ライフサイエンスコーパス: FU

1 FU has not been reported for lowland tropical rainforest

2 FU HVPG but not BL HVPG predicted hepatic decompensation

3 zed to receive either a single-dose of 2,000 FU NK (NSK-SD, Japan Bio Science Laboratory Co., Ltd) or

4 During 1y-FU in 1687 (45.9%) pts recurrence of AF occurred.

5 eoxy-2'-fluorouridine [(R)- or (S)-C5'-Me-2'-FU, respectively] revealed that the stereochemical orien

6 5-FU induced intestinal damage observed by shortened villi

7 5-FU is known to gradually lose its efficacy in treating c

8 5-FU was first entrapped in PLGA core by solvent evaporati

9 5-FU-based combinatory chemotherapeutic regimens have been

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

11 ipidomic analysis on 5-FU-resistant (DLD-1/5-FU) and -sensitive (DLD-1) colorectal cancer cells using

12 05% calcipotriol ointment combined with 5% 5-FU cream were compared with Vaseline plus 5-FU for the f

13 The nanobeacons comprise a 5-FU intercalated DNA hairpin, which is labeled with a nea

14 S 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 r

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

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

18 g with improved stress hematopoiesis after 5-FU treatment, and this results in HSC exhaustion over ti

19 DC-0941 may suppress disease relapse after 5-FU-based gastric cancer chemotherapy.

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

21 r inhibitory effect of combined CB-839 and 5-FU administration.

22 ms of action, doxorubicin, paclitaxel, and 5-FU all induce rapid and robust upregulation of atypical

23 ination of a neutralizing OPN antibody and 5-FU dramatically inhibited tumor growth.

24 vity to methylmethane sulfonate, H2O2, and 5-FU from DRC.

25 he synergistic effects of calcipotriol and 5-FU treatment in optimally activating a CD4+ T cell-media

26 abiliary local delivery of gemcitabine and 5-FU was performed by using a microporous balloon with (ei

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

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

29 M12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/Akt signal

30 ffect than free form of these proteins and 5-FU.

31 howed enhanced efficacy with cisplatin and 5-FU.

32 ssue +/- 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 < .05

33 dUTP is incorporated by DNA polymerases as 5-FU in the genome; however, it remains unclear how either

34 ion stress-inducing chemotherapies such as 5-FU.

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

36 into immunodeficient mice was inhibited by 5-FU.

37 MagMBs delivering the combined 5-FU/SDT treatment produced a reduction in cell viability

38 igning new combination regimens containing 5-FU or gemcitabine, we could identify more effective drug

39 m and measured their capacities to convert 5-FU to dihydro-fluorouracil, the product of DPD catabolis

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

41 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor

42 r sensitivity to the chemotherapeutic drug 5-FU.

43 ble nanogel entrapped with 5-fluororuacil (5-FU) coated with eucalyptus oil, topically applied onto t

44 mbination, indicating that 5-fluorouracil (5-FU) + irinotecan (IRI) + bevacizumab (BEV) and regorafen

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

46 ne and in combination with 5-fluorouracil (5-FU) and cisplatin.

47 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyuridine (FdUrd, flox

48 ing chemotherapies such as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivi

49 ted cytotoxicity of SN-38, 5-fluorouracil (5-FU) and mitoxantrone, but not that of gemcitabine, capec

50 alogues of cytotoxic drugs 5-fluorouracil (5-FU) and monomethyl auristatin E (MMAE) are partially act

51 ctal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combinati

52 d myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC fu

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

54 ncer chemotherapeutic drug 5-fluorouracil (5-FU) by prolonging S phase, generating DNA strand breaks,

55 ent, the pyrimidine analog 5-fluorouracil (5-FU) has become an integral component of many cancer trea

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

57 ults in chemoresistance to 5-fluorouracil (5-FU) in different cell lines and in mice.

58 combination of CB-839 and 5-fluorouracil (5-FU) induces PIK3CA-mutant tumor regression in xenograft

59 5-Fluorouracil (5-FU) is a chemotherapeutic drug widely used to treat colo

60 5-Fluorouracil (5-FU) is a standard treatment option for colorectal cancer

61 5-Fluorouracil (5-FU) is an anticancer agent whose main side effects inclu

62 tion of the cytotoxic drug 5-fluorouracil (5-FU) is generally considered to result from thymidylate s

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

64 ancer (CRC) treatment with 5-fluorouracil (5-FU) is the first line of therapy for this debilitating d

65 ffect of the anticancer drug fluorouracil (5-FU) on HCT116 cancer spheroids.

