ライフサイエンスコーパス: 5-fluorouracil

1 h available anti-cancer drugs (imiquimod and 5-fluorouracil).

2 of spheroids to different concentrations of 5-fluorouracil.

3 cells in the presence of a chemical mutagen, 5-fluorouracil.

4 n cells were more sensitive to cisplatin and 5-fluorouracil.

5 lerance to toxic analogs 5-fluorouridine and 5-fluorouracil.

6 somal stress-inducing agent actinomycin D or 5-fluorouracil.

7 iamminedichloroplatinum(II), hydroxyurea, or 5-fluorouracil.

8 utant p53-expressing cell lines resistant to 5-fluorouracil.

9 the colorectal cancer chemotherapeutic agent 5-fluorouracil.

10 SI tumors do not benefit from treatment with 5-fluorouracil.

11 f cancer cells to the chemotherapeutic agent 5-fluorouracil.

12 y used colorectal chemotherapeutic compound, 5-fluorouracil.

13 ptible to the lethal effect of high doses of 5-fluorouracil.

14 e from HSCs, we treated Hmgb3(-/Y) mice with 5-fluorouracil.

15 state conditions and after cytoablation with 5-fluorouracil.

16 rts a prodrug 5-flucytosine into a cytotoxic 5-fluorouracil.

17 ersistent anemia was induced by hemolysis or 5-fluorouracil.

18 phenotype in Vero cells were generated using 5-fluorouracil.

19 dosage levels of the chemotherapeutic agent 5-fluorouracil.

20 red resistance to the chemotherapeutic agent 5-fluorouracil.

21 -bromo derivative and coupled with protected 5-fluorouracil.

22 agents, including cisplatin, sorafenib, and 5-fluorouracil.

23 o sensitizes tumour cells to doxorubicin and 5-Fluorouracil.

24 elated apoptosis-inducing ligand (TRAIL) and 5-fluorouracil.

25 creasing UBE2C expression in the presence of 5-fluorouracil.

26 ic agents, namely, cisplatin, docetaxel, and 5-fluorouracil.

27 c injury induced by serial administration of 5-fluorouracil.

28 oside analogs, ribavirin, 5-azacytidine, and 5-fluorouracil.

29 bination is due to the in situ generation of 5-fluorouracil.

30 onditions of stress hematopoiesis induced by 5-fluorouracil.

31 5-Fluorouracil 1% administered topically 4 times daily f

32 Direct coupling of N(6)-protected 5-fluorouracil 15 with cyclopentenyl intermediate 13, fo

33 was performed on COLO205 cells treated with 5-fluorouracil (3.1, 31, or 310 muM) and oxaliplatin (0.

34 to docetaxel (15-fold), cisplatin (13-fold), 5-fluorouracil (31-fold), camptothecin (7-fold), and gem

35 r maximal resection, 37 patients received IP 5-fluorouracil, 35 of whom also received IP chromic phos

36 t plan included neoadjuvant CRT (cisplatin + 5-fluorouracil/45 Gy) followed 6 to 8 weeks later by a t

37 5,6-dihydro-5-fluorouracil (5-DHFU) is a metabolite of the chemother

38 r, treatment with the chemotherapeutic agent 5-fluorouracil (5-FU) also induces GzmB production in HS

39 5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, f

40 aluate AUY922, alone and in combination with 5-fluorouracil (5-FU) and cisplatin.

41 y, we examined whether antineoplastic agents 5-fluorouracil (5-FU) and dacarbazine (DTIC) sensitize m

42 pyrimidine chemotherapeutic agents including 5-fluorouracil (5-FU) and elevated expression of dUTPase

43 rtant role in the antineoplastic activity of 5-fluorouracil (5-FU) and in the anabolism of its oral p

44 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyur

45 ation stress-inducing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to

46 argued that colorectal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effect

47 y in combination regimens, specifically with 5-fluorouracil (5-FU) and oxaliplatin, in CRC.

