ライフサイエンスコーパス: pancreatic tumor

1 d assessment of subclonal variation within a pancreatic tumor.

2 ed tumor initiating cell (TIC) population in pancreatic tumor.

3 the maintenance of amino acid levels within pancreatic tumors.

4 efficiently enhance chemotherapy delivery to pancreatic tumors.

5 ells could be efficacious for the therapy of pancreatic tumors.

6 sphorylated KRAS in a panel of primary human pancreatic tumors.

7 ceptor subtype 2 (SSTR2) upregulated in some pancreatic tumors.

8 dentification of strategies to target CIN in pancreatic tumors.

9 e blood of mice engrafted with primary human pancreatic tumors.

10 his specific Vav is ectopically expressed in pancreatic tumors.

11 entified in various tumors, including cystic pancreatic tumors.

12 he number of tumor-initiating cells (TIC) in pancreatic tumors.

13 very of MUC4 antibodies to mucin4-expressing pancreatic tumors.

14 gene is mutated to an oncogenic form in most pancreatic tumors.

15 se have not been compared with pre-malignant pancreatic tumors.

16 en limits the growth of lung tumors, but not pancreatic tumors.

17 n2 is upregulated in 60% of human metastatic pancreatic tumors.

18 tions have been identified in resected human pancreatic tumors.

19 y led to the development of undifferentiated pancreatic tumors.

20 ghts into designing novel therapies to treat pancreatic tumors.

21 he HGF-dependent growth of lung, breast, and pancreatic tumors.

22 cytidine, GEM) which is used in treatment of pancreatic tumors.

23 ity of TR3 inhibitors to block the growth of pancreatic tumors.

24 survival, angiogenesis, and highly invasive pancreatic tumors.

25 s recruitment of macrophages into orthotopic pancreatic tumors.

26 resent in the microenvironment of orthotopic pancreatic tumors.

27 uced macrophage infiltration into orthotopic pancreatic tumors.

28 tivated form of KRAS and develop spontaneous pancreatic tumors.

29 tic devices that are implanted directly onto pancreatic tumors.

30 c driving force for Brca2-deficiency-induced pancreatic tumors.

31 , as well as reduced phospho-Smad2 levels in pancreatic tumors.

32 oplasms (IPMNs) are the most frequent cystic pancreatic tumors.

33 atures of infiltrating immune cells in human pancreatic tumors.

34 ributes to the supply of free amino acids in pancreatic tumors.

35 tent antimetastatic agents for Vav1-positive pancreatic tumors.

36 ere used to build a tissue microarray of 161 pancreatic tumors (113 resections and 48 biopsies).

37 own about the role and regulation of hdm2 in pancreatic tumors, a large proportion (50-75%) of which

38 and/or pmTOR-positive human PDACs and mouse pancreatic tumors also shared some histopathological sim

39 Inhibition of PKCiota expression in pancreatic tumors also significantly reduces tumor angio

40 s found to be expressed extensively in human pancreatic tumor and stromal cells.

41 T cells and myeloid suppressor cells in the pancreatic tumor and tumor draining lymph nodes.

42 ssociated with the differentiation status in pancreatic tumors and cell lines.

43 echniques to paired-end sequencing data from pancreatic tumors and confirm a previous finding of BFB

44 ed a mouse model of Brca2-deficiency-induced pancreatic tumors and found that excessive reactive nitr

45 hip between Tif1gamma and Smad4 signaling in pancreatic tumors and found that Pdx1-Cre; LSL-Kras(G12D

46 brosis in the aggressiveness of SMAD4 mutant pancreatic tumors and highlight STAT3 and mechanics as k

47 of genetically engineered Kras-driven mouse pancreatic tumors and human pancreatic cancer cells to i

48 a complete growth inhibition of AsPC1 human pancreatic tumors and improved survival of SCID beige mi

49 carcinoma (PDA) accounts for the majority of pancreatic tumors and is among the leading causes of can