66 tment with the RNA mutagen 5-fluorouracil (5-FU) than wild-type (WT)-ExoN(+), suggestive of decreased

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

68 d cancer cells compared to 5-fluorouracil (5-FU) treated cells.

69 llular stress triggered by 5-fluorouracil (5-FU) treatment potentiates the effects of the loss of Dok

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

71 st for the highest DW (i.e., fluorouracil (5-FU)) and K(OW) (i.e., lovastatin (LOVS)) compounds, indi

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

73 apies such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamma-irradiation directly or indir

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

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

76 th Rose Bengal (RB) and/or 5-fluorouracil (5-FU), were assessed as a delivery vehicle for the targete

77 0g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduc

78 xia reduces sensitivity to 5-fluorouracil (5-FU)-chemotherapy for colorectal cancer (CRC).

79 anoparticles modified with 5-fluorouracil (5-FU)-intercalated nanobeacons that serve as an ON/OFF mol

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

81 inetics of and response to 5-fluorouracil (5-FU).

82 the chemotherapeutic agent 5-fluorouracil (5-FU).

83 rescribed anti-cancer drug 5-fluorouracil (5-FU).

84 ctor alpha (TNF-alpha) and 5-Fluorouracil (5-FU).

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

86 Initially, 5-Fluorouracil(5-FU)/Belotecan/Oxaliplatinum and Tegafur/Gimeracil (TS-1)

87 uridine is substituted by 5-fluorouridine (5-FU), reveals a covalent bond between the isomerized targ

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

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

90 ene with increased p53 occupancy following 5-FU treatment of cells.

91 pression of ADAM12-L in BC cells following 5-FU treatment results in the acquisition of resistance to

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

93 tions in developing BOK as a biomarker for 5-FU resistance and have the potential for the development

94 cally improve predictive genetic tests for 5-FU sensitivity, especially in individuals of non-Europea

95 c variations in DPYD increase the risk for 5-FU toxicity, however, there is not a clear consensus abo

96 Furthermore, 5-FU increased RAGE and NFkappaB NLS immunostaining in ent

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

98 5-FU resistant colon cancer cells (HCT116 5-FU Res).

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

100 ing a vasospastic role of 5-fluoruracil in 5-FU associated optic neuropathy.

101 strated that FOXM1 plays a pivotal role in 5-FU resistance at least partially through the regulation

102 udy reveals a significant role of FOXM1 in 5-FU resistance.

103 t miR-210, were significantly increased in 5-FU resistant CRCs.

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

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

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

107 eptors expression were markedly reduced in 5-FU-SLN(4) treated mice compared with 5FU and liver and k

108 nositide 3-kinase (PI3K) increased both in 5-FU-tolerant subpopulations according to the 5-FU dose, a

109 pression by Ezh2 predicts poor survival in 5-FU-treated cancers.

110 ance to chemotherapy regimens that include 5-FU.

111 s indicating that genomically incorporated 5-FU plays a major role in the antineoplastic effects of F

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

113 ovalent bond between enzyme and isomerized 5-FU we propose a Michael addition mechanism for pseudouri

114 The SLN-loaded 5-FU was developed by utilizing a Strategic and unique Met

115 raltitrexed), which induces uracil but not 5-FU accumulation, thus indicating that genomically incorp

116 equence, may decrease the effectiveness of 5-FU an antitumor drug in carriers.

117 Sequential administration of 5-FU and a PI3K inhibitor, GDC-0941, targeted the downstre

118 ally enhances the therapeutic potential of 5-FU and irinotecan to eradicate chemotherapy-resistant me

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

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

121 ese results suggest that administration of 5-FU followed by GDC-0941 may suppress disease relapse aft

122 splayed efficient and steady state flux of 5-FU from the biodegradable nanogles into the skin, while

123 in vitro and reduced the effectiveness of 5-FU in the inhibition of tumor growth in a mouse xenograf

124 mor growth and limits the effectiveness of 5-FU in vivo.

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

126 ydrogenase (DPD) is a major determinant of 5-FU response and toxicity.

127 ific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU the

128 5-FU and, in turn, increased anabolism of 5-FU to cytotoxic nucleotides, resulting in more severe cl

129 UPP1 facilitated the conversion of 5-FU to its active compound, thereby enhancing the inhibit

130 LN), capable of delivering high payload of 5-FU to treat CRC.

131 stent with clinical association studies of 5-FU toxicity, the D949V substitution reduced enzyme activ

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

133 ug activation of a propargyl derivative of 5-FU was shown in a colorectal zebrafish xenograft model t

134 tecting strategy by the adjunct therapy of 5-FU with Resveratrol.

