ライフサイエンスコーパス: genomic instability

1 t mice showed a defect in ATR activation and genomic instability.

2 ithelium led to impaired colonic healing and genomic instability.

3 ication and transcription, which can lead to genomic instability.

4 NBS1 and plays a central role in preventing genomic instability.

5 escence by restoring SKP2 expression display genomic instability.

6 types, hypoxia was associated with elevated genomic instability.

7 turb DNA replication progression, leading to genomic instability.

8 boundaries core fragility regions leading to genomic instability.

9 the stalling of replication forks and cause genomic instability.

10 ersensitivity to replication inhibitors, and genomic instability.

11 ables BRCA1-deficient cells to avoid further genomic instability.

12 ess-inducing agents and displayed pronounced genomic instability.

13 linical subtypes, cellular proliferation and genomic instability.

14 likely tumor evolution, rather than ongoing genomic instability.

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

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

17 plication, repair and recombination to avoid genomic instability.

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

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

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

21 oxidative stress, chromatin remodeling, and genomic instability.

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

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

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

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

26 ave been identified as endogenous sources of genomic instability.

27 esions intensifies, progressively leading to genomic instability.

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

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

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

31 fic transcriptional signature, and increased genomic instability.

32 ta-dependent tumor progression by preventing genomic instability.

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

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

35 enome replication is a significant source of genomic instability.

36 urodegeneration is driven at least partly by genomic instability.

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

38 ontribution to defective DNA methylation and genomic instability.

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

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

41 due to poor tumor cellularity and extensive genomic instability.

42 licit DNA replication stress and may promote genomic instability.

43 replication stress, double-strand break, and genomic instability.

44 -stranded DNA) create DNA damage and lead to genomic instability.

45 ed replication stress-induced DNA damage and genomic instability.

46 s, representing a mechanism of Z-DNA-induced genomic instability.

47 plication collisions, causing DNA damage and genomic instability.

48 AX expression, Lys(382)-p53 acetylation, and genomic instability.

49 region, with the risk of creating indels and genomic instability.

50 s, leading to DNA double-stranded breaks and genomic instability.

51 tivation-induced cytidine deaminase-mediated genomic instability.

52 e the repair pathway is chosen, and prevents genomic instability.

53 ve a g/sBRCA1/2, or whose tumor demonstrates genomic instability.

54 association with prognosis and its impact in genomic instability.

55 ve frameshifts during TLS, which can lead to genomic instability.

56 res drives telomere shortening and, in turn, genomic instability.

57 distinct molecular subgroup associated with genomic instability.

58 ly been considered to reflect cancer somatic genomic instabilities.

59 eatment of breast cancers that are driven by genomic instability(3).

60 umours and is associated with high levels of genomic instability(4-6).

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

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

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

64 s or deletions, making them a major cause of genomic instability, a driving force of many diseases of

65 oliferative tumors, characterized by extreme genomic instability, absence of immune infiltration, and

66 with stage III-IV EOC with g/sBRCA1/2 and/or genomic instability and a partial or complete response t

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

68 targeting miR-23a and miR-155 reversed this genomic instability and accelerated mucosal healing.

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

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

71 show that Cds1 inhibition of Mus81 promotes genomic instability and allows mcm4-dg cells to evade ce

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

73 asis for R-loop-mediated gene regulation and genomic instability and briefly discusses methods for id

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

75 ting DNA polymerases have been implicated in genomic instability and cancer development, but the mech

76 However, little is known about its impact on genomic instability and cancer immunity.

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

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

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

80 trategies for anti-Plk4 intervention against genomic instability and cancer.

81 esions such as double strand breaks prevents genomic instability and carcinogenesis.

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

83 that can lead to chromosome rearrangements, genomic instability and cell death.

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

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

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

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

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

89 , CRL4 or RBBP7 delay mitotic exit, increase genomic instability and enhance sensitivity to paclitaxe

90 oblasts and transformed fibroblasts, through genomic instability and expression of a specific transcr

91 DNA rereplication leads to genomic instability and has been implicated in the patho

92 ons in R-loop metabolism have been linked to genomic instability and have been implicated in human di

93 DNA, they can promote replication stress and genomic instability and have been implicated in several

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

95 Genomic instability and high mutation rates cause cancer

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

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

98 Genomic instability and immune evasion are hallmarks of

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

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

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

102 isruption of RAD51 recruitment, resulting in genomic instability and induction of EMT.

