ライフサイエンスコーパス: chemosensitivity

1 nd provide a therapeutic strategy to restore chemosensitivity.

2 ndothelial-cell FAK as a regulator of tumour chemosensitivity.

3 nse, thereby affecting tumor progression and chemosensitivity.

4 l cell fate as reflected in dysregulation in chemosensitivity.

5 ividually migrating cells exhibit diminished chemosensitivity.

6 echanism by which endothelial cells regulate chemosensitivity.

7 eat sensitization, conductive properties and chemosensitivity.

8 loop inhibits LC aggressiveness and enhances chemosensitivity.

9 imetric monitoring of cell proliferation and chemosensitivity.

10 h while Axl knockdown more robustly improved chemosensitivity.

11 l regulation of RRM2 influencing gemcitabine chemosensitivity.

12 in in PARC post-translational processing and chemosensitivity.

13 hereby maintaining OCT4 levels and enhancing chemosensitivity.

14 ablate the suppressive effects of hypoxia on chemosensitivity.

15 which expression levels were correlated with chemosensitivity.

16 protein (IAP) expression and enhancement of chemosensitivity.

17 t "reversing" such a signature might restore chemosensitivity.

18 eolytic degradation, and their loss leads to chemosensitivity.

19 o-SCT depends on patient characteristics and chemosensitivity.

20 anisms and brain areas seemingly involved in chemosensitivity.

21 -155 renders cells to apoptosis and enhances chemosensitivity.

22 ored the p21 level and reversed ID1-enhanced chemosensitivity.

23 echanism contributing to central respiratory chemosensitivity.

24 n of genes controlling growth, survival, and chemosensitivity.

25 but nonetheless differ in their influence on chemosensitivity.

26 ses IAP/MDR1 down-regulation, apoptosis, and chemosensitivity.

27 iated tumor cell behaviors but also enhances chemosensitivity.

28 iciency in xenograft models led to increased chemosensitivity.

29 d postsynaptic neurons contribute to the CO2 chemosensitivity.

30 bition of NF-kappaB activity correlated with chemosensitivity.

31 molecular mechanisms underlying respiratory chemosensitivity.

32 These results suggest that DcR2 regulates chemosensitivity.

33 that DcR2 is a p53 target gene and regulates chemosensitivity.

34 chanosensitivity, thermal sensitivity and O2 chemosensitivity.

35 orated into DNA as a potential mechanism for chemosensitivity.

36 t role for membrane transport in determining chemosensitivity.

37 critical determinant for tumorigenicity and chemosensitivity.

38 loss of p53-dependent caspase activation and chemosensitivity.

39 n are either chemosensitive or they modulate chemosensitivity.

40 efine the role of the Notch pathway in B-ALL chemosensitivity.

41 cells were sufficient for the prediction of chemosensitivity.

42 ances UMPS activity, cell proliferation, and chemosensitivity.

43 OSE-derived organoids exhibited differential chemosensitivity.

44 itivity, and blocking 5-HT reuptake enhanced chemosensitivity.

45 P3 as a predictive biomarker of breast tumor chemosensitivity.

46 n of Cancer-Stem-Cell markers, and increased chemosensitivity.

47 ous 5-HT did not enable latent intrinsic RTN chemosensitivity.

48 iferation and the enhancement of cancer cell chemosensitivity.

49 n of cancer stem cell markers, and increased chemosensitivity.

50 uroendocrine marker expression and increases chemosensitivity.

51 l chemoreflex sensitivity but not peripheral chemosensitivity.

52 ynaptic transmission in studies of intrinsic chemosensitivity.

53 as reduces tumor cell invasion and enhances chemosensitivity.

54 where deiodinases control cell division and chemosensitivity.

55 us they have a key role in determining tumor chemosensitivity.

56 pendent changes in breathing and respiratory chemosensitivity.

57 by astrocytes in central respiratory CO2 /pH chemosensitivity.

58 ibition, decreased metastasis, and increased chemosensitivity.

59 al therapeutic approach for increasing tumor chemosensitivity.

60 both genetic and functional levels improves chemosensitivity.

61 meostatic process called central respiratory chemosensitivity.

62 d essential central mediators of respiratory chemosensitivity.

63 ange of lung tumors with different intrinsic chemosensitivities.

64 90-buffered mutants, exacerbating FA-related chemosensitivities.

