ライフサイエンスコーパス: drug sensitivity

1 pply MiSL to pinpoint genetic biomarkers for drug sensitivity.

2 ce that RNA editing could selectively affect drug sensitivity.

3 otentially linking upregulation to increased drug sensitivity.

4 ortant determinants of cation permeation and drug sensitivity.

5 n (Y652W) into S620T hERG1 partially rescued drug sensitivity.

6 s displayed decreased stemness and increased drug sensitivity.

7 ia (CLL) cells, thereby also affecting their drug sensitivity.

8 breast cancer cell line was found to restore drug sensitivity.

9 ith a unique epigenetic signature to predict drug sensitivity.

10 n profoundly influence parasite genetics and drug sensitivity.

11 f these lncRNAs exhibited a clear phenotype: drug sensitivity.

12 effects of NOX-A12 on CLL cell migration and drug sensitivity.

13 e diagnostic tools for tuberculosis (TB) and drug sensitivity.

14 e HGF receptor MET abrogates HGF's rescue of drug sensitivity.

15 tem to study the interplay of metabolism and drug sensitivity.

16 several parasite lines to test the effect on drug sensitivity.

17 sion of NICD1 reversed the action of DAPT on drug sensitivity.

18 und impact in their metabolism, biology, and drug sensitivity.

19 , elevated VTA BDNF may be a risk factor for drug sensitivity.

20 lls lacking H3K4 methylation have antifungal drug sensitivity.

21 expression can affect platelet function and drug sensitivity.

22 EN in PTEN-null breast cancer cells restored drug sensitivity.

23 inkages between genetic profile and targeted-drug sensitivity.

24 age, and gene-expression-based predictors of drug sensitivity.

25 e confounding effects of tumor CIN status on drug sensitivity.

26 of APP played a pivotal role in determining drug sensitivity.

27 whereas most other mutations did not affect drug sensitivity.

28 cell-specific dynamic signaling pathways and drug sensitivity.

29 markers, such as EVA1 and MAL2, and restored drug sensitivity.

30 tosis, cell differentiation, and therapeutic drug sensitivity.

31 to evaluate the effect of betaIII-tubulin on drug sensitivity.

32 lant exposure is positively related to later drug sensitivity.

33 l model for studying mechanisms of cisplatin drug sensitivity.

34 mon, previously unappreciated determinant of drug sensitivity.

35 igenetic silencing of p73 directly modulates drug sensitivity.

36 f these strains including immune evasion and drug sensitivity.

37 notypes, better cancer prognosis, and better drug sensitivity.

38 tumorigenesis as well as in chemotherapeutic drug sensitivity.

39 relationship between ICL repair capacity and drug sensitivity.

40 structure in those associated with wild-type drug sensitivity.

41 n between individuals, including disease and drug sensitivity.

42 ate was directly correlated with the in vivo drug sensitivity.

43 ere functional and exhibited family-specific drug sensitivity.

44 umorigenesis, as well as in chemotherapeutic drug sensitivity.

45 he expression level of slo is a predictor of drug sensitivity.

46 er revert the malignant phenotype or enhance drug sensitivity.

47 ergy status of the cell, PXR regulation, and drug sensitivity.

48 nts, mutations can have important effects on drug sensitivity.

49 t component of tumor fitness and can predict drug sensitivity.

50 cing unique growth physiologies and reducing drug sensitivity.

51 , decreased HOX gene expression and restored drug sensitivity.

52 OK2, miR-193a, and others) restored platinum drug sensitivity.

53 i-cancer treatment can uncover biomarkers of drug sensitivity.

54 erturbed genes cooperatively associated with drug sensitivity.

55 ns on tumorigenesis, cancer progression, and drug sensitivity.

56 related modules as top differential ones for drug sensitivity.

57 el to study the effects of the cell cycle on drug sensitivity.

58 ought to represent a biomarker predictive of drug sensitivity.

59 nd high MYC expression predicts anti-mitotic drug sensitivity.

60 nisms, establishing an individual profile of drug sensitivity.

61 nt channels can exhibit dramatically reduced drug sensitivity.

62 etween parasite isolates that exhibit varied drug sensitivities.

63 s, including life span, budding pattern, and drug sensitivities.