50 the normal pancreas, is highly expressed in pancreatic tumors and is sufficient to induce neoplastic

51 trix metalloproteinases 1 (TIMP1) in primary pancreatic tumors and metastases using both in vitro tec

52 tein, is expressed at high levels in CAFs of pancreatic tumors and other solid tumors, and also in an

53 hat gamma-T3 can inhibit the growth of human pancreatic tumors and sensitize them to gemcitabine by s

54 ptor (VDR) is expressed in stroma from human pancreatic tumors and that treatment with the VDR ligand

55 extrusion, cell death, and reduce orthotopic pancreatic tumors and their metastases.

56 the activating KRAS mutations that occur in pancreatic tumors and their putative precursors, pancrea

57 was to test if Dyn2 is upregulated in human pancreatic tumors and to define its role in cell migrati

58 , hCNT1 expression was frequently reduced in pancreatic tumors and tumor cell lines.

59 nes in genomic DNA from 38 breast tumors, 48 pancreatic tumors, and 10 non-BRCA1/BRCA2 hereditary bre

60 sitions was studied in mice bearing IP human pancreatic tumors, and compared to that of the intraveno

61 omography for detection of smaller than 3-cm pancreatic tumors, and for T staging, while they are equ

62 multiple tumor types, including over 80% of pancreatic tumors, and increased levels of Lsm1 protein

63 pression is markedly down-regulated in human pancreatic tumors, and Pdx1-driven Tif1gamma inactivatio

64 Pancreatic tumors are renowned for their extremely hypox

65 proteins, which are abundant in desmoplastic pancreatic tumor, are as potent as growth factors in inh

66 Pancreatic tumors arise in an appropriate MUC1-tolerant

67 review intends to describe recent studies on pancreatic tumor-associated stroma and potential opportu

68 hat the presence of a solid area in a cystic pancreatic tumor at cross-sectional imaging should raise

69 ta-catenin results in the formation of large pancreatic tumors at a high frequency in adult mice.

70 loaded PEG-PDLA micelles or nanoemulsions to pancreatic tumor bearing mice resulted in complete tumor

71 evelopment of drug resistance was studied in pancreatic tumor bearing mice.

72 SiGdNP were tested in cynomolgus monkeys and pancreatic tumor-bearing mice models, respectively.

73 Saliva exosomes from pancreatic tumor-bearing mice modulate NK cell phenotype

74 ing, and histology studies were performed on pancreatic tumor-bearing mice to evaluate the ability an

75 Pancreatic tumor-bearing mice with luciferase-transduced

76 MCs and tumors of everolimus-treated CA20948 pancreatic tumor-bearing rats.

77 Pretreatment K(trans) measurement in pancreatic tumors can predict response to antiangiogenic

78 aberrant Ras signaling promotes uncontrolled pancreatic tumor cell growth remains to be fully elucida

79 , RalGAP suppression caused mTORC1-dependent pancreatic tumor cell invasion.

80 the radioligands were characterized with the pancreatic tumor cell line AR42J in vitro, including ass

81 Orthotopic implantation of a pancreatic tumor cell line expressing SHH (Capan-2) and

82 ate that the surface binding of TM601 to the pancreatic tumor cell line Panc-1 is dependent on the ex

83 ancer cells and a low-passage cultured human pancreatic tumor cell line using clonogenic and DNA dama

84 were isolated from mouse tissues and primary pancreatic tumor cell lines and analyzed by reverse-tran

85 nfirming the significant differences between pancreatic tumor cell lines and small intestinal cell li

86 ern blot and immunohistochemical analyses in pancreatic tumor cell lines and tumor tissues compared w

87 First, pharmacotherapeutic studies using pancreatic tumor cell lines as models for small intestin

88 Using human pancreatic tumor cell lines BxPC3 and Capan-1, which exp

89 factor (TF) expression in 4 different human pancreatic tumor cell lines for the purpose of producing

90 ing RNA-mediated down-regulation of SRPK1 in pancreatic tumor cell lines resulted in a dose-dependent

91 In pancreatic tumor cell lines stably transfected with the

92 w CTGF influences tumor growth, we generated pancreatic tumor cell lines that overexpress different l

93 utical 64Cu-CB-TE2A-sst2-ANT using AR42J rat pancreatic tumor cell membranes.

