ライフサイエンスコーパス: gemcitabine

1 from 14 to 18 months by adding erlotinib to gemcitabine.

2 l under nutrient withdrawal, with or without gemcitabine.

3 infused with an admixture of paclitaxel and gemcitabine.

4 temness and showed synergistic activity with gemcitabine.

5 pharmacokinetic interaction between IVC and gemcitabine.

6 ion may be the mechanism of sensitization to gemcitabine.

7 ckade of IGF sensitized pancreatic tumors to gemcitabine.

8 further upregulated by the chemotherapy drug gemcitabine.

9 tumor effects of DNA damaging agents such as gemcitabine.

10 or stroma and tumor growth and resistance to gemcitabine.

11 ic cancer previously treated with first-line gemcitabine.

12 ifene treatment alone or in combination with gemcitabine.

13 -inferior to and superior to paclitaxel plus gemcitabine.

14 d tumor growth as compared with BEZ, DOX, or gemcitabine.

15 oresistance to the current standard therapy, gemcitabine.

16 c NU7441 release and pH-dependent release of gemcitabine.

17 ity sensitizes inherently resistant cells to gemcitabine.

18 ing pathway showed heightened sensitivity to gemcitabine.

19 s for sensitizing pancreatic cancer cells to gemcitabine.

20 ped by introducing a linker between HNPs and gemcitabine.

21 was combined with the chemotherapeutic drug gemcitabine.

22 randomly assigned to one of two study arms: gemcitabine 1,000 mg/m(2) days 1, 8, 15, every 4 weeks p

23 mmended phase II dose is MK-8776 200 mg plus gemcitabine 1,000 mg/m(2) on days 1 and 8 of a 21-day cy

24 Neoadjuvant gemcitabine (1,000 mg/m(2) intravenously [IV] on days 1

25 All patients received gemcitabine 1000 mg/m(2) as a 30-min intravenous infusio

26 4, 75 mg/m(2) docetaxel) or with addition of gemcitabine (1000 mg/m(2) days 1 and 8 intravenously, 75

27 s 1 and 8), docetaxel (75 mg/m(2) on day 1), gemcitabine (1200 mg/m(2) on days 1 and 8), or pemetrexe

28 itabine (paclitaxel 175 mg/m(2) on day 1 and gemcitabine 1250 mg/m(2) on days 1 and 8) given intraven

29 mcitabine (cisplatin 75 mg/m(2) on day 1 and gemcitabine 1250 mg/m(2) on days 1 and 8) or paclitaxel

30 (18.9%) and a decline in paclitaxel (38.7%), gemcitabine (17.0%), and vinorelbine (5.7%; all P < .05)

31 ted for immobilization of an anticancer drug gemcitabine (2',2'-difluoro-2'-deoxycytidine, GEM) which

32 ria can metabolize the chemotherapeutic drug gemcitabine (2',2'-difluorodeoxycytidine) into its inact

33 Gemcitabine, 5-fluorouracil, hydroxyurea, doxorubicin an

34 f 24.2 months-longer than that reported with gemcitabine (6-13 months).

35 /m(2) on day 1 every 3 weeks, or intravenous gemcitabine 675 mg/m(2) on days 1 and 8 and intravenous

36 een on days 2, 3, and 5 after treatment with gemcitabine, a chemotherapeutic agent that is powerfully

37 uction as a possible resistance mechanism to gemcitabine, adding to complexity and multiple paths to

38 Gemcitabine administration after resection of pancreatic

39 y as compared to the current first line drug gemcitabine after heat mediated controlled release.

40 stant tumors, but adjuvant administration of gemcitabine after tumor resection prolonged survival.

41 clitaxel/gemcitabine (PAG) or nab-paclitaxel/gemcitabine (AG).