64 lly among P. falciparum strains with varying drug sensitivities.

65 sis, an in silico screening of a database of drug sensitivities across 39 cancer cell lines (JFCR39),

66 osis, chemokine release, gene induction, and drug sensitivity across divergent epithelial cell lines.

67 GemR cells to gemcitabine, reaching parental drug sensitivity after 10 treatment cycles.

68 e of matrix stiffness in growth kinetics and drug sensitivity against standard chemotherapy in vivo.

69 Data for laboratory isolates, including drug sensitivities and 24-mycobacterial interspersed rep

70 three strains of gametocytes with different drug sensitivities and geographical origins, 3D7, HB3 an

71 itation by developing GEMs based on in vitro drug sensitivities and microarray analyses of the NCI-60

72 e harbor multiple IMPDH enzymes with varying drug sensitivities and offer an assay to monitor the inh

73 erstanding the differences between intrinsic drug sensitivity and acquired resistance in the context

74 A549 cells, suggesting a correlation between drug sensitivity and basal phospho-Akt levels independen

75 n, inactivation rates, G-protein modulation, drug sensitivity and cell surface expression.

76 the levels of RAD6 could lead to changes in drug sensitivity and damage-induced mutagenesis.

77 ral biomarkers for clinical determination of drug sensitivity and drug efficacy in nucleotide triphos

78 ient-derived melanoids for prognostic use of drug sensitivity and further underscoring the beneficial

79 is of great interest to jointly analyze the drug sensitivity and gene expression data from the same

80 ovides a unique resource incorporating large drug sensitivity and genomic datasets to facilitate the

81 e of a mitochondrial MSH that is involved in drug sensitivity and implicate the induction of mitochon

82 ures predictive of tumor phenotypes, such as drug sensitivity and invasive or metastatic potential.

83 a that inhibition of autophagy will increase drug sensitivity and kill more cancer cells.

84 These cells demonstrate >100-fold reduced drug sensitivity and maintain viability via engagement o

85 ering ~500-fold in drug response, determined drug sensitivity and marker segregation in clonally deri

86 Interspecies differences in drug sensitivity and mechanistic profiles, low predictiv

87 The method is exemplified by application to drug sensitivity and microRNA expression data from a pan

88 Drug sensitivity and resistance are conventionally quant

89 Here we combine comprehensive drug sensitivity and resistance profiling of patient cel

90 Drug sensitivity and resistance testing on diagnostic le

91 Our results explain the basis for drug sensitivity and resistance to an exceptionally pote

92 es three subtypes of lung SCC that differ in drug sensitivity and shows a novel mechanism of miR-29b

93 Adequate infrastructure for testing drug sensitivity and sufficient evidence of first-line r

94 n of miR-23b cluster or miR-125a-5p enhanced drug sensitivity and suppressed invasiveness of NSCLC ce

95 reprograms melanoma metabolism to influence drug sensitivity and survival.

96 that melanosomal regulatory genes influence drug sensitivity and that the presence of mature melanos

97 Epigenomic subpopulations in cancer impact drug sensitivity and the clonal dynamics of cancer evolu

98 Fanconi anemia, has yielded new insights to drug sensitivity and treatment of sporadic cancers, such

99 s interact, we investigated their effects on drug sensitivity and viral fitness.

100 ed ABCC4 from the plasma membrane, increased drug sensitivity, and abrogated MPP1-dependent hematopoi

101 OM permeability, lipopolysaccharide levels, drug sensitivity, and cell death in stationary phase.

102 detect a population which shows differential drug sensitivity, and imply that treatment of patients c

103 pression of PTEN in PTEN-null cells restored drug sensitivity, and knockdown of PTEN promoted drug re

104 expected to reduce cardiac I Kr and enhance drug sensitivity, and represent a potential mechanism un

105 dictive of the kinds of mutations, the tumor drug sensitivity, and the treatment outcome.