48 ads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion o

49 a topical TSLP inducer, in combination with 5-fluorouracil (5-FU) as an immunotherapy for actinic ke

50 ity of the anti-cancer chemotherapeutic drug 5-fluorouracil (5-FU) by prolonging S phase, generating

51 oxo-C12-(L)-HSL reduces the apparent IC50 of 5-fluorouracil (5-FU) from 1 micromol/L to 80 nmol/L (12

52 since its development, the pyrimidine analog 5-fluorouracil (5-FU) has become an integral component o

53 cases (93%): mitomycin C (MMC) in 271 (63%), 5-fluorouracil (5-FU) in 129 (30%), and no antifibrotic

54 RNA-chk transfection and the anticancer drug 5-fluorouracil (5-FU) in those cell lines.

55 5-fluorouracil (5-FU) is a widely used anticancer drug t

56 5-fluorouracil (5-FU) is a widely used chemotherapeutic

57 The antimetabolite 5-fluorouracil (5-FU) is one of the most widely used che

58 hough colorectal cancer (CRC) treatment with 5-fluorouracil (5-FU) is the first line of therapy for t

59 5-Fluorouracil (5-FU) is the most widely used antimetabo

60 FU) is a metabolite of the chemotherapy drug 5-fluorouracil (5-FU) of importance for biological studi

61 failure of oxaliplatin (FOLFOX) compared to 5-fluorouracil (5-FU) or no chemotherapy for adjuvant tr

62 sensitive to treatment with the RNA mutagen 5-fluorouracil (5-FU) than wild-type (WT)-ExoN(+), sugge

63 ) is a target for pemetrexed and the prodrug 5-fluorouracil (5-FU) that inhibit the protein by bindin

64 We treated mice with 5-fluorouracil (5-FU) to isolate a quiescent and undiffe

65 n these NPs-treated cancer cells compared to 5-fluorouracil (5-FU) treated cells.

66 Furthermore, cellular stress triggered by 5-fluorouracil (5-FU) treatment potentiates the effects

67 However, after 5-fluorouracil (5-FU) treatment, there was a rapid incre

68 modulator to reduce host toxicity caused by 5-fluorouracil (5-FU) without impairing its antitumor ac

69 species using three chemotherapeutic drugs: 5-fluorouracil (5-FU), 5-fluoro-2'-deoxyuridine (FUDR),

70 divergent mechanisms of action [gemcitabine, 5-fluorouracil (5-FU), and cisplatin] in pancreatic canc

71 the healthy muVM to a vasotoxic cancer drug, 5-Fluorouracil (5-FU), in comparison with an in vivo mou

72 RTOG) 98-11 [A Phase III Randomized Study of 5-Fluorouracil (5-FU), Mitomycin, and Radiotherapy Versu

73 hemotherapy induces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite o

74 functionalised with Rose Bengal (RB) and/or 5-fluorouracil (5-FU), were assessed as a delivery vehic

75 tes resistance to the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activ

76 pression of miR-520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis

77 ve CMT (radiation: 5040 centi-Gray (cGy) and 5-fluorouracil (5-FU)-based chemotherapy) followed by TM

78 oprotein E (ApoE) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 ce

79 Hypoxia reduces sensitivity to 5-fluorouracil (5-FU)-chemotherapy for colorectal cancer

80 produce miR-21 exhibit significantly reduced 5-fluorouracil (5-FU)-induced G2/M damage arrest and apo

81 d with dark-gold nanoparticles modified with 5-fluorouracil (5-FU)-intercalated nanobeacons that serv

82 to 5-FU for >100 passages, we established a 5-fluorouracil (5-FU)-tolerant line, MKN45/5FU.

83 bine and approximately 1000 times lower than 5-fluorouracil (5-FU).

84 atopoietic recovery after myeloablation with 5-fluorouracil (5-FU).

85 to recovery from the cell-cycle-active drug 5-fluorouracil (5-FU).

86 ffect on pharmacokinetics of and response to 5-fluorouracil (5-FU).

87 k was increased by the chemotherapeutic drug 5-fluorouracil (5-FU).

88 -140 were more resistant to methotrexate and 5-fluorouracil (5-FU).

89 esistance to chemotherapeutic drugs, such as 5-fluorouracil (5-FU).

90 insensitivity to the chemotherapeutic agent 5-Fluorouracil (5-FU).

91 groups that were given either gemcitabine or 5-fluorouracil (5-FU).