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

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

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

138 oing standard CRT (50.4 Gy and 2 cycles of 5-FU-based chemotherapy) were compared with those undergoi

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

140 5-FU, and clearly reduced the toxicity of 5-FU.

141 ion and slightly increases the toxicity of 5-FU.

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

143 pecific ADAM12-L inhibition could optimize 5-FU-based chemotherapy of BC, thereby preventing BC recur

144 r how either genomically incorporated U or 5-FU contributes to killing.

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

146 les for therapeutic strategies to overcome 5-FU resistance.

147 nanogel conjugates with the phosphorylated 5-FU nucleoside Floxuridine and demonstrated their enhance

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

149 alcipotriol plus 5-FU versus Vaseline plus 5-FU led to an 87.8% versus 26.3% mean reduction in the nu

150 Importantly, calcipotriol plus 5-FU treatment induced TSLP, HLA class II, and natural kil

151 Four-day application of calcipotriol plus 5-FU versus Vaseline plus 5-FU led to an 87.8% versus 26.3

152 pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, enteric glia activation, intes

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

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

155 evelopment of BOK-mimetics for sensitizing 5-FU-resistant cancers.

156 ing them from the lethal effects of serial 5-FU treatment.

157 eficient mice are more resistant to serial 5-FU treatments.

158 DPYD alleles are protective against severe 5-FU toxicity, and, as a consequence, may decrease the eff

159 phosphorylation to significantly suppress 5-FU-tolerant subpopulations and tumor propagation of orth

160 d postoperative HAI combined with systemic 5-FU (HAI group) and 54 (55%) had received "modern" system

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

162 Surprisingly, we find that 5-FU and FUDR act through bacterial ribonucleotide metabol

163 We found that 5-FU does not induce apoptosis rather vascular hyperpermea

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

165 We provide evidence that 5-FU induces reactive gliosis and reduction of enteric neu

166 These results show that 5-FU lesions that escape UNG repair activate HR, which pro

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

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

169 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells was

170 Here, we demonstrate that 5-FU-generated colon carcinoma debris stimulates the growt

171 significant difference in IOP between the 5-FU and the placebo group at 8 years.

172 U-tolerant subpopulations according to the 5-FU dose, and in gastric submucosal orthotopic xenografts

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

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

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

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

177 ity and efficacy of the cancer therapeutic 5-FU.

178 that ADAM12-L mediates chemoresistance to 5-FU and 5-FU-induced recurrence of BC by enhancing PI3K/A

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

180 impairment leads to increased exposure to 5-FU and, in turn, increased anabolism of 5-FU to cytotoxi

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

182 sing the gastric cancer cell line MKN45 to 5-FU for >100 passages, we established a 5-fluorouracil (5

183 Relative sensitivity to 5-FU for cells expressing DPYD variations was also measure

184 ed independently of acquired resistance to 5-FU in human colon cancer cells.

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

186 s2(-/-) HSC gene expression in response to 5-FU revealed a significant overlap with the molecular pro

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

188 ly inhibited tumor growth in comparison to 5-FU while area-under plasma concentration-time curve (AUC

189 Resistance to 5-FU, and a decreased number of genomic mutations, was eff

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

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

192 esults in the acquisition of resistance to 5-FU.

193 ntagonists sensitized hypoxic CRC cells to 5-FU.

194 inding, leading to increased resistance to 5-FU.

195 and may contribute to tumor resistance to 5-FU.

196 quency of complete resolution with topical 5-FU treatment and the rate of OSSN recurrence.

197 Topical 5-FU was used as primary therapy in 44 patients with OSSN.

198 /- 0.02 uM) was 2.3 fold low compared with 5-FU (17.7 +/- 0.03 uM).

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

200 e (U5MT), TRMT2A, and its interaction with 5-FU metabolites incorporated within tRNAs, lead to an add

201 been previously reported to associate with 5-FU toxicity in clinical association studies, which have

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

203 taneous tumor growth in mice compared with 5-FU.

204 5FU-SLN(4) was 3.6 fold high compared with 5-FU.

205 f FOXM1, thiostrepton, in combination with 5-FU.

206 on comprised 1,886 patients (XELOX, n = 944; FU/FA, n = 942).

207 tin using the oxaliplatin, folinic acid, and FU (OFF) regimen.