106 ient, in terms of their malignant potential, drug sensitivity, and their potential to metastasize and

107 ltiple biomarkers that contribute jointly to drug sensitivity, and to identify combination therapies

108 nhibition of IL-10 signaling correlates with drug sensitivity; and (6) addition of exogenous IL-10 or

109 e find that differences in general levels of drug sensitivity are driven by biologically relevant pro

110 data tend to exhibit improved prediction of drug sensitivity as compared with genomic and transcript

111 known drug-target relationships and overall drug sensitivity as compared with genomic or transcripto

112 tated or deleted in human tumors, may impact drug sensitivity, as exemplified by triple-negative brea

113 However, a drug sensitivity assay suggested that extremely low leve

114 7Ysr39tk supermutant was also confirmed by a drug sensitivity assay, in which the 50% inhibitory conc

115 yped with the Env proteins in a single-round drug sensitivity assay.

116 Drug sensitivity assays revealed resistance to oseltamiv

117 ractory to sodium stibogluconate in in-vitro drug sensitivity assays.

118 -pencyclovir ((3)H-PCV), and (3)H-GCV and by drug sensitivity assays.

119 -state acetylcholine release as indicated by drug sensitivity assays.

120 Quantitatively predicting changes in drug sensitivity associated with residue mutations is a

121 ging the latest knowledge on mutation-cancer drug sensitivity associations and the results from large

122 apy may have future application in restoring drug sensitivity at relapse.

123 matically analyze mutations affecting cancer drug sensitivity based on individual genomic profiles.

124 cused on identifying molecular biomarkers of drug sensitivity based on queries of specific anticancer

125 e that neoplastic cells exhibit differential drug sensitivity based on their residence in specific ce

126 The UPR was shown to be required for altered drug sensitivity, because the BiP-overexpressing cell li

127 d R5 cells, establishing that differences in drug sensitivities between sublines were independent of

128 ontrivial, complex ways to the difference in drug sensitivity between Emu-myc Arf-/- and Emu-myc p53-

129 apoptotic regulators that are predictive of drug sensitivity (BIM, caspase-3, BCL-XL) and resistance

130 ing pocket with Ala has a dramatic effect on drug sensitivity, but that the channel remains fully dru

131 idly detects bacterial growth and determines drug sensitivity by measuring changes in the suspension'

132 we found that most cells can be rescued from drug sensitivity by simply exposing them to one or more

133 Thus, parasites selected for decreased drug sensitivity can appear long after predicted exposur

134 Herein we ask whether or not drug sensitivity can be designed into Klp61F.

135 ted in both drug resistance and personalized drug sensitivity can be predicted in a high-throughput f

136 he traditional view, circadian variations in drug sensitivity cannot be attributed to the changes in

137 embrane domains, whose regulation may affect drug sensitivity, cellular metabolism and growth.

138 Figure 2 demonstrates resistance to drug sensitivity conferred by co-culture with some strom

139 mechanism nor the uniformity of anti-mitotic drug sensitivity connected with mutant KRAS expression a

140 tion coefficients (PCCs) >0.4, where reduced drug sensitivity correlated with ABCG2 expression, as we

141 of alterations in cell-surface antigens and drug sensitivity correlated with iron availability.

142 f-of-principle case, we showed that in vitro drug sensitivity could predict both a clinical response

143 olecular markers of drug response, cell line drug sensitivity data are integrated with large genomic

144 Using in vitro drug sensitivity data coupled with Affymetrix microarray

145 GDSC currently contains drug sensitivity data for almost 75 000 experiments, des

146 Such drug sensitivity data for cancer cell lines provide sugg

147 aluated using microarray gene expression and drug sensitivity data from human and canine cancer cell

148 Comparisons of gene essentiality with drug sensitivity data suggest potential resistance mecha

149 clinical platform generating a compendium of drug sensitivity data totalling >4,000 assays testing 16

150 Using in vitro drug sensitivity data, coupled with microarray data, we

151 sues (n=60), and integrated with genomic and drug sensitivity data.

152 intly analyze the paired gene expression and drug sensitivity datasets measured across the same panel

153 he utility of our package in comparing large drug sensitivity datasets, such as the Genomics of Drug

154 The increased drug sensitivity did not extend to epothilone A, a drug

155 fying genetic biomarkers of synthetic lethal drug sensitivity effects provides one approach to the de

156 On the basis of drug sensitivity experiments for resolving the kinetic c

157 signaling dynamics correlated strongly with drug sensitivity for 14 of the drugs, 9 of which had no

158 he simulations predicted the ranked order of drug sensitivity for indomethacin, aspirin, MRS-2179 (a

159 ies also reveal unique signature patterns of drug sensitivity for inhibition of tyrosine autophosphor

160 ossibility of identifying genomic markers of drug sensitivity for novel compounds on novel cell lines

161 s a simple semiempirical method to determine drug sensitivity for positive secondary ions.

