ライフサイエンスコーパス: drug resistance

1 cer evolution, intratumor heterogeneity, and drug resistance.

2 rocesses that contribute to the emergence of drug resistance.

3 which suggested an association of BMK1 with drug resistance.

4 extrinsic as well as intrinsic mechanisms of drug resistance.

5 or malignancy, and leads to the emergence of drug resistance.

6 public health problem that is exacerbated by drug resistance.

7 reatment access, and the role of second-line drug resistance.

8 ion and progression, bacterial dynamics, and drug resistance.

9 treatment regimens, and growing evidence of drug resistance.

10 cs are unsustainable due to the emergence of drug resistance.

11 aminidase inhibitors has declined because of drug resistance.

12 ci that contribute to artemisinin or partner drug resistance.

13 nt response is limited by the development of drug resistance.

14 altered cellular metabolism, metastasis, and drug resistance.

15 at can control the development and spread of drug resistance.

16 its E3 ubiquitin ligase activity to HDR and drug resistance.

17 esign of additional combinations that bypass drug resistance.

18 rug development efforts to overcome acquired drug resistance.

19 nt target), side-effects and are implicit in drug resistance.

20 of inhibitors that target this mechanism of drug resistance.

21 ucleus, increased expression of pERK1/2, and drug resistance.

22 re considered a potent cause of antimalarial drug resistance.

23 d to rapidly increasing population levels of drug resistance.

24 cer evolution, progression, and emergence of drug resistance.

25 nition, are less likely to be susceptible to drug resistance.

26 pression, cancer stemness, tumor growth, and drug resistance.

27 Cs, so as to overcome both breast cancer and drug resistance.

28 l to metastatic tumor cell dissemination and drug resistance.

29 ces (2.1%) indicated evidence of transmitted drug resistance.

30 t a therapeutic strategy to prevent acquired drug resistance.

31 the effect humoral immunity has on evolving drug resistance.

32 valuation of baseline and treatment-emergent drug resistance.

33 ed cisplatin treatment frequently results in drug resistance.

34 MGB1 and its isoforms in epileptogenesis and drug resistance.

35 ion of genotypic testing for cytomegalovirus drug resistance.

36 de that is essential for their viability and drug resistance.

37 nists, thereby circumventing HER3-associated drug resistance.

38 environment in engendering heterogeneity and drug resistance.

39 e reducing the risk of generating additional drug resistance.

40 acy in BRCA-deficient patients is limited by drug resistance.

41 e been correlated with tumor progression and drug resistance.

42 eatment, but its effectiveness is limited by drug resistance.

43 TKI resistance and to discover mechanisms of drug resistance.

44 ithelial cells and promote proliferation and drug resistance.

45 F) correlates with invasion, senescence, and drug resistance.

46 ibed mutations as potentially responsible of drug resistance.

47 the regulation of apoptosis, DNA repair and drug resistance.

48 arget EGFR to reduce the risks of developing drug resistance.

49 cannot be mutated by the parasite to evolve drug resistance.

50 it coordinately mediates immune evasion and drug resistance.

51 nts is often countered by the acquisition of drug resistance.

52 herapy or a combination of drugs to overcome drug resistance.

53 each sector contributes to the emergence of drug resistance.

54 are associated with high economic costs and drug resistance.

55 at can overcome persistence and, indirectly, drug resistance.

56 the potential for overcoming issues such as drug resistance.

57 and confer it with aggressive phenotype and drug resistance.

58 d is correlated with disease progression and drug resistance.

59 e of mechanotransduction in the evolution of drug resistance.

60 amide, which is being threatened by emerging drug resistance.

61 r cells, consistent with the role of hPXR in drug resistance.

62 microenvironment and development of acquired drug resistance.

63 ant role of CAF exosomes in chemotherapeutic drug resistance.

64 persistence, followed by the development of drug resistance.

65 including cases of acquisition of additional drug resistance.