103 astasis, reprogram energy metabolism, induce genomic instability and inflammation, and trigger evasio

104 Inactivation of mammalian Rev3l results in genomic instability and invokes cell death and senescenc

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

106 ion of focal structural variants, leading to genomic instability and Met amplification.

107 Deletion of Norad in mice results in genomic instability and mitochondrial dysfunction, leadi

108 tive humoral immunity and to protect against genomic instability and neoplastic transformation.

109 criptional R-loops and DNA damage leading to genomic instability and neurodegeneration in SMA.

110 nscriptional R-loops and DNA damage to avert genomic instability and neurodegeneration in SMA.

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

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

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

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

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

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

117 l insights into how oxidative stress affects genomic instability and phenotypic evolution in aerobic

118 rthermore, Vcpip1 knockout mice are prone to genomic instability and premature aging.

119 e in VHL, SET2, PBRM1 and BAP1, may engender genomic instability and promote defects in DNA repair pa

120 2 nuclear basket proteins show AID-dependent genomic instability and replication defects that were su

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

122 d examines the consequences of both inducing genomic instability and suppressing safeguard mechanisms

123 to identify additional driver mechanisms for genomic instability and targeted strategies to exploit t

124 her defects in DNA replication contribute to genomic instability and the diverse differentiation pote

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

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

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

128 s of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion

129 of BCCIP function was sufficient to trigger genomic instability and tumorigenesis.

130 counteract DNA replication stress to prevent genomic instability and tumorigenesis.

131 ophagy initiation and maturation to suppress genomic instability and tumorigenesis.

132 Cells depleted for BGL3 displayed genomic instability and were sensitive to DNA-damaging r

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

134 forks by nucleases can cause fork collapse, genomic instability, and cell death.

135 functional telomeres activate DDR signaling, genomic instability, and cellular senescence, but the li

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

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

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

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

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

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

142 iversification of driver genes and increased genomic instability are features of later stages.

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

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

145 Regions of genomic instability are not random and often co-localize

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

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

148 y, these findings highlight TRIM37-dependent genomic instability as a putative driver event in 17q23-

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

150 her mechanisms, R337H increases the level of genomic instability, as evidenced by a higher number of

151 ion repair (HDR) and caused androgen-induced genomic instability, as indicated by frequent occurrence

152 ns and provide possible explanations for the genomic instability, as well as the osteolytic phenotype

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

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

155 Other historical and recent instances of genomic instability, at the same time, suggest multiple

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

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

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

159 R loops arising during transcription induce genomic instability, but how cells respond to the R loop

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

161 ind that the overexpression of TRIM37 causes genomic instability by delaying centrosome maturation an

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

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

164 Eukaryotic DNA methylation prevents genomic instability by regulating the expression of onco

165 Genomic instability can be a hallmark of both human gene

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

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

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

169 Genomic instability can trigger cellular responses that

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

171 eotide variants (SNVs), but showed prevalent genomic instability caused by widespread occurrence of R

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

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

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

175 Cancer genomic instability contributes to the phenomenon of int

176 Genomic instability contributes to tumorigenesis through

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

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

179 a (FA) DNA damage-response pathway result in genomic instability, developmental defects, hematopoieti

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

181 s) are recognized as a significant source of genomic instability, driving genome variability and evol

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

183 aging to study the consequences of increased genomic instability during aging in budding yeast and id

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

185 that disease heterogeneity is due to ongoing genomic instability during progression.

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

187 l carcinoma through loss of SIM2s, increased genomic instability, EMT, and metastasis.

188 ochondrial dysfunction, telomere shortening, genomic instability, epigenetic changes, protein aggrega

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

190 Genomic instability (GI) predisposes cells to malignant

191 Genomic instability (GIN), an increased tendency to acqu

192 Although genomic instability has been extensively studied in cell

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

194 Genomic instability has previously been associated with

195 Studies of genomic instability have historically focused on intrins

196 s ovarian carcinoma, where it contributes to genomic instability; however, the timing of LINE-1 activ

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

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

199 aintaining mitotic integrity and the lack of genomic instability in ARID1A-mutated cancers.

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

201 Furthermore, genomic instability in cancer cells accelerates the gene

202 ese results support the value of aggravating genomic instability in cancer cells to enable immunologi

203 pede DNA synthesis and are a major source of genomic instability in cancer cells.

204 However, the extent of such genomic instability in cancer models has received limite

205 e way for investigating mechanisms promoting genomic instability in cancer.

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

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

208 ngle-stranded DNA that represent a source of genomic instability in mammalian cells(1-4).

209 y induced DNA damage could not only increase genomic instability in metastasizing cancer cells but co

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

211 nase inhibitors, increase AID expression and genomic instability in normal and neoplastic B cells.