65 n the 27 patients (34%) with high peripheral chemosensitivity, 3-year survival was 41% (95% CI 22% to

66 y results in increased chromosome damage and chemosensitivity after irofulven treatment.

67 xenograft model that enable patient-specific chemosensitivity analyses.

68 F1 and RNA pol III-mediated transcription in chemosensitivity and apoptosis.

69 wth and cancer stem cell expansion, restores chemosensitivity and blocks metastatic spread, thus prov

70 agents, suggesting that FAN1 mutations cause chemosensitivity and bone marrow failure.

71 morphological basis for impaired respiratory chemosensitivity and central sleep apnoea in this disord

72 r that may manifest with reduced respiratory chemosensitivity and central sleep apnoea.

73 itivity) and to a semantic confusion between chemosensitivity and chemoreception (the mechanism by wh

74 d in NTS neurons and contribute to intrinsic chemosensitivity and control of breathing.

75 F patients demonstrated augmented peripheral chemosensitivity and decreased BRS (all P<0.01 versus re

76 iR200c expression significantly enhanced the chemosensitivity and decreased the metastatic potential

77 increased loop gain-consequent to increased chemosensitivity and delay-the strength of spontaneous o

78 Both cell lines showed improved in vitro chemosensitivity and Dox uptake at HT.

79 this phosphatase may increase neuroblastoma chemosensitivity and DUSP26 is a novel therapeutic targe

80 ation, leading to a dramatic augmentation of chemosensitivity and enhanced apoptosis.

81 y is reflected in cell-to-cell variations in chemosensitivity and expression of drug-resistance prote

82 1R translation start site enhance radio- and chemosensitivity and impair Atm function.

83 mal tumor subtype, by altering tumor growth, chemosensitivity and metastatic potential in vivo.

84 tion, although they exhibited differences in chemosensitivity and migratory abilities, suggesting tha

85 d the positive impact of oxidative stress on chemosensitivity and prognosis of ovarian cancer patient

86 genomic features driving tumour initiation, chemosensitivity and progression are incompletely charac

87 d the novel insight into the role of IPO4 in chemosensitivity and provide a clinical translational po

88 isplay antitumor effect in NPC, and enhanced chemosensitivity and radiosensitivity in NPC.

89 Treatment may be adjusted according to the chemosensitivity and radiosensitivity of the tumor tissu

90 f p53 in part explains its ability to confer chemosensitivity and radiosensitivity upon tumor cells.

91 critical for the development of microfluidic chemosensitivity and resistance assay (CSRA) platforms t

92 GCT evolution, and may provide insights into chemosensitivity and resistance in other cancers.

93 Poor chemosensitivity and the development of chemoresistance

94 so found that suggested associations between chemosensitivity and the endocrine, paracrine ligand-rec

95 gin by describing the need for central CO(2) chemosensitivity and the problems that the field has fac

96 rties of AML blasts thus appear to influence chemosensitivity and therefore may be therapeutic target

97 rapamycin-mediated cell cycle regulation and chemosensitivity and thus significantly potentiates the

98 rain P(CO(2)) presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation

99 y of ectopically expressed wtBRCA1 to induce chemosensitivity and to inhibit estrogen receptor transc

100 an intra- or interspecies manner to predict chemosensitivity and treatment outcome in canine OS.

101 acidification on neurons recorded in vitro (chemosensitivity) and to a semantic confusion between ch

102 tion with poor prognosis disease, documented chemosensitivity, and a minimal tumor burden at the time

103 sors or oncogenes, induce chemoresistance or chemosensitivity, and are major posttranscriptional gene

104 5-HT synthesis in culture reduced RTN neuron chemosensitivity, and blocking 5-HT reuptake enhanced ch

105 on, increased apoptosis, mitotic arrest, and chemosensitivity, and cooperated with chemotherapy to si

106 sites of disease (nodal or organ), previous chemosensitivity, and goals of treatment (long-term dise

107 rized by impaired cardiac function, enhanced chemosensitivity, and greater sympathetic restraint at r

108 g7 appears to be a valid strategy to enhance chemosensitivity, and it could indeed improve outcomes i

109 p53 is a major determinant of chemosensitivity, and its levels are increased following

110 schemia with respect to cell cycle kinetics, chemosensitivity, and molecular dependencies that may be

111 status, predicted chemoresistance, predicted chemosensitivity, and predicted endocrine sensitivity id

112 ly regulates breast cancer cell survival and chemosensitivity, and the pathways involved.

