ライフサイエンスコーパス: genetic instability

1 ers , and Fbw7 loss in cultured cells causes genetic instability .

2 nd transcription, and lead to cell death and genetic instability.

3 mes, and this correlates with aneuploidy and genetic instability.

4 SBs) are highly toxic lesions that can drive genetic instability.

5 evolve rapidly and can mobilize and trigger genetic instability.

6 ide insight into how RNA:DNA hybrids lead to genetic instability.

7 ycle progression and give rise to pronounced genetic instability.

8 ed, mTOR-mediated cell-cycle progression and genetic instability.

9 and mobilization of these elements triggers genetic instability.

10 edispose these regions to disease-associated genetic instability.

11 developmental defects, tumor propensity, and genetic instability.

12 activity, which is associated with increased genetic instability.

13 humans characterized by premature aging and genetic instability.

14 ence of the role of TEs in human disease and genetic instability.

15 ay lead to an accumulation of DNA damage and genetic instability.

16 uses cancers in animals, in part by inducing genetic instability.

17 ock replication and transcription and induce genetic instability.

18 nd synthesis as the likely mechanism for the genetic instability.

19 cancers, and loss of BRCA2 function leads to genetic instability.

20 checkpoints that arrest growth and suppress genetic instability.

21 ption may increase the risk of Z-DNA-related genetic instability.

22 s preceded by mutations in genes that confer genetic instability.

23 uent and require careful management to avoid genetic instability.

24 t, in general, only a small disadvantage for genetic instability.

25 ecies (ROS), a major cause of DNA damage and genetic instability.

26 roteins, the impairment of which can lead to genetic instability.

27 es, into the ancestral diploid strain caused genetic instability.

28 to the mechanisms underlying hypoxia-induced genetic instability.

29 aluable tools to study DNA structure-induced genetic instability.

30 Only DSBs increased the overall genetic instability.

31 n of repeated, strong selection enriches for genetic instability.

32 on of stalled forks without rescue can cause genetic instability.

33 er genomes for the precise analysis of their genetic instability.

34 ainder are candidates to contribute to human genetic instability.

35 enomes, representing an endogenous source of genetic instability.

36 telomere-shortened epithelial field prone to genetic instability.

37 delity of chromosome segregation and promote genetic instability.

38 r refining the classification of tumors with genetic instability.

39 rid structures involved in transcription and genetic instability.

40 e-3, is directly responsible for Myc-induced genetic instability.

41 , and they make major contributions to human genetic instability.

42 ly important for controlling mutagenesis and genetic instability.

43 n proposed to affect FEN1 activity and cause genetic instability.

44 d transcription in regulating Top1-dependent genetic instability.

45 evelopment of resistance to chemotherapy and genetic instability.

46 yploids missegregate chromosomes and undergo genetic instability.

47 DSB repair pathways that is highly prone to genetic instability.

48 enome at risk of retrotransposition-mediated genetic instability.

49 e used to determine their capacity to induce genetic instabilities.

50 so study the effect of chromosomal and other genetic instabilities.

51 etabolism, and have revealed new targets for genetic instability(7-11), including essential genes.

52 Genetic instability, a hallmark feature of human cancers

53 rophoresis indicated that mensacarcin causes genetic instability, a hallmark of early apoptosis.

54 Genetic instability, a heritable increase in the rate of

55 Consistent with a causative role of AID in genetic instability, AID(-/-) leukemia had a lower frequ

56 adly documented in early UC, contributing to genetic instability, altered gene expression and tumor p

57 lonal evolution in BCR-ABL1 ALL by enhancing genetic instability and aberrant somatic hypermutation,

58 es malignant transformation through inducing genetic instability and activating oncogenic pathways su

59 BER enzymes lead to elevated mutagenesis and genetic instability and are frequently found in cancer c

60 most all human cancers, perhaps facilitating genetic instability and cancer initiation and progressio

61 are most probably associated with increased genetic instability and cancer, phenotypes not observed

62 blethal doses, and yet UV irradiation causes genetic instability and cancer, suggesting that chromoso

63 by neurological dysfunction and/or increased genetic instability and cancer.

