ライフサイエンスコーパス: gemcitabine

1 rom these cells had increased sensitivity to gemcitabine.

2 to two chemotherapeutics: 5-Fluorouracil and Gemcitabine.

3 immediate surgery and 6 courses of adjuvant gemcitabine.

4 PH20 had moderate effects on tumor uptake of gemcitabine.

5 at with the first-line chemotherapeutic drug gemcitabine.

6 s, and are significantly more efficient than Gemcitabine.

7 invasive and adhesive and more resistant to gemcitabine.

8 when compared to animals treated with low IV gemcitabine.

9 d cell-extrinsic mechanisms of resistance to gemcitabine.

10 t-derived xenograft mouse model treated with gemcitabine.

11 growth was suppressed to the same degree as gemcitabine.

12 ycolysis, and increased their sensitivity to gemcitabine.

13 ing pathway showed heightened sensitivity to gemcitabine.

14 potential of doxycycline in combination with gemcitabine.

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

16 knockdown cells had increased sensitivity to gemcitabine.

17 -EGFR inhibitor afatinib in combination with gemcitabine.

18 ancer stem-like properties and resistance to gemcitabine.

19 liferation and primes cells for apoptosis by gemcitabine.

20 knockdown were smaller and more sensitive to gemcitabine.

21 ant having 1,000-fold reduced sensitivity to gemcitabine.

22 h before coinjection of (18)F-FAC and (14)C-gemcitabine.

23 Treatment was gemcitabine 1,000 mg/m(2) intravenously followed by erib

24 of a localized BTC to receive either GEMOX (gemcitabine 1,000 mg/m(2) on day 1 and oxaliplatin 85 mg

25 mg/m(2) [arm A] or 125 mg/m(2) [arm C]) plus gemcitabine 1,000 mg/m(2) or a standard schedule of 3 we

26 mg/m(2) [arm B] or 125 mg/m(2) [arm D]) plus gemcitabine 1,000 mg/m(2).

27 e intention to receive four 21-day cycles of gemcitabine (1,000 mg/m(2) days 1 and 8) with AZD1775 (o

28 to form a complex with gemcitabine at copper:gemcitabine (1:4).

29 of liver metastases, to receive intravenous gemcitabine 1000 mg/m(2) and intravenous carboplatin (ar

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

31 Patients received 21-day cycles of gemcitabine (1000 mg/m(2) body surface area, administere

32 nly) administered intravenously on day 1 and gemcitabine (1000 mg/m(2)) administered intravenously on

33 ndomly assigned (1:1) to receive intravenous gemcitabine (1000 mg/m(2)) on day 1 and day 8, or gemcit

34 the concentration curve [AUC] 4, day 1) plus gemcitabine (1000 mg/m(2), days 1 and 8) every 3 weeks o

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

36 Standard therapies such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamm

37 erexpressed ZIP4 had increased resistance to gemcitabine, 5-fluorouracil, and cisplatin, whereas AsPC

38 arm A consisted of cisplatin 25 mg/m(2) and gemcitabine 600 mg/m(2) intravenously on days 3 and 10;

39 rgeting the very mechanisms of resistance to gemcitabine, a commonly used chemotherapeutic agent.

40 sensitizes MDA-MB-231 breast cancer cells to gemcitabine, a nucleoside analog used in chemotherapy fo

41 Gemcitabine, a nucleotide analog that inhibits RNR, has

42 Here, we show that gemcitabine, a standard chemotherapy for various solid t

43 Despite its widespread use, gemcitabine achieves responses in less than 10% of patie

44 Gemcitabine activated caspase-3 and synergized with AZD1

45 herapy, we explored the effects of long-term gemcitabine administration on the tumor microenvironment

46 urine syngeneic cell line growth compared to gemcitabine/afatinib alone treatment.

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

48 70 were randomly assigned to treatment with gemcitabine alone (36 patients) or gemcitabine plus berz

49 osertib and 14.7 weeks (90% CI 9.7-36.7) for gemcitabine alone (hazard ratio 0.57, 90% CI 0.33-0.98;

50 s were observed in ten (28%) patients in the gemcitabine alone group and nine (26%) patients in the g

51 There was one treatment-related death in the gemcitabine alone group due to sepsis and one treatment-

52 rophil count (14 [39%] of 36 patients in the gemcitabine alone group vs 16 [47%] of 34 patients in th

53 group and 43.0 weeks (IQR 23.2-69.1) in the gemcitabine alone group.

