ライフサイエンスコーパス: pancreatic cancer cell line

1 pancreatic adenocarcinoma xenografts and 11 pancreatic cancer cell lines).

2 ransiently expressed in the MIA PaCa-2 human pancreatic cancer cell line.

3 e to NT was determined in L3.6, a metastatic pancreatic cancer cell line.

4 was overexpressed ectopically in a MYB-null pancreatic cancer cell line.

5 nocarcinomas and is amplified in a subset of pancreatic cancer cell lines.

6 t, and NF-kappaB was determined in six human pancreatic cancer cell lines.

7 in a panel of ten genetically diverse human pancreatic cancer cell lines.

8 in human pancreatic adenocarcinomas and some pancreatic cancer cell lines.

9 of pharmacologic inhibition of MEK on human pancreatic cancer cell lines.

10 hibit to various degrees the growth of three pancreatic cancer cell lines.

11 its growth inhibitory activity against human pancreatic cancer cell lines.

12 s in mediating cytotoxicity in four invasive pancreatic cancer cell lines.

13 EGF expression were variable among different pancreatic cancer cell lines.

14 vel for maspin and S100P in a large panel of pancreatic cancer cell lines.

15 ibroblasts and in a panel of bona fide human pancreatic cancer cell lines.

16 rbation of the MKK4 expression in breast and pancreatic cancer cell lines.

17 even after hypoxia treatment in six of seven pancreatic cancer cell lines.

18 ells, but was not expressed in a majority of pancreatic cancer cell lines.

19 se-type plasminogen activator, in metastatic pancreatic cancer cell lines.

20 activation of NF-kappaB in metastatic human pancreatic cancer cell lines.

21 itis and which were also highly expressed in pancreatic cancer cell lines.

22 nvasive pancreatic cancer tissues but not in pancreatic cancer cell lines.

23 ect of 2-ME on apoptosis in a panel of human pancreatic cancer cell lines.

24 ancreatic adenocarcinoma patients and 71% of pancreatic cancer cell lines.

25 fect of PDEdelta knockdown in a set of human pancreatic cancer cell lines.

26 ot activate a TGFbeta-responsive reporter in pancreatic cancer cell lines.

27 were expressed in ASPC-1 and COLO-357 human pancreatic cancer cell lines.

28 d photodynamic therapy on a variety of human pancreatic cancer cell lines.

29 tive (BxPC3) and -negative (MIAPaCa-2) human pancreatic cancer cell lines.

30 s of loss or gain of S100A4 were examined in pancreatic cancer cell lines.

31 identified in innately gemcitabine-resistant pancreatic cancer cell lines.

32 l cycle progression and apoptosis in several pancreatic cancer cell lines.

33 n PanINs, pancreatic cancers, and in several pancreatic cancer cell lines.

34 T5C) as favoring the mesenchymal identity in pancreatic cancer cell lines.

35 p-regulated in prostate, kidney, breast, and pancreatic cancer cell lines.

36 of the interaction between tRNA and MEK2 in pancreatic cancer cell lines.

37 itro activity screen in Panc-1 and MiaPaCa-2 pancreatic cancer cell lines.

38 enhance TRAIL-mediated cytotoxicity in human pancreatic cancer cell lines.

39 ed elevated AGR2 expression in seven of nine pancreatic cancer cell lines.

40 ne or radiation therapy were measured in two pancreatic cancer cell lines.

41 rogated in leukemic, skin, kidney, lung, and pancreatic cancer cell lines.

42 a Ras-signaling-dependent manner in various pancreatic cancer cell lines.

43 target gene expression and cell survival in pancreatic cancer cell lines.

44 ent inhibitor of brain, breast, ovarian, and pancreatic cancer cell lines.

45 using RNA interference in lung, breast, and pancreatic cancer cell lines.

