ライフサイエンスコーパス: 5-FU

1 5-FU treatment increased the fraction of ribosome-free L

2 5-FU treatment was toxic and did not improve survival.

3 5-FU was first entrapped in PLGA core by solvent evapora

4 5-FU-based combinatory chemotherapeutic regimens have be

5 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P

6 adjuvant FOLFOX [DFS at 3 years: 14% vs 38% (5-FU) vs 45% (no-chemo), OS at 3 years: 58% vs 70% (5-FU

7 .005% calcipotriol ointment combined with 5% 5-FU cream were compared with Vaseline plus 5-FU for the

8 s 45% (no-chemo), OS at 3 years: 58% vs 70% (5-FU) vs 84% (no-chemo)].

9 The nanobeacons comprise a 5-FU intercalated DNA hairpin, which is labeled with a n

10 Capecitabine (CAP) is a 5-FU pro-drug approved for the treatment of several canc

11 Of these, 60 patients received adjuvant 5-FU chemotherapy after surgery and the other 60 did not

12 y DPYD) rapidly degrades 85% of administered 5-FU, and as such, limits the amount of drug available f

13 Although DPYD variants may affect 5-FU metabolism, they do not completely explain the repo

14 s using small inhibitory RNAs did not affect 5-FU cytotoxicity.

15 ents (27/47) after FOLFOX, 29% (12/41) after 5-FU, and 32% (13/41) after no chemotherapy (P = 0.011).

16 Mice were sacrificed 3 days after 5-FU challenge.

17 ing with improved stress hematopoiesis after 5-FU treatment, and this results in HSC exhaustion over

18 GDC-0941 may suppress disease relapse after 5-FU-based gastric cancer chemotherapy.

19 uired to achieve a protective effect against 5-FU toxicity, but exogenous administration of Urd is no

20 , providing further evidence for alternative 5-FU protein targets.

21 s in bacterial deoxynucleotide pools amplify 5-FU-induced autophagy and cell death in host cells, an

22 tissue +/- 0.033 vs 0.260 mg/g +/- 0.030 and 5-FU: 0.660 mg/g +/- 0.060 vs 0.52 mg/g +/- 0.050, P < .

23 the synergistic effects of calcipotriol and 5-FU treatment in optimally activating a CD4+ T cell-med

24 showed enhanced efficacy with cisplatin and 5-FU.

25 larger and higher blebs than the control and 5-FU-treated groups (P < 0.05).

26 ve primary was comparable between FOLFOX and 5-FU but lower in the no-chemotherapy group (P < 0.0001)

27 DAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt sign

28 trabiliary local delivery of gemcitabine and 5-FU was performed by using a microporous balloon with (

29 n therapy with chemotherapy (gemcitabine and 5-FU) plus RF hyperthermia, (b) chemotherapy only, (c) R

30 tivity to methylmethane sulfonate, H2O2, and 5-FU from DRC.

31 OC cell growth, was more active than LR and 5-FU, and showed a TS/DHFR expression pattern similar to

32 the effect of saracatinib on oxaliplatin and 5-FU efficacy in CRC cells.

33 isms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and robust upregulation of atypica

34 effect than free form of these proteins and 5-FU.

35 te levels and the accumulation of uracil and 5-FU in the genome, events that activate the ATR- and AT

36 est (doxorubicin) or G1-phase growth arrest (5-FU).

37 FdUTP is incorporated by DNA polymerases as 5-FU in the genome; however, it remains unclear how eith

38 ation stress-inducing chemotherapies such as 5-FU.

39 t IL-6, heme oxygenase-1, and NO, attenuated 5-FU-MSC-induced immunosuppression.

40 contributing to the synergy observed between 5-FU and oxaliplatin in the clinic.

41 n was altered upon treatment with FdUMP, but 5-FU toxicity seemed to be largely RNA-based, being resc

42 ular mechanisms underlying p53 activation by 5-FU remain largely obscure.

43 findings suggested that immunosuppression by 5-FU-MSC is mediated by a combination of elevated IL-1ra

44 unctional role of ABCB5 in colorectal cancer 5-FU resistance.