54 acceptable toxicity and superior efficacy to gemcitabine alone in high-grade serous ovarian cancer.

55 ignificantly improved survival compared with gemcitabine alone in patients with metastatic pancreatic

56 rthotopic pancreatic tumor-bearing mice with gemcitabine alone or in combination with a CXCR4 antagon

57 hloride, and oxaliplatin (FOLFIRINOX) versus gemcitabine alone, presented at the 2018 ASCO Annual Mee

58 ing survival when compared to treatment with gemcitabine alone.

59 FOLFIRINOX or gemcitabine along with nab-paclitaxel were used in 165 (

60 Ribonucleotide reductase inhibitors such as gemcitabine also arrest cells in S phase by preventing d

61 Results: Tumor-to-muscle ratios of (14)C-gemcitabine and (18)F-FAC correlated well across all PDX

62 lternative strategy that relies on combining gemcitabine and a novel programmed death-ligand 1 (PD-L1

63 the setting of TGFbeta signaling deficiency, gemcitabine and anti-PD-1 led to a robust CD8(+) T-cell

64 Combined gemcitabine and anti-PD-1 treatment in transgenic models

65 herapeutics not currently used to treat AML, gemcitabine and cabazitaxel, have broad anti-leukemic ac

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

67 afety and activity data for trilaciclib plus gemcitabine and carboplatin chemotherapy in patients wit

68 d tolerability of combining trilaciclib with gemcitabine and carboplatin chemotherapy.

69 osuppression endpoints with trilaciclib plus gemcitabine and carboplatin in patients with metastatic

70 ib 240 mg/m(2) on days 1 and 8 (group 2), or gemcitabine and carboplatin on days 2 and 9 plus trilaci

71 rve 2 mug x h/mL) on days 1 and 8 (group 1), gemcitabine and carboplatin plus intravenous trilaciclib

72 nd potentiated the cytotoxic effects of both gemcitabine and cisplatin in PDAC cell lines.

73 Although the combination of gemcitabine and cisplatin is a standard regimen of choic

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

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

76 further sensitized RECQ1-deficient cells to gemcitabine and increased cell death.

77 Drugs such as gemcitabine and irinotecan elicit their therapeutic effe

78 expression in PDA primary cells, potentiated gemcitabine and JQ1 cytotoxicity in cell culture, and Ge

79 Combination therapy consisting of gemcitabine and MN-siPDL1 in a syngeneic murine pancreat

80 Gemcitabine and once daily radiation (GD) is a well-supp

81 Either gemcitabine and once daily radiation or a cisplatin-base

82 e in PDAC cells, thus reducing the effect of gemcitabine and other nucleoside analogues on cancer cel

83 We aimed to assess whether gemcitabine and oxaliplatin chemotherapy (GEMOX) would i

84 and efficacy of AZD1775 in combination with gemcitabine and radiation in patients with newly diagnos

85 AZD1775 in combination with gemcitabine and radiation therapy was well tolerated at

86 ed dose of AZD1775 given in conjunction with gemcitabine and radiation.

87 All patients were treated with gemcitabine and S-1 (GS)-based chemotherapies with/witho

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

89 ice were given injections of PD1 antibody or gemcitabine and survival was monitored.

90 ed the interaction of CDK4/6 inhibitors with gemcitabine and taxanes that are employed in the treatme

91 We found that anti-tumoral activity of gemcitabine and the Wee1 kinase inhibitor AZD1775 in ost

92 cytosine) has close structural similarity to gemcitabine and thus offers the potential to image drug

93 portant in vitro cytotoxicity differences to gemcitabine, and a genome-wide CRISPR/Cas9 genetic scree

94 bited CA9 with SLC-0111, incubated them with gemcitabine, and assessed pHi, metabolic flux, and cytot

95 ncreatic tumors, increases their response to gemcitabine, and significantly extends survival of mice.

96 se IB data from a trial that used cisplatin, gemcitabine, and veliparib treatment demonstrated a high

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

98 These data establish cisplatin and gemcitabine as a standard approach in gBRCA/PALB2+ PDAC.

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

100 Animals were injected with PEGPH20 and (14)C-gemcitabine as described above to validate increased dru

101 n tumour biopsies from patients treated with gemcitabine, assessed by immunostaining and image analys

102 copper (II) gluconate to form a complex with gemcitabine at copper:gemcitabine (1:4).

