells to acquire genetic alt

202 amage in senescent cells is thought to cause genomic instability, eventually allowing secondary hits

203 gene regulation and has been associated with genomic instability, genetic diseases and cancer progres

204 ions is distributed among coexisting clones, genomic instability has important therapeutic implicatio

205 Genomic instability has previously been associated with

206 Genomic instability has profound effects on cellular phe

207 Studies of genomic instability have historically focused on intrins

208 ir genetic mode of action, and their role in genomic instability have not been established.

209 mportant to devise methods to overcome their genomic instability, immune reactivity, and tumorigenic

210 r example, overexpression of Mdm2 results in genomic instability in a p53-independent manner.

211 and HLTF, cause nascent DNA degradation and genomic instability in BRCA1/2-deficient cells upon repl

212 egulation of the transcription machinery and genomic instability in cancer.

213 ng a possible route for tetraploidy-mediated genomic instability in carcinogenesis.

214 g that additional defects must contribute to genomic instability in dividing iECs.

215 , a polyketide-peptide genotoxin that causes genomic instability in eukaryotic cells by induction of

216 c insight into how G34R mutation may promote genomic instability in glioma.

217 ne-induced replication stress contributes to genomic instability in human cancer.

218 We investigated whether genomic instability in human colorectal cancer (CRC) cel

219 Bruton's tyrosine kinase inhibitors increase genomic instability in normal and neoplastic B cells by

220 defect causative in TH1 immunodeficiency and genomic instability in patients with WAS.

221 ntenance were detected and may contribute to genomic instability in SS.

222 RNS-induced DNA lesions cause genomic instability in the absence of Brca2.

223 Here we show that TGFbeta also promotes genomic instability in the form of DNA double strand bre

224 APC loss leads to a DNA damage signature and genomic instability in the liver and that additional los

225 nked to the degree of TH cell deficiency and genomic instability in the XLT/WAS clinical spectrum.

226 and appear to be responsible for the bulk of genomic instability in these tumors.

227 hanistic insight into the molecular basis of genomic instability in tumour cells containing significa

228 morigenesis by promoting immortalization and genomic instability in two phases.

229 ich shows that loss of H2Bub1 contributes to genomic instability in yeast.

230 are associated with defective DNA repair and genomic instability, including the most common inherited

231 expression is associated with DNA damage and genomic instability independent of Pol I transcription.

232 Filia depletion causes ESC genomic instability, induces resistance to apoptosis, an

233 long-range DNA end-joining while suppressing genomic instability inherently associated with DSBs are

234 Genomic instability is a frequently occurring feature of

235 Genomic instability is a fundamental feature of human ca

236 Genomic instability is a hallmark of human cancer, and r

237 bpopulations of larger size, especially when genomic instability is shared among a limited number of

238 ntly formed telomere fusions trigger rampant genomic instability leading to cell death or tumorigenes

239 peutic targets against ATL and might explain genomic instability leading to the pathogenesis of ATL.

240 cell nuclear antigen, is critical to prevent genomic instability, little is known about how the stead

241 vivo methods suffer from a lack of control, genomic instability, low efficiency and narrow mutationa

242 Osteosarcoma is associated with massive genomic instability, making it problematic to identify d

243 deleterious consequences of triplex-induced genomic instability may be averted by activating apoptos

244 othesize that cancers with extreme levels of genomic instability may be teetering on the brink of a t

245 oss leads to abnormal centrosome numbers and genomic instability mediated by NDRG1.

246 othesis that HPV oncogenes contribute to the genomic instability observed in HPV-associated malignanc

247 rks listed above, as well as the patterns of genomic instability observed in human cancers, proposes

248 ring transcription, transcription-associated genomic instability occurs in normal and malignant cells

249 ng the replication stress and increasing the genomic instability of cancer cells.

250 Loss of HR accounts for the genomic instability of EOCs and for their cellular hyper

251 orm 2 differently account for 2/3(rd) of the genomic instability of hCEB1 in two G4-stabilizing condi

252 The high genomic instability of non-small cell lung cancer tumors

253 t cells afford cytoprotection in the face of genomic instability, oncogene activation, microenvironme

254 d to chromosomal rearrangements resulting in genomic instability or cell death.