42 5.5 months (95% CI, 22.7 to 27.9 months) for gemcitabine alone (hazard ratio, 0.82; 95% CI, 0.68 to 0

43 to receive six cycles of either 1000 mg/m(2) gemcitabine alone administered once a week for three of

44 , 223 patients received 1000 mg/m2 weekly of gemcitabine alone and 219 patients received 1000 mg/m2 o

45 ine-erlotinib and erlotinib maintenance with gemcitabine alone at the second randomization, and toxic

46 with gemcitabine and capecitabine than with gemcitabine alone in advanced or metastatic pancreatic c

47 Gemcitabine alone is recommended for patients with ECOG

48 Therapy with a Trk inhibitor together with gemcitabine also increased survival of KPC mice.

49 unds, NU7441 - a potent radiosensitizer, and gemcitabine - an FDA approved chemotherapeutic drug for

50 these, 366 were randomly assigned to receive gemcitabine and 364 to gemcitabine plus capecitabine.

51 Mice given a combination of gemcitabine and a JAK2 inhibitor formed smaller tumors a

52 Mice with pancreatic tumors were given gemcitabine and a Janus kinase 2 (JAK2) inhibitor; tumor

53 imed to determine the efficacy and safety of gemcitabine and capecitabine compared with gemcitabine m

54 The doublet regimen of gemcitabine and capecitabine is preferred in the absence

55 INTERPRETATION: The adjuvant combination of gemcitabine and capecitabine should be the new standard

56 own better survival and tumour response with gemcitabine and capecitabine than with gemcitabine alone

57 f adjuvant combination chemotherapy compared gemcitabine and capecitabine with gemcitabine monotherap

58 He was briefly treated with gemcitabine and carboplatin, but this was discontinued a

59 ly assigned them to receive necitumumab plus gemcitabine and cisplatin (n=545) or gemcitabine and cis

60 ab plus gemcitabine and cisplatin (n=545) or gemcitabine and cisplatin (n=548).

61 gemcitabine and cisplatin group than in the gemcitabine and cisplatin alone group (median 11.5 month

62 ngs show that the addition of necitumumab to gemcitabine and cisplatin chemotherapy improves overall

63 12%) of 538 patients in the necitumumab plus gemcitabine and cisplatin group and 57 (11%) of 541 pati

64 More patients in the necitumumab plus gemcitabine and cisplatin group had grade 3-4 hypomagnes

65 significantly longer in the necitumumab plus gemcitabine and cisplatin group than in the gemcitabine

66 [9%] of 538 patients in the necitumumab plus gemcitabine and cisplatin group vs six [1%] of 541 in th

67 nd cisplatin group vs six [1%] of 541 in the gemcitabine and cisplatin group) and grade 3 rash (20 [4

68 in group and 57 (11%) of 541 patients in the gemcitabine and cisplatin group; these were deemed to be

69 ceived doxorubicin versus those who received gemcitabine and docetaxel (46.3% [95% CI 37.5-54.6] vs 4

70 doxorubicin group and 80 (63%) of 128 in the gemcitabine and docetaxel group.

71 This study compared gemcitabine and docetaxel versus doxorubicin as first-li

72 in and 25 [20%] of 126 patients who received gemcitabine and docetaxel), febrile neutropenia (26 [20%

73 atment groups (129 to doxorubicin and 128 to gemcitabine and docetaxel).

74 ious adverse events in patients who received gemcitabine and docetaxel, fever (18 [12%] and 19 [15%])

75 ST6Gal-I also promoted resistance to gemcitabine and enabled the formation of stably resistan

76 xic effects of the chemotherapeutical agents gemcitabine and etoposide distinctively.

77 dem mass spectrometry (LC-MS/MS) analysis of gemcitabine and its metabolites extracted from tumor tis

78 l was associated with undergoing combination gemcitabine and nab-paclitaxel [time ratio (TR) = 1.26,

79 Moreover, treatment with gemcitabine and nab-paclitaxel significantly reduces the

80 wed trends in PFS favoring pertuzumab in the gemcitabine and paclitaxel cohorts, meriting further exp

81 voring pertuzumab was more pronounced in the gemcitabine and paclitaxel cohorts.

82 P1 upregulation as a resistance mechanism to gemcitabine and provide a rationale for combining chemo/

83 ) compared with 46% (150/322 patients) after gemcitabine and radiation, and 52% (66/128 patients) aft

84 hile TIMP1 inhibition resensitized tumors to gemcitabine and radiotherapy.

85 control the intracellular concentrations of gemcitabine and several other US Food and Drug Administr

86 Combination of gemcitabine and the FASN inhibitor orlistat significantl

87 was 16.0 months (Folfirinox) vs 16.5 months (gemcitabine) and 14.5 months (others) with 3-year surviv

88 (23%) received docetaxel, 283 (19%) received gemcitabine, and 497 (33%) received pemetrexed.