64 Misregulation of RAD51 is associated with genetic instability and cancer.

65 lation of 8-oxoG in the genomic DNA leads to genetic instability and carcinogenesis and is thought to

66 H6 complex, which potentially contributes to genetic instability and carcinogenesis.

67 n suppresses chemical- and radiation-induced genetic instability and carcinogenesis.

68 nt cells, thereby suppressing epigenetic and genetic instability and contributing to long-term senesc

69 Reasoning that the combination of genetic instability and cytokine hypersensitivity might

70 enotypes; analogous defects may underlie the genetic instability and diseases associated with RecQ4 d

71 We evaluated genetic instability and DNA repair defects by direct and

72 mportance as these adducts may contribute to genetic instability and elevated cancer risk associated

73 Solid tumors possess a high degree of genetic instability and emergence of treatment resistanc

74 In addition, we describe genetic instability and exceptional phenotypic changes t

75 suited for 'difficult' cell lines displaying genetic instability and high levels of epigenetic silenc

76 mechanistic explanation for the accelerating genetic instability and increased ROS stress in cancer c

77 hat it can be used to study the evolution of genetic instability and infer tumor evolutionary history

78 Tumor progression is associated with genetic instability and L1 mutants.

79 Defects in DNA damage responses may underlie genetic instability and malignant progression in melanom

80 lasmids due to phenotypic noise generated by genetic instability and natural population dynamics.

81 imensions, dysregulation of which results in genetic instability and neuro- and ciliopathies.

82 ing many single-guide RNAs (sgRNAs) triggers genetic instability and phenotype loss, due to the prese

83 repair or DNA-damage checkpoints can lead to genetic instability and predispose lymphocytes undergoin

84 Further, we observed a dose response in genetic instability and PTTG expression (GI Index low do

85 ble to estimate the relative contribution of genetic instability and selection to the process of tumo

86 Disruption of UVRAG increases genetic instability and sensitivity of cells to irradiat

87 osed that centrosome amplification can drive genetic instability and so tumorigenesis.

88 s of spontaneous damage is likely to promote genetic instability and thus carcinogenesis.

89 -rearrangements correlates with the level of genetic instability and thus could be used as a predicti

90 al, unexpected role in mediating Myc-induced genetic instability and transformation in mammalian cell

91 th of Atg7-deficient Lgr5(+)ISC but promotes genetic instability and tumor formation.

92 an early oncogenic event that contributes to genetic instability and tumor progression by sustaining

93 PE1 endonuclease activity, which may promote genetic instability and tumorigenesis.

94 ess-efficient cell cycle control can lead to genetic instability and tumorigenesis.

95 isruption of this pathway is associated with genetic instability and tumorigenesis.

96 However, notorious genetic instability and underlying neuropathogenicity ha

97 ering p53 functionality, are associated with genetic instability, and are present in aggressive CLL.

98 er characterized by chromosomal aberrations, genetic instability, and cancer predisposition, all of w

99 ther SIGIRR controls cell-cycle progression, genetic instability, and colon tumor initiation by modul

100 peration among NF-kappaB-driven prosurvival, genetic instability, and immune evasion mechanisms in DL

101 junction with DNA repair gene dysregulation, genetic instability, and inflammation.

102 initiation by promoting cell proliferation, genetic instability, and miRNA dysregulation.

103 of information to study genome organization, genetic instability, and polymorphisms, as well as a kno

104 at sequence also elicits profound mutagenic, genetic instability, and recombination behaviors.

105 e balance of angiogenesis, cell death rates, genetic instability, and replication rates give rise to

106 imarily because of insufficient attenuation, genetic instability, and reversion to a less-attenuated

107 ns that can functionally promote DNA damage, genetic instability, and tumorigenesis.