162 ion may come from diverse sources, including drug sensitivities, gene ontology biological processes,

163 OS, providing a mechanistic link between the drug sensitivity, gene expression, and pathogenesis phen

164 ature of cancer, but its global influence on drug sensitivity has not been examined.

165 Predictive models of in vitro drug sensitivity have previously been constructed using

166 Analysis of gene set enrichment and drug sensitivity identified an immune-evasion subtype th

167 revented core complex formation and restored drug sensitivity, impairing the signaling pathways invol

168 A, acbA, smlA, and atg8) resulted in altered drug sensitivity, implicating novel pathways in cisplati

169 otential solution to this may lie in finding drug sensitivities in the resistant population, termed c

170 e, MDR1, has previously been associated with drug sensitivities in two breeds from the collie lineage

171 We measured gene expression and drug sensitivity in 15 pediatric T-ALL cell lines to fin

172 w targeting apoptotic programmes can restore drug sensitivity in a genotype-dependent manner.

173 onine beta-synthase (CYS4) that causes multi-drug sensitivity in a vineyard strain of Saccharomyces c

174 The Genomics of Drug Sensitivity in Cancer (GDSC) and Cancer Cell Line E

175 The Genomics of Drug Sensitivity in Cancer (GDSC) database (www.cancerRx

176 to understand the mechanisms that determine drug sensitivity in cancer and normal cells.

177 ensitivity datasets, such as the Genomics of Drug Sensitivity in Cancer and the Cancer Cell Line Ency

178 e largest public resource for information on drug sensitivity in cancer cells and molecular markers o

179 tematic identification of genomic markers of drug sensitivity in cancer cells" by Garnett and colleag

180 ovides new insights into the determinants of drug sensitivity in cancer cells.

181 ores the important role of hCtr1 in platinum-drug sensitivity in cancer chemotherapy.

182 models and models generated from Genomics of Drug Sensitivity in Cancer database shows the ability of

183 small interfering RNA against PP2A/C reduced drug sensitivity in E1A-expressing cells.

184 .Z.2 as a mediator of cell proliferation and drug sensitivity in malignant melanoma, holding translat

185 ntibodies may provide a surrogate measure of drug sensitivity in patients with drug-induced immune cy

186 e show that variability in general levels of drug sensitivity in pre-clinical cancer models confounds

187 utated-B-RAF inhibitors and possibly restore drug sensitivity in resistant tumors.

188 ts in physiological abnormalities or affects drug sensitivity in selected populations (e.g., those wi

189 tory strains that show little differences in drug sensitivity in standard in vitro assays exhibit sub

190 t of proteins that effectively reconstituted drug sensitivity in the cell-free screen and included a

191 Ornithine uptake and the modulation of drug sensitivity in Trypanosoma brucei.

192 ion by E1B-55K for cell cycle regulation and drug sensitivity in tumor cells has not been examined.

193 c residues inducing the greatest increase in drug sensitivity in vivo and in vitro.

194 nisms, including consequences for inhibitory drug sensitivity, insights that may inform the developme

195 and determined the impact of these genes on drug sensitivity, irradiation sensitivity, and genome ma

196 Nonetheless, drug sensitivity is equivalent in the mutant pdr5 and th

197 The role of TME in modulating tumor drug sensitivity is increasingly recognized and targetin

198 ough which mutants of p53 may induce loss of drug sensitivity is via the NF-kappaB2 pathway.

199 Of 4 drug-sensitivity loci selected for validation, 2 showed

200 alse-positive associations, we identified 16 drug-sensitivity loci, only 3 of which had been previous

201 This model, developed using FM-HCR and drug sensitivity measurements in 24 human lymphoblastoid

202 e resource for cancer researchers, providing drug sensitivity, molecular and phenotypic data for a ra

203 an in cancer cells, may be attributed to low drug sensitivity, nevertheless the study invited close a

204 MAR revealed heterogeneity in drug sensitivity not only between different tumors, but

205 es lacking SMARCB1 are vital determinants of drug sensitivity, not just to TOP2A-targeted agents, but

206 toward WT tumors, confirming the collateral drug sensitivities observed in vitro.