89 Tumors were resected and mice were given gemcitabine, and tumor recurrence patterns and survival

90 y evaluated the combination of bendamustine, gemcitabine, and vinorelbine (BeGEV) as induction therap

91 g age, low baseline cancer antigen 19-9, and gemcitabine as a radiosensitizer were associated with a

92 r antigen 19-9 level less than 200 U/mL, and gemcitabine as a radiosensitizer were associated with a

93 Simulations identified daily 0.5-1 mg/kg gemcitabine as an optimal protocol to maximize antitumor

94 n-inferior to or superior to paclitaxel plus gemcitabine as first-line therapy for patients with meta

95 Gemcitabine, as a single agent or in combination therapy

96 etastatic pancreatic adenocarcinoma for whom gemcitabine-based chemotherapy had failed were randomize

97 etastatic pancreatic adenocarcinoma for whom gemcitabine-based chemotherapy had failed.

98 c adenocarcinoma is moderately responsive to gemcitabine-based chemotherapy, the most widely used sin

99 The gemcitabine-based combinations and treatments recommende

100 uctal adenocarcinoma previously treated with gemcitabine-based therapies.

101 s with metastatic pancreatic cancer for whom gemcitabine-based therapy had failed.

102 tients with advanced pancreatic cancer after gemcitabine-based therapy is not clearly defined.

103 uctal adenocarcinoma previously treated with gemcitabine-based therapy were randomly assigned (1:1) u

104 uctal adenocarcinoma who previously received gemcitabine-based therapy.

105 months (IQR 30-46) in the patients receiving gemcitabine, busulfan, and melphalan and 34 months (25-5

106 ect to the secondary survival endpoints, the gemcitabine, busulfan, and melphalan cohort had signific

107 ed in a 1-2:1 ratio with the patients in the gemcitabine, busulfan, and melphalan group by sex, age,

108 65 patients (24.6%, 95% CI 14.2-35.0) in the gemcitabine, busulfan, and melphalan group had stringent

109 INTERPRETATION: Gemcitabine, busulfan, and melphalan is a comparatively

110 c 11, 2013, we enrolled 74 patients into the gemcitabine, busulfan, and melphalan trial.

111 ts with measurable disease at ASCT receiving gemcitabine, busulfan, and melphalan who achieved string

112 For only the patients treated with gemcitabine, busulfan, and melphalan, grade 3 or worse a

113 study a new high-dose combination of infused gemcitabine, busulfan, and melphalan.

114 The patient received adjuvant chemotherapy (Gemcitabine) but expired 10 months after surgery.

115 he prodrug was 4.3 times less cytotoxic than gemcitabine, but exhibited 11-fold improvement in cellul

116 ise in cytotoxicity causing it to outperform gemcitabine by 26%.

117 of replication stress, through aphidicolin, gemcitabine, camptothecin or hydroxyurea exposure, activ

118 Moreover, gemcitabine can promote the stemness of pancreatic cance

119 nd natural killier (NK) cells in addition to gemcitabine chemotherapy to prevent tumor recurrence.

120 nded further when combined with warfarin and gemcitabine chemotherapy.

121 igned (1:1) to receive either cisplatin plus gemcitabine (cisplatin 75 mg/m(2) on day 1 and gemcitabi

122 Regimens were nivolumab 10 mg/kg plus gemcitabine-cisplatin (squamous) or pemetrexed-cisplatin

123 herapy (pemetrexed-cisplatin [LUX-Lung 3] or gemcitabine-cisplatin [LUX-Lung 6]), stratified by EGFR

124 e response rates for nivolumab 10 mg/kg plus gemcitabine-cisplatin, nivolumab 10 mg/kg plus pemetrexe

125 nificant difference in overall survival with gemcitabine compared with gemcitabine plus erlotinib use

126 If non-inferiority of cisplatin plus gemcitabine compared with paclitaxel plus gemcitabine wa

127 On the basis of the gemcitabine concentration and [(18)F]FLT excretion measu

128 Gemcitabine constitutes one of the backbones for chemoth

129 to induce HAC loss revealed that paclitaxel, gemcitabine, dactylolide, LMP400, talazoparib, olaparib,

130 mor angiogenesis, leakiness, blood flow, and Gemcitabine delivery.