103 with cholangiocarcinoma after progression on gemcitabine-based chemotherapy are urgently needed.

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

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

106 pants receiving no induction chemotherapy or gemcitabine-based induction chemotherapy and 14.9 months

107 roup, 18 participants received no therapy or gemcitabine-based induction chemotherapy and 22 received

108 nvironment and that patients who progress on gemcitabine-based regimens may benefit from multidrug im

109 of neoadjuvant therapy in FOLFIRINOX-based, gemcitabine-based, and combination of the two, and subse

110 We focused on 5-Fluorouracil and Gemcitabine because based on our exclusion criteria, the

111 ere randomly assigned to receive carboplatin-gemcitabine-bevacizumab (standard group).

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

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

114 on, and showed similar therapeutic effect to gemcitabine but at one-third the molar dose.

115 the molecular mechanism of sensitization to gemcitabine by the CHK1i MK8776.

116 cil (5-FU) and mitoxantrone, but not that of gemcitabine, capecitabine, cisplatin or oxaliplatin.

117 uorouracil and mitoxantrone, but not that of gemcitabine, capecitabine, cisplatin, or oxaliplatin.

118 by type of on-study chemotherapy (taxane or gemcitabine-carboplatin), PD-L1 expression at baseline (

119 d in 6 CCA cell lines treated with Cisplatin-Gemcitabine (CG) seeking changes in cell viability.

120 cinoma cell lines treated with cisplatin and gemcitabine (CG) seeking changes in cell viability.

121 ues) from patients who underwent surgery and gemcitabine chemotherapy and analyzed them by immunohist

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

123 nces drug delivery and efficacy of cytotoxic gemcitabine chemotherapy.

124 We administered adjuvant gemcitabine/cisplatin chemotherapy.

125 model of murine pancreatic cancer, liposomal gemcitabine combined with local hyperthermia induced cel

126 Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E(2) rel

127 esentation and immune checkpoint expression, gemcitabine consistently increased the synthesis of CCL/

128 nfirmed the presence of a liquid crystalline gemcitabine-copper mixture.

129 he selective ATR inhibitor, berzosertib, and gemcitabine could show acceptable toxicity and superior

130 eover, afatinib alone or in combination with gemcitabine decreased stemness and tumorspheres by reduc

131 Gemcitabine delivery to pancreatic ductal adenocarcinoma

132 of targeted intra-arterial (IA) delivery of gemcitabine directly into the pancreas in an orthotopic

133 Our study shows targeted IA injection of gemcitabine directly into the pancreas, via its arterial

134 With 5% of the free gemcitabine dose (5 rather than 100 mg/kg), tumor growth

135 PDAC and suggests new avenues for improving gemcitabine efficacy.

136 C, however, nearly all patients treated with gemcitabine either fail to respond or rapidly develop re

137 Addition of CHK1i 18 h after gemcitabine elicited cell division cycle 7 (CDC7)- and c

138 assessed the tolerability and efficacy of a gemcitabine-eribulin combination in this population.

139 Gemcitabine-eribulin treatment response and survival for

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

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

142 Gemcitabine extended survival of KPC/Cdh11(+/-) and KPC/

143 juvant chemotherapy (NAC) with cisplatin and gemcitabine followed by CRT.

144 ed to three cycles of NAC with cisplatin and gemcitabine followed by standard CRT with weekly cisplat

145 has a synergistic effect in combination with gemcitabine for killing pancreatic cancer cells.

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

147 erapeutic agent alone or in combination with gemcitabine for the treatment of CCA.

148 ptamethines 1 were synthesized, which have a gemcitabine fragment attached to the meso-position of th

149 Resistance to nucleoside analog gemcitabine frequently used in first-line therapy is an

150 d-temozolomide (TMZ) complexes combined with gemcitabine (GEM) and decitabine (DAC) to improve the ef

151 the chemotherapeutic drugs cyclophosphamide, gemcitabine (GEM) and oxaliplatin (OXP) for 24 hours in

152 was adopted for detection and assessment of Gemcitabine (GEM) as an anti-cancer drug based on evalua

153 se 3 (PGM3), is associated with the onset of gemcitabine (GEM) resistance in PC.