94 in vitro binding affinity assay to AR42J rat pancreatic tumor cell membranes.

95 system resulted in significant inhibition of pancreatic tumor cell proliferation in vitro and orthoto

96 We used a Panc02 pancreatic tumor cell transplant model in diet-induced o

97 On the other hand, pancreatic tumor cell-derived sonic hedgehog (SHH) acts

98 ough different imaging studies in a panel of pancreatic tumor cells (HPAC, BxPC-3, and Panc-1) both i

99 -3beta positively affected p53 expression in pancreatic tumor cells after mAb16D10 binding.

100 om patients with PDAC tumor infiltrates lyse pancreatic tumor cells after selective stimulation with

101 vo, siG12D LODER impeded the growth of human pancreatic tumor cells and prolonged mouse survival.

102 Our data demonstrate that pancreatic tumor cells are susceptible to sorafenib + HD

103 a potent regulator of matrix degradation by pancreatic tumor cells as depletion of Vav1 by siRNA-med

104 ly enhanced the tumor-initiating capacity of pancreatic tumor cells by activating the transcription f

105 Pancreatic tumor cells derived from CCN2 shRNA-expressin

106 When human head and neck or pancreatic tumor cells ectopically expressing mir-210 we

107 -1alpha) after chemical stimulation of human pancreatic tumor cells encapsulated in 3D alginate spots

108 10 inhibited the proliferation of only human pancreatic tumor cells expressing 16D10 plasma membrane

109 In pancreatic tumor cells expressing mutant active K-RAS, P

110 STAT3 was phosphorylated constitutively in pancreatic tumor cells from KC mice with loss or mutatio

111 s a demonstration of the technology's value, pancreatic tumor cells from Panc-1 cell lines and patien

112 The lethality of sorafenib was enhanced in pancreatic tumor cells in a synergistic fashion by pharm

113 Src on incidence, growth, and metastasis of pancreatic tumor cells in an orthotopic model.

114 ssion and secretion was increased in hypoxic pancreatic tumor cells in vitro, and we observed colocal

115 mulated the growth of Kras(G12D)/Tp53(R172H) pancreatic tumor cells in vivo and in vitro.

116 how that glutamine metabolization by hypoxic pancreatic tumor cells is necessary for their survival.

117 s directed at aberrant signaling pathways in pancreatic tumor cells may improve the poor outcome of p

118 RNA interference knockdown of DRD2 in pancreatic tumor cells reduced growth of xenograft tumor

119 Pan02 murine pancreatic tumor cells that secrete TGF-beta were transd

120 that azathioprine could also inhibit Vav1 in pancreatic tumor cells to reduce its proinvasive functio

121 Src expression in L3.6pl human pancreatic tumor cells was reduced by stable expression

122 ed, we have found that treatment of cultured pancreatic tumor cells with azathioprine inhibited Vav1-

123 ithelial mesenchymal transition, invasion of pancreatic tumor cells, and regulation of tumor growth i

124 lony-stimulating factor-secreting allogeneic pancreatic tumor cells, induces T-cell immunity to cance

125 demonstrate that shRNA silencing of LDLR, in pancreatic tumor cells, profoundly reduces uptake of cho

126 ession alters metastatic properties of human pancreatic tumor cells, stable clones of BxPC-3 cells ov

127 bits proliferation, and induces apoptosis in pancreatic tumor cells.

128 ajor driver of invasive matrix remodeling by pancreatic tumor cells.

129 ted the rapid growth and metastasis of human pancreatic tumor cells.

130 ta T cells and Her2/neu (ERBB2) expressed by pancreatic tumor cells.