66 ntibiotics, which result in side effects and drug resistance.

67 ioblastoma cell proliferation, apoptosis and drug resistance.

68 ntly affects drug clearance and the onset of drug resistance.

69 A alkylation and establishes a mechanism for drug resistance.

70 lex, and essential in tumour development and drug resistance.

71 ssential to bacterial growth, metabolism and drug resistance.

72 mising strategies to impede the evolution of drug resistance.

73 ell membrane and significantly contribute to drug resistance.

74 tionally design new combinations that bypass drug resistance.

75 ectiveness is thwarted by rapid emergence of drug resistance.

76 iation in carriage duration: serotype (17%), drug-resistance (9%) and other significant locus effects

77 arasite lineages, which then acquire partner drug resistance across the Greater Mekong subregion, thr

78 roportions of failure, relapse, and acquired drug resistance (ADR) for 4 dosing schedules: daily thro

79 eria-positive cultures to ascertain acquired drug resistance (ADR).

80 , which induces apoptosis and reverses multi-drug resistance against ovarian cancer cells through dow

81 c drugs and their high propensity to develop drug resistance, alternative strategies are required to

82 influence self-renewal, differentiation and drug resistance, although the pathways underlying these

83 For example, increasing drug resistance among gram-positive bacteria is responsi

84 Cases of drug resistance among these pathogens have become more f

85 s with isolated NNRTI-associated transmitted drug resistance and 49 matched controls.

86 initiate key steps in microbial evolution of drug resistance and cancer progression.

87 nce complicated by poor adherence leading to drug resistance and disease relapse.

88 o release of MCL cells from TME, reversal of drug resistance and enhanced anti-MCL activity in MCL pa

89 The patterns of drug resistance and factors driving emergence of resista

90 We independently analyzed HCV drug resistance and HCV RNA measurement results that wer

91 ProGENI gives new insight into mechanisms of drug resistance and identifies genes that may be targete

92 nding of glutamine metabolism involvement in drug resistance and immuno-response, we investigated the

93 a-tumour genetic heterogeneity (ITH) fosters drug resistance and is a critical hurdle to clinical tre

94 c spectrum, and underlies key traits such as drug resistance and metastasis.

95 poorer predicted patient survival, acquired drug resistance and metastasis.

96 mechanisms for understanding anti-angiogenic drug resistance and presents an expanded role of growth

97 the multistage nature of the acquisition of drug resistance and provides a framework for understandi

98 urable and is characterized by high rates of drug resistance and relapse.

99 nalysis offers deeper perspectives on cancer drug resistance and suggests new biomarkers and treatmen

100 eals a novel regulatory mechanism underlying drug resistance and suggests that TRIB2 functions as a r

101 Underlying drug resistance and the acquisition of drug resistance d

102 Given the serious problem of drug resistance and the adverse side effect profiles of

103 netic methods used to study the emergence of drug resistance and the spread of resistant viruses.

104 ntries has also contributed to the spread of drug resistance and threatens long-term eradication goal

105 GNA13 levels modulate drug resistance and TIC-like phenotypes in patient-deriv

106 the cleavage of caspase-3 and HuR to promote drug resistance and tumor growth.

107 y the tumor microenvironment contributing to drug resistance and tumor recurrence.

108 file in S. flexneri 2457T, including induced drug resistance and virulence gene expression.

109 d growth factor signaling, which may promote drug resistance, and decreased antigen presentation and

110 Current antiviral drugs are susceptible to drug resistance, and developing new antivirals is essent

111 haracteristics including invasive migration, drug resistance, and epithelial-to-mesenchymal transitio

112 chemotherapeutic efficacy, address risks of drug resistance, and improve patient compliance by enabl

113 i, demonstrate that this can result in multi-drug resistance, and indicate that vigilance will be req

114 n cancer correlates with aggressive disease, drug resistance, and poor prognosis.