212 that clonal haematopoiesis is a biomarker of genomic instability in other tissues.

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

214 lts in replication stress (RS) that leads to genomic instability in premalignant lesions.

215 To address the importance of genomic instability in prostate carcinogenesis and tumor

216 nized and widespread mechanism of reversible genomic instability in S. aureus associated with SCV gen

217 hybrids (R-loops) and DNA damage leading to genomic instability in SMA mice and patient cells.

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

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

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

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

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

223 stability (CIN) is one of the major forms of genomic instability in various human cancers and is reco

224 USP15 knockout mice exhibit genomic instability in vivo.

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

226 ion, neurohormonal stress, angiogenesis, and genomic instability, in an effort to understand common m

227 tly controlled during development to prevent genomic instability, inappropriate gene activation and o

228 plication was incompletely reprogrammed, and genomic instability increased during replicative stress.

229 numbers of 53BP1 nuclear bodies, a marker of genomic instability induced by replication stress.

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

231 Genomic instability, involving chromosome number and str

232 Genomic instability is a frequently occurring feature of

233 Genomic instability is a hallmark of cancer, and has a c

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

235 Genomic instability is a key hallmark of cancer that ari

236 There is increasing evidence that genomic instability is a prerequisite for cancer progres

237 As a result, genomic instability is currently considered an enhancer

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

239 his host-pathogen interaction contributes to genomic instability is unknown.

240 Cancer is characterized by genomic instability leading to deletion or amplification

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

242 ence through a program involving generalized genomic instability manifested by DNA single- and double

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 ancm mutant embryos have increased levels of genomic instability (measured as the number of cells wit

246 nsive telomere fusion that drives widespread genomic instability, mitotic arrest, hyperactivation of

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

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

249 Here, we review the state of knowledge of genomic instability of cancer models and discuss its bio

250 homeostasis with important implications for genomic instability of cancer stromal cells and beyond.

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 id and hematopoietic tumors often experience genomic instability, oncogene activation, increased prot

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

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

256 R-loop structures have been associated with genomic instability phenotypes.

257 kpoints, elucidation of factors enabling the genomic instability present in this subtype has the pote

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

259 e propagation of cells with a high degree of genomic instability remain unclear.

260 case comprising MCM2 to MCM7(3,4)-that cause genomic instability render female mouse embryos markedly

261 , depending on the protocol used, can induce genomic instability resulting in large-scale changes lik

262 with the PARP inhibitor olaparib, increases genomic instability, resulting in cell growth inhibition

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

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

265 and replication stress are major sources of genomic instability, selective ATR inhibition has been r

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

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

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

269 ith the nine biological hallmarks of ageing: genomic instability, telomere attrition, epigenetic alte

270 zed by a unique molecular profile and higher genomic instability than noncarrier tumours.

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

272 spersed duplications and creates hotspots of genomic instability that appear to be an ancient propert

273 eveal a pathway by which HPV may promote the genomic instability that drives oncogenesis.

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

275 ypia, accumulation of somatic mutations, and genomic instability, the etiologies of which remain uncl

276 Changes in gene copy number contribute to genomic instability, the onset and progression of cancer

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

278 gous loss of Bap1 in murine pancreata causes genomic instability, tissue damage, and pancreatitis wit

279 This drives surviving cells, potentiated by genomic instability, to acquire rescuing mutations, whic

280 key sensor and suppressor of R loop-induced genomic instability, uncovering a signaling circuitry th

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

282 es cellular proliferation and suppression of genomic instability under normal growth conditions.

283 y neutrophils control epithelial fitness and genomic instability via delivery of miR-23a-and miR-155-

284 ients and thus emphasize the central role of genomic instability vis-a-vis tumor aggressiveness.

285 Genomic instability was rescued by simultaneous depletio

286 can experience discrete episodes of systemic genomic instability, when the entire genome becomes vuln

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

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

289 her show that IL-22 increases DNA damage and genomic instability, which can accelerate cellular trans

290 damage is the driving force for mutation and genomic instability, which can both lead to cell death o

291 Such aberrant repair leads to increased genomic instability, which is exacerbated at chromosome

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

293 prone DNA-repair pathways, causing increased genomic instability, which may be responsible for their

294 of cancer development is the acquisition of genomic instability, which results from the inaccurate r

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

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

297 HGSOC tumors exhibit genomic instability with frequent alterations in the pro

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

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

300 talled replication forks are main sources of genomic instability, yet the molecular mechanisms for pr