45 ) or type of pre/postoperative chemotherapy (5-FU-leucovorin vs. FOLFOX/FOLFIRI vs. bevacizumab) (P=0

46 performed better than standard chemotherapy (5-FU and oxaliplatin).

47 MagMBs delivering the combined 5-FU/SDT treatment produced a reduction in cell viabilit

48 oups were as follows: unchallenged controls, 5-FU-challenged mice (450 mg/kg, i.p) with or without th

49 tem and measured their capacities to convert 5-FU to dihydro-fluorouracil, the product of DPD catabol

50 well as free parent drugs (CPT, 5-Fu and CPT/5-FU mixture (1:1)).

51 to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumo

52 ents with a defect in the MMR system (dMMR), 5-FU therapy was associated to reduced survival (DFS; HR

53 son with irinotecan, topotecan, doxorubicin, 5-FU, gemcitabine, docetaxel, oxaliplatin, cytoxan and c

54 heart, liver, and bone, compared with either 5-FU or cyclophosphamide.

55 mutant RasV12, but not the WT Ras, enhanced 5-FU-induced apoptosis in 293T cells.

56 otherapeutic agent for HCC, 5-flouorouracil (5-FU), are known to modulate p53.

57 dable nanogel entrapped with 5-fluororuacil (5-FU) coated with eucalyptus oil, topically applied onto

58 h the chemotherapeutic agent 5-fluorouracil (5-FU) also induces GzmB production in HSCs.

59 5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, floxuridine) have

60 lone and in combination with 5-fluorouracil (5-FU) and cisplatin.

61 therapeutic agents including 5-fluorouracil (5-FU) and elevated expression of dUTPase is negatively c

62 e antineoplastic activity of 5-fluorouracil (5-FU) and in the anabolism of its oral prodrug, capecita

63 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyuridine (FdUrd, fl

64 ucing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensiti

65 rectal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combina

66 regimens, specifically with 5-fluorouracil (5-FU) and oxaliplatin, in CRC.

67 ted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC

68 inducer, in combination with 5-fluorouracil (5-FU) as an immunotherapy for actinic keratosis.

69 cancer chemotherapeutic drug 5-fluorouracil (5-FU) by prolonging S phase, generating DNA strand break

70 reduces the apparent IC50 of 5-fluorouracil (5-FU) from 1 micromol/L to 80 nmol/L (12-fold) in a colo

71 pment, the pyrimidine analog 5-fluorouracil (5-FU) has become an integral component of many cancer tr

72 omycin C (MMC) in 271 (63%), 5-fluorouracil (5-FU) in 129 (30%), and no antifibrotic in 28 (7%).

73 tion and the anticancer drug 5-fluorouracil (5-FU) in those cell lines.

74 5-fluorouracil (5-FU) is a widely used anticancer drug that disrupts pyr

75 5-fluorouracil (5-FU) is a widely used chemotherapeutic drug for the tre

76 The antimetabolite 5-fluorouracil (5-FU) is one of the most widely used chemotherapy drugs.

77 cancer (CRC) treatment with 5-fluorouracil (5-FU) is the first line of therapy for this debilitating

78 ite of the chemotherapy drug 5-fluorouracil (5-FU) of importance for biological studies.

79 iplatin (FOLFOX) compared to 5-fluorouracil (5-FU) or no chemotherapy for adjuvant treatment of color

80 eatment with the RNA mutagen 5-fluorouracil (5-FU) than wild-type (WT)-ExoN(+), suggestive of decreas

81 r pemetrexed and the prodrug 5-fluorouracil (5-FU) that inhibit the protein by binding at its active

82 We treated mice with 5-fluorouracil (5-FU) to isolate a quiescent and undifferentiated mesenc

83 ted cancer cells compared to 5-fluorouracil (5-FU) treated cells.

84 cellular stress triggered by 5-fluorouracil (5-FU) treatment potentiates the effects of the loss of D

85 duce host toxicity caused by 5-fluorouracil (5-FU) without impairing its antitumor activity.