115 ntly needed to monitor the spread of partner drug resistance, and to recommend alternative treatments

116 s and compensatory evolution, coselection of drug resistances, and population bottlenecks and clonal

117 e rate, the cases of recurrence and acquired drug resistance are concerning and highlight the need fo

118 The molecular mechanisms that cause drug resistance are naturally occurring in less suscepti

119 resources rates of emerging and transmitted drug resistance are not regularly assessed.

120 Successful drug delivery and overcoming drug resistance are the primary clinical challenges for

121 Recurrence and chemotherapeutic drug resistance are two of the most prominent factors th

122 Although their mechanisms of drug resistance are well studied, the virulence factors

123 ted mortality, were stratified by underlying drug resistance, as well as by health sector to understa

124 gnificant human immunodeficiency virus (HIV) drug resistance, assays to detect these mutations have b

125 to facilitate the placement of an important drug-resistance associated insertion at the position at

126 MDR and XDR tuberculosis caused by acquired drug resistance, assuming no fitness cost of resistance

127 utlier AML responded and exhibited intrinsic drug resistance at relapse.

128 thermore, we are able to reverse established drug resistance based on the model prediction by modulat

129 s in the absolute prevalence of pretreatment drug resistance between 2015 and 2016 ranged from 0.3% i

130 The addition of LDR significantly reduced drug resistance both in vitro and in computational model

131 SC) have been implicated in the emergence of drug resistance but mechanisms and intervention points a

132 findings demonstrate that SALL4 could induce drug resistance by enhancing DDR and DNA repair through

133 there is an opportunity to better understand drug resistance by exploiting these techniques to provid

134 resistant parasites retards the evolution of drug resistance by intensifying competitive interactions

135 r intrinsic high expression of TRIB2 induces drug resistance by promoting phospho-AKT (at Ser473) via

136 e demonstrate a novel approach in addressing drug resistance by taking inhibitors against which resis

137 teractions and revert cell adhesion-mediated drug resistance (CAM-DR) to the same levels as SOX11(-)

138 Drug resistance can be transmitted.

139 with targeted drugs, which by selecting for drug resistance can drive metastatic progression, this s

140 cellular states in cancer has been linked to drug resistance, cancer progression and the presence of

141 Acquired drug resistance caused 80% of incident XDR tuberculosis

142 stance is increasingly compounded by partner drug resistance, causing high failure rates of artemisin

143 The emergence of drug resistance continues to be a major hurdle towards i

144 ns and unpublished datasets for pretreatment drug-resistance data in individuals in LMICs initiating

145 Data were matched with the UK HIV Drug Resistance Database (UKHIVDRB) to assess cumulative

146 of MDR tuberculosis strains, with increasing drug-resistance, drives the MDR tuberculosis epidemic in

147 lying drug resistance and the acquisition of drug resistance during treatment were included.

148 dherence difficulties contribute to acquired drug resistance during treatment.

149 idemiological studies, and to understand how drug resistance emerges and spreads.

150 r most consistently associated with platinum drug resistance, emphasizing the need to directly measur

151 cancer, such as progression, metastasis and drug resistance etc., cannot be fully understood by gene

152 wledge of the mechanisms by which antifungal drug resistance evolves in experimental populations and

153 cer (or renal cell carcinoma, RCC); however, drug resistance frequently occurs via subsequent activat

154 spread of human immunodeficiency virus (HIV) drug resistance from antiretroviral roll-out programs re

155 depends on the chromosomal neighborhood of a drug-resistance gene inserted at different positions of

156 l-time adaptive changes in expression of the drug-resistance gene.

157 Human immunodeficiency virus type 1 (HIV-1) drug resistance genotyping is recommended to help in the

158 ysaccharide O2 serotype strains in all major drug resistance groups correlating with a paucity of ant

159 orrelate with stem cell pluripotency, cancer drug resistance, GSL storage disorders and other disease

160 However, the rapid development of drug resistance has been a major hurdle in gemcitabine t

161 tremendously decreased, and transmission of drug resistance has merely stabilized in recent years.