108 accumulation of DNA damage in living cells, genetic instability, and tumorigenesis.

109 Problems related to immune rejection, genetic instability, and tumorigenicity must be solved.

110 leads to the development of spindle defects, genetic instability, and tumors.

111 Although genetic instability appeared to have occurred in most tu

112 Genetic instabilities are believed to be one of the majo

113 sociated replication stress, DNA damage, and genetic instability are detectable in CLDs before any ne

114 The mechanisms responsible for this genetic instability are poorly understood.

115 Energy metabolism, obesity, and genetic instability are regulated in part by the relatio

116 Overall, this study identified genetic instability as a predictive biomarker for sensit

117 red in biopsies and does not reveal the same genetic instability as conventional genome assays opens

118 y in resistance to targeted therapy, discuss genetic instability as one of its causes, and detail app

119 Z-miRNA axis promotes cell proliferation and genetic instability, as indicated by comet assays that s

120 nical DNA structures have been implicated in genetic instability associated with human disease.

121 ch cellular factor(s) is responsible for the genetic instability associated with initiating and susta

122 of new genes and are an important source of genetic instability associated with rare and common dise

123 Genetic instability associated with shortened telomeres

124 3 mutations and that E2F1 contributes to the genetic instability associated with transformation and t

125 re against FFA production that could lead to genetic instability at industrial scale.

126 Genetic instability at palindromes and spaced inverted r

127 These data highlight the importance of genetic instability at the chromosome level in the devel

128 monstrate that HIF-1alpha is responsible for genetic instability at the nucleotide level by inhibitin

129 Although genetic instability, because of inheritance of specific

130 This limits genetic instability both in time and to localized genome

131 ion of the non-B DNA structures enhanced the genetic instabilities, both within the repeat sequences

132 ar CGG*CCG or CTG*CAG repeat tracts on their genetic instabilities, both within the repeats and in th

133 he tumors revealed widespread aneuploidy and genetic instability, both hallmarks of nearly all solid

134 ex formation in human minisatellite leads to genetic instability but also address the fundamental que

135 ic Ras activity potentiates cyclin E-induced genetic instability but only when cyclin E is susceptibl

136 'random' ribonucleotide incorporation causes genetic instability, but new evidence suggests there may

137 of the heterogeneity may be attributable to genetic instability, but recent data emphasize that deve

138 ination, higher than normal levels can yield genetic instability by disrupting the normal interplay o

139 f-function of p53 cancer mutants in inducing genetic instability by inactivating critical tumor suppr

140 In summary, NO/RNS stimulates genetic instability by inhibiting BRCA1 expression and s

141 se that p53-dependent loss of Fbxw7 leads to genetic instability by mechanisms that might involve the

142 sion of homologous recombination may lead to genetic instability by shifting the balance between the

143 Hypoxia promotes genetic instability by undefined mechanisms.

144 Small lesions without genetic instability can take a very long time to inactiv

145 ase genes WRN and BLM respectively cause the genetic instability/cancer predisposition syndromes Wern

146 The genetic instability caused by BRCA1 deficiency, however,

147 Genetic instability caused by mutations in the p53 gene

148 uman breast cancer, including high levels of genetic instability, cell cycle defects, poor differenti

149 eases, the expanded repeats display dramatic genetic instability, changing in size when transmitted t

150 replication and, ultimately, leading to the genetic instability characteristic of CFSs.

151 tress characteristic of CFSs, leading to the genetic instability characteristic of this regions.

152 Of note, overexpression of Aurora-A led to genetic instability, characterized by centrosome amplifi

153 These imposed genetic instabilities did not reduce the time required f

154 nce of continued BCR-ABL activity leading to genetic instability, DNA damage, and impaired DNA repair

155 As genetic instability drives disease or loss of cell fitne

156 mitotic exit, thus protecting cells against genetic instability during cell division.