86 hree chemotherapeutic drugs: 5-fluorouracil (5-FU), 5-fluoro-2'-deoxyuridine (FUDR), and camptothecin

87 isms of action [gemcitabine, 5-fluorouracil (5-FU), and cisplatin] in pancreatic cancer cells.

88 to a vasotoxic cancer drug, 5-Fluorouracil (5-FU), in comparison with an in vivo mouse model.

89 hase III Randomized Study of 5-Fluorouracil (5-FU), Mitomycin, and Radiotherapy Versus 5-Fluorouracil

90 ces Notch-1, as oxaliplatin, 5-fluorouracil (5-FU), or SN-38 (the active metabolite of irinotecan) in

91 with Rose Bengal (RB) and/or 5-fluorouracil (5-FU), were assessed as a delivery vehicle for the targe

92 o the chemotherapeutic agent 5-fluorouracil (5-FU), which at low concentrations activates p53 by indu

93 520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and red

94 n: 5040 centi-Gray (cGy) and 5-fluorouracil (5-FU)-based chemotherapy) followed by TME from 1988 to 2

95 ) COG 133 mimetic peptide in 5-fluorouracil (5-FU)-challenged Swiss mice and IEC-6 cell monolayers.

96 poxia reduces sensitivity to 5-fluorouracil (5-FU)-chemotherapy for colorectal cancer (CRC).

97 xhibit significantly reduced 5-fluorouracil (5-FU)-induced G2/M damage arrest and apoptosis that is c

98 nanoparticles modified with 5-fluorouracil (5-FU)-intercalated nanobeacons that serve as an ON/OFF m

99 0 passages, we established a 5-fluorouracil (5-FU)-tolerant line, MKN45/5FU.

100 prescribed anti-cancer drug 5-fluorouracil (5-FU).

101 mately 1000 times lower than 5-fluorouracil (5-FU).

102 ery after myeloablation with 5-fluorouracil (5-FU).

103 m the cell-cycle-active drug 5-fluorouracil (5-FU).

104 by the chemotherapeutic drug 5-fluorouracil (5-FU).

105 esistant to methotrexate and 5-fluorouracil (5-FU).

106 motherapeutic drugs, such as 5-fluorouracil (5-FU).

107 o the chemotherapeutic agent 5-Fluorouracil (5-FU).

108 given either gemcitabine or 5-fluorouracil (5-FU).

109 pyrimidine uptake antagonist 5-fluorouracil (5-FU).

110 okinetics of and response to 5-fluorouracil (5-FU).

111 h the chemotherapeutic agent 5-fluorouracil (5-FU).

112 ng resistance to the mutagen 5-fluorouracil (5-FU): nsp12-M611F and nsp12-V553I.

113 cizumab (1.25 mg, 25 mg/mL), 5-fluorouracil (5-FU; 5 mg, 50 mg/mL), or balanced salt solution (BSS; 0

114 effect of the anticancer drug fluorouracil (5-FU) on HCT116 cancer spheroids.

115 test for the highest DW (i.e., fluorouracil (5-FU)) and K(OW) (i.e., lovastatin (LOVS)) compounds, in

116 ctal cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence

117 t uridine is substituted by 5-fluorouridine (5-FU), reveals a covalent bond between the isomerized ta

118 o-5-deoxyuridine (5-dFUrd) to 5-fluouridine (5-FU), a potent thymidine synthase inhibitor, which bloc

119 The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literatu

120 FU)+irinotecan+folinic acid] than to FOLFOX (5-FU+oxaliplatin+folinic acid), not only between isogeni

121 ranscripts, and reduction of IL-10 following 5-FU treatment, each of which were partially abrogated b

122 expression of ADAM12-L in BC cells following 5-FU treatment results in the acquisition of resistance

123 gene with increased p53 occupancy following 5-FU treatment of cells.