46 nalyze global gene expression patterns in 14 pancreatic cancer cell lines, 17 resected infiltrating p

47 xpression in pancreatic adenocarcinoma (10), pancreatic cancer cell lines (7), chronic pancreatitis (

48 changes in gene expression profiles of four pancreatic cancer cell lines after treatment with the de

49 Pancreatic cancer cell lines also secreted adrenomedulli

50 mistry and was expressed by 100% (8 of 8) of pancreatic cancer cell lines analyzed by reverse transcr

51 , we stably overexpressed S100P in the Panc1 pancreatic cancer cell line and identified the consequen

52 In the present study, using a CFTR-defective pancreatic cancer cell line and its derived subline expr

53 Additionally, six pancreatic cancer cell lines and a spleen subcapsular in

54 interference or pharmacologic inhibitors in pancreatic cancer cell lines and analyses of xenograft t

55 ated (3)H-gemcitabine transport was lower in pancreatic cancer cell lines and correlated with cytotox

56 n of this gene was identified in six of nine pancreatic cancer cell lines and correlated with increas

57 We therefore examined 10 pancreatic cancer cell lines and corresponding primary t

58 promoter was observed in all BNIP3-negative pancreatic cancer cell lines and eight of 10 pancreatic

59 ts receptors in human pancreatic tissues and pancreatic cancer cell lines and examined the effects of

60 eless critical for invasion in seven of nine pancreatic cancer cell lines and for metastasis as asses

61 e orthotopic and heterotopic implantation of pancreatic cancer cell lines and freshly isolated patien

62 mRNA was undetectable in a high fraction of pancreatic cancer cell lines and in primary pancreatic d

63 molecular forms of the secretin receptor in pancreatic cancer cell lines and in primary tumors.

64 r having its fourth intron retained in three pancreatic cancer cell lines and in tumor tissue, but no

65 inhibits maturation of the microRNA let-7 in pancreatic cancer cell lines and increases their prolife

66 ed the effects of SINE analogs in a panel of pancreatic cancer cell lines and nontransformed human pa

67 Moreover, in a panel of pancreatic cancer cell lines and normal pancreas, we obs

68 Sp1 expression and activity was detected in pancreatic cancer cell lines and pancreatic cancer tissu

69 rantly hypomethylated in a large fraction of pancreatic cancer cell lines and primary pancreatic carc

70 ayed a high prevalence of hypomethylation in pancreatic cancer cell lines and primary pancreatic carc

71 s can mediate growth inhibitory responses in pancreatic cancer cell lines and raise the possibility t

72 using genomic DNA from exosomes derived from pancreatic cancer cell lines and serum from patients wit

73 ressed the growth of a subset of KRAS-mutant pancreatic cancer cell lines and that concurrent phospha

74 the high rates of cellular proliferation in pancreatic cancer cell lines and the host desmoplastic r

75 ted directly with high cavin-1 expression in pancreatic cancer cell lines and tumor specimens (P < 0.

76 yses, we assessed expression of KLF4alpha in pancreatic cancer cell lines and tumor tissue samples; x

77 e 16.5-kb mitochondrial genome (mtDNA) in 15 pancreatic cancer cell lines and xenografts.

78 roblastoma, colorectal, breast, cervical and pancreatic cancer cell lines and xenografts.

79 tic cancer specimens, normal pancreas, human pancreatic cancer cell lines, and an endothelial cell li

80 We studied CD44v6 signaling in several pancreatic cancer cell lines, and its role in tumor grow

81 Mirk has been shown to lead to apoptosis in pancreatic cancer cell lines, and thus to inhibit their

82 Rac1 was activated in four out of five pancreatic cancer cell lines, and was activated by signa

83 erative and antiapoptotic effects of PG on a pancreatic cancer cell line, AR42J.

84 Using HPAF-II, a well-differentiated pancreatic cancer cell line as our model system, we show

85 e growth inhibition and apoptosis in a human pancreatic cancer cell line (AsPC-1).

86 BMP-2 stimulated the growth of two pancreatic cancer cell lines (ASPC-1 and CAPAN-1).

87 Using two human pancreatic cancer cell lines, AsPc-1 and Capan-2, we hav

88 that the drug inhibited 50% growth of seven pancreatic cancer cell lines at 10(-7) mol/L, whereas cl

89 The system was validated in three model pancreatic cancer cell lines before being applied to pri

90 and blocked proliferation in a subset of the pancreatic cancer cell lines both in vitro and in vivo.