154 combined delivery of microRNA (miR-345) and gemcitabine (GEM) to treat pancreatic cancer (PC).

155 we show that a multidose clinical regimen of gemcitabine (GEM) treatment enhances the immunosuppressi

156 tes synergistic tumor growth inhibition with gemcitabine (Gem), a first- or second-line chemotherapeu

157 Using three common chemotherapeutic drugs, gemcitabine (GEM), irinotecan (IRIN), and a prodrug form

158 t on apoptosis; however, in combination with gemcitabine given during the last 2 days of treatment, d

159 Gemcitabine (GMT) is a nucleoside analog used in the tre

160 , tumor samples from animals treated with IA gemcitabine had significantly lower residual cancer cell

161 n in tumor growth as seen with IA treatment, gemcitabine had to be given IV at over 300x the dose (hi

162 A limitation of liposomal gemcitabine has been the low loading efficiency.

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

164 echanisms of CHK1i-mediated sensitization to gemcitabine have been proposed, but their role was ruled

165 luding ethambutol, isoniazid, ephedrine, and gemcitabine in biological matrices was further demonstra

166 d to reported circulation of 16 min for free gemcitabine in mice), and free drug was not detected wit

167 ession significantly reduced accumulation of gemcitabine in pancreatic cancer cells, increased growth

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

169 Deoxycytidine inhibited the processing of gemcitabine in PDAC cells, thus reducing the effect of g

170 udy shows a benefit of adding berzosertib to gemcitabine in platinum-resistant high-grade serous ovar

171 sly been shown to have equivalent potency to gemcitabine in the pancreatic cancer cell line MIA PaCa-

172 croenvironment and facilitated resistance to gemcitabine in tumor cells.

173 The combination of VE-822 and gemcitabine in vitro was synergistic, inhibited cell pro

174 selective blockade sensitizes tumor cells to gemcitabine in vitro, and genetic ablation of p110gamma

175 g CA9, in combination with administration of gemcitabine, in mouse models of pancreatic cancer.

176 administration of SLC-0111 and injection of gemcitabine increased intratumor acidosis and increased

177 Brief gemcitabine incubation irreversibly inhibited ribonucleo

178 zes pancreatic cancer cells to Etoposide and Gemcitabine induced apoptosis.

179 in cells under hypoxic conditions, decreased gemcitabine-induced glycolysis, and increased their sens

180 l cycle checkpoint activation in response to gemcitabine-induced replication stress.

181 nuclease subunit (MUS81) and RECQ1 increased gemcitabine-induced, replication-associated DNA double-s

182 r xenograft tumors in mice, and injection of gemcitabine inhibited tumor growth and significantly inc

183 Gemcitabine is a drug of choice in the treatment of huma

184 Gemcitabine is a fluoropyrimidine analogue that is used

185 Gemcitabine is a widely used chemotherapeutic drug, but

186 The deoxynucleoside analogue gemcitabine is among the most effective therapies to tre

187 Cisplatin and gemcitabine is an effective regimen in advanced gBRCA/PA

188 Purpose Gemcitabine is standard of care in the adjuvant treatmen

189 Gemcitabine largely ablates the function of CDK4/6 inhib

190 e data suggest that long-term treatment with gemcitabine leads to extensive reprogramming of the panc

191 In KPC-derived tumors, PEGPH20 raised (14)C-gemcitabine levels (tumor-to-muscle ratio of 1.9 vs. 2.4

192 We further modified tumor gemcitabine levels with injectable PEGylated recombinant

193 mpared tumor (18)F-FAC PET images with (14)C-gemcitabine levels, established ex vivo, in 3 mouse mode

194 Three repeated treatments of activatable gemcitabine liposomes plus ultrasound hyperthermia regre

195 The optimized gemcitabine liposomes released 60% and 80% of the gemcit

196 The resulting gemcitabine liposomes were efficacious against both muri

197 d compared against doxorubicin liposomes and gemcitabine liposomes.

198 ression of genes in PC cells associated with gemcitabine metabolism, antioxidant defense, and cancer

199 ct of these genetic alterations by measuring gemcitabine metabolites, reactive oxygen species product

200 n side effect associated with nab-paclitaxel gemcitabine (Nab-Gem) therapy.