92 ce of the known pyrimidine uptake antagonist 5-fluorouracil (5-FU).

93 al treatment with the chemotherapeutic agent 5-fluorouracil (5-FU).

94 of the commonly prescribed anti-cancer drug 5-fluorouracil (5-FU).

95 tations conferring resistance to the mutagen 5-fluorouracil (5-FU): nsp12-M611F and nsp12-V553I.

96 jections of bevacizumab (1.25 mg, 25 mg/mL), 5-fluorouracil (5-FU; 5 mg, 50 mg/mL), or balanced salt

97 ee thymine (T) analogs including uracil (U), 5-fluorouracil (5FU) and 5-hydroxymethyluracil (5hmU) on

98 5-Fluorouracil (5FU) and oxaliplatin are standard therap

99 Doxorubicin (DOX) and 5-fluorouracil (5FU) are two commonly used chemotherapy

100 I-like therapy including the drugs CPT11 and 5-fluorouracil (5FU) damaged host immunocompetence in a

101 The chemotherapeutic drug 5-fluorouracil (5FU) disrupts DNA synthesis by inhibitin

102 5-fluorouracil (5FU) is an effective anti-cancer drug, y

103 pared the effects of the nucleoside analogue 5-fluorouracil (5FU) on cell cycle progression and clono

104 IOP-lowering medications, bleb needling with 5-fluorouracil (5FU) or further glaucoma surgery, and th

105 When treated with 5-fluorouracil (5FU), the Fgfr1 CKO mice showed defects

106 rocytosine (5FC) to form the anticancer drug 5-fluorouracil (5FU).

107 We find that hTDG removes 5-fluorouracil 78-fold faster than uracil, and 5-chlorou

108 Transfected cells were treated with 5-fluorouracil, a chemotherapeutic that decreases hTERT

109 is and pyrimidine nucleotide metabolism, and 5-fluorouracil activity.

110 GEMs for breast cancer patients treated with 5-fluorouracil, Adriamycin (doxorubicin), and cyclophosp

111 suggests that IP chromic phosphate P 32 and 5-fluorouracil after maximal surgical resection of PMC o

112 g 5-fluorocytosine (5FC) into the chemotoxin 5-fluorouracil, after delivery by infusion into the loco

113 cers with MSI suggest a lack of benefit from 5-fluorouracil alone, the benefit of the current standar

114 --anti-inflammatory ibuprofen and anticancer 5-fluorouracil--along with many other compounds found on

115 Mutants sensitive to 5-fluorouracil, an anticancer drug are under-represented

116 is known to enhance transdermal delivery of 5-fluorouracil, an important systemic antitumor drug.

117 CD also converts 5-fluorocytosine (5FC) to 5-fluorouracil, an inhibitor of DNA synthesis and RNA fu

118 alues 6 and 7 muM for the pyrimidine analogs 5-fluorouracil and 4-thiouracil, respectively.

119 llowing treatment with the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a

120 t) values obtained with the uracil analogues 5-fluorouracil and 5-iodouracil were over 20- to 30-fold

121 In 5-fluorouracil and carboplatin-paclitaxel models, CNTO 5

122 Docetaxel, when combined with 5-fluorouracil and cisplatin, prolongs overall survival

123 own of GRP78 also sensitizes glioma cells to 5-fluorouracil and CPT-11.

124 In this study, the photochemical fate of 5-fluorouracil and cyclophosphamide was investigated in

125 The use of cytotoxic substances, such as 5-fluorouracil and cyclophosphamide, is carefully contro

126 Finally, 5-fluorouracil and docetaxel were shown to cause apoptot

127 ncluding important anticancer agents such as 5-fluorouracil and flutamide, and is extendable to any d

128 5-Fluorouracil and interferon alpha2b have been found to

129 eading explanation for the cardiotoxicity of 5-fluorouracil and may be the underlying the mechanism o

130 est that capecitabine can be substituted for 5-fluorouracil and oxaliplatin for cisplatin.

131 ould benefit from adjuvant chemotherapy with 5-fluorouracil and oxaliplatin.

132 T(17) intron repeat, sensitizes the cells to 5-fluorouracil and oxaliplatin.We investigated whether H

133 re resistant to CRT following treatment with 5-fluorouracil and radiation.