124 In addition, a pulse enhancement (PE) for 5-FU and LOVS was not present in wastewater effluent.

125 tic variations in DPYD increase the risk for 5-FU toxicity, however, there is not a clear consensus a

126 tically improve predictive genetic tests for 5-FU sensitivity, especially in individuals of non-Europ

127 colon cancer cell line protected cells from 5-FU-induced apoptosis.

128 Facile racemic syntheses of 5-DHFU from 5-FU or uracil, using p-methoxybenzyl protecting groups

129 Cancer cell lines were also rescued from 5-FU toxicity with uridine rather than thymidine.

130 Further, 5-FU-mediated p53 expression was reduced with concurrent

131 ated closely with resistance to gemcitabine, 5-FU, and cisplatin.

132 associated with survival in the group given 5-FU.

133 ) with neoadjuvant radiochemotherapy (40 Gy, 5-FU, cisplatin) or chemotherapy (MAGIC or FLOT) for cT3

134 Patients were excluded if 5-FU was used as adjuvant therapy, if they did not compl

135 s a population of potently immunosuppressive 5-FU-MSCs that have the potential to be exploited to rem

136 linositide 3-kinase (PI3K) increased both in 5-FU-tolerant subpopulations according to the 5-FU dose,

137 No change in 5-FU sensitivity was observed for R80A/E82A-ExoN(-) rela

138 sting a vasospastic role of 5-fluoruracil in 5-FU associated optic neuropathy.

139 not miR-210, were significantly increased in 5-FU resistant CRCs.

140 ny functional relevance to p53 modulation in 5-FU-treated cells.

141 re protein did not play a detectable role in 5-FU-mediated caspase-7 activation in the absence of fun

142 ls of p-Akt and restored 5-FU sensitivity in 5-FU-resistant BC cells.

143 repression by Ezh2 predicts poor survival in 5-FU-treated cancers.

144 hus indicating that genomically incorporated 5-FU plays a major role in the antineoplastic effects of

145 mage response and repair processes influence 5-FU and FdUrd toxicity in ovarian cancer cells.

146 n of 5'-deoxy-5-fluorouridine (5'-DFUR) into 5-FU.

147 Irradiating 5-FU and LOVS in hydrophobic (HPO), transphilic (TPI), a

148 covalent bond between enzyme and isomerized 5-FU we propose a Michael addition mechanism for pseudou

149 arterial infusion (HAI) and intravenous (IV) 5-FU compared with standard modern adjuvant IV chemother

150 Saracatinib did not modulate 5-FU efficacy but antagonized oxaliplatin in a schedule-

151 We examined these 5-FU-resistant MSCs (5-FU-MSCs) free from hematopoietic components for CFU fi

152 Compared with untreated MSCs, 5-FU-MSCs demonstrated potent immunosuppression of Con A

153 with IC(50) = 0.10 muM (cisplatin, 1.6 muM; 5-FU, 4.7 muM).

154 obtained prior to and following neoadjuvant 5-FU-based chemoradiation therapy in a series of colorec

155 (raltitrexed), which induces uracil but not 5-FU accumulation, thus indicating that genomically inco

156 The anti-tumor activity of 5-FU has been attributed in part to its ability to induc

157 re, cGAMP improved the antitumor activity of 5-FU, and clearly reduced the toxicity of 5-FU.

158 Sequential administration of 5-FU and a PI3K inhibitor, GDC-0941, targeted the downst

159 These results suggest that administration of 5-FU followed by GDC-0941 may suppress disease relapse a

160 to 5-FU and, in turn, increased anabolism of 5-FU to cytotoxic nucleotides, resulting in more severe

161 and rate-limiting step in the catabolism of 5-FU.

162 ecific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU t

163 Degradation of 5-FU and LOVS were inhibited by wastewater effluent to a

164 be causally associated with major degrees of 5-FU sensitivity.

165 In rabbits, local delivery of 5-FU immediately after RF ablation provided a significan

166 ehydrogenase (DPD) is a major determinant of 5-FU response and toxicity.

167 nsequence, may decrease the effectiveness of 5-FU an antitumor drug in carriers.

