ライフサイエンスコーパス: FU

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

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

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

4 5-FU treatment was toxic and did not improve survival.

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

6 5-FU-based combinatory chemotherapeutic regimens have been

7 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P)

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

9 05% calcipotriol ointment combined with 5% 5-FU cream were compared with Vaseline plus 5-FU for the f

10 45% (no-chemo), OS at 3 years: 58% vs 70% (5-FU) vs 84% (no-chemo)].

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

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

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

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

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

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

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

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

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

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

21 red to achieve a protective effect against 5-FU toxicity, but exogenous administration of Urd is not

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

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

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

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

26 levels and the accumulation of uracil and 5-FU in the genome, events that activate the ATR- and ATM-

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

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

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

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

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

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

33 howed enhanced efficacy with cisplatin and 5-FU.

34 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

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

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

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

38 ndings suggested that immunosuppression by 5-FU-MSC is mediated by a combination of elevated IL-1ra,

39 ctional role of ABCB5 in colorectal cancer 5-FU resistance.

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

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

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

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

44 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor

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

46 n with irinotecan, topotecan, doxorubicin, 5-FU, gemcitabine, docetaxel, oxaliplatin, cytoxan and cis

47 art, liver, and bone, compared with either 5-FU or cyclophosphamide.

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

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

50 5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, floxuridine) have a

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

52 5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyuridine (FdUrd, flox

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

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

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

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

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

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

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

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

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

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

63 latin (FOLFOX) compared to 5-fluorouracil (5-FU) or no chemotherapy for adjuvant treatment of colorec

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

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

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

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

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

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

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

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

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

73 se III Randomized Study of 5-Fluorouracil (5-FU), Mitomycin, and Radiotherapy Versus 5-Fluorouracil,

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

75 0g conferred resistance to 5-fluorouracil (5-FU)- or oxaliplatin-induced apoptosis in vitro and reduc

76 al cancer patients following fluorouracil (5-FU)-based chemoradiation therapy and provide evidence fo

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

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

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

83 tely 1000 times lower than 5-fluorouracil (5-FU).

84 y after myeloablation with 5-fluorouracil (5-FU).

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

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

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

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

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 nscripts, and reduction of IL-10 following 5-FU treatment, each of which were partially abrogated by

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

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

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

98 a population of potently immunosuppressive 5-FU-MSCs that have the potential to be exploited to remit

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

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

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

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

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

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

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

106 ge response and repair processes influence 5-FU and FdUrd toxicity in ovarian cancer cells.

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

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

109 terial infusion (HAI) and intravenous (IV) 5-FU compared with standard modern adjuvant IV chemotherap

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

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

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

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

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

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

116 differences in the cytotoxic mechanisms of 5-FU and FdUrd and suggest that combining FdUrd and PARP i

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

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

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

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

121 ncentrations ( approximately 25 microM) of 5-FU in both models, as a single agent, and induced surviv

122 odels, IEC-6 cells were exposed to 1 mM of 5-FU in glutamine free media with or without the ApoE pept

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

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

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

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

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

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

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

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

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

135 5-FU, and clearly reduced the toxicity of 5-FU.

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

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

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

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

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

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

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

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

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

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

146 preciable fraction of patients who receive 5-FU suffer severe adverse toxicities, which in extreme ca

147 Subsequently, patients received 5-FU based chemoradiation.

148 ave worse outcomes than those who received 5-FU or no chemotherapy.

149 el ApoE COG 133 mimetic peptide can reduce 5-FU-induced intestinal changes and potentially benefit mu

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

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

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

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

154 Subconjunctival 5-FU injection was performed postoperatively in 119 patien

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

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

157 FdUMP[10] was better tolerated than 5-FU or cytarabine plus doxorubicin and did not affect nor

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

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

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

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

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

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

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

165 Our findings suggested that 5-FU treatment identifies a population of potently immunos

166 r in the FOLFOX group (2.5 cm) than in the 5-FU (3.0 cm) or no-chemotherapy (3.5 cm) groups, (P = 0.0

167 was achieved in 48 subjects (55.8%) in the 5-FU and 33 subjects (39.3%) in the placebo group (P = 0.0

168 0%) completed 8 years follow-up, 86 in the 5-FU and 84 in the placebo group.