134 e substrates, azathioprine/6-mercaptopurine, 5-fluorouracil and sulindac.

135 he oral cavity of mice receiving concomitant 5-fluorouracil and x-ray radiation.

136 rsensitive to high concentrations of uracil, 5-fluorouracil, and 4-thiouracil in the growth medium.

137 ivatives (including thymine, 5-formyluracil, 5-fluorouracil, and 5-nitrouracil) and some DNA and RNA

138 using omeprazole, following gamma-radiation, 5-fluorouracil, and dextran sulphate sodium (DSS).

139 cal treatments for OSSN include mitomycin C, 5-fluorouracil, and interferon alpha2b.

140 which different combinations of oxaliplatin, 5-fluorouracil, and irinotecan were investigated for met

141 ination chemotherapy, FOLFIRI (folinic acid, 5-fluorouracil, and irinotecan) in a 3D printed fluidic

142 Chemoradiation consisted of: cisplatinum, 5-fluorouracil, and radiation to a median dose of 50.4 G

143 enrollment, a history of ever use of topical 5-fluorouracil, and total occupational time spent outdoo

144 Here, we show that doxorubicin, 5-fluorouracil, and UV and ionizing radiation elicit cha

145 tral venous catheters externally coated with 5-fluorouracil are a safe and effective alternative to c

146 tudies of the toxicity of photobyproducts of 5-fluorouracil are needed to determine the true risk to

147 totoxic effects of the chemotherapeutic drug 5-fluorouracil, as shown by increased apoptosis (P<0.05)

148 EMT, invasion, migration, and resistance to 5-fluorouracil, as well as metastasis of xenograft tumor

149 es C) plus local chemotherapy (cisplatin and 5-fluorouracil), (b) chemotherapy alone, (c) RF hyperthe

150 n cancers (N = 528) from patients treated in 5-fluorouracil-based adjuvant therapy trials were analyz

151 the regimen combining interferon-alpha with 5-fluorouracil-based chemoradiation.

152 ned with external beam radiation therapy and 5-fluorouracil-based chemotherapy for definitive treatme

153 ors without MSI, but have a poor response to 5-fluorouracil-based chemotherapy.

154 Ploidy did not predict the benefit of 5-fluorouracil-based treatment.

155 rectal cancer is preoperative, long course (5-fluorouracil-based) CRT.

156 otolysis resulted in quick transformation of 5-fluorouracil but minimal mineralization.

157 y Gram-positive organisms were cultured from 5-fluorouracil catheters, whereas Gram-positive bacteria

158 ministration-approved drug and metabolite of 5-fluorouracil, causes DNA damage that is repaired by ba

159 modality therapy using radiation therapy and 5-fluorouracil chemotherapy.

160 chemotherapy agents, including doxorubicin, 5-fluorouracil, cisplastin, melphalan, mitoxantrone, and

161 noma and planned neoadjuvant chemoradiation (5- fluorouracil, cisplatin, 40Gy) followed by 2-field tr

162 Furthermore, they are safer compared to 5-fluorouracil, cisplatin and betulinic acid on NIH/3T3,

163 l (5-FU), Mitomycin, and Radiotherapy Versus 5-Fluorouracil, Cisplatin and Radiotherapy in Carcinoma

164 luorouracil/cisplatin followed by concurrent 5-fluorouracil/cisplatin and radiotherapy had a higher c

165 agents, the use of induction therapy in the 5-fluorouracil/cisplatin arm, or other factors.

166 showed that patients treated with induction 5-fluorouracil/cisplatin followed by concurrent 5-fluoro

167 inoma cell lines to the cytotoxic effects of 5-fluorouracil combined with leucovorin and to the thymi

168 y of functional HSCs after administration of 5-fluorouracil compared with wild-type mice, which may b

169 ant to 5-fluoroorotate and hypersensitive to 5-fluorouracil, consistent with loss of UMPS, but remain

170 o determine the true risk to human health of 5-fluorouracil contamination of surface water, given its

171 Chemosensitivity experiments with 5-fluorouracil, cytosine arabinoside (araC), and mercapt

172 Most patients receiving intravenous 5-fluorouracil develop side effects.

173 ated inhibition in cell proliferation, while 5-fluorouracil did not.