255 lay loss of NF2, which co-occurs either with genomic instability or recurrent SMARCB1 mutations.

256 as consistently associated with a particular genomic instability pattern characterized by hundreds of

257 gnal but not to an immediate increase in the genomic instability phenotype.

258 the mechanisms by which TACC3 contributes to genomic instability, potentially leading to cancer devel

259 Genomic instability promotes colon carcinogenesis by ind

260 es a variety of cellular stresses, including genomic instability, proteotoxic and oxidative stresses,

261 ith canonical DNA repair pathways to prevent genomic instability remains unknown.

262 This situation can cause genomic instability resulting from improper segregation

263 The underlying cause is genomic instability resulting from the deficiency in rep

264 These cancers often exhibit genomic instability, resulting in chromosomal rearrangem

265 e show that the histone H4 alterations cause genomic instability, resulting in increased apoptosis an

266 great promise in cell-based therapy, but the genomic instability seen in culture hampers their full a

267 These patterns mirror the genomic instability seen in some mitochondria.

268 Cancers with higher levels of genomic instability showed a corresponding increase in f

269 exploratory analyses showed that a BRCA-like genomic instability signature (n = 32) discriminated res

270 UNX3 inactivation as aggravating factors for genomic instability.Significance: RUNX3 inactivation in

271 le-strand break repair pathway that leads to genomic instabilities similar to those observed in cance

272 the animal not exposed to radiation, causing genomic instability, stress responses and altered apopto

273 The genomic instability syndrome Fanconi anemia is caused by

274 Fanconi anemia and Bloom syndrome are genomic instability syndromes caused by mutations in pro

275 s in senescent cells could contribute to the genomic instability that allows senescence bypass and tu

276 es chromosome end-to-end fusions, initiating genomic instability that can be cancer promoting.

277 Mutation or dysregulation of MSH2 causes genomic instability that can lead to cancer.

278 es and also averts the cell-cycle errors and genomic instability that could result from mistimed degr

279 ter membrane permeabilization (MOMP) promote genomic instability that drives tumorigenesis, providing

280 Cancer is a disease associated with genomic instability that often results from oncogene act

281 They also signify high levels of genomic instability that sensitize cancer cells to addit

282 chromosome mis-segregation leads to further genomic instability that ultimately causes cell-cycle ar

283 ized by radiation-induced and age-associated genomic instability that was partially reversed by short

284 ement 1 (LINE-1 or L1) is capable of causing genomic instability through the activity of the L1 ORF2

285 ITH and genomic instability thus have the potential to be useful

286 omitant induction of Hsp90 lead to increased genomic instability under DNA-damaging conditions.

287 drive extreme locus- and cell-type-specific genomic instability under replication stress, resulting

288 Furthermore, telomere loss and genomic instability were observed at a higher frequency

289 which plays a crucial role in DNA damage and genomic instability, were reported to be associated with

290 mors of epithelial origin, extreme levels of genomic instability, where more than 75% of the genome i

291 nt manner, endogenous p21 prevents a type of genomic instability which is not triggered by endogenous

292 ing GQ are known to result in DNA breaks and genomic instability, which are prominent in Werner and B

293 ed homologous recombination (HR) can lead to genomic instability, which greatly increases the threat

294 An underlying hallmark of cancers is their genomic instability, which is associated with a greater

295 s in mice via a gain of function that drives genomic instability, which is frequently observed in hum

296 hepatocytes bearing micronuclei, a marker of genomic instability, which is suppressed by IL6 blockade

297 signaling, defective cell cycle control, and genomic instability, which was rescued by WT GINS1.

298 ell cycle progression and the development of genomic instability with aneuploidy.

299 pair genes, which suggests an association of genomic instability with therapeutic resistance.

300 factors such as reactive oxygen species and genomic instability, yet an emerging challenge is to rec