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

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

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

5 d into immunodeficient mice was inhibited by 5-fluorouracil.

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

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

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

9 onditions of stress hematopoiesis induced by 5-fluorouracil.

10 of spheroids to different concentrations of 5-fluorouracil.

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

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

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

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

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

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

17 utate, photodynamic therapy, colchicine, and 5-fluorouracil.

18 y used colorectal chemotherapeutic compound, 5-fluorouracil.

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

20 rmediate for oxaliplatin and the largest for 5-fluorouracil.

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

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

23 the colorectal cancer chemotherapeutic agent 5-fluorouracil.

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

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

26 5-Fluorouracil 1% administered topically 4 times daily f

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

28 itron emission tomography (PET) agent [(18)F]5-fluorouracil ([(18)F]FU).

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

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

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

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

33 t drugs or drug combination, indicating that 5-fluorouracil (5-FU) + irinotecan (IRI) + bevacizumab (

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

35 5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, f

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

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

38 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyur

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

40 lectively potentiated cytotoxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of

41 , the protected analogues of cytotoxic drugs 5-fluorouracil (5-FU) and monomethyl auristatin E (MMAE)

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

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

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

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

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

47 l proliferation via a chemotherapeutic agent 5-fluorouracil (5-Fu) eliminated fast-cycling stem cells

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

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

50 eletion of Bok results in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mic

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

52 Moreover, the combination of CB-839 and 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regres

53 5-Fluorouracil (5-FU) is a chemotherapeutic drug widely

54 5-Fluorouracil (5-FU) is a standard treatment option for

55 5-fluorouracil (5-FU) is a widely used chemotherapeutic

56 5-Fluorouracil (5-FU) is an anticancer agent whose main

57 lecular mode of action of the cytotoxic drug 5-fluorouracil (5-FU) is generally considered to result

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

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

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

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

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

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

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

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

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

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

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

69 Standard therapies such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamma-irradiation

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

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

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

73 lon cancer recurrence after therapy, such as 5-fluorouracil (5-FU), remains a challenge in the clinic

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

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

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

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

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

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

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

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

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

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

87 -140 were more resistant to methotrexate and 5-fluorouracil (5-FU).

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

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

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

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

92 tumor necrosis factor alpha (TNF-alpha) and 5-Fluorouracil (5-FU).

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

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

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

96 Initially, 5-Fluorouracil(5-FU)/Belotecan/Oxaliplatinum and Tegafur

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

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

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

102 as a prodrug, which is converted into toxic 5-fluorouracil (5FU) upon uptake into fungal cells.

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

104 5-Fluorouracil (800 mg/m(2) intravenous infusion on days

105 weeks followed by 1 week off (or intravenous 5-fluorouracil, 800 mg/m(2) per day on days 1-5), and a

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

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

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

109 T cell lines BON1 and QGP1 were treated with 5-fluorouracil alone or in combination with decitabine o

110 on: This preclinical study demonstrated that 5-fluorouracil alone or in combination with decitabine o

111 Results: Treatment with 5-fluorouracil alone or in combination with decitabine o

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

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

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

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

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

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

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

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

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

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

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

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

124 We focused on 5-Fluorouracil and Gemcitabine because based on our excl

125 vely or negatively to two chemotherapeutics: 5-Fluorouracil and Gemcitabine.

126 5-Fluorouracil and interferon alpha2b have been found to

127 which cancer patients received oxaliplatin, 5-fluorouracil and irinotecan via chronomodulated schedu

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

129 lectively potentiated cytotoxicity of SN-38, 5-fluorouracil and mitoxantrone, but not that of gemcita

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 Bacterial conversion of 5-FC to 5-fluorouracil and subsequently to fluorouridine monopho

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 IP4 had increased resistance to gemcitabine, 5-fluorouracil, and cisplatin, whereas AsPC-1 cells with

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

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

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

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

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

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

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

149 patients with stage III/IV PDAC treated with 5-fluorouracil based therapy (n = 176).

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

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

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

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

154 h DNA-damaging agents (i.e., oxaliplatin and 5-fluorouracil), but not with PARPi therapy.