113 umor growth and its role as a determinant of chemosensitivity are poorly understood.

114 Neurons with appropriate chemosensitivity are spread throughout the brainstem; th

115 hemichannels, causally linked to respiratory chemosensitivity, are directly modulated by CO2.

116 e dose of adenosine used and on the level of chemosensitivity as determined by the ventilatory respon

117 We report a phenotypic chemosensitivity assay for epithelial ovarian cancer bas

118 n and Hamburger to produce a viable cellular chemosensitivity assay in the 1970s, and continues to th

119 For instance, the ATP-based chemosensitivity assay was developed in the early 1990s

120 0 value, which is an important indicator for chemosensitivity assay.

121 uated through a combination of transport and chemosensitivity assays, using the L5178 mouse T lymphom

122 ed tumor cell viability and induced dramatic chemosensitivity both in vitro and in vivo.

123 c and BCL-XL protein expression and enhanced chemosensitivity, both in vitro and in vivo.

124 s shown to result in the desired increase in chemosensitivity, but with a decrease in net production

125 uble-strand breaks and that BRCA1 may affect chemosensitivity by controlling cell cycle checkpoints,

126 a possible link between pH(i) regulation and chemosensitivity by following the pH(i) measurements on

127 rther demonstrating that modulation of tumor chemosensitivity by GSI is Notch specific.

128 post-transcriptional regulation of RRM2 and chemosensitivity by let-7a and that the manipulation of

129 ndicate that miR-96 regulates DNA repair and chemosensitivity by repressing RAD51 and REV1.

130 uggests a new strategy to modulate cisplatin chemosensitivity by targeting the PRIMPOL pathway.

131 We studied whether augmented peripheral chemosensitivity carries independent prognostic signific

132 In this study, we compared chemosensitivity, cell cycle distribution, and apoptosis

133 nsferability of 2D/3D cancer cell line-based chemosensitivity data and underline the importance of in

134 In this study, we integrate chemosensitivity data from a large-scale pharmacogenomic

135 ge scale features of the gene expression and chemosensitivity data, such as tissue of origin and othe

136 To apply this approach to chemosensitivity data, we identify genes whose basal exp

137 s migrated up the gradient, and the measured chemosensitivity (defined as the average cell velocity a

138 d peripheral (P=0.01) and central (P=0.0006) chemosensitivity, depressed low-frequency component of h

139 induction of this microRNA, thereby limiting chemosensitivity due to microRNA-mediated feedback inhib

140 ET is a well-established surrogate for tumor chemosensitivity early during therapy.

141 ID1-mediated chemosensitivity enhancement was in part due to ID1 supp

142 Chemosensitivity experiments with 5-fluorouracil, cytosi

143 uroendocrine cancer characterized by initial chemosensitivity followed by emergence of chemoresistant

144 High peripheral chemosensitivity (>0.72 L. min(-1).

145 The field of CO(2) chemosensitivity has developed considerably in recent ye

146 n acute myeloid leukemia (AML) parameters of chemosensitivity have been restricted mainly to the rapi

147 ether, they impact apoptosis, proliferation, chemosensitivity, immune response, and the population of

148 l results showed that cell proliferation and chemosensitivity in 3D cell culture format can be monito

149 tein overexpressed in cancer, might increase chemosensitivity in acute myeloid leukemia (AML).

150 Nutlin-3a in cells with mutant p53 enhances chemosensitivity in an E2F1-dependent manner.

151 s recently emerged as a genetic predictor of chemosensitivity in anaplastic oligodendrogliomas.

152 may offer a therapeutic target for enhancing chemosensitivity in blast cells.

153 Although it is known that chemosensitivity in BRCA1-associated cancers is associat

154 o differentially impact let-7 biogenesis and chemosensitivity in gemcitabine-sensitive versus -resist

155 and tumor cell invasion, but also increases chemosensitivity in HA-treated CSCs.

156 t also decreases IAP expression and enhances chemosensitivity in HA-treated HNSCC cells.

157 ets for enhancing YAP-mediated apoptosis and chemosensitivity in HNSCCs.

158 ate a novel molecular mechanism that defines chemosensitivity in IDH-mutated gliomas.

159 that down-regulation of Bcl-2 would restore chemosensitivity in leukemic cells.

