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 s suppressor genes, telomere shortening, and genetic instability).

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

4 developmental defects, tumor propensity, and genetic instability.

5 activity, which is associated with increased genetic instability.

6 humans characterized by premature aging and genetic instability.

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

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

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

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

11 ock replication and transcription and induce genetic instability.

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

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

14 checkpoints that arrest growth and suppress genetic instability.

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

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

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

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

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

20 delity of chromosome segregation and promote genetic instability.

21 to the mechanisms underlying hypoxia-induced genetic instability.

22 Only DSBs increased the overall genetic instability.

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

24 otherapeutic response and the development of genetic instability.

25 derstanding the relationship between age and genetic instability.

26 eosome assembly of trinucleotide repeats and genetic instability.

27 nes and tumor suppressor genes, but promotes genetic instability.

28 has implications for anticancer therapy and genetic instability.

29 es or oncogenes but promote the emergence of genetic instability.

30 ly important for controlling mutagenesis and genetic instability.

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

32 d transcription in regulating Top1-dependent genetic instability.

33 evelopment of resistance to chemotherapy and genetic instability.

34 yploids missegregate chromosomes and undergo genetic instability.

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

36 enome at risk of retrotransposition-mediated genetic instability.

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

38 r refining the classification of tumors with genetic instability.

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

40 rid structures involved in transcription and genetic instability.

41 evolve rapidly and can mobilize and trigger genetic instability.

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

43 ycle progression and give rise to pronounced genetic instability.

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

45 and mobilization of these elements triggers genetic instability.

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

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

48 ed to explain the mechanisms of the observed genetic instabilities.

49 ells age there is a marked increase in their genetic instability (a hallmark of cancer), which is ind

50 Genetic instability, a hallmark feature of human cancers

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

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

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

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

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

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

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

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

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

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

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

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

63 t pathway has the potential to contribute to genetic instability and chromosomal aberrations during t

64 e literature over the relative importance of genetic instability and clonal expansion during progress

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 ur findings demonstrate that NAC counteracts genetic instability and suggest that genetic instability

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

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

86 of DNA metabolism and is thought to mediate genetic instability and transcription of expanded trinuc

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

88 ymocyte proliferation; however, it increases genetic instability and triggers gamma-irradiation-induc

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

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

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

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

93 ow deregulation of AuroraA can contribute to genetic instability and tumorigenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Although genetic instability appeared to have occurred in most tu

108 Genetic instability appears to be required for a normal

109 Genetic instabilities are believed to be one of the majo

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

111 tive forces responsible for the emergence of genetic instability are not clear.

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

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

114 The trigger for these events is likely the genetic instability arising from centrosome amplificatio

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

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

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

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

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

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

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

122 Genetic instability associated with shortened telomeres

123 3 mutations and that E2F1 contributes to the genetic instability associated with transformation and t

124 his review focuses on mouse assays detecting genetic instability at endogenous loci.

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 oidy is often caused by a particular type of genetic instability, called chromosomal instability, whi

145 Together, our data show that a high level of genetic instability can result from environmental impedi

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

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

148 The genetic instability caused by BRCA1 deficiency, however,

149 Genetic instability caused by mutations in the p53 gene

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

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

152 The genetic instability characteristic of cancer cells may b

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

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

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

156 al G insertion, suggesting that the observed genetic instability contributed to pathogenicity.

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

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

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

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

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

162 However, intrinsic genetic instability enables these immunodeficiency virus

163 8-hydroxy-2'-deoxyguanosine levels and, as a genetic instability endpoint, DNA deletions.

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

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

166 SBs) within a triplet repeat sequence on its genetic instabilities (expansions and deletions) related

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

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

169 Hypoxia promotes genetic instability for tumor progression.

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

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

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

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

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

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

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

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

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

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

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

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

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

183 results identify a potential new pathway of genetic instability in cancer: hypoxia-induced reduction

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

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

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

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

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

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

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

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

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

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

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

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

198 se findings, we propose a novel mechanism of genetic instability in the tumor microenvironment mediat

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

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

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

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

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

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

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

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

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

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

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

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

211 iotherapy response and could be a source for genetic instability, increased angiogenesis, and metasta

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

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

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

215 The combination of clonal expansion and genetic instability is a better predictor of cancer outc

216 Genetic instability is a common mechanism by which cance

217 Genetic instability is a defining characteristic of canc

218 Genetic instability is a feature of chronic lymphocytic

219 Genetic instability is a hallmark of aneuploidy in buddi

220 Genetic instability is a hallmark of cancer; the hypoxic

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

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

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

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

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

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

227 teracts genetic instability and suggest that genetic instability may be a consequence of oxidative st

228 In addition, this stress-induced genetic instability may represent a conceptual parallel

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

230 To test whether genetic instability might accelerate tumor progression,

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

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

233 Cells with mutations conferring genetic instability normally have a reduced somatic fitn

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

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

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

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

238 The genetic instability of (GAC*GTC)n (where n = 6-74) was i

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

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

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

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

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

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

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

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

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

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

249 a subset of ctf4Delta-interacting genes with genetic instability of their own.

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

251 nsights into the molecular mechanisms of the genetic instability of this tract as possibly related to

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

253 Transcription stimulates the genetic instability of trinucleotide repeat sequences.

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

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

263 e growing) cells and, second, that transient genetic instability, producing both point mutation and g

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

265 Genetic instability, provoked by exogenous mutagens, is

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

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

268 r findings suggest that H-DNA is a source of genetic instability resulting from DSBs and demonstrate

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

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

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

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

276 e findings suggest a new route to MMR-driven genetic instability that does not rely primarily on the

277 These observations define a type of genetic instability that has significant implications fo

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

284 60 observed in many human tumors can promote genetic instability via defective pericentric heterochro

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

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

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

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

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

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

291 In small compartments, genetic instability, which confers a selective disadvant

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