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

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

157 motherapy), or cetuximab plus a platinum and 5-fluorouracil (cetuximab with chemotherapy).

158 es hematologic recovery in mice treated with 5-fluorouracil chemotherapy.

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

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

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

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

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

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

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

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

167 tiple actinic keratosis lesions on the head, 5% fluorouracil cream was the most effective of four fie

168 nts were randomly assigned to treatment with 5% fluorouracil cream, 5% imiquimod cream, methyl aminol

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

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

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

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

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

174 erapeutic drugs that activate p53, including 5-fluorouracil, etoposide and cisplatin.

175 e TRMT2A-tRNA crosslinking in vivo following 5-Fluorouracil exposure is also intriguing, as it sugges

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

177 motherapy combinations including FOLFIRINOX (5-fluorouracil, folinic acid [leucovorin], irinotecan, a

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

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

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

181 Spheroids were treated with 5-Fluorouracil for five days through continuous perfusio

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

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

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

191 nucleoside analogues, such as ribavirin and 5-fluorouracil, have been ineffective at inhibiting CoVs

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

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

194 preclinical in vitro findings indicate that 5-fluorouracil in combination with epigenetic modifiers

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

196 more than 30 years, of carmofur's mysterious 5-fluorouracil-independent antitumor activity.

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

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

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

200 ida albicans infection and more sensitive to 5-fluorouracil-induced granulocytic regeneration.

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

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

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

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

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

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

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

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

209 Subconjunctival 5-fluorouracil injections were given postoperatively, as

210 ss was also exacerbated by stress induced by 5-fluorouracil injections.

211 ownstream gene-targets, and interaction with 5-fluorouracil, irinotecan, and oxaliplatin.

212 and safety, pembrolizumab plus platinum and 5-fluorouracil is an appropriate first-line treatment fo

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

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

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

216 5-Fluorouracil is effective and well tolerated as a prim

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

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

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

220 luding relaxin (RLN), FOLFOX (combination of 5-fluorouracil, leucovorin, and oxaliplatin), and IL-12,

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

222 r patients with resectable disease, modified 5-fluorouracil, leucovorin, irinotecan and oxaliplatin (

223 nd 14.9 months for those receiving induction 5-fluorouracil, leucovorin, irinotecan, and oxaliplatin

224 peutic regimen FOL-F-IRIN-OX (combination of 5-fluorouracil, leucovorin, irinotecan, and oxaliplatin)

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

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

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

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

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

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

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

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

233 5-fluorouracil, often given with leucovorin, is the most

234 38 (the active metabolite of irinotecan) and 5-fluorouracil on cell proliferation under hypoxic condi

235 r rectum who had received RCT (45-50 Gy with 5-fluorouracil or capecitabine) were included and random

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

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 glaucoma incisional surgery, intraoperative 5-fluorouracil, or follow-up <1 month.

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

241 ation with chemotherapy [C26 oxaliplatin and 5-fluorouracil (oxfu)] and to evaluate the potential of

242 mab alone, pembrolizumab plus a platinum and 5-fluorouracil (pembrolizumab with chemotherapy), or cet

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

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

245 reclinical study, we explored the effects of 5-fluorouracil plus the DNA methyltransferase inhibitor

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

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

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

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

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

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

252 5-Fluorouracil-resistant TYMS T51S, G52S (TYMS(SS)) is r

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

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

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

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

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

258 28 fractions during 5.5 weeks, with infusion 5-fluorouracil, surgery in 4 to 6 weeks, and 4 courses o

259 Novel conjugates of ferrocene with uracil, 5-fluorouracil, tegafur, or acyclovir are reported.

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

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

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

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

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

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

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

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

268 racil) degradation metabolites in predicting 5-fluorouracil toxicity and the role of the agmatine pat

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

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

271 sues were collected from 53 stage II and 54 (5-fluorouracil-treated) stage III patients.

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

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

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

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

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

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

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

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

280 HSC more vulnerable to serial myeloablative 5-fluorouracil treatment.

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

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

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

284 In mice treated with topical 5-fluorouracil, use of STAR particles increased the effi

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

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

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

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

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

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

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

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

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

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

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