162 rgence of human immunodeficiency virus (HIV) drug resistance has tremendously decreased, and transmis

163 ng are pivotal to limiting the threat of HIV drug resistance (HIVDR) accumulation,and allow for optim

164 The emergence of HIV drug resistance (HIVDR) as antiretroviral treatment prog

165 However, HIV drug resistance (HIVDR) data among HIV-1-infected young

166 opment of human immunodeficiency virus (HIV) drug resistance (HIVDR) in many low- and middle-income c

167 apy (ART) can lead to increased rates of HIV drug resistance (HIVDR) mutations in treated and also in

168 Human immunodeficiency virus drug resistance (HIVDR) plays a major role in pediatric

169 antiretroviral therapy (ART) programs to HIV drug resistance (HIVDR), we used an individual-level mod

170 sidered the prevalence of pretreatment NNRTI drug resistance in 2017.

171 When modeling the effect of drug resistance in a heterogeneous cancer cell populatio

172 Evading persistent drug resistance in cancer and bacteria is quintessential

173 NRF2 accumulation promote cell survival and drug resistance in cancer cells.

174 The development of drug resistance in cancer poses a major clinical problem

175 This fractional killing contributes to drug resistance in cancer.

176 s, which could give rise to the emergence of drug resistance in cases of drug pressure weakening.

177 97S) and HER2 (C805S) that mediated acquired drug resistance in drug-sensitive EGFR or HER2 exon 20 i

178 Mechanisms of drug resistance in gram-negative bacteria (GNB) are nume

179 changes, associated with the development of drug resistance in high-grade serous ovarian cancer, wer

180 provides a novel strategy to block TICs and drug resistance in HNSCCs.

181 ansmission model to project the emergence of drug resistance in India due to incorrect tuberculosis m

182 The key drivers of drug resistance in LMICs are reviewed here, and recommen

183 a critical role in oxidative stress-mediated drug resistance in mantle cell lymphoma (MCL); however,

184 oenvironment are key drivers associated with drug resistance in many cancers.

185 itical role in cell wall biosynthesis of and drug resistance in methicillin-resistant Staphylococcus

186 erapy on CAFs and how they may contribute to drug resistance in neighboring cancer cells is not well

187 ion of apoptotic vulnerabilities to overcome drug resistance in ovarian and other cancers.High-grade

188 malignant transformation and development of drug resistance in ovarian cancer.

189 eat need to discover new compounds to combat drug resistance in parasitic nematodes.

190 ffective tools for limiting the emergence of drug resistance in pathogens.

191 Pretreatment drug resistance in people initiating or re-initiating an

192 hain reaction assays at loci associated with drug resistance in Plasmodium falciparum isolated from s

193 tly empower serial monitoring strategies for drug resistance in the clinic as well as the development

194 acellular regulated kinase-1/2 signaling and drug resistance in the presence of its ligand CXCL12.

195 ry into the roles for acquired versus innate drug resistance in this setting.

196 newal agonist, and promotes immunomodulatory drug resistance in vitro.

197 together with cytotoxic drugs could overcome drug-resistance in glycolytic cancers.

198 suggest that AG can be exploited to diminish drug-resistance in Mtb through redox-based interventions

199 dinate not only MCL tumor dispersal but also drug resistance, including bortezomib resistance, via pl

200 Drug resistance is a major problem in antibacterial chem

201 Drug resistance is an almost inevitable consequence of c

202 oma (MM) patients; however, the emergence of drug resistance is common.

203 human immunodeficiency virus type 1 (HIV-1) drug resistance is critical for assessing ART effectiven

204 INTERPRETATION: Pretreatment drug resistance is increasing at substantial rate in LMI

205 st probably in the commensal niche, and that drug resistance is not a primary determinant of success

206 Drug resistance is one of the major problems in targeted

207 Since drug resistance is rooted mainly in tumor cell heterogen

208 tion of this transporter besides its role in drug resistance is still unclear.