157 . coelicolor shows a bias toward one type of genetic instability during this particular assault from

158 tected by GAPF providing strong evidence for genetic instability early in Myc-induced tumorigenesis a

159 However, intrinsic genetic instability enables these immunodeficiency virus

160 8-hydroxy-2'-deoxyguanosine levels and, as a genetic instability endpoint, DNA deletions.

161 sults in a disruption of cell cycle control, genetic instability, enhanced cell motility, and apoptot

162 methylation plays a similar role to that of genetic instability, enhancing the ability of cancer cel

163 n human tumors and have been associated with genetic instability favoring tumor progression.

164 We report an altered pattern of genetic instability for Streptomyces coelicolor when the

165 We report a previously unobserved form of genetic instability for Streptomyces coelicolor, the rep

166 Hypoxia promotes genetic instability for tumor progression.

167 ms are thought to progress to cancer through genetic instability generating cellular diversity and cl

168 was greatest in Bi-Tg thyrocytes with a mean genetic instability (GI) index of 35.8+/-2.6%, as well a

169 y diploid mutants exhibit G2/M delay, severe genetic instability (GIN), and reduced viability.

170 d Baller-Gerold syndromes), characterized by genetic instability, growth deficiency, and predispositi

171 Tumors are characterized by properties of genetic instability, heterogeneity, and significant olig

172 Cells from patients with AT show genetic instability, hypersensitivity to radiation, and

173 ot' regions in the genome are susceptible to genetic instability, implicating them in diseases.

174 -DNA-forming sequences induce high levels of genetic instability in both bacterial and mammalian cell

175 ith DCTPP1 deficiency causing DNA damage and genetic instability in both chromosomal and mitochondria

176 There is an emerging concept that acquired genetic instability in cancer cells can arise from the d

177 cribes "chromothripsis," a new mechanism for genetic instability in cancer cells.

178 into the effect of hypoxia on DNA repair and genetic instability in cancer.

179 contribute to uncontrolled cell division and genetic instability in cancer.

180 ing numerous human neurological diseases and genetic instability in cancer.

181 s mutations in mammalian homologues initiate genetic instability in cancer.

182 tient/cancer-specific as well as the overall genetic instability in cancer.

183 the tumor microenvironment can contribute to genetic instability in cancer.

184 roid follicular cells and observed increased genetic instability in cells overexpressing PTTG compare

185 The mechanism underlying genetic instability in DFF/CAD-deficient cells, at least

186 Here we have used this approach to evolve genetic instability in diploid cells of the budding yeas

187 We conclude that single genetic events cause genetic instability in diploid yeast cells, and propose

188 leoside pool can significantly contribute to genetic instability in DNA mismatch repair-defective hum

189 werful mechanism that can initiate bursts of genetic instability in eukaryotes, including humans.

190 TNF-alpha induced ROS-dependent genetic instability in Fancc-/- but not in WT cells.

191 this delay, there is no dramatic increase in genetic instability in flies with extra centrosomes, and

192 genetic and epigenetic changes that lead to genetic instability in gastric epithelial cells.

193 In addition to increasing genetic instability in growing cells, Top1 activity in t

194 s (aneuploidy), which is a prevalent form of genetic instability in human cancers.

195 rs/destabilizers may allow the regulation of genetic instability in human genomes.

196 rring intra-molecular triplex (H-DNA) caused genetic instability in mammals largely in the form of DN

197 and cell-cycle checkpoint pathways, initiate genetic instability in many sporadic and hereditary canc

198 ncy triggers replicative stresses leading to genetic instability in mice carrying a mammary specific

199 ip between PTTG expression and the degree of genetic instability in normal and tumorous thyroid sampl

200 nsight into the molecular defects leading to genetic instability in patients with ataxia-telangiectas

201 Deciphering the contribution of genetic instability in somatic cells is critical to our

202 predicted with high accuracy the underlying genetic instability in the original and in three indepen

203 ip between PTTG expression and the degree of genetic instability in thyroid cancers (R2=0.80, P=0.007

204 dered arguments concerning the importance of genetic instability in tumorigenesis and the number of m

205 y provides a further basis for understanding genetic instability in tumors and may guide the design o

206 role in HTLV-induced cell proliferation and genetic instability in vitro and facilitate viral persis

207 ith genetic instability in vivo, and induces genetic instability in vitro.