168 is in vitro and reduced the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenogr

169 nd improved the antiproliferative effects of 5-FU on colon cancer cells, accompanied by a reduction o

170 cant protection against the toxic effects of 5-FU, a G1/S cell cycle arrest phenotype, and accumulate

171 e is protective against the toxic effects of 5-FU.

172 atically reduces the therapeutic efficacy of 5-FU.

173 Our work provides pre-clinical evidence of 5-FU delivery to tumours and anti-tumour efficacy follow

174 displayed efficient and steady state flux of 5-FU from the biodegradable nanogles into the skin, whil

175 FU and in very low yield by hydrogenation of 5-FU; however, a practical chemical synthesis is not ava

176 47; p < 0.01 respectively), independently of 5-FU treatment.

177 uracil BER in the cell killing mechanism of 5-FU.

178 e differences in the cytotoxic mechanisms of 5-FU and FdUrd and suggest that combining FdUrd and PARP

179 concentrations ( approximately 25 microM) of 5-FU in both models, as a single agent, and induced surv

180 models, IEC-6 cells were exposed to 1 mM of 5-FU in glutamine free media with or without the ApoE pe

181 is in a colorectal cancer xenograft model of 5-FU monotherapy.

182 has been prepared by enzymatic reduction of 5-FU and in very low yield by hydrogenation of 5-FU; how

183 ted with a first-line combination regimen of 5-FU, oxaliplatin, and bevacizumab (FOLFOX-bevacizumab),

184 sistent with clinical association studies of 5-FU toxicity, the D949V substitution reduced enzyme act

185 on of thymidylate synthase (TS), a target of 5-FU.

186 rotecting strategy by the adjunct therapy of 5-FU with Resveratrol.

187 ation and slightly increases the toxicity of 5-FU.

188 of 5-FU, and clearly reduced the toxicity of 5-FU.

189 ion mechanism may aid in the clinical use of 5-FU-based chemotherapy.

190 For this, the role of HAX-1 on 5-FU treatment was examined in HepG2 cells expressing HC

191 specific ADAM12-L inhibition could optimize 5-FU-based chemotherapy of BC, thereby preventing BC rec

192 han 10-fold higher than that of cisplatin or 5-FU, was independent of the oxidation state (Au(III), 6

193 cell line treated with either doxorubicin or 5-FU showed a concentration-dependent reduced cell proli

194 ear how either genomically incorporated U or 5-FU contributes to killing.

195 ncreased incorporation of 5'-DFUR-originated 5-FU nucleotides into nucleic acids.

196 herapy and was synergistic with oxaliplatin, 5-FU, and SN-38.

197 t for primary CRC was FOLFOX in 77 patients, 5-FU in 169 patients, and no chemotherapy in 95 patients

198 d nanogel conjugates with the phosphorylated 5-FU nucleoside Floxuridine and demonstrated their enhan

199 Importantly, calcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural k

200 Four-day application of calcipotriol plus 5-FU versus Vaseline plus 5-FU led to an 87.8% versus 26

201 ng a T. brucei-specific DHODH inhibitor plus 5-FU may prove to be an effective therapeutic strategy.

202 5-FU cream were compared with Vaseline plus 5-FU for the field treatment of actinic keratosis in a r

203 calcipotriol plus 5-FU versus Vaseline plus 5-FU led to an 87.8% versus 26.3% mean reduction in the

204 perimental cancer cell lines did not predict 5-FU sensitivity or resistance.

205 n between HCV core and HAX-1, which promotes 5-FU mediated p53-dependent caspase-7 activation and hep

206 PT/5-FU co-treatment was more effective in Caco-2 cells.

207 from cancer cells treated with radiolabeled 5-FU were labeled, species with alternative molecular we

208 appreciable fraction of patients who receive 5-FU suffer severe adverse toxicities, which in extreme

209 Subsequently, patients received 5-FU based chemoradiation.

210 have worse outcomes than those who received 5-FU or no chemotherapy.

211 d gemcitabine, but not in those who received 5-FU.