209 hat breast cancer initiation, recurrence and drug resistance is supported by breast cancer stem cells

210 Overcoming drug resistance is the key to successful treatment of EO

211 vention of both persister cell formation and drug resistance leads ultimately to mycobacterial cell d

212 barriers to drug delivery and selection for drug resistance limit survival outcomes in cancer patien

213 ady been tested in clinical trials, however, drug resistance limits clinical efficacy.

214 enges and limitations persist in identifying drug-resistance loci in malaria.

215 We assessed Plasmodium falciparum drug resistance markers in parasites collected in 2012,

216 ence of the initial parasite populations and drug resistance markers revealed no clinically significa

217 g that isolated NNRTI-associated transmitted drug resistance may not be a risk factor for virological

218 estigated in multiple clinical settings, but drug resistance may reduce their benefit.

219 ioblastoma stem cell (GSC) proliferation and drug resistance may reveal opportunities for therapeutic

220 ic resistance remarkably rapidly, with multi drug-resistance (MDR) rates exceeding 60%.

221 dy unifies TME-mediated de novo and acquired drug resistance mechanisms and provides a novel combinat

222 ion of in vivo outcomes and investigation of drug resistance mechanisms for advancement of personaliz

223 Drug resistance mechanisms include altered drug-target i

224 rug resistance to CIBM is inevitable and the drug resistance mechanisms still remain to be elucidated

225 nce implicates a key role for non-mutational drug resistance mechanisms underlying the survival of re

226 e, we describe such a method for elucidating drug resistance mechanisms using genome-wide chemical mu

227 tance through stepwise selection of multiple drug-resistance mechanisms.

228 entry independent of antigenic evolution or drug resistance might address these problems.

229 l ultrasensitive assays able to detect HIV-1 drug-resistance minority variants (DRMVs) not detectable

230 mary HIV infection, the presence of minority drug resistance mutations (DRM) may be a consequence of

231 viral drugs (ARVs), data are emerging on the drug resistance mutations (DRMs) selected by the most wi

232 The presence of transmitted drug resistance mutations (TDRMs) in antiretroviral trea

233 We detected associations between TAMs and drug resistance mutations both between and within studie

234 Drug resistance mutations emerge in genetic sequences of

235 would open the door to identify all putative drug resistance mutations in cancer models.

236 which contains the major immune epitopes and drug resistance mutations.

237 ded additional information on genotyping and drug resistance mutations.

238 allows the detection of both known and novel drug resistance mutations.

239 Sequences were analyzed for transmitted drug resistance mutations.

240 %) of the 38 clusters accumulated additional drug-resistance mutations through emergence or fixation

241 ent outcomes; however, all cases of acquired-drug resistance (n = 1) and recurrence (n = 3) occurred

242 -growing number of fungal strains exhibiting drug resistance necessitates the development of novel an

243 terials, whether they would induce bacterial drug resistance needs to be determined, which requires f

244 Knowledge of which molecular changes confer drug resistance of influenza A(H7N9) viruses (group 2NA)

245 conjunction with docetaxel (DTX) to overcome drug resistance of triple negative breast cancer (TNBC).

246 the influence of Mycobacterium tuberculosis drug resistance on the outcomes of patients with TBM enr

247 oes not provide satisfactory efficacy due to drug resistance or reduced EGFR level.

248 fication of molecular mechanisms involved in drug resistance or sensitization is imperative.

249 ing cassette transporter family, pleiotropic drug resistance (PDR) transporters play essential functi

250 th infections due to pathogens with a "usual drug resistance" phenotype that will be responsive to wi

251 In addition, the emergence of drug resistance poses new threats to longer-term use and

252 Acquired drug resistance prevents cancer therapies from achieving

253 ulness is being seriously compromised by the drug resistance problem.