160 ing a proapoptotic protein that is linked to chemosensitivity in many settings, is upregulated throug

161 Acid-sensing ion channels (ASICs) mediate chemosensitivity in nociceptive terminals, where pH valu

162 p53 tumor suppressor, a central mediator of chemosensitivity in normal cells, is functionally inacti

163 he expression of miR-140 was associated with chemosensitivity in osteosarcoma tumor xenografts.

164 Consistent with the reported platinum chemosensitivity in patients with Brca1-associated ovari

165 d their mechanosensitivity, excitability and chemosensitivity in response to the stable prostacyclin

166 athways that control tumor cell survival and chemosensitivity in the absence of functional p53.

167 uce apoptosis in malignant cells and enhance chemosensitivity in the absence of p53, suggesting this

168 and an enhancement in caspase-3 activity and chemosensitivity in the breast tumor cells.

169 Interim PET can assess chemosensitivity in these lymphomas, but it does not pre

170 To define the primary stimulus for chemosensitivity in these neurones, the response to hype

171 r pH (pH(i)) may be the primary stimulus for chemosensitivity in these putative central respiratory c

172 d potential therapeutic target for enhancing chemosensitivity in this disease.

173 l mutation burden and significantly enhanced chemosensitivity in TNBC and suggests that functional RN

174 n turn increases TAM-dependent anti-estrogen chemosensitivity in vitro and in vivo.

175 lk2 as a clinically important determinant of chemosensitivity, in support of the candidacy of Plk2 as

176 about its function in human tumor growth and chemosensitivity independently of up-regulation of p53 p

177 Chemosensitivity is a key mechanism for the regulation o

178 tors may contribute, it is uncertain whether chemosensitivity is altered, hyperventilation is maintai

179 Central respiratory chemosensitivity is an essential mechanism that, via reg

180 Mainly, during CHF the CB chemosensitivity is enhanced leading to increases in ven

181 e that, although not attributable to central chemosensitivity, may possibly have peripheral chemorefl

182 gainst these same tumor cell lines to relate chemosensitivity more precisely to biochemical pathways.

183 f apoptosis by many DNA-damaging agents, the chemosensitivity of 5-FU for patients with advanced colo

184 o inhibit Sirt1 activity and to increase the chemosensitivity of androgen-refractory prostate cancer

185 : Inhibition of Notch signaling enhances the chemosensitivity of B-ALL cells, suggesting Notch inhibi

186 of the RNF168/53BP1 pathway could alter the chemosensitivity of BRCA1 deficient tumors.

187 TRAIL by 5-aza-CdR is critical for enhancing chemosensitivity of breast cancer cells to Adriamycin.

188 ther, our data suggest that miR-621 enhances chemosensitivity of breast cancer cells to PTX/CBP chemo

189 Based on these developments, chemosensitivity of cancer cell colonies under different

190 orm, thus promoting apoptosis and increasing chemosensitivity of cancer cells to common antitumor dru

191 and humanized mouse models and enhances the chemosensitivity of cancer cells, consistent with the ro

192 substituted histone H2AX enhanced radio- and chemosensitivity of cancer cells.

193 ing demalonylation of TPI at Lys56 increases chemosensitivity of CDCP1+ CSCSs and delays recurrence o

194 antitative platform for the investigation of chemosensitivity of cells cultured in the 3D environment

195 overexpression of miR-218 in H1299 increased chemosensitivity of cells to cisplatin treatment through

196 ering a potential explanation for the marked chemosensitivity of certain cancers that express abundan

197 We then compared the chemosensitivity of clones derived from these two cell l

198 a-secretase inhibitors (GSI) may enhance the chemosensitivity of colon cancer cells.

199 mal-epithelial transition (MET) and enhanced chemosensitivity of CRCs to oxaliplatin.

200 tations of existing assays in evaluating the chemosensitivity of dissociated tumor cells, we develope

201 y downregulates MGMT expression and restores chemosensitivity of DNA-alkylating drugs in mouse models

202 ovative therapeutic agents for enhancing the chemosensitivity of doxorubicin while providing concurre

203 rease the long-term survival and improve the chemosensitivity of GBM in vitro, its role in malignant

204 ally, actopaxin down-regulation enhanced the chemosensitivity of HCC cells towards oxaliplatin treatm

205 p16 and gigaxonin play an important role in chemosensitivity of head and neck cancers through ubiqui

206 stratification and methods for assessing the chemosensitivity of HL through imaging studies and bioma

207 vitamin D status might be important for the chemosensitivity of HL.