91 (>5-fold) induced after 5Aza-dC treatment in pancreatic cancer cell lines but not in a nonneoplastic

92 n-1 nuclear factors in IL-13Ralpha2-positive pancreatic cancer cell lines but not in IL-13Ralpha2-neg

93 in human pancreatic adenocarcinoma and human pancreatic cancer cell lines but not in normal pancreati

94 ylated in pancreatic cancer are expressed in pancreatic cancer cell lines, but not in normal pancreat

95 ombinant immunotoxin) is highly cytotoxic to pancreatic cancer cell lines, but with limited activity

96 dney epithelial cell line Hs715.K; and human pancreatic cancer cell line Bx-PC3).

97 normal PZ-HPV-7 prostate cells) and for the pancreatic cancer cell line BxPC-3 (but not for normal S

98 ium conditioned by a highly metastatic human pancreatic cancer cell line BxPC-3 [BxPC-3 conditioned m

99 se in normal human pancreas and in the human pancreatic cancer cell lines BxPC-3, Capan-1, MIA PaCa-2

100 beit attenuated, responses are seen in other pancreatic cancer cell lines, BxPC-3 and AsPC-1.

101 Two pancreatic cancer cell lines, BxPC-3 and MIA PaCa-2 were

102 proximal Fanconi pathway was screened in 21 pancreatic cancer cell lines by an assay of Fancd2 monou

103 se CpGs were 100% hypomethylated in 11 of 12 pancreatic cancer cell lines by methylation-specific pol

104 induces the expression of TbetaRII in human pancreatic cancer cell lines by modulating the transcrip

105 sion of the PSCA mRNA transcript in 14 of 19 pancreatic cancer cell lines by reverse transcription-PC

106 , and one was the 6174delT mutation from the pancreatic cancer cell line CAPAN-1, for which normal ti

107 her constitutive or regulated manner, in the pancreatic cancer cell line Capan-1, which expresses onl

108 cond, cisplatin selection of a BRCA2-mutated pancreatic cancer cell line, Capan-1, led to five differ

109 We have found that different pancreatic cancer cell lines coexpress high-level TRAIL-

110 utations; one of which was identified in the pancreatic cancer cell line COLO357.

111 ifferentially methylated in a panel of eight pancreatic cancer cell lines compared with normal pancre

112 pendent validation experiment using five new pancreatic cancer cell lines confirmed that an inverse c

113 a2+/- mouse cells and Capan-1 cells, a human pancreatic cancer cell line deficient of BRCA2, were mor

114 Pancreatic cancer cell lines derived from these mice exp

115 ell viability and clonogenic survival in all pancreatic cancer cell lines examined, but not in nontum

116 l lines, MIA PaCa-2, a gemcitabine-resistant pancreatic cancer cell line, exhibited relatively restri

117 reverse transcription-PCR: only 1 (5%) of 19 pancreatic cancer cell lines expressed HIP/PAP-I transcr

118 Importantly, neither of the vaccinating pancreatic cancer cell lines expressed HLA-A2, A3, or A2

119 Pancreatic cancer cell lines expressed variable levels o

120 Here, we show that pancreatic cancer cell lines expressed various levels of

121 d during arachidonic acid (AA) metabolism in pancreatic cancer cell lines expressing COX-2 or 5-LOX.

122 o showed excellent cytotoxicity against four pancreatic cancer cell lines, expressing three to four m

123 In a panel of pancreatic cancer cell lines, expression of total and ac

124 Pancreatic cancer cell lines frequently coexpressed all

125 we compared the gene expression patterns of pancreatic cancer cell lines growing in tissue culture w

126 In pancreatic cancer cell lines, Hh inhibition with cyclopa

127 The dissection of differential response of pancreatic cancer cell lines holds promise for future th

128 The pancreatic cancer cell lines Hs766T and PL11 were defect

129 A pancreatic cancer cell line (Hs766T) that exhibited a "n

130 We used two pancreatic cancer cell lines, IL-13Ralpha2-negative HPAF

131 over 50% when tested against a panel of four pancreatic cancer cell lines in vitro.

132 d equivalent activity to gemcitabine against pancreatic cancer cell lines in vitro.