174 ting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin, and cyclophosphamide) gener

175 ore resistant to preoperative paclitaxel and 5-fluorouracil-doxorubicin-cyclophosphamide combination

176 hundred sixty-three patients (57%) received 5-fluorouracil during surgery.

177 tor eukaryotic initiation factor 4E, such as 5-fluorouracil, etoposide, and quercetin, dramatically i

178 he C-6 proton of 1-(beta-d-erythrofuranosyl)-5-fluorouracil (FEU), a phosphodianion truncated product

179 survival to and less toxicity than adjuvant 5-fluorouracil/folinic acid in patients with resected pa

180 f leucovorin calcium, and then 2400 mg/m2 of 5-fluorouracil for 4 cycles) followed by 5.5 weeks of ex

181 lactide-co-glycolide), polycaprolactone, and 5-fluorouracil for delivering the anti-cancer drug in a

182 s retinoic acid, dexamethasone, doxorubicin, 5'-fluorouracil, forskolin), sodium dodecyl sulfate (+co

183 ort the in vitro bioorthogonal generation of 5-fluorouracil from a biologically inert precursor by he

184 ctive when compared to the doublet cisplatin-5-fluorouracil from the British and Italian perspectives

185 ncer patients were treated concurrently with 5-Fluorouracil (FU) and radiation for 5 to 6 weeks.

186 5-Fluorouracil (FU) has been widely used for more than f

187 designed and synthesized for recognition of 5-fluorouracil (FU), an antitumor chemotherapy agent, by

188 hymidylate synthase inhibitory metabolite of 5-fluorouracil (FU), is most closely correlated with the

189 ved a general higher sensitivity to FOLFIRI [5-fluorouracil(FU)+irinotecan+folinic acid] than to FOLF

190 Local site infection occurred in 1.4% of the 5-fluorouracil group and 0.9% of the chlorhexidine and s

191 elated bloodstream infection occurred in the 5-fluorouracil group, whereas two episodes were noted in

192 ne in plasma and tissues efficiently reduced 5-fluorouracil host toxicity and altered the anesthetic

193 Gemcitabine, 5-fluorouracil, hydroxyurea, doxorubicin and paclitaxel

194 erapy, yet development of drug resistance to 5-fluorouracil in colorectal cancer cells is the primary

195 tance to repeat treatments with cytoablative 5-fluorouracil in vivo compared with WT HSCs.

196 During 5-fluorouracil-induced anemia, both reticulocyte and red

197 tizes squamous cell carcinoma (SCC) cells to 5-fluorouracil-induced apoptosis and melanoma cells to U

198 o repopulate upon adoptive transfer or after 5-fluorouracil-induced damage.

199 f megakaryocyte damage and release of PF4 on 5-fluorouracil-induced marrow failure was then examined.

200 very of the BM myeloid compartment following 5-Fluorouracil-induced myelo-ablation was much slower in

201 -) BM cells showed hyper proliferation after 5-fluorouracil-induced myeloablation.

202 ruited into an increased cycling state after 5-fluorouracil-induced myelosuppression.

203 utant mice showed enhanced susceptibility to 5-fluorouracil-induced myelosuppression.

204 tin-treated mice significantly and modulated 5-fluorouracil-induced thrombocytosis strongly, suggesti

205 ating the blood-brain barrier - thioTEPA and 5-fluorouracil - influence the normal process of cell pr

206 The antimetabolite drug, 5-fluorouracil, inhibits microbial growth.

207 id recovery after sub-lethal irradiation and 5-fluorouracil injection.

208 stia and underwent Nd:YAG LGP, followed by a 5-fluorouracil injection.

209 amma-radiation, or 2 injections of 400 mg/kg 5-fluorouracil, INS-GAS mice exhibited significantly inc

210 ell migration, as shown by BrdU analysis and 5-fluorouracil insensitivity, and by scratch wound assay

211 as tumour regeneration after treatment with 5-fluorouracil is blocked.

212 three-drug regimen docetaxel, cisplatin and 5-fluorouracil is considered cost-effective when compare

213 aring taxane-containing ICT to cisplatin and 5-fluorouracil is discussed.