208 nstrate that PTTG expression correlates with genetic instability in vivo, and induces genetic instabi

209 uclease activity in vitro and confers strong genetic instability in vivo, but does not affect yMutLal

210 t together may facilitate the development of genetic instability in vivo, provides insights into why

211 x, Msh2-Msh3, are required for Z-DNA-induced genetic instability in yeast and human cells.

212 egregation-induced aneuploidy but also other genetic instabilities including DNA damage and loss of k

213 cDNA resolution can lead to various forms of genetic instability including the generation of chimeric

214 Oxidative stress and genetic instability, including DNA deletions, are involv

215 icrobes under growth-limiting stress causing genetic instability, including occasional adaptive mutat

216 ad excellent infectivity without evidence of genetic instability, induced durable immunity, and prime

217 n form of malignant glioma, characterized by genetic instability, intratumoral histopathological vari

218 ropriate repeat tracts; also, numerous prior genetic instability investigations invoke a role for the

219 results integrate DNA damage resulting from genetic instability, IR, or chemotherapeutic agents, to

220 Genetic instability is a common mechanism by which cance

221 Genetic instability is a defining characteristic of canc

222 Genetic instability is a feature of chronic lymphocytic

223 Genetic instability is a hallmark of aneuploidy in buddi

224 Genetic instability is a hallmark of cancer; the hypoxic

225 er, specifically to the colorectum, in which genetic instability is a primary etiologic factor.

226 umber of breast stem cells and TSGs exist or genetic instability is involved as a driving force of th

227 the mechanisms involved in non-B DNA-induced genetic instability is needed.

228 The mechanism for Myc-induced genetic instability is not well understood.

229 agmentation, one of the main contributors to genetic instability, is intimately linked to DNA replica

230 ure of most if not all cancers is a striking genetic instability, leading to ongoing accrual of mutat

231 es (eg, of retinoic acid receptor-beta, p53, genetic instability, loss of heterozygosity, and cyclin

232 Two major classes of genetic instability, microsatellite instability (MSI) an

233 To test whether genetic instability might accelerate tumor progression,

234 These results suggest that enhanced genetic instability might be one of the mechanisms by wh

235 systemic DNA damage, contributes early on to genetic instability necessary for progression to inflamm

236 The genetic instabilities of (CCTG.CAGG)(n) tetranucleotide

237 ence of negative superhelical density on the genetic instabilities of long GAA.TTC, CGG.CCG, and CTG.

238 Thus, the genetic instabilities of the CCTG*CAGG repeats may be me

239 Thus, by inhibiting transcription, the genetic instability of (GAC*GTC)49 repeats did not signi

240 pression might be involved in the remarkable genetic instability of ATLL cells.

241 ranscription may therefore contribute to the genetic instability of c-MYC in B-cell malignancies.

242 A, E2F1 and DP1, creating conditions for the genetic instability of cells.

243 lation of genetic alterations and subsequent genetic instability of cells.

244 Intrinsic genetic instability of RNA viruses may lead to the accum

245 This result suggests that the genetic instability of such regions is often the cause r

246 stalled replication forks as a mechanism for genetic instability of the (GAA*TTC)n sequence.

247 ates erroneous DSB repair as a mechanism for genetic instability of the (GAA*TTC)n sequence.

248 We conclude that genetic instability of the PIG-A gene is not a factor in

249 cVDPV emerges due to the genetic instability of the Sabin viruses used in the ora

250 ase elongation and thereby contribute to the genetic instability of these repeat tracts.

251 te to our understanding of FEN1 in mediating genetic instability of TNR sequences.

252 Transcription stimulates the genetic instability of trinucleotide repeat sequences.

253 cancer is the extremely high mutability and genetic instability of tumor cells.

