ライフサイエンスコーパス: chemosensitivity

1 in in PARC post-translational processing and chemosensitivity.

2 hereby maintaining OCT4 levels and enhancing chemosensitivity.

3 ablate the suppressive effects of hypoxia on chemosensitivity.

4 which expression levels were correlated with chemosensitivity.

5 protein (IAP) expression and enhancement of chemosensitivity.

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

7 uroendocrine marker expression and increases chemosensitivity.

8 o-SCT depends on patient characteristics and chemosensitivity.

9 anisms and brain areas seemingly involved in chemosensitivity.

10 -155 renders cells to apoptosis and enhances chemosensitivity.

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

12 l chemoreflex sensitivity but not peripheral chemosensitivity.

13 echanism contributing to central respiratory chemosensitivity.

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

15 but nonetheless differ in their influence on chemosensitivity.

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

17 iated tumor cell behaviors but also enhances chemosensitivity.

18 ynaptic transmission in studies of intrinsic chemosensitivity.

19 iciency in xenograft models led to increased chemosensitivity.

20 d postsynaptic neurons contribute to the CO2 chemosensitivity.

21 bition of NF-kappaB activity correlated with chemosensitivity.

22 molecular mechanisms underlying respiratory chemosensitivity.

23 These results suggest that DcR2 regulates chemosensitivity.

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

25 iferation and the enhancement of cancer cell chemosensitivity.

26 chanosensitivity, thermal sensitivity and O2 chemosensitivity.

27 orated into DNA as a potential mechanism for chemosensitivity.

28 t role for membrane transport in determining chemosensitivity.

29 critical determinant for tumorigenicity and chemosensitivity.

30 as reduces tumor cell invasion and enhances chemosensitivity.

31 loss of p53-dependent caspase activation and chemosensitivity.

32 n are either chemosensitive or they modulate chemosensitivity.

33 cells were sufficient for the prediction of chemosensitivity.

34 where deiodinases control cell division and chemosensitivity.

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

36 a region not generally associated with CO(2) chemosensitivity.

37 may contribute to the maturation of hypoxic chemosensitivity.

38 ntrol, prognosis, and the role of peripheral chemosensitivity.

39 including apoptosis and altered chemotherapy chemosensitivity.

40 pendent changes in breathing and respiratory chemosensitivity.

41 by astrocytes in central respiratory CO2 /pH chemosensitivity.

42 ibition, decreased metastasis, and increased chemosensitivity.

43 al therapeutic approach for increasing tumor chemosensitivity.

44 both genetic and functional levels improves chemosensitivity.

45 meostatic process called central respiratory chemosensitivity.

46 d essential central mediators of respiratory chemosensitivity.

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

48 nse, thereby affecting tumor progression and chemosensitivity.

49 l cell fate as reflected in dysregulation in chemosensitivity.

50 ividually migrating cells exhibit diminished chemosensitivity.

51 echanism by which endothelial cells regulate chemosensitivity.

52 eat sensitization, conductive properties and chemosensitivity.

53 loop inhibits LC aggressiveness and enhances chemosensitivity.

54 imetric monitoring of cell proliferation and chemosensitivity.

55 h while Axl knockdown more robustly improved chemosensitivity.

56 l regulation of RRM2 influencing gemcitabine chemosensitivity.

57 ange of lung tumors with different intrinsic chemosensitivities.

58 90-buffered mutants, exacerbating FA-related chemosensitivities.

59 ilation (78+/-2% versus 50+/-8%), peripheral chemosensitivity (0.6+/-0.4 versus 0.2+/-0.1 L/min per p

60 s, impaired autonomic balance, and increased chemosensitivity (0.80 and 0.75 versus 0.34 L. min(-1).

61 /-0.1 L/min per percent SaO(2)), and central chemosensitivity (2.9+/-0.2 versus 2.0+/-0.2 L. min(-1).

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

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

64 ion seems to contribute to the regulation of chemosensitivity and apoptotic commitment of human tumor

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

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

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

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

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

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

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

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

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

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

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

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

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

78 1R translation start site enhance radio- and chemosensitivity and impair Atm function.