131 ADCmean in A549 xenografts 1 or 2 days after gemcitabine did not seem to be of therapy-related biolog

132 ion and inflammation in vivo, while standard gemcitabine did not.

133 Nucleoside analogs such as gemcitabine diphosphate and clofarabine nucleotides targ

134 The addition of bevacizumab to gemcitabine-docetaxel for first-line treatment of metast

135 citabine-docetaxel plus placebo (n = 54) and gemcitabine-docetaxel plus bevacizumab (n = 53).

136 abine-docetaxel plus placebo) to 6.7 months (gemcitabine-docetaxel plus bevacizumab).

137 In all, 107 patients were accrued: gemcitabine-docetaxel plus placebo (n = 54) and gemcitab

138 ect an increase in median PFS from 4 months (gemcitabine-docetaxel plus placebo) to 6.7 months (gemci

139 Gemcitabine-docetaxel remains a standard first-line trea

140 Nuclear YAP enhances gemcitabine effectiveness by down-regulating multidrug t

141 Targeted inhibition of STAT3 combined with gemcitabine enhances in vivo drug delivery and therapeut

142 erall survival, progression-free survival of gemcitabine-erlotinib and erlotinib maintenance with gem

143 Finally, treatment of gemcitabine-exposed CAFs with an inhibitor of exosome re

144 ins in modulating cancer stemness induced by gemcitabine exposure based on PPIs map.

145 OR and PI3K/Akt pathways were verified after gemcitabine exposure.

146 OVA on ranks with Dunn test), while standard gemcitabine failed to significantly reduce tumor growth.

147 t investigator's choice of either rituximab, gemcitabine, fludarabine, chlorambucil, or cytarabine.

148 ntly, the IC50 for NSAH is within twofold of gemcitabine for growth inhibition of multiple cancer cel

149 d for nonsquamous NSCLC and carboplatin plus gemcitabine for squamous histology.

150 Median OS times for gemcitabine, G+T240, and G+T340 were 6.9, 8.7, and 9.2 m

151 s erlotinib 100 mg once per day (GemErlo) or gemcitabine (Gem) alone for six cycles.

152 This non-invasive RF combined with gemcitabine (Gem) chemotherapy enhanced drug uptake and

153 temporal scheduling of doxorubicin (DOX) and gemcitabine (GEM) on drug synergy.

154 The first drug, gemcitabine (GEM, 40wt%), was loaded in positively-charg

155 pirubicin, cyclophosphamide, paclitaxel, and gemcitabine (gemcitabine group; n=1576) or to epirubicin

156 compared with 25.5 months (22.7-27.9) in the gemcitabine group (hazard ratio 0.82 [95% CI 0.68-0.98],

157 een in three patients in the paclitaxel plus gemcitabine group (interstitial pneumonia, anaphylaxis,

158 neutropenia) and four in the cisplatin plus gemcitabine group (pathological bone fracture, thrombocy

159 months (IQR 14.4-26.8) in the cisplatin plus gemcitabine group and 15.9 months (10.7-25.4) in the pac

160 11 patients (six in the gemcitabine group and five in the control group) were in

161 tment groups at 10 years (65% [63-68] in the gemcitabine group vs 65% [62-67] in the control group),

162 .9 months (10.7-25.4) in the paclitaxel plus gemcitabine group, the hazard ratio for progression-free

163 adverse events in 196 of 366 patients in the gemcitabine group.

164 clophosphamide, paclitaxel, and gemcitabine (gemcitabine group; n=1576) or to epirubicin, cyclophosph

165 When this study was developed, gemcitabine had shown significant activity in metastatic

166 Gemcitabine has been the first line systemic treatment f

167 Therefore, gemcitabine has not been added to standard adjuvant chem

168 nase inhibitor erlotinib in combination with gemcitabine has shown efficacy in the treatment of advan

169 nd gemcitabine] v 10.7 months [cisplatin and gemcitabine]; HR, 1.46; P = .02).