133 Adrenomedullin was up-regulated in pancreatic cancer cell lines, in which supernatants redu

134 GN193198 produces similar responses in other pancreatic cancer cell lines including AsPC-1 and MIA Pa

135 Our treatment of the human pancreatic cancer cell line L3.6pl with the VEGFR-1 liga

136 protein response was investigated in a human pancreatic cancer cell line, L3.6pl.

137 tor receptor-1 (VEGFR-1) expression on human pancreatic cancer cell lines mediates cell migration and

138 In pancreatic cancer cell lines, methylation of ppENK, a ge

139 potent antitumor activity against the human pancreatic cancer cell line MIA PaCa-2 with growth inhib

140 rthermore, PARP-1 mutant overexpression in a pancreatic cancer cell line (MIA PaCa-2) increased sensi

141 The pancreatic cancer cell line, MIA PaCa-2 is not responsiv

142 , trypsinogen activation by caerulein in the pancreatic cancer cell line, MIA PaCa-2 without zymogen

143 itivity responses in a poorly differentiated pancreatic cancer cell line, MIA PaCa-2.

144 In contrast to gemcitabine-sensitive pancreatic cancer cell lines, MIA PaCa-2, a gemcitabine-

145 cted GSK-3beta inhibitors were tested in the pancreatic cancer cell lines MiaPaCa-2, BXPC-3, and HupT

146 ncer cell lines Calu-6 and SKLU-1; and human pancreatic cancer cell line MIAPaCa2) were more sensitiv

147 mparisons between pancreatic adenocarcinoma, pancreatic cancer cell lines, normal pancreas, and chron

148 BA145 induced robust autophagy in pancreatic cancer cell line PANC-1 and exhibited cell pr

149 As a proof-of-principle, the pancreatic cancer cell line Panc-1 was investigated for

150 was reported to be up-regulated in the human pancreatic cancer cell line PANC-1 when cells were stabl

151 Thus downregulation of GPC1 in the human pancreatic cancer cell line PANC-1, using antisense appr

152 STAT3 transcription factor at Tyr705 in the pancreatic cancer cell lines PANC-1 and MIAPaCa-2 as wel

153 Pancreatic cancer cell lines PANC-1, MIA PaCa-2, and BxP

154 stably integrated into the genome of a human pancreatic cancer cell line (PANC-1) that has wild-type

155 Aliquots of solubilized proteins from a pancreatic cancer cell line (Panc-1) were subjected to t

156 examined by methylation-specific PCR using a pancreatic cancer cell line (Panc-1).

157 -kappaB activation and cell proliferation in pancreatic cancer cell lines (Panc-1 and MiaPaCa-2).

158 tro targeting efficacy, tested against three pancreatic cancer cell lines (PANC-1, AsPC-1, and MIA Pa

159 ed signal transduction cascade in five human pancreatic cancer cell lines (Panc-1, MDAPanc-28, HS766T

160 the tumorigenicity of a nonmetastatic human pancreatic cancer cell line, PANC-1, in an orthotopic nu

161 Cells of a pancreatic cancer cell line, Panc-1, up-regulate MMP act

162 salivary biomarkers by implanting the mouse pancreatic cancer cell line Panc02 into the pancreas of

163 mice xenografted with A431, HuCCT1, and the pancreatic cancer cell line Panc430, maximal growth arre

164 50% in Colo357 cells but also in a different pancreatic cancer cell line, Panc89.

165 cumin inhibited the proliferation of various pancreatic cancer cell lines, potentiated the apoptosis

166 eal was conducted in a cohort of low-passage pancreatic cancer cell lines, primary patient-derived xe

167 Pancreatic cancer cell lines (PsPC-1 and BXPC-3) and a n

168 or pathways restored ciliogenesis in a mouse pancreatic cancer cell line, raising the possibility tha

169 e-expression of SMARCA4 in SMARCA4-deficient pancreatic cancer cell lines reduced cell growth and pro

170 and Bcl-2 are predominantly overexpressed in pancreatic cancer cell lines, respectively.