214 5-Fluorouracil is effective and well tolerated as a prim

215 5-Fluorouracil is inactivated by dihydropyrimidine dehyd

216 The analysis showed that 5-fluorouracil is incorporated into a large number of me

217 for the current studies, 1-ethyloxycarbonyl-5-fluorouracil, is known to enhance transdermal delivery

218 m of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA following

219 e benefit of the current standard treatment, 5-fluorouracil, leucovorin, and oxaliplatin, in this sub

220 These mice were given cisplatin or 5-fluorouracil/leucovorin and oxaliplatin (FOLFOX), and

221 y shows additive killing with complement and 5-fluorouracil/leucovorin in vivo, suggesting a new ther

222 Adjuvant chemoradiation with 5-fluorouracil/leucovorin significantly improves disease

223 Coating of central venous catheters with 5-fluorouracil may reduce the risk of catheter infection

224 cyclin D1 in colon cancer cells reduced the 5-fluorouracil-mediated DDR.

225 il and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metabolite.

226 ization, bystander effects, and formation of 5-fluorouracil metabolites.

227 ll lines to several other anticancer agents (5-fluorouracil, mitomycin C, doxorubicin, colchicine, vi

228 y rate than patients treated with concurrent 5-fluorouracil/mitomycin C and radiotherapy.

229 fore and after treatment with doxorubicin or 5-fluorouracil/mitomycin C.

230 enous catheter externally coated with either 5-fluorouracil (n = 480) or chlorhexidine and silver sul

231 5-fluorouracil, often given with leucovorin, is the most

232 38 (the active metabolite of irinotecan) and 5-fluorouracil on cell proliferation under hypoxic condi

233 By contrast, combination of 2-MeO-E(2) with 5-fluorouracil only had a partial additive effect agains

234 Similar results were obtained when 5-fluorouracil or 5-fluoro-2'-deoxyuridine was used inst

235 agents vincristine and taxotere but not with 5-fluorouracil or doxorubicin.

236 In this study, stress induced by 5-fluorouracil or phenylhydrazine revealed a delay in th

237 efects are observed in feathers treated with 5-fluorouracil or taxol but not with doxorubicin or arab

238 with an appropriate cytotoxic chemotherapy (5-fluorouracil) or tyrosine kinase inhibitor (erlotinib)

239 e in cytotoxicity to doxorubicin, cisplatin, 5-fluorouracil, or etoposide.

240 motherapies used in colorectal cancer (CRC) (5-fluorouracil, oxaliplatin and irinotecan).

241 t individual death responses of CRC cells to 5-fluorouracil/oxaliplatin.

242 hich, after a successful trabeculectomy with 5-Fluorouracil, phacoemulsification with posterior chamb

243 oxaliplatin (IROX) compared with those given 5-fluorouracil plus oxaliplatin (FOLFOX; cycle 1 mean gr

244 icacy of chemoradiotherapy, with CRLX101 and 5-fluorouracil producing the highest therapeutic efficac

245 ticancer therapeutics, such as cisplatin and 5-fluorouracil, reportedly exert, at least partially, th

246 lowly cycling HSPC compartment and increased 5-fluorouracil resistance but not a decreased serial rep

247 l line had the opposite effect and increased 5-fluorouracil resistance.

248 and reduced the viability of self-renewing, 5-fluorouracil-resistant Aldefluor positive [Aldefluor(+

249 olonosphere formation of unsorted and sorted 5-fluorouracil-resistant CSCs.

250 5-Fluorouracil-resistant TYMS T51S, G52S (TYMS(SS)) is r

251 erapy (45 Gy in 25 fractions with concurrent 5-fluorouracil) restricted to patients with involvement

252 ole-rifampicin (RR, 0.14 [95% CI, .05-.36]), 5-fluorouracil (RR, 0.34 [95% CI, .14-.82]), and chlorhe

253 Repeat challenge with 5-fluorouracil showed that Ghr was dispensable for HSC a

254 somal stress-inducing agent actinomycin D or 5-fluorouracil significantly decreased the c-myc mRNA le

255 5-Fluorouracil subjects the hemopoietic system to acute

256 ncreased response to the nucleoside analogue 5-fluorouracil, suggesting that lower levels of this met

257 28 fractions during 5.5 weeks, with infusion 5-fluorouracil, surgery in 4 to 6 weeks, and 4 courses o

258 Next, (5-fluorouracil)-templated molecularly imprinted polymer

259 the metabolic subtype were more sensitive to 5-fluorouracil than the other subtypes.