201 ry outcome) is the FDA/EMEA approved dose of gemcitabine-nab-paclitaxel along-with ATRA (45 mg/m(2) o

202 stromal-targeting agent in combination with gemcitabine-nab-paclitaxel chemotherapy using a two-step

203 osing ATRA as a stromal-targeting agent with gemcitabine-nab-paclitaxel is safe and tolerable.

204 ive chemotherapy with mFOLFIRINOX (Arm 1) or gemcitabine/nab-paclitaxel (Arm 2).

205 neoadjuvant SOC chemotherapy (FOLFIRINOX or gemcitabine/nab-paclitaxel) followed by chemoradiation (

206 ncluding docetaxel (microtubule stabilizer), gemcitabine (nucleoside analogue) and GDC-0980 (PI3K/mTO

207 rkably enhanced the effects of cisplatin and gemcitabine on basal-like bladder cancer both in vivo an

208 ther 100 and 125 mg/m(2) in combination with gemcitabine on days 1, 8, and 15 every 28 days is well t

209 41 enhanced the growth inhibitory effects of gemcitabine or cisplatin when used in combination in bla

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

211 sistant cells to DNA damaging agents such as gemcitabine or hydroxyurea by inhibition of HR.

212 xercise-induced vascular remodeling improves gemcitabine or other chemotherapy efficacy in patients,

213 ollowed by surgery and 4 courses of adjuvant gemcitabine or to immediate surgery and 6 courses of adj

214 d with carboplatin-paclitaxel or carboplatin-gemcitabine) or the most active non-bevacizumab regimen:

215 given injections of antibody against CDH11, gemcitabine, or small molecule inhibitor of CDH11 (SD133

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

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

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

219 Gemcitabine-platinum combination chemotherapy initiated

220 ment with gemcitabine alone (36 patients) or gemcitabine plus berzosertib (34 patients).

221 free survival was 22.9 weeks (17.9-72.0) for gemcitabine plus berzosertib and 14.7 weeks (90% CI 9.7-

222 follow-up was 53.2 weeks (25.6-81.8) in the gemcitabine plus berzosertib group and 43.0 weeks (IQR 2

223 epsis and one treatment-related death in the gemcitabine plus berzosertib group due to pneumonitis.

224 lone group vs 16 [47%] of 34 patients in the gemcitabine plus berzosertib group) and decreased platel

225 e alone group and nine (26%) patients in the gemcitabine plus berzosertib group.

226 chemotherapy (nab-paclitaxel; paclitaxel; or gemcitabine plus carboplatin) or placebo plus chemothera

227 chemotherapy (gemcitabine plus cisplatin or gemcitabine plus carboplatin, depending on cisplatin eli

228 y 4 weeks; or standard-of-care chemotherapy (gemcitabine plus cisplatin or gemcitabine plus carboplat

229 ens were as follows: trabectedin in HG-MLPS; gemcitabine plus dacarbazine in LMS; high-dose prolonged

230 SS; etoposide plus ifosfamide in MPNST; and gemcitabine plus docetaxel in UPS.

231 tabine (1000 mg/m(2)) on day 1 and day 8, or gemcitabine plus intravenous berzosertib (210 mg/m(2)) o

232 eucovorin], irinotecan, and oxaliplatin) and gemcitabine plus nab-paclitaxel remain the mainstay of t

233 elate with survival in patients treated with gemcitabine plus nab-paclitaxel.

234 tigated in an additional cohort treated with gemcitabine plus nab-paclitaxel.

235 Gemcitabine plus nanoparticle albumin-bound (NAB) paclit

236 Importantly, dinaciclib, in combination with gemcitabine, produced a robust and sustained inhibition

237 itized p53-/- cells to the nucleoside analog gemcitabine, raising the future perspective of using Mdm

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

239 administration of SLC-0111 and injection of gemcitabine reduced numbers of B cells in tumors.

240 consideration in the clinical management of gemcitabine-refractory PDAC.

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

242 Moreover, DHS overcame both gemcitabine resistance in pancreatic cancer and cisplati

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

244 w insight into mechanisms that contribute to gemcitabine resistance in PDAC and suggests new avenues

245 ithelial-to-mesenchymal phenotype and confer gemcitabine resistance of PDAC cells induced by CAF-deri

246 composition of the tumor stroma, conferring gemcitabine resistance to cancer-associated fibroblasts

247 rly, high SOX2 expression is associated with gemcitabine resistance whereas down-regulation of SOX2 s

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

249 Using acquired gemcitabine resistant pancreatic cell lines, we revealed

250 tential for clinical use in the treatment of gemcitabine-resistant human pancreatic cancer.