208 e nucleoside transporter, in determining the chemosensitivity of human pancreatic cancer cells to gem

209 lations of E1A-induced immunosensitivity and chemosensitivity of human tumor cells.

210 eathing conditions do not exhibit CO2 and O2 chemosensitivity of lung breathing, similar to water-bre

211 target of PKCzeta in regulating survival and chemosensitivity of lung cancer cells.

212 at potential as an approach to improving the chemosensitivity of melanoma cells.

213 valuated the ability of BDNF to decrease the chemosensitivity of NB cells to a number of common chemo

214 e tumor cell kill by enhancing the intrinsic chemosensitivity of P450-expressing tumor cells by chemi

215 e G1/S transition and enhanced apoptosis and chemosensitivity of pancreatic cancer cells.

216 engineers the intensity and heterogeneity of chemosensitivity of primary cells from multiple myeloma

217 To evaluate whether the chemosensitivity of primary central nervous system lymph

218 We conclude that chemosensitivity of raphe neurones can occur independent

219 ) receptors enables or potentiates intrinsic chemosensitivity of RTN neurons, as exogenous 5-HT did n

220 te that a non-TASK K+ current contributes to chemosensitivity of RTN neurons, which are profoundly pH

221 BCSCs attenuating self-renewal and restored chemosensitivity of the BCSCs.

222 In addition, TS1058 restored chemosensitivity of the resistant RKO-HTStet cell line t

223 eatment regimens according to the individual chemosensitivity of the tumor tissue.

224 ry supplement, cholecalciferol) improves the chemosensitivity of tumors by reducing the rate of tumor

225 eplication forks are thought to underlie the chemosensitivity of tumors deficient in the hereditary b

226 To test this hypothesis, we examined the chemosensitivity of two prime candidate chemoreceptor ne

227 ee monitoring system to directly analyze the chemosensitivity of undissociated tumor tissue.

228 in and stathmin 1 may be related to the high chemosensitivity of WT.

229 is not due to persistent changes in hypoxic chemosensitivity or central neural integration.

230 have an important role in the development of chemosensitivity or chemoresistance in different types o

231 e in HT29 cells did not substantially affect chemosensitivity or the amount of DNA damage incurred de

232 ether this is due to biologic differences in chemosensitivity or to treatment or socioeconomic differ

233 ating this pathway was sufficient to enhance chemosensitivity, overcoming DNp73-mediated drug resista

234 77% (66% to 89%) in 53 patients with normal chemosensitivity (P=0.0002).

235 In a large population of altitude visitors, chemosensitivity parameters (high desaturation and low v

236 by PACER can serve as testable hypotheses on chemosensitivity pathways and help further study the mec

237 em to more reliably predict patient-specific chemosensitivity patterns and to monitor antitumor effic

238 impedance spectroscopy to obtain individual chemosensitivity patterns.

239 gins of this disease and associated with the chemosensitivity phenotype, as well as the rare progress

240 a subset of compounds genomic approaches to chemosensitivity prediction are feasible.

241 ar mechanisms underlying the altered central chemosensitivity present in a variety of disorders such

242 being developed to predict patient-specific chemosensitivity profiles before treatment in the clinic

243 cancer cell lines (the NCI-60) for which the chemosensitivity profiles of thousands of chemical compo

244 ciated with vesicle shedding correlates with chemosensitivity profiles.

245 hether trastuzumab trigger receptor-enhanced chemosensitivity (REC) when combined with chemotherapy w

246 Cellular mechanisms of central pH chemosensitivity remain largely unknown.

247 But, how it modulates cellular chemosensitivity remains poorly characterized.

248 RNAs led to differential RRM2 expression and chemosensitivity responses in a poorly differentiated pa

249 ncentration from 10 mM to 2 mM reduced CO(2) chemosensitivity significantly from 0.007 +/- 0.002 Hz m

250 inical translational potential to enhance CC chemosensitivity since the IPO4-CEBPD-PRKDC axis is acti

251 induced correlating closely with activity in chemosensitivity studies.