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

170 roliferation and migration, 24 h after the 5-FU challenge.

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

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

173 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

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

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

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 inflammatory infiltrates were seen in the 5-FU-challenged group, findings that were partially amelio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 ent refractory and exhibited resistance to 5-FU-induced apoptosis in a colorectal cancer xenograft mo

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

194 ls expressing S534N were more resistant to 5-FU-mediated toxicity compared with cells expressing WT D

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

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

197 ntagonists sensitized hypoxic CRC cells to 5-FU.

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

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

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

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

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

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

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

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

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

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

208 al mesorectal excision surgery, and adjuvant FU chemotherapy, or the same schedule of CRT used postop

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

210 (SPM5) was performed between patient BL- and FU-PET data as well as between patients and 15 PiB-negat

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

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

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

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

215 The 5-year OS for XELOX and FU/FA were 77.6% and 74.2%, respectively.

216 -5-yl)methane (TTM) cross-linking monomer at FU:Ade-BTM:TTM = 1:2:3 mol ratio.

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

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

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

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

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

222 when compared with induction plus concurrent FU plus cisplatin (CDDP), but did not significantly impa

223 DFS and OS versus induction plus concurrent FU/CDDP, and it has borderline significance for CFS, CF,

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

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

226 , and surgical downstaging compared with CVI FU.

227 re treated concurrently with 5-Fluorouracil (FU) and radiation for 5 to 6 weeks.

228 nthesized for recognition of 5-fluorouracil (FU), an antitumor chemotherapy agent, by RNA-type (nucle

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

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

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

232 % of patients with neoadjuvant fluorouracil (FU) -based chemoradiotherapy (CRT).

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

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

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

236 rent chemoradiation (CCR) with fluorouracil (FU) plus mitomycin (MMC) decreased colostomy failure (CF

237 igned to preoperative CRT with fluorouracil (FU), total mesorectal excision surgery, and adjuvant FU

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

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

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

241 ow-up were randomly assigned to either FULV (FU 500 mg/m(2) by intravenous [IV] bolus weekly for 6 we

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

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

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

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

246 s predict toxicity from bolus and infusional FU monotherapy.

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

248 standard chemoradiotherapy using infusional FU at 225 mg/m(2)/d.

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

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

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

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

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

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

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

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

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

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

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

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

261 GJ-398 significantly inhibited the growth of FU-DDLS-1 and LiSa-2 cells with a concomitant suppressio

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

263 Thus, increased similarity of FU hypometabolism with BL amyloid deposition was found (

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

265 erization complex stoichiometry involved one FU molecule and two molecules of the Ade-BTM functional

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

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

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

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

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

271 FS and OS were statistically better for RT + FU/MMC versus RT + FU/CDDP (5-year DFS, 67.8% v 57.8%; P

272 Therefore, RT + FU/MMC remains the preferred standard of care.

273 istically better for RT + FU/MMC versus RT + FU/CDDP (5-year DFS, 67.8% v 57.8%; P = .006; 5-year OS,

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

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

276 The FU, cisplatin, and IFN alpha-2b plus radiotherapy regime

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

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

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

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

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

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

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

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

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

286 s were randomly assigned to XELOX and 942 to FU/FA (Mayo Clinic, n = 664; Roswell Park, n = 278).

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

288 overall survival (OS) for XELOX compared to FU/FA was 0.87 (95% CI, 0.72 to 1.05; P = .1486).

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

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

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

292 ld AD underwent baseline (BL) and follow-up (FU) examination with [(18)F] FDG-PET and [(11)C] PiB-PET

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

294 CCR with FU/MMC has a statistically significant, clinically meani

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

296 n did not improve the survival compared with FU monotherapy.

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

298 *3/*3 or *3/*4 (poor risk) were treated with FU/RT plus weekly intravenous irinotecan at 50 mg/m(2).

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

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

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