207 We determined drug sensitivities of the subtypes in primary tumors usi

208 e, we show that COXEN can accurately predict drug sensitivity of bladder cancer cell lines and clinic

209 insights into the mechanisms underlying the drug sensitivity of cancer cell lines.

210 teractions and mutation loads to explain the drug sensitivity of cancer cells.

211 actions serve as biomarkers that predict the drug sensitivity of cell lines in screens across 195 dru

212 We then examine the drug sensitivity of cell-to-cell spread of HIV, a mode o

213 terogeneous leukemia-initiating capacity and drug sensitivity of CML LTHSCs and suggest that high MPL

214 and PP2Acalpha phosphatases in the selective drug sensitivity of del(5q) MDS.

215 manipulation of SALL4 expression can affect drug sensitivity of endometrial cancer cells to carbopla

216 p53 status to the biological properties and drug sensitivity of human cancer.

217 We therefore assessed drug sensitivity of I(Kur) generated in vitro in CHO and

218 eflected in altered frequency, kinetics, and drug sensitivity of mIPSCs.

219 ssion (P < .001), perhaps reflecting greater drug sensitivity of more aggressive disease.

220 Gant61 monotherapy did not alter the drug sensitivity of naive cells, but could reverse the r

221 thus resulting in successful restoration of drug sensitivity of OVCAR8/ADR cells to Pgp-transportabl

222 ence that synonymous mutations can alter the drug sensitivity of proteins.

223 ize a functional assay to assess the ex vivo drug sensitivity of single multiple myeloma cells based

224 region fine-tunes calcium responsiveness and drug sensitivity of the anchored phosphatase.

225 These results suggest that the drug sensitivity of the mutant Pdr5 is attributable to t

226 st that the altered signaling properties and drug sensitivity of these EGFR mutants that have been ob

227 of CgAP1 also phenotypically suppressed the drug sensitivity of two Yap1p-regulated transporter muta

228 For most drugs, sensitivity of skin testing is higher in immediat

229 rug action that influence treatment outcome: drug sensitivity or drug resistance.

230 an EGFR mutation known to be associated with drug sensitivity or objective clinical benefit from trea

231 crochannel resonator, accurately defined the drug sensitivity or resistance of glioblastoma and B-cel

232 hibit L. donovani infection, irrespective of drug sensitivity or resistance.

233 externalizing traits, consumption drive, and drug sensitivity or tolerance) that combine with key env

234 Linking molecular profiles with drug sensitivity patterns identifies novel biomarkers, i

235 genes that most likely explain the observed drug sensitivity patterns.

236 n identifying molecular mediators for cancer drug sensitivity (pharmaco-epigenomics).

237 However, despite the null-like drug sensitivity phenotype, chemical cross-linking analy

238 cally diverse locations and possess distinct drug sensitivity phenotypes.

239 s (DREAM) project, we analyzed a total of 44 drug sensitivity prediction algorithms.

240 This study establishes benchmarks for drug sensitivity prediction and identifies approaches th

241 of random forest based methods in NCI-DREAM drug sensitivity prediction challenge.

242 To assess the preclinical feasibility of drug sensitivity prediction, several studies have measur

243 For designing a drug sensitivity predictive model from such a database,

244 rug to treat this cancer type that mimic the drug sensitivity profile in PDX model, further confirmin

245 Here, we evaluate the in vitro drug sensitivity profile of normally-developing P. falci

246 cells-of-origin may critically determine the drug sensitivity profiles of mammary neoplasia.

247 Analysis of the resulting drug sensitivity profiles provides novel information on

248 tion, high-throughput drug perturbation, and drug sensitivity profiles, enabling drug classification

249 By comparing drug sensitivity profiles, we predicted BUB1B(S) cells t

250 showed that our prediction agrees with their drug-sensitivity profiles.