252 uman prostate cancer cells, characterized by chemosensitivity, susceptibility to apoptosis, decreased

253 der to achieve high predictive value of cell chemosensitivity test for clinical efficacy, cancer cell

254 Chemosensitivity testing identified vorinostat as a pote

255 ased diagnostics and therapeutics (including chemosensitivity testing) and greatly expands the value

256 s are considered to be the gold-standard for chemosensitivity testing, and leads identified with thes

257 gions within the brain to coordinate central chemosensitivity, the discovery of long-term and short-t

258 indicate differences in 5-fluorouracil-based chemosensitivity; this is consistent with in vitro studi

259 f miR-155 in regulation of cell survival and chemosensitivity through down-regulation of FOXO3a in br

260 ween mutant and wild-type status of p53, and chemosensitivity to alkylating agents, while extending t

261 f FDA-approved drugs as capable of restoring chemosensitivity to anti-EGFR-based therapy for the trea

262 Using this platform, we predicted chemosensitivity to bortezomib and melphalan, two clinic

263 nce and whether inhibiting PKM2 augments the chemosensitivity to cisplatin and reduces BC growth and

264 showed that TIMP-2 overexpression increased chemosensitivity to cytotoxic drugs.

265 ithelial-mesenchymal transition process, and chemosensitivity to cytotoxic drugs.

266 Finally, anti-xCT vaccination increased CSC chemosensitivity to doxorubicin in vivo, indicating that

267 tion and spheroid cell survival and restored chemosensitivity to Ewing sarcoma spheroids.

268 HD6 knockdown in human cancer cells enhances chemosensitivity to genotoxic anticancer drugs, whereas

269 hat inhibition of the MAPK pathway increases chemosensitivity to glucocorticoids and possibly other a

270 CSR in HF patients is predicted by increased chemosensitivity to hypercapnia and is associated with w

271 terminal pro-B-type natriuretic peptide, and chemosensitivity to hypercapnia, which was the only inde

272 n levels directly correlated with paclitaxel chemosensitivity to mitosis, while also identifying addi

273 , yielding a potential target for increasing chemosensitivity to multiple drugs.

274 diosyncratic action on receptors involved in chemosensitivity to oxygen, but well-established pathoph

275 g correlation between miR-621 expression and chemosensitivity to paclitaxel plus carboplatin (PTX/CBP

276 s overexpressing KISS1 were found to enhance chemosensitivity to paclitaxel.

277 of miR-621 promoted apoptosis and increased chemosensitivity to PTX and CBP both in cultured breast

278 d with sham, and its inhibition increased GB chemosensitivity to temozolomide.

279 ged as the dominant predictor of cancer cell chemosensitivity to the hybrid agent (Pearson correlatio

280 acid transporters positively correlated with chemosensitivity to their respective drug substrates.

281 ractive targets to confer enhanced radio and chemosensitivity to tumor cells.

282 implicated in chemoresistance, also induced chemosensitivity to vincristine and melphalan.

283 lective inhibition of ALDH3A1 could increase chemosensitivity toward cyclophosphamide in ALDH3A1 expr

284 ssion and activity and subsequently enhanced chemosensitivity towards cisplatin, taxol and tamoxifen

285 ween increased HMGA2 expression and enhanced chemosensitivity towards topoisomerase II inhibitor, dox

286 We assessed peripheral chemosensitivity (ventilatory response to hypoxia using

287 rine, doxorubicin, and vincristine, and this chemosensitivity was attenuated by exogenous expression

288 The effect of PD-L1 on chemosensitivity was confirmed in MC38 murine tumor xeno

289 Chemosensitivity was indicated by augmentation of AP fir

290 Chemosensitivity was measured in HCT-116, a human colore

291 The effect of 5-HT on RTN neuron chemosensitivity was not explained by a mechanism whereb

292 The CO2 chemosensitivity was reduced but not eliminated by block

293 hen Ad-Bid and cisplatin were used together, chemosensitivity was restored in p53-null H358 cells, in

294 y the Bcl-2 family is a known determinant of chemosensitivity, we compared the constitutive levels of

295 To further understand how E1A enhances chemosensitivity, we have made use of a human colon carc

296 as inhibition of Notch-1 with siRNA enhanced chemosensitivity whereas overexpression of NICD increase

297 p73 exhibit distinct functions-p73 mediates chemosensitivity while p63 promotes proliferation and ce

298 Chemosensitivity with one CB was similar to that in inta

299 ocrine therapy, (2) chemoresistance, and (3) chemosensitivity, with independent validation (198 patie

300 arance, as a potential surrogate for in vivo chemosensitivity, would have prognostic relevance in AML