171 wever, transfection of Smad4 into the BxPC-3 pancreatic cancer cell line restored TGFbeta responsiven

172 RNAi-mediated depletion of PR55alpha in pancreatic cancer cell lines resulted in diminished phos

173 constructs that were overexpressed in human pancreatic cancer cell lines S2-013 and Panc-1.

174 used to analyze gene expression profiles of pancreatic cancer cell lines, short-term cultures of nor

175 Over 70% of the human pancreatic cancer cell lines studied in vitro secreted c

176 ine pancreatic cancer model, using the human pancreatic cancer cell line, Suit-2.

177 nstrated that NQO(1) was up-regulated in the pancreatic cancer cell lines tested but present in very

178 ion revealed expression of 5-LOX mRNA in all pancreatic cancer cell lines tested including, PANC-1, A

179 ited sub-micromolar IC(50) values in all the pancreatic cancer cell lines tested using MTT and colony

180 cement of cell kill in a panel of breast and pancreatic cancer cell lines that are insensitive to the

181 was investigated using isogenically matched pancreatic cancer cell lines that differed only in expre

182 of multiple members of erbB family in three pancreatic cancer cell lines that express varying levels

183 In pancreatic cancer cell lines that retained methylation o

184 In Ras mutant pancreatic cancer cell lines, the phosphorylation and di

185 ility, we analyzed the proteomes of 10 human pancreatic cancer cell lines to a depth of >8,700 quanti

186 In our study, more than 80% of the human pancreatic cancer cell lines used exhibited constitutive

187 stance, we generated a gemcitabine-resistant pancreatic cancer cell line using stepwise selection and

188 icing of the CCK-B receptor mini-gene in the pancreatic cancer cell line was reversed by transfection

189 The expression of 5-LOX protein in pancreatic cancer cell lines was demonstrated by Western

190 TGFbeta on the BxPC-3, MiaPaCa-2, and PANC-1 pancreatic cancer cell lines was evaluated by [3H]thymid

191 t, the clonogenic ability of Panc1 and AsPc1 pancreatic cancer cell lines was reduced 8- to 12-fold b

192 A panel of 39 pancreatic cancer cell lines was tested for Wnt dependen

193 Using mouse models and human pancreatic cancer cell lines, we investigated whether pr

194 schistosome parasitic flatworm larvae and a pancreatic cancer cell line were deconvoluted in a subtr

195 Pancreatic cancer cell lines were genetically manipulate

196 ivation of specific signaling pathways, four pancreatic cancer cell lines were infected with an adeno

197 When breast and pancreatic cancer cell lines were treated with imetelsta

198 Mirk was an active kinase in each pancreatic cancer cell line where it was detected.

199 recently shown to be absent after hypoxia in pancreatic cancer cell lines whereas its overexpression

200 nging from >0.1 to 13 ng/mL] to six of eight pancreatic cancer cell lines, whereas no cytotoxicity (I

201 resistant (PIR) clones from the human CAPAN1 pancreatic cancer cell line, which carries the protein-t

202 mutant p53(R273H/P309S), and the MIA PaCa-2 pancreatic cancer cell line, which contains mutant p53(R

203 We have identified two categories of pancreatic cancer cell lines, which are either sensitive

204 Treatment of two pancreatic cancer cell lines, which express glypican-1,

205 extensive growth stimulation in six of seven pancreatic cancer cell lines, which was completely inhib

206 cted our studies using paired isogenic human pancreatic cancer cell line with differences in metastat

207 Treatment of BNIP3-negative pancreatic cancer cell lines with a DNA methylation inhi

208 , flow cytometry analysis was performed in 3 pancreatic cancer cell lines with different expression l

209 metry assays in BXPC-3 and PANC-1 cells, two pancreatic cancer cell lines with high and low TF expres

210 otein and messenger RNA were up-regulated in pancreatic cancer cell lines with high metastatic potent

211 bited the growth of human breast, colon, and pancreatic cancer cell lines with micromolar potency.

212 ession observed after treatment of different pancreatic cancer cell lines with the methylase inhibito

213 a-T3 inhibited the in vitro proliferation of pancreatic cancer cell lines with variable p53 status an

214 e 10-fold more potent against the MIA PaCa-2 pancreatic cancer cell line, with IC50 values of ~10 nM.