170 erse panel of cell lines and human tumors to gemcitabine in 3D spheroid, mouse xenografts, and patien

171 liferation and enhanced cellular response to gemcitabine in a FKBP51-AKT-dependent manner.

172 Targeted therapy of HGF in combination with gemcitabine in a preclinical model of PDAC reduces prima

173 Gemcitabine in combination with a CD40 agonist induced T

174 PDAC xenografts were less sensitive to gemcitabine in hypoglycemic mice compared with hyperglyc

175 a synergistic effect of FASN inhibitors with gemcitabine in pancreatic cancer cells in culture and or

176 widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glyc

177 of vandetanib when used in combination with gemcitabine in patients with advanced pancreatic cancer.

178 d median overall survival when combined with gemcitabine in patients with locally advanced and metast

179 ry and increased the antitumor properties of gemcitabine in PDAC mice.

180 1 localization, and enhanced the efficacy of gemcitabine in prolonging the survival of KP(fl/fl)C mic

181 hemotherapeutics cisplatin or cisplatin plus gemcitabine in the core and pooled siRNAs that target mu

182 se assays confirmed pH responsive release of gemcitabine in vitro.

183 Gemcitabine increased inflammatory cytokines including T

184 Co-treatment of PDAC cells with lumican and gemcitabine increased mitochondrial damage, reactive oxy

185 oroquine or autophagy inhibitor 3MA enhanced gemcitabine-induced apoptosis, suggesting that autophagy

186 Inhibition of gemcitabine-induced autophagy in cancer cells by treatme

187 Additionally, KD of ST6Gal-I potentiates gemcitabine-induced DNA damage as measured by comet assa

188 resistance and reducing MYC levels decreases gemcitabine-induced neuroendocrine marker expression and

189 sms, such as competing gemcitabine uptake or gemcitabine-induced thymidylate synthase inhibition, and

190 Gemcitabine inhibited accumulation of CD11b+Gr1intF4/80i

191 Gemcitabine is a widely used chemotherapeutic drug, but

192 Gemcitabine is commonly used to treat pancreatic ductal

193 [(18)F]FLT-PET imaging of tumor response to gemcitabine is of crucial importance.

194 Purpose Gemcitabine is standard of care in the adjuvant treatmen

195 Cisplatin and gemcitabine is the standard first-line chemotherapy regi

196 The ESPAC-3 trial showed that adjuvant gemcitabine is the standard of care based on similar sur

197 Currently, the first line treatment, gemcitabine, is only effective in 23.8% of patients.

198 NK cells but not T cells were required for gemcitabine-mediated antitumor responses.

199 a2-6 sialic acids by neuraminidase, enhances gemcitabine-mediated cell death assessed via clonogenic

200 ST6Gal-I KD in S2-013 cells increases gemcitabine-mediated DNA damage, indicating that suppres

201 6Gal-I KD also alters mRNA expression of key gemcitabine metabolic genes, RRM1, RRM2, hENT1, and DCK,

202 our observations of retention time shifts of gemcitabine/metabolites on PGC are not consistent with c

203 NTERPRETATION: The addition of vandetanib to gemcitabine monotherapy did not improve overall survival

204 f gemcitabine and capecitabine compared with gemcitabine monotherapy for resected pancreatic cancer.

205 y compared gemcitabine and capecitabine with gemcitabine monotherapy in 730 evaluable patients with r

206 e most effective administration schedule for gemcitabine monotherapy.

207 his observation, patients receiving adjuvant gemcitabine (n = 107) with elevated serum glucose levels

208 cisplatin and gemcitabine or paclitaxel and gemcitabine; nonsquamous patients received cisplatin and

209 idine analogues, such as 2'deoxycytidine and gemcitabine, occurs through a saturable process that is

210 ombination with irradiation or chemotherapy (gemcitabine or docetaxel).

211 r tolerance; alternatively, monotherapy with gemcitabine or fluorouracil plus folinic acid can be off

212 to 1, and favorable comorbidity profile, and gemcitabine or fluorouracil should be offered to patient

213 logy were randomly assigned to cisplatin and gemcitabine or paclitaxel and gemcitabine; nonsquamous p

214 ve treatment, and adjuvant chemotherapy with gemcitabine or S-1, an oral fluoropyrimidine derivative,

215 In mice given adjuvant gemcitabine or vehicle, gemcitabine significantly inhibi

216 ize for the observed increase in response to gemcitabine over time.