212 ovel ApoE COG 133 mimetic peptide can reduce 5-FU-induced intestinal changes and potentially benefit

213 attenuated the levels of p-Akt and restored 5-FU sensitivity in 5-FU-resistant BC cells.

214 SGs, but the cumulative dose of sensitizing 5-FU and radiation was higher in SG2.

215 cting them from the lethal effects of serial 5-FU treatment.

216 -deficient mice are more resistant to serial 5-FU treatments.

217 d DPYD alleles are protective against severe 5-FU toxicity, and, as a consequence, may decrease the e

218 Subconjunctival 5-FU injection was performed postoperatively in 119 pati

219 se phosphorylation to significantly suppress 5-FU-tolerant subpopulations and tumor propagation of or

220 ved postoperative HAI combined with systemic 5-FU (HAI group) and 54 (55%) had received "modern" syst

221 We tested 5-FU sensitivity in yeast and human cancer cell models i

222 al cells, and was >10 times more potent than 5-FU, the current therapy for CRC.

223 FdUMP[10] was better tolerated than 5-FU or cytarabine plus doxorubicin and did not affect n

224 These results demonstrate that 5-FU treatment triggers a ribosomal stress response so t

225 Surprisingly, we find that 5-FU and FUDR act through bacterial ribonucleotide metab

226 We found that 5-FU does not induce apoptosis rather vascular hyperperm

227 It highlights that 5-FU may have the potential to cause arterial vasospasm

228 In this study, we observed that 5-FU induces expression of the ADAM12 isoform ADAM12-L b

229 Here we report that 5-FU treatment leads to p53 stabilization and activation

230 These results show that 5-FU lesions that escape UNG repair activate HR, which p

231 We also show that 5-FU metabolites do not block the first round of DNA syn

232 Our findings suggested that 5-FU treatment identifies a population of potently immun

233 proliferation and migration, 24 h after the 5-FU challenge.

234 no significant difference in IOP between the 5-FU and the placebo group at 8 years.

235 ler in the FOLFOX group (2.5 cm) than in the 5-FU (3.0 cm) or no-chemotherapy (3.5 cm) groups, (P = 0

236 s was achieved in 48 subjects (55.8%) in the 5-FU and 33 subjects (39.3%) in the placebo group (P = 0

237 0.0%) completed 8 years follow-up, 86 in the 5-FU and 84 in the placebo group.

238 number of medications was 0.65 drops in the 5-FU versus 0.93 drops in the placebo group (P = 0.06).

239 Mean IOP at 8 years was 13.7 mmHg in the 5-FU versus 14.4 mmHg in the placebo group (P = 0.24).

240 vy inflammatory infiltrates were seen in the 5-FU-challenged group, findings that were partially amel

241 re definitions of IOP >21 mmHg (11.6% of the 5-FU group vs. 16.7% of the placebo group; P = 1.00), IO

242 group; P = 1.00), IOP >17 mmHg (23.3% of the 5-FU group vs. 31% of the placebo group; P = 0.78), and

243 p; P = 0.78), and IOP >14 mmHg (46.5% of the 5-FU group vs. 58.3% of the placebo group; P = 0.37).

244 teins by small interfering RNA prevented the 5-FU-induced p53 activation and reversed the 5-FU-induce

245 5-FU-induced p53 activation and reversed the 5-FU-induced G1/S arrest.

246 -FU-tolerant subpopulations according to the 5-FU dose, and in gastric submucosal orthotopic xenograf

247 ab prolonged bleb survival compared with the 5-FU and control groups (16.0 +/- 1.3 days vs. 6.9 +/- 0

248 intraocular proliferation compared with the 5-FU in a parallel study (P = 0.014).

249 icity and efficacy of the cancer therapeutic 5-FU.

250 We examined these 5-FU-resistant MSCs (5-FU-MSCs) free from hematopoietic

251 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oli

252 sis that PT sensitizes colon cancer cells to 5-FU and we examine the underlying mechanism(s) by which

253 ly increased the sensitivity of HCC cells to 5-FU in vitro and a lentivirus delivering AEG-1 siRNA in

254 ed resistant colon cancer stem-like cells to 5-FU treatment.