208 onstant of the complex of the MIP cavity and FU, piezoelectric microgravimetry (PM) under both batch-

209 DFS rates were 63% and 56% in the XELOX and FU/FA groups, respectively (hazard ratio [HR], 0.80; 95%

210 r OS rates were 73% and 67% in the XELOX and FU/FA groups, respectively (HR, 0.83; 95% CI, 0.70 to 0.

211 or a new colorectal cancer in the XELOX and FU/FA groups, respectively, received drug treatment for

212 -5-yl)methane (TTM) cross-linking monomer at FU:Ade-BTM:TTM = 1:2:3 mol ratio.

213 RSA, at 98.1% versus 98.0%, respectively, at FU.

214 Investigator-assessed success was similar at FU (84.7% versus 84.1%) and LFU (82.0% versus 81.7%).

215 aily on days 1 to 14 every 3 weeks, or bolus FU/FA, as the Mayo Clinic or Roswell Park regimens, for

216 XELOX improved OS compared with bolus FU/FA in patients with resected stage III colon cancer a

217 (fu) ), we estimate that the contribution by FU to annual transpiration at this site has a median val

218 its use in bolus, infusional, or combination FU.

219 nfusional FU (ECF) before and after combined FU and radiotherapy (ECF arm).

220 erative FU plus LV before and after combined FU and radiotherapy (FU plus LV arm) or postoperative ep

221 ous intravenous infusional fluorouracil (CVI FU; 225 mg/m(2), 5 days per week), with or without intra

222 downstaging were identified between the CVI FU and capecitabine regimens or between the two regimens

223 , and surgical downstaging compared with CVI FU.

224 hy (PET) agent [(18)F]5-fluorouracil ([(18)F]FU).

225 mor recurrence, outcomes after fluorouracil (FU) -based treatment are expected to have improved over

226 e chemoradiotherapy with bolus fluorouracil (FU) and leucovorin (LV) compared with surgery alone.

227 vival benefit with second-line fluorouracil (FU) and oxaliplatin using the oxaliplatin, folinic acid,

228 Combination regimens and oral fluorouracil (FU) therapy are now standard.

229 e randomly assigned to receive fluorouracil (FU) -based chemotherapy either alone or in combination w

230 on cancer randomly assigned to fluorouracil (FU) or FU plus oxaliplatin in National Surgical Adjuvant

231 igher sensitivity to FOLFIRI [5-fluorouracil(FU)+irinotecan+folinic acid] than to FOLFOX (5-FU+oxalip

232 Fluourouracil (FU) is a mainstay of chemotherapy, although toxicities a

233 indicating suitability of the former two for FU determination in blood plasma or serum (~500 nM).

234 these sites is induced by the kinase Fused (FU), a known downstream effector of SMO.

235 Attenuation of FRS2 protein in FU-DDLS-1 and LiSa-2 cell lines decreased the phosphoryl

236 In turn, activation of SMO induces FU to act on its downstream targets.

237 rative epirubicin, cisplatin, and infusional FU (ECF) before and after combined FU and radiotherapy (

238 s predict toxicity from bolus and infusional FU monotherapy.

239 d to receive biweekly mFOLFOX6 or infusional FU/LV until progression.

240 ucovorin, and oxaliplatin) versus infusional FU/leucovorin (LV) in this setting.

241 administered as mFOLFOX6, versus infusional FU/LV in patients with advanced pancreatic cancer previo

242 aring oxaliplatin-based chemotherapy with IV FU, statistically significant interactions were not obse

243 al fluoropyrimidine therapy compared with IV FU; noninferiority was supported in both age populations

244 Fluorouracil plus leucovorin (FU + LV) adjuvant chemotherapy reduced the risk of recur

245 in three high-grade liposarcoma cell lines: FU-DDLS-1, LiSa-2, and SW872.

246 templated molecularly imprinted polymer (MIP-FU) films were deposited on indium-tin oxide (ITO) or Au

247 confirm the FU template presence in the MIP-FU film and its subsequent release by extraction with me

248 ransform infrared (FT-IR) spectra of the MIP-FU films were recorded to confirm the FU template presen

249 y (CI), and PM] were integrated with the MIP-FU recognition unit.

250 multicenter trial to evaluate the benefit of FU and oxaliplatin administered as modified FOLFOX6 (mFO

251 The PFS benefit of FU plus LV added to panitumumab maintenance, reported in

252 on historical data related to the benefit of FU-based adjuvant therapy in such patients.

253 emains a need to identify further markers of FU toxicity for all regimens.