217 mg/m(2) on days 1 and 8) or paclitaxel plus gemcitabine (paclitaxel 175 mg/m(2) on day 1 and gemcita

218 sites of action of four drugs (palbociclib, gemcitabine, paclitaxel and actinomycin D) to illustrate

219 o treatment with PEGPH20 plus nab-paclitaxel/gemcitabine (PAG) or nab-paclitaxel/gemcitabine (AG).

220 ingle-agent topotecan, weekly paclitaxel, or gemcitabine), patients were randomly assigned to also re

221 ition was combined with the chemotherapeutic gemcitabine, pervasive apoptosis was observed in intesti

222 There was no interference to gemcitabine pharmacokinetics by IVC administration.

223 mcitabine (vandetanib group) or placebo plus gemcitabine (placebo group) according to pre-generated s

224 lone and 219 patients received 1000 mg/m2 of gemcitabine plus 100 mg/d of erlotinib.

225 were reported by 226 of 359 patients in the gemcitabine plus capecitabine group compared with 481 gr

226 median overall survival for patients in the gemcitabine plus capecitabine group was 28.0 months (95%

227 y assigned to receive gemcitabine and 364 to gemcitabine plus capecitabine.

228 ndard chemotherapy for metastatic disease is gemcitabine plus cisplatin based on a single positive ra

229 retroperitoneal lymph nodes was treated with gemcitabine plus cisplatin, but after two cycles neutrop

230 ediate adjuvant chemotherapy (four cycles of gemcitabine plus cisplatin, high-dose methotrexate, vinb

231 Fixed-dose rate gemcitabine plus docetaxel achieves objective response i

232 -13.5 months) for the 219 patients receiving gemcitabine plus erlotinib (HR, 1.19; 95% CI, 0.97-1.45;

233 rall survival with gemcitabine compared with gemcitabine plus erlotinib used as maintenance therapy.

234 For second-line therapy, gemcitabine plus NAB-paclitaxel should be offered to pat

235 d to patients with first-line treatment with gemcitabine plus NAB-paclitaxel, ECOG PS 0 to 1, and fav

236 aliplatin; favorable comorbidity profile) or gemcitabine plus nanoparticle albumin-bound (NAB) -pacli

237 eucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nanoparticle albumin-bound paclitaxel (

238 leucovorin, irinotecan, and oxaliplatin and gemcitabine plus nanoparticle albumin-bound paclitaxel)

239 ADRB2 blockade together with gemcitabine reduced NGF expression and nerve density, an

240 osomal irinotecan is approved by the FDA for gemcitabine-refractory metastatic pancreatic cancer.

241 We assessed whether a cisplatin plus gemcitabine regimen was non-inferior to or superior to p

242 identified potential secretory biomarkers of gemcitabine resistance (response) in the transgenic KRas

243 e ST6Gal-I as a critical player in imparting gemcitabine resistance and as a potential target to rest

244 tween alterations in lipogenesis pathway and gemcitabine resistance by utilizing tissues from the gen

245 s pathway manipulation can help overcome the gemcitabine resistance in pancreatic cancer by regulatin

246 In a colon cancer mouse model, gemcitabine resistance was induced by intratumor Gammapr

247 e cells and cooperates with TGFbeta to drive gemcitabine resistance.

248 l role for the ST6Gal-I sialyltransferase in gemcitabine resistance.

249 , these features enable this KDC to bypass a gemcitabine-resistance mechanism found in pancreatic can

250 Gemcitabine-resistant MiaPaCa-2 cells display higher ST6

251 that most significantly correlated with poor gemcitabine response in pancreatic cancer patients.

252 ression of nucleoside transporters affecting gemcitabine response, and an immune stimulatory microenv

253 sion with poor survival in patients and poor gemcitabine responsiveness in cell lines.