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

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

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

82 By comparing chemosensitivity and proteins in different tumors (prima

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

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

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

86 BRCA1 may also enhance chemosensitivity and repair of DNA damage through bindin

87 nsfer or 5aza2dC treatment markedly enhances chemosensitivity and rescues the apoptotic defects assoc

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

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

90 levance of particular genetic alterations to chemosensitivity and survival.

91 Poor chemosensitivity and the development of chemoresistance

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 0 value, which is an important indicator for chemosensitivity assay.

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

118 an algorithm for classification of cell line chemosensitivity based on gene expression profiles alone

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

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

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

122 Dihydrocodeine administration decreased chemosensitivity by 42% (P=0.05), which correlated with

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

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

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

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

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

128 Modulation of peripheral chemosensitivity can reduce or abolish abnormal respirat

129 We studied whether augmented peripheral chemosensitivity carries independent prognostic signific

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

131 These CDK inhibition and chemosensitivity data indicate that the distinct mode of

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

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

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

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

136 tin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4

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

138 g eIF4E (REF/Myc/4E) significantly increased chemosensitivity; either soluble antisense cyclin D1 oli

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

140 Chemosensitivity experiments with 5-fluorouracil, cytosi

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

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

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

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

145 pendent, which in turn influences tumor cell chemosensitivity in a cell cycle-dependent fashion.

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

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

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

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

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

151 ctivation as an adjuvant approach to promote chemosensitivity in colorectal tumor cells to treatment

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

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

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

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

156 thm in breathing, metabolism and ventilatory chemosensitivity in humans.

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

158 <.05 by the log rank test), suggesting that chemosensitivity in leukemic blasts may be regulated by

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 However, the increase in chemosensitivity in PC-3 cells was statistically identic

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

167 s that certain molecular markers may predict chemosensitivity in some tumor types, particularly anapl

168 Enhanced chemosensitivity in telomere dysfunctional cells was lin

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

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

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

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

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

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

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

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

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

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

179 In multivariate analyses, augmented chemosensitivity independently predicted death (hazard r

180 also a strong predictor of increased central chemosensitivity (independently of clinical parameters),

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

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

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

184 Chemosensitivity is not an all-or-none neuronal property

185 or-none neuronal property, and the degree of chemosensitivity may be relevant to the role neurons pla

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

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

188 Hypoxic and hypercapnic chemosensitivity (n=38), heart rate variability (n=34),

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 rmal germ cells as a factor in the exquisite chemosensitivity of germ cell cancer has been high-light

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

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

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

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

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

214 Similarly, the chemosensitivity of KB-8-5 cells to colchicine was resto

215 ed G(0)-G(1) checkpoint control affected the chemosensitivity of LNCaP cells.

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

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

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

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

220 We previously quantified chemosensitivity of neurons from the medullary raphe usi

221 ic neoplasms and the previously demonstrated chemosensitivity of oligodendrogliomas, a combined appro

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

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

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

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

226 We conclude that chemosensitivity of raphe neurones can occur independent

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

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

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

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

231 However, the degree of chemosensitivity of these neurons was less than medullar

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

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

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

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

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

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

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

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

240 77% (66% to 89%) in 53 patients with normal chemosensitivity (P=0.0002).

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

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

243 impedance spectroscopy to obtain individual chemosensitivity patterns.

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

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

246 The accuracy of chemosensitivity prediction was considerably better than

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

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

249 ciated with vesicle shedding correlates with chemosensitivity profiles.

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

251 Cellular mechanisms of central pH chemosensitivity remain largely unknown.

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

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

254 nd to be the principal determinant governing chemosensitivity specifically to agents that induced dou

255 induced correlating closely with activity in chemosensitivity studies.

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

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

258 Chemosensitivity testing identified vorinostat as a pote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 t cells displayed a dose-dependent, enhanced chemosensitivity to MTIs in both monolayer and soft agar

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

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

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

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

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 Peripheral chemosensitivity was assessed with the transient hypoxia

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

289 Chemosensitivity was indicated by augmentation of AP fir

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

291 wtBRCA1-induced chemosensitivity was partially reversed by expression of

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