254 namic electropolymerization from solution of FU, Ade-BTM, and tris([2,2'-bithiophen]-5-yl)methane (TT

255 er randomly assigned to fluorouracil (FU) or FU plus oxaliplatin in National Surgical Adjuvant Breast

256 r, TE/VITRO were able to rule in or rule out FU CSPH (AUROC, 0.86-0.92) in most patients, especially

257 ntravenous cisplatin 60 mg/m(2) (day 1) plus FU 1,000 mg/m(2) (days 1-4) every 21 days or carboplatin

258 survival was 12.3 months for cisplatin plus FU (95% CI, 9.2 to 17.7 months) compared with 20 months

259 were randomly assigned: 46 to cisplatin plus FU and 45 to carboplatin plus paclitaxel.

260 erse events were noted in the cisplatin plus FU arm (62%) compared with the carboplatin plus paclitax

261 5% CI, 3.3 to 9.0 months) for cisplatin plus FU compared with 8.1 months (95% CI, 6.6 to 8.8 months)

262 (95% CI, 39.4% to 73.7%) for cisplatin plus FU versus 59% (95% CI, 42.1% to 74.4%) for carboplatin p

263 mly assigned to receive either postoperative FU plus LV before and after combined FU and radiotherapy

264 fore and after combined FU and radiotherapy (FU plus LV arm) or postoperative epirubicin, cisplatin,

265 eived mFOLFOX6 and 11% of those who received FU/LV.

266 tive chemoradiotherapy regimen that replaced FU plus LV with a potentially more active systemic thera

267 Overall, our data provide evidence for a SMO/FU positive regulatory loop nested within a multikinase

268 not improve survival compared with standard FU and LV before and after radiotherapy.

269 We demonstrate that FU occurs in all six genera and that dew-derived water m

270 Our results indicate that FU is likely to be a common strategy and may have signif

271 '-bithienyl)methane moiety of Ade-BTM by the FU titrant, in benzonitrile, at 352 nm excitation.

272 he MIP-FU films were recorded to confirm the FU template presence in the MIP-FU film and its subseque

273 quency and severity of SHb and Vb during the FU were assessed every two weeks by the MOAS.

274 FU, (c) predictors of SHb and Vb during the FU.

275 disease-free survival rates were 39% in the FU plus LV arm and 37% in the ECF arm ( Plogrank = .94;

276 -year overall survival rates were 44% in the FU plus LV arm and 44% in the ECF arm ( Plogrank = .69;

277 In the FU/FA group, no statistically significant associations w

278 lysis: 242 in the XELOX group and 256 in the FU/FA group.

279 from study due to adverse events than in the FU/LV arm (20% v 2%), whereas the use of postprogression

280 sion therapy was significantly higher in the FU/LV arm (25% v 7%; P = .015).

281 The stability constant of the FU-Ade-BTM complex of 1:2 stoichiometry was K = 2.17(+/-

282 The impact of oxaliplatin added to FU + LV on the time course of recurrence and survival re

283 lly derived estimates of leaf conductance to FU (k(fu) ), we estimate that the contribution by FU to

284 ents and patients concurrently randomized to FU + LV with or without oxaliplatin; the latter analyses

285 D), and overall survival (OS) with regard to FU-based adjuvant regimens.

286 hemosensor was appreciably more sensitive to FU than to their common interferences.

287 After adjusting for time to FU, increasing N1 and P1 IT were both associated with de

288 intensifier gate delay; focused ultrasound (FU) power; and imaging depth) and the image qualities (i

289 lude and underwent 2 standardized follow-up (FU) visits within 5 years following a baseline examinati

290 848 and 99(12%) were deceased at follow-up (FU).

291 solution of signs and symptoms at follow-up (FU; Day 14 +/- 1) and late follow-up (LFU; Day 21- 28),

292 before (baseline [BL]) and after (follow-up [FU]) IFN-free therapy.

293 tion facilitated by gravity), foliar uptake (FU) may be a significant process in determining how fore

294 nts) to examine the polymorphisms in various FU monotherapy and combination therapy regimens.

295 owland tropical rainforests; we test whether FU occurs in six common Amazonian tree genera in lowland

296 y postpone recurrence or death compared with FU + LV alone).

297 .98; 95% CI, 0.78 to 1.24 comparing ECF with FU plus LV).

298 also predictors of AF recurrence during 1-y-FU.

299 dent predictors for AF recurrence during 1-y-FU.

300 th complete follow-up one year after CA (1-y-FU; n = 3679).

301 stics, (b) violent behaviour during a 1-year FU, (c) predictors of SHb and Vb during the FU.