254 nces of heavy (V(H)) and light chains showed genetic instability of V(H) chains with only the hp-B6.1

255 This genetic instability of wt HAV in cell culture is a major

256 esponsible for the expansions and deletions (genetic instabilities) of repeating tri-, tetra- and pen

257 counteract the negative effect of tumor cell genetic instability on the outcome of immunotherapy targ

258 xpansion represents a major disadvantage for genetic instability only when inactivation of the tumor

259 carcinomas, but are not sufficient to induce genetic instability or metastases with high penetrance.

260 Genetic instability plays a central role in the developm

261 defects in DNA repair may lead to cancer and genetic instabilities, Pol beta has been extensively stu

262 the next TSG, whereas the same lesions with genetic instability pose a much greater risk for cancer

263 emonstrate a role for overexpressed cIAP1 in genetic instability, possibly by interfering with mitoti

264 Different genetic instability processes result in characteristic n

265 es can form G-quadruplexes, which can affect genetic instability, promoter activity, RNA splicing, RN

266 Genetic instability, provoked by exogenous mutagens, is

267 mal recessive human disease characterized by genetic instability, radiosensitivity, immunodeficiency

268 lity and safety stem from the possibility of genetic instability related to over-engineering the viru

269 hese advantages, OPV has the disadvantage of genetic instability, resulting in rare and sporadic case

270 monstrate that BER deficiency, which induces genetic instability, results in dramatic changes in gene

271 uplexes, which can affect promoter activity, genetic instability, RNA splicing, translation, and neur

272 strand break repair pathway that can promote genetic instabilities similar to those observed in cance

273 by inactivation of the SbcC protein; and by genetic instability studies with plasmids containing lon

274 yeloma (MM) is a malignancy characterized by genetic instability, suggesting a disruption of checkpoi

275 evel of predisposing conditions, initiation, genetic instability, susceptibility to host immune respo

276 Follicular thyroid tumours exhibited greater genetic instability than papillary tumours (27.6% (n=9)

277 Inactivation of cross-link repair leads to genetic instability that is restricted to PGCs within th

278 idence indicates that Fbw7 ablation promotes genetic instability that is suppressed by p53, and we sh

279 cess (low-grade pathway) and through greater genetic instability that leads to rapid metastasis witho

280 is an example of a catastrophic induction of genetic instability that may initiate or advance the cou

281 d the loss of DNA repair capacity results in genetic instability that may lead to a decline of cellul

282 checkpoint is thought to play a key role in genetic instability that predisposes cells to malignant

283 By inducing genetic instability, they can accelerate the evolution o

284 a critical target of viral HBx for promoting genetic instability through formation of defective spind

285 60 observed in many human tumors can promote genetic instability via defective pericentric heterochro

286 Consistent with this, genetic instability was greatest in Bi-Tg thyrocytes wit

287 y can have deleterious consequences, such as genetic instability, we discuss the mechanisms that may

288 As expression of RHAMM in MM contributes to genetic instability, we tested effects of RHAMM.

289 To further investigate PTTG's role in genetic instability, we transfected FTC133 thyroid folli

290 Here we show that the increase in genetic instability when GAA serves as the lagging stran

291 ese mechanisms lead to somatic mutations and genetic instability, which are hallmarks of cancer.

292 ces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage

293 Genetic instability, which includes both numerical and s

294 including Barrett's adenocarcinoma (BAC) is genetic instability, which is associated with developmen

295 Genetic instability, which leads to an accumulation of v

296 A key feature in the pathogenesis of OSCC is genetic instability, which results in altered expression

297 tribute to the phenomenon of hypoxia-induced genetic instability within the tumor microenvironment.

298 bolishes recruitment by Ub-Fancd2 and causes genetic instability without affecting ICL repair.

299 st androgen-based therapies, and an inherent genetic instability would enable the tumor to develop th

300 e hypothesized that expansion of clones with genetic instability would predict progression to esophag