260 e mutagenic nucleoside analogs ribavirin and 5-fluorouracil than the WT virus, whereas the lower-fide

261 y the correlation between sensitivity toward 5-fluorouracil therapy and uPAR expression level was inv

262 Dichotomized by use of 5-fluorouracil, there was increased risk of death in pat

263 luorocytosine into the toxic anticancer drug 5-fluorouracil, thereby producing tumor-specific antitum

264 as found to react with the excited states of 5-fluorouracil, thus enhancing direct photolysis rates.

265 lized targeted CONs for targeted delivery of 5-fluorouracil to breast cancer cells.

266 estigated as alternatives to mitomycin C and 5-fluorouracil to reduce inflammation and subsequent ble

267 te-inhibited by uracil and 4-thiouracil, but 5-fluorouracil toxicity transpires via an alternative me

268 ue to DYRK3-deficiency also were observed in 5-fluorouracil-treated mice expressing a compromised ery

269 res of these mice were delayed recovery from 5-fluorouracil treatment and diminished multilineage rec

270 aired reconstitution capacity as assessed by 5-fluorouracil treatment and long-term transplantation.

271 els of TS and p53 mRNAs were unaltered after 5-fluorouracil treatment as assessed by real-time qRT-PC

272 Decreases in hTERT gene expression caused by 5-fluorouracil treatment could be visualized in living 2

273 5-Fluorouracil treatment of colon carcinoma HCT116 cells

274 Only upon 5-fluorouracil treatment was HSPC-depleted bone marrow c

275 rthermore, using serial transplantations and 5-fluorouracil treatment, we demonstrate that HSCs do no

276 btype appeared to have greater benefits with 5-fluorouracil treatment.

277 e expression in tumor cells before and after 5-fluorouracil treatment.

278 t mice are significantly more susceptible to 5-fluorouracil treatment.

279 nograft tumor initiation and was superior to 5-fluorouracil treatment.

280 Hdac8-deficient mice challenged with serial 5-fluorouracil treatment.

281 nces PDA cell sensitivity to oxaliplatin and 5-fluorouracil under physiologic low oxygen conditions.

282 mitis were not significantly associated with 5-fluorouracil use.

283 The phototransformation product of 5-fluorouracil was also identified.

284 Of importance, the anticancer drug 5-fluorouracil was an excellent substrate for TbU3, and

285 cant amounts of bicarbonate (close to 2 mM), 5-fluorouracil was rapidly removed (within 1 day) throug

286 eline uPAR expression and sensitivity toward 5-fluorouracil was revealed, thus illustrating the possi

287 Also, screening of Dam MTase inhibitor 5-fluorouracil was successfully investigated using this

288 An anticancer drug (5-fluorouracil) was conjugated to the surface of gold na

289 A cytostatic drug (5-fluorouracil) was introduced into the microsystem with

290 Central venous catheters coated with 5-fluorouracil were noninferior to chlorhexidine and sil

291 Treatment doses for doxorubicin and 5-fluorouracil were selected to cause comparable cytotox

292 tency of the cytotoxic agents paclitaxel and 5-fluorouracil when given in combination.

293 apeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early steps of antimetabo

294 Neither cisplatin nor 5-fluorouracil, which are used to treat head and neck ca

295 ice were given intraperitoneal injections of 5-fluorouracil, which blocked gastric cell proliferation

296 SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic st

297 ability after treatment with 1,4-dioxane and 5-fluorouracil, which proves that it can be used for tru

298 Clinical trials comparing cisplatin and 5-fluorouracil with or without a taxane followed by radi

299 tral venous catheters externally coated with 5-fluorouracil with those coated with chlorhexidine and

300 ogenitors following bone marrow depletion by 5-fluorouracil, with the pro-B and pre-B cell pools stil