254 iagnostics and is capable of providing rapid drug resistance profiles while performing species identi

255 tion of combination therapy across diseases, drug resistance rates continue to rise, leading to faili

256 the implications of nongenetic mechanisms of drug resistance recently reported in the literature, and

257 esponsible for integrating the stemness with drug resistance remain poorly understood.

258 mechanisms that couple glycolysis to cancer drug resistance remain unclear.

259 Overcoming acquired drug resistance remains a core challenge in the clinical

260 Drug resistance remains an elusive problem in cancer the

261 the past 80 years, increasing antimicrobial drug resistance requires a major and rapid intervention.

262 o Xpert as an initial diagnostic test and to drug resistance screening.

263 molecular genotyping to assess antimalarial drug resistance selection and spread in the Greater Meko

264 r countries despite improvements in acquired drug resistance shown by the Green Light Committee-suppo

265 riptomic changes in potential key drivers of drug resistance, such as KLF4.

266 alibrated a compartmental model to data from drug resistance surveys and WHO tuberculosis reports to

267 Transmitted drug resistance (TDR) may compromise response to antiret

268 low-cost human immunodeficiency virus (HIV) drug resistance tests that are able to provide timely ac

269 values revealed that Huh7 cells had a higher drug resistance than Hep-G2 cells and doxorubicin had a

270 order to clarify the molecular mechanisms of drug resistance, the DNA methylation and transcriptomic

271 l point of isolation, genetic background and drug resistance, the patterns for the emergence of drug

272 ency and ability to evade acquired bacterial drug resistance, there is a lack of knowledge on their s

273 underlying molecular mechanism of GR-driven drug resistance, these data suggest that inhibitors of b

274 red by anticancer therapeutics, resulting in drug resistance through cell-nonautonomous microenvironm

275 We describe here a mechanism of acquired drug resistance through the tumor microenvironment, whic

276 ticancer therapeutics not least by promoting drug resistance throughout the targeted tumor.

277 ctal cancer chemotherapy, yet development of drug resistance to 5-fluorouracil in colorectal cancer c

278 However, drug resistance to CIBM is inevitable and the drug resis

279 we show that BMK1 pathway contributes to the drug resistance to CIBM.

280 the molecular mechanisms underlying acquired drug resistance to current targeted therapies, and may h

281 atory signaling mechanisms that can engender drug resistance to individual targeted drugs.

282 substantially with higher prevalence of HIV drug resistance to NNRTI in ART initiators.

283 Africa where the prevalence of pretreatment drug resistance to NNRTIs is high.

284 HIV-1 drug resistance to older thymidine analogue nucleoside r

285 ophylaxis lead to high rates of pretreatment drug resistance to regimens most commonly used in childr

286 ition may be explored to prevent or overcome drug resistance to single targeting agents.

287 Transmitted HIV drug resistance was determined using World Health Organi

288 sis had been taken in the past 6 months, but drug resistance was suspected.

289 e for the new regimen because of second-line drug resistance, we projected a change in incidence of -

290 yearly increases in the odds of pretreatment drug resistance were 23% (95% CI 16-29) in southern Afri

291 esistance, the patterns for the emergence of drug resistance were conserved globally.

292 whom variants with isolated NNRTI-associated drug resistance were transmitted are at increased risk o

293 ells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted ap

294 eared virus in 2-18 days with no evidence of drug resistance, while 41 of 93 (44%) treated subjects e

295 ity in nuanced clinical contexts of acquired drug resistance with a more favorable therapeutic index.

296 To assess the prevalence of drug resistance within a specified region at any specifi

297 sampling year to prevalence of pretreatment drug resistance within geographical regions.

298 DS Society Conference, and the International Drug Resistance Workshop for the period Jan 1, 2001, to

299 prescribing contributes to the generation of drug resistance worldwide, and is particularly common in

300 Acquired drug resistance would cause less than 30% of incident MD