254 ion models demonstrated a robust increase in gemcitabine responsiveness upon inhibition of fatty acid

255 reated with ormeloxifene in combination with gemcitabine restored the tumor-suppressor miR-132 and in

256 RM2, hENT1, and DCK, leading to an increased gemcitabine sensitivity ratio, an indicator of gemcitabi

257 n treatment-naive cells along with a reduced gemcitabine sensitivity ratio, suggesting that chronic c

258 Further, CAFs exposed to gemcitabine significantly increase the release of extrac

259 mice given adjuvant gemcitabine or vehicle, gemcitabine significantly inhibited local recurrence of

260 Despite this, metronomic gemcitabine significantly inhibited tumor angiogenesis a

261 pyrimidine biosynthesis, in combination with gemcitabine, strongly diminishes tumor burden.

262 bicin, cyclophosphamide, and paclitaxel plus gemcitabine (the same chemotherapy regimen as the other

263 und that CAFs are intrinsically resistant to gemcitabine, the chemotherapeutic standard of care for P

264 atic cancer who were previously treated with gemcitabine therapy and with an Eastern Cooperative Onco

265 f drug resistance has been a major hurdle in gemcitabine therapy leading to unsatisfactory patient ou

266 e of lung carcinoma xenografts in mice after gemcitabine therapy.

267 In combination with gemcitabine, these compounds demonstrate an in vivo phar

268 els of dCTP diminish the effective levels of gemcitabine through molecular competition.

269 multidrug transporters as well by converting gemcitabine to a less active form, both leading to its i

270 INTERPRETATION: The addition of gemcitabine to anthracycline and taxane-based adjuvant c

271 trial testing whether adding capecitabine or gemcitabine to docetaxel followed by doxorubicin plus cy

272 demonstrate that it can selectively deliver gemcitabine to malignant cells expressing tumor-associat

273 her group, with the addition of 1250 mg/m(2) gemcitabine to the paclitaxel cycles, administered intra

274 mcitabine sensitivity ratio, an indicator of gemcitabine toxicity.

275 In gemcitabine-treated mice, neoadjuvant PD-1 blockade foll

276 but depriving PDAC cells of nutrients before gemcitabine treatment attenuated this effect.

277 Molecular markers downstream of gemcitabine treatment in preclinical models may provide

278 Gemcitabine treatment of patient-derived xenograft tumor

279 ng pathways in pancreatic cancer cells after gemcitabine treatment using iTRAQ labeling LC-MS/MS, bec

280 ed in vitro by either nutrient withdrawal or gemcitabine treatment, but depriving PDAC cells of nutri

281 revealed that H1975 xenografts responded to gemcitabine treatment, whereas A549 growth was not affec

282 tophagy is a protective cellular response to gemcitabine treatment.

283 metabolic pathways improves the efficacy of gemcitabine treatment.

284 mors reflected mechanisms, such as competing gemcitabine uptake or gemcitabine-induced thymidylate sy

285 arcinoma xenografts, and in combination with gemcitabine using a well-tolerated multidose schedule, t

286 erapy (median OS, 7.6 months [paclitaxel and gemcitabine] v 10.7 months [cisplatin and gemcitabine];

287 omly assigned 1:1 to receive vandetanib plus gemcitabine (vandetanib group) or placebo plus gemcitabi

288 randomization for the 223 patients receiving gemcitabine was 13.6 months (95% CI, 12.3-15.3 months) a

289 Systemic exposure to gemcitabine was 14 times lower in the metronomic groups

290 us gemcitabine compared with paclitaxel plus gemcitabine was achieved, we would then test for superio

291 Randomized crossover after progression on gemcitabine was allowed.

292 001, psuperiority=0.009, thus cisplatin plus gemcitabine was both non-inferior to and superior to pac

293 Gemcitabine was infused at 1875 mg/m(2) for 3 h for 2 da

294 r who had experienced treatment failure with gemcitabine were randomly assigned 1:1 to the JAK1/JAK2

295 esigned to investigate the potential role of gemcitabine when added to anthracycline and taxane-conta

296 act cancer in combination with cisplatin and gemcitabine, which remains the standard of care.

297 In vivo the formulation outperformed free gemcitabine with a 62% reduction in tumor weight in panc

298 However, median cumulative payments for gemcitabine with nab-paclitaxel were highest overall [me

299 resumably related to a direct competition of gemcitabine with the radiotracer for cellular uptake.

300 Furthermore, metronomic gemcitabine yielded a 40%-50% decrease in tumor mass at