251 aCa-2 cell line is largely unaffected in the gemcitabine-resistant line.

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

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

254 ssion patterns of numerous genes involved in gemcitabine sensitivity are down regulated in the resist

255 he GLI-SOX2 signaling axis for regulation of gemcitabine sensitivity in vitro and in animal models.

256 Gemcitabine showed a synergetic effect with hYP7-DC in v

257 In vivo, the combination of VE-822 and gemcitabine significantly enhanced tumor growth inhibiti

258 Afatinib in combination with gemcitabine significantly reduced Kras(G12D/+); Pdx-1 Cr

259 offers survival benefits superior to that of gemcitabine single agent, but the treatment-related side

260 These results suggest that gemcitabine successfully primes PDAC tumors for immune c

261 re randomly assigned into 3 groups receiving gemcitabine: systemic intravenous (IV) injection (low: 0

262 ere on cell lines of increased resistance to gemcitabine that have been generated from this line, wit

263 adiotherapy, which consisted of 3 courses of gemcitabine, the second combined with 15 x 2.4 Gy radiot

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

265 ed chemoresistant pancreatic cancer cells to gemcitabine, thereby improving the effectiveness of chem

266 ther synergizes with the antineoplastic drug gemcitabine to effectively suppress pineoblastoma in our

267 , LIF-neutralizing antibodies synergize with gemcitabine to eradicate established pancreatic tumors i

268 addition of NAC consisting of cisplatin and gemcitabine to standard CRT is not superior and is possi

269 Cs) they are significantly more resistant to gemcitabine toxicity than those grown in monoculture.

270 other fibroblasts, protected PDAC cells from gemcitabine toxicity.

271 gnaling, via JNK, inhibits expression of the gemcitabine transporter ENT1, so that cells take up smal

272 al kinase (JNK), inhibited expression of the gemcitabine transporter ENT1, which reduced gemcitabine

273 duction, and sphere formation in vehicle- or gemcitabine-treated monocultures and co-cultured PC cell

274 by 59% and of fibroblasts by 24% compared to gemcitabine treatment alone.

275 The authors show that gemcitabine treatment causes profound changes in the pan

276 AM-1 promotes tumor growth and resistance to gemcitabine treatment in vivo but not in vitro.

277 Collectively, gemcitabine treatment increases the release of sVCAM-1 f

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

279 d mechanistic evidence that a combination of gemcitabine treatment with targeted inhibition of both t

280 tage II PDAC patients (all of them underwent gemcitabine treatment), indicating that reduced SOX2 exp

281 Human PDAC tissues with gemcitabine treatment, autochthonous mouse tumors from K

282 ism did not occur with concurrent CHK1i plus gemcitabine treatment, providing support for delayed adm

283 e tumor, thereby promoting the resistance to gemcitabine treatment.

284 eater DNA damage accumulation in response to gemcitabine treatment.

285 ve in sensitizing pancreatic cancer cells to gemcitabine treatment.

286 f SOX2 sensitizes pancreatic cancer cells to gemcitabine treatment.

287 olecule-1 (sVCAM-1) increases in response to gemcitabine treatment.

288 cer was an independent prognostic factor for gemcitabine treatment.

289 FAC PET was shown to be a good surrogate for gemcitabine uptake and, when combined with MR, to succes

290 gemcitabine transporter ENT1, which reduced gemcitabine uptake by pancreatic cancer cells.

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

292 of Raman G-band intensity when treated with gemcitabine versus the pretreated tumor; the Raman G-ban

293 nd muscle uptake of both (18)F-FAC and (14)C-gemcitabine was obtained ex vivo.

294 elarin), a phosphoramidate transformation of gemcitabine, was the first anti-cancer ProTide to enter

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

296 r drug payloads (docetaxel, cabazitaxel, and gemcitabine) were successfully generated and tested in d

297 phase II trial to investigate cisplatin and gemcitabine with or without veliparib in gBRCA/PALB2+ PD

298 antially higher than prior results combining gemcitabine with radiation therapy and warrants addition

299 tabine liposomes released 60% and 80% of the gemcitabine within 1 and 5 min, respectively, at 42 degr

300 onidase (PEGPH20) to test whether changes in gemcitabine would be tracked by (18)F-FAC.