ライフサイエンスコーパス: 5-FU

1 5-FU induced intestinal damage observed by shortened vil

2 5-FU is known to gradually lose its efficacy in treating

3 5-FU treatment was toxic and did not improve survival.

4 5-FU was first entrapped in PLGA core by solvent evapora

5 5-FU-based combinatory chemotherapeutic regimens have be

6 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P

7 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells was mainly associated with

8 lipidomic analysis on 5-FU-resistant (DLD-1/5-FU) and -sensitive (DLD-1) colorectal cancer cells usi

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

10 .005% calcipotriol ointment combined with 5% 5-FU cream were compared with Vaseline plus 5-FU for the

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

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

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

14 YMS expression was also observed in acquired 5-FU resistant colon cancer cells (HCT116 5-FU Res).

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

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

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

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

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

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

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

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

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

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

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

26 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 < .

27 mor inhibitory effect of combined CB-839 and 5-FU administration.

28 mbination of a neutralizing OPN antibody and 5-FU dramatically inhibited tumor growth.

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

30 showed enhanced efficacy with cisplatin and 5-FU.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 ucositis and enteric neurotoxicity caused by 5-FU (450 mg/kg, IP, single dose).

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

48 d into immunodeficient mice was inhibited by 5-FU.

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

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

51 esigning new combination regimens containing 5-FU or gemcitabine, we could identify more effective dr

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

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

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

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

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

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

58 eir sensitivity to the chemotherapeutic drug 5-FU.

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

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

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

62 combination, indicating that 5-fluorouracil (5-FU) + irinotecan (IRI) + bevacizumab (BEV) and regoraf

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

64 5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, floxuridine) have

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

66 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyuridine (FdUrd, fl

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

68 iated cytotoxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of gemcitabine, cap

69 analogues of cytotoxic drugs 5-fluorouracil (5-FU) and monomethyl auristatin E (MMAE) are partially a

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

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

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

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

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

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

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

77 esults in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mice.

78 he combination of CB-839 and 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regression in xenograf

79 5-Fluorouracil (5-FU) is a chemotherapeutic drug widely used to treat co

80 5-Fluorouracil (5-FU) is a standard treatment option for colorectal canc

81 5-Fluorouracil (5-FU) is an anticancer agent whose main side effects inc

82 action of the cytotoxic drug 5-fluorouracil (5-FU) is generally considered to result from thymidylate

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

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

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

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

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

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

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

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

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

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

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

94 erapies such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamma-irradiation directly or ind

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

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

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

98 rence after therapy, such as 5-fluorouracil (5-FU), remains a challenge in the clinical setting.

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

100 520g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and red

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

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

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

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

105 0 passages, we established a 5-fluorouracil (5-FU)-tolerant line, MKN45/5FU.

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

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

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

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

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

111 factor alpha (TNF-alpha) and 5-Fluorouracil (5-FU).

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

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

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

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

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

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

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

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

120 Initially, 5-Fluorouracil(5-FU)/Belotecan/Oxaliplatinum and Tegafur/Gimeracil (TS-

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

122 Resistance to 5-Fluoruracil (5-FU) has been linked to elevated expression of the main

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

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

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

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

127 cations in developing BOK as a biomarker for 5-FU resistance and have the potential for the developme

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

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

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

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

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

133 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in e

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

135 ed 5-FU resistant colon cancer cells (HCT116 5-FU Res).

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

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

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

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

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

141 study reveals a significant role of FOXM1 in 5-FU resistance.

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

143 eceptors expression were markedly reduced in 5-FU-SLN(4) treated mice compared with 5FU and liver and

144 ) species were significantly up-regulated in 5-FU-resistant cells in MALDI-TOF analysis.

145 onstrated that FOXM1 plays a pivotal role in 5-FU resistance at least partially through the regulatio

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

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

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

149 stance to chemotherapy regimens that include 5-FU.

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

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

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

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

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

155 The SLN-loaded 5-FU was developed by utilizing a Strategic and unique M

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

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

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

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

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

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

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

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

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

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

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

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

168 UPP1 facilitated the conversion of 5-FU to its active compound, thereby enhancing the inhib

169 rgoing standard CRT (50.4 Gy and 2 cycles of 5-FU-based chemotherapy) were compared with those underg

170 dergoing extended CRT (54 Gy and 6 cycles of 5-FU-based chemotherapy).

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

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

173 drug activation of a propargyl derivative of 5-FU was shown in a colorectal zebrafish xenograft model

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

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

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

177 tumor growth and limits the effectiveness of 5-FU in vivo.

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

179 atically reduces the therapeutic efficacy of 5-FU.

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

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

182 47; p < 0.01 respectively), independently of 5-FU treatment.

183 We investigated the mechanism of 5-FU resistance using comprehensive lipidomic approaches

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

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

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

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

188 (SLN), capable of delivering high payload of 5-FU to treat CRC.

189 ically enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant

190 ion of CB-839 and capecitabine, a prodrug of 5-FU, was well tolerated at biologically-active doses.

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

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

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

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

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

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

197 We performed lipidomic analysis on 5-FU-resistant (DLD-1/5-FU) and -sensitive (DLD-1) color

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

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

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

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

202 at FOXM1 can also potentially regulate other 5-FU targets, such as TYMS, thymidine kinase 1 (TK-1) an

203 cules for therapeutic strategies to overcome 5-FU resistance.

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

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

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

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

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

209 5-FU cream were compared with Vaseline plus 5-FU for the field treatment of actinic keratosis in a r

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

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

212 ce pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, int

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

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

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

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

217 Subsequently, patients received 5-FU based chemoradiation.

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

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

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

221 development of BOK-mimetics for sensitizing 5-FU-resistant cancers.

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

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

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

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

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

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

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

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

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

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

232 Here, we demonstrate that 5-FU-generated colon carcinoma debris stimulates the gro

233 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric n

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

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

236 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells wa

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

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

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

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

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

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

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

244 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

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

246 0.0%) completed 8 years follow-up, 86 in the 5-FU and 84 in the placebo group.

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

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

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

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

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

252 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).

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

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

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

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

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

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

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

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

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

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

263 antagonists sensitized hypoxic CRC cells to 5-FU.

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

265 ntly inhibited tumor growth in comparison to 5-FU while area-under plasma concentration-time curve (A

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

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

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

269 d primary tissues that acquire resistance to 5-FU down-regulate BOK expression.

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

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

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

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

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

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

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

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

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

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

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

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

282 53(-/-) cells increased their sensitivity to 5-FU treatment.

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

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

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

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

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

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

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

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

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

292 of FOXM1, thiostrepton, in combination with 5-FU.

293 +/- 0.02 uM) was 2.3 fold low compared with 5-FU (17.7 +/- 0.03 uM).

294 cutaneous tumor growth in mice compared with 5-FU.

295 f 5FU-SLN(4) was 3.6 fold high compared with 5-FU.

296 ase (U5MT), TRMT2A, and its interaction with 5-FU metabolites incorporated within tRNAs, lead to an a

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

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

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

300 ection of debris and systemic treatment with 5-FU increased plasma OPN levels in tumor-bearing mice.