255 ve sensitivity of colorectal cancer cells to 5-FU, using FISH with probes targeted to nascent mRNAs t

256 th and sensitized colorectal cancer cells to 5-FU-induced cell killing.

257 antagonists sensitized hypoxic CRC cells to 5-FU.

258 st that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K

259 This arrest is not due to 5-FU lesions blocking DNA polymerase delta but instead d

260 PD impairment leads to increased exposure to 5-FU and, in turn, increased anabolism of 5-FU to cytoto

261 S protein as a target, was hypersensitive to 5-FU.

262 posing the gastric cancer cell line MKN45 to 5-FU for >100 passages, we established a 5-fluorouracil

263 ined independently of acquired resistance to 5-FU in human colon cancer cells.

264 ate tumor growth but increases resistance to 5-FU treatment in vivo.

265 Resistance to 5-FU, and a decreased number of genomic mutations, was e

266 Despite the cross-resistance to 5-FU, more than 90% tumor reduction is achieved in vivo

267 The lack of understanding of resistance to 5-FU, therefore, remains a significant impediment in max

268 tment refractory and exhibited resistance to 5-FU-induced apoptosis in a colorectal cancer xenograft

269 , Dok1/Dok2 deficiency induces resistance to 5-FU-induced hematopoietic stem cell exhaustion.

270 ut toxicity and in the face of resistance to 5-FU.

271 results in the acquisition of resistance to 5-FU.

272 binding, leading to increased resistance to 5-FU.

273 on and may contribute to tumor resistance to 5-FU.

274 ells expressing S534N were more resistant to 5-FU-mediated toxicity compared with cells expressing WT

275 n may show enhanced apoptosis in response to 5-FU also in vivo.

276 ptional profile is predictive of response to 5-FU in a small number of patient colon tumor tissues.

277 ocs2(-/-) HSC gene expression in response to 5-FU revealed a significant overlap with the molecular p

278 s mutations promote apoptosis in response to 5-FU treatment and imply that tumors with Ras mutations

279 s phosphorylation on serine15 in response to 5-FU, a situation that favors apoptosis over growth arre

280 atively correlated with clinical response to 5-FU-therapy.

281 (ATP7B), can accurately predict response to 5-FU.

282 Relative sensitivity to 5-FU for cells expressing DPYD variations was also measu

283 53(-/-) cells increased their sensitivity to 5-FU treatment.

284 howed significantly increased sensitivity to 5-FU with G2/M arrest.

285 e that Ras mutations increase sensitivity to 5-FU-induced apoptosis at least in part through the nega

286 HCV-core or FL gene were more susceptible to 5-FU-induced growth inhibition than control cells, where

287 Topical 5-FU was used as primary therapy in 44 patients with OSS

288 requency of complete resolution with topical 5-FU treatment and the rate of OSSN recurrence.

289 unbound TS protein in many cancers and, upon 5-FU treatment of the colon cancer cell line, HCT116, ev

290 ells, accompanied by a reduction of in vitro 5-FU cytotoxicity in aggressive SW-620 cancer cells.

291 ubicin and did not affect normal HSCs, while 5-FU dramatically impaired their ability to engraft.

292 ploited as a therapeutic strategy along with 5-FU-based combinatorial chemotherapy for HCC, a highly

293 e been previously reported to associate with 5-FU toxicity in clinical association studies, which hav

294 atment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner,

295 A combination of siRNA-chk with 5-FU treatment resulted in a larger reduction of cell vi

296 s delivering AEG-1 siRNA in combination with 5-FU markedly inhibited growth of HCC cells xenotranspla

297 contrast, we showed that Ras interferes with 5-FU-induced expression of gelsolin, a protein with know

298 markedly synergized with FdUrd but not with 5-FU in ovarian cancer cell lines.

299 etuximab should be explored in patients with 5-FU-resistant colon cancer harboring wild-type KRAS.

300 ent strategies, especially for patients with 5-FU-resistant tumors expressing ER-beta protein.