251 y protein KCR1, which markedly reduces I(Kr) drug sensitivity, protects HERG through glucosyltransfer

252 perturbation gene expression signatures and drug sensitivity provide a powerful framework to develop

253 For problem use of illicit and prescription drugs, sensitivity ranged from 0.82 (CI, 0.76 to 0.87) f

254 e stage- and strain-dependent differences in drug sensitivity reflect differential response lag times

255 aches integrated cistrome, transcriptome and drug sensitivity relationships to reveal that NCOR1 func

256 Existing approaches to predicting drug sensitivity rely primarily on profiling of cancer c

257 he relationship between p53-driven genes and drug sensitivity remains controversial.

258 regarding somatic mutation for prediction of drug sensitivity remains controversial.

259 osphorylation-related signaling networks and drug sensitivity/resistance in the era of precision onco

260 mors, find that many of these associate with drug sensitivity/resistance, and highlight the importanc

261 Notably, drug sensitivity results directly from tgp1(+) expressio

262 ently of tuberculin skin test and index-case drug sensitivity results.

263 cellular events, including stress responses, drug sensitivity, sexual reproduction, and virulence.

264 Thus, genome-informed drug sensitivity studies identify a subset of GBMs likel

265 Results from drug sensitivity studies with beta-lactamase enzymes are

266 suppressing genes on the basis of the shared drug sensitivity suppression and similar genetic interac

267 monstrated that the function of HSP-16.48 in drug sensitivity surprisingly was independent of chapero

268 tecting rifampin resistance using phenotypic drug sensitivity testing (DST) as the reference standard

269 ically relevant time scale some weeks before drug sensitivity testing (DST) data are available, and t

270 Drug sensitivity testing of CTC lines with multiple muta

271 Subsequent drug sensitivity testing revealed over 100-fold increase

272 Parasite clearance half-life and in vitro drug sensitivity testing were performed using standard m

273 plications, including regenerative medicine, drug sensitivity testing, gene expression profiling and

274 ntry of high tuberculosis burden should have drug-sensitivity testing on isolates to ensure appropria

275 isen from diploid cell lines displayed lower drug sensitivity than their diploid parental cells only

276 to identify previously occult biomarkers of drug sensitivity that can aid in the identification of p

277 oproteins provide information for predicting drug sensitivity that is not available from the correspo

278 stimulation; this mutant retained wild-type drug sensitivity that was unaffected by PKA.

279 ance the generation of important insights to drug sensitivity that will lead to improved precision me

280 d and distinct roles in stress responses and drug sensitivity through the Hog1 MAPK system.

281 We exploited breed phylogeny and reports of drug sensitivity to survey other purebred populations th

282 e with lentiviral TR4 siRNA led to increased drug sensitivity to the two commonly used chemotherapeut

283 s a significant improvement in prediction of drug sensitivity using genes identified by ProGENI compa

284 Drug sensitivity was also different.

285 This enhanced drug sensitivity was associated with a severe impairment

286 Drug sensitivity was restored with co-treatment of eithe

287 To identify additional genes influencing drug sensitivity, we used CYS4 as a covariate and conduc

288 es using in vitro transformation assays, and drug sensitivities were validated with the use of assays

289 Similar levels of drug sensitivity were displayed by the three most common

290 us or MYC expression levels and anti-mitotic drug sensitivity when surveying a large database of anti

291 pidermis and cuticle layers causes increased drug sensitivity, which could aid the growing use of C.

292 of KCNA5 generated a channel with wild-type drug sensitivity, which indicated that P532 is not a dru

293 ned inhibition, is sufficient to enhance AML drug sensitivity, which provides a novel therapeutic str

294 increased AKT phosphorylation and decreased drug sensitivity, which was attenuated by GLI1 inhibitio

295 Knockdown of CDK6 restored drug sensitivity, while enforced overexpression of CDK6

296 rtefactual correlations between genotype and drug sensitivity, while obscuring valuable biological in

297 to identify patient subclasses according to drug sensitivity will lead to a more personalized medici

298 patient samples revealed a wide diversity of drug sensitivities, with 70% of the clinical specimens e

299 branch point (BP) region strongly influence drug sensitivity, with additional functional BPs reducin

300 lary subunits can potentially strongly alter drug sensitivity without obvious functional changes in g