131 llular signaling pathways obtained using rat pancreatic tumor cells.

132 e liver that increases its susceptibility to pancreatic tumor cells.

133 ed signaling has proproliferative effects on pancreatic tumor cells.

134 e low-density lipoprotein receptor (LDLR) in pancreatic tumor cells.

135 ed in animals injected with S100A4-deficient pancreatic tumor cells.

136 d in significantly higher numbers in primary pancreatic tumors compared to blood samples from patient

137 show that HOTAIR expression is increased in pancreatic tumors compared with non-tumor tissue and is

138 TR3 was overexpressed in human pancreatic tumors compared with nontumor tissue.

139 nes with high metastatic potential and human pancreatic tumors compared with normal pancreatic tissue

140 ose of MET mRNA, in patients with metastatic pancreatic tumors, compared with nonmetastatic tumors; t

141 s), the most abundant cells in the stroma of pancreatic tumors, contribute to the tumor's invasion, m

142 Here, we examine the hypothesis that pancreatic tumor-derived exosomes are mechanistically in

143 hat we have recently learned about CTCs from pancreatic tumors, describing advances in their isolatio

144 ary, we identified MYB as novel regulator of pancreatic tumor desmoplasia, which is suggestive of its

145 o cooperates with activated K-Ras to promote pancreatic tumor development.

146 For the pancreatic tumors, ELP brachytherapy (n=6) induced signi

147 ndicate that hornerin is highly expressed in pancreatic tumor endothelium and alters tumor vessel par

148 0 fused-type protein, is highly expressed on pancreatic tumor endothelium in a vascular endothelial g

149 In pancreatic tumors established in NOD SCID mice, c-Met in

150 Pancreatic tumors exhibit enhanced autophagy as compared

151 termined whether different zones of the same pancreatic tumor exhibited differential expression of ge

152 We also describe relationships between the pancreatic tumor extracellular matrix, the vasculature,

153 To induce formation of pancreatic tumor foci, we electroporated oncogenic plasm

154 ligand targeted MSNs preferentially bind to pancreatic tumors for payload delivery.

155 ormed on a tissue microarray of 229 resected pancreatic tumors from RTOG9704 and scored as having no

156 gated the hypothesis that SHH, secreted from pancreatic tumors, functions in a paracrine manner to in

157 the Her2/Vgamma9 antibody reduced growth of pancreatic tumors grafted into SCID-Beige immunocompromi

158 ll patients had a borderline or unresectable pancreatic tumor (group 1) or oligometastatic disease (d

159 lox/lox);GPC1(-/-) mice exhibited attenuated pancreatic tumor growth and invasiveness, decreased canc

160 esults suggest that deguelin suppresses both pancreatic tumor growth and metastasis by inducing apopt

161 esults suggest that deguelin suppresses both pancreatic tumor growth and metastasis by inducing apopt

162 etformin and rapamycin significantly reduced pancreatic tumor growth and mTOR-related signaling.

163 erstanding of the mechanisms responsible for pancreatic tumor growth and progression, and also indica

164 tudies established that penfluridol inhibits pancreatic tumor growth by autophagy-mediated apoptosis.

165 ng gammadelta T cell receptors (TCR) promote pancreatic tumor growth by inhibiting activation of T ce

166 ug delivery system to inhibit advanced stage pancreatic tumor growth in an orthotopic mouse model.

167 ed proliferation of cancer cells and de novo pancreatic tumor growth in mice.

168 hat metformin and rapamycin can both inhibit pancreatic tumor growth in obese, prediabetic mice throu

169 enhance AIG in vitro was linked to enhanced pancreatic tumor growth in vivo when these cells were im

170 cer, PARI silencing was sufficient to reduce pancreatic tumor growth in vivo.

171 r cell proliferation in vitro and orthotopic pancreatic tumor growth in vivo.

172 athepsins B and S are critical for promoting pancreatic tumor growth, angiogenesis, and invasion in v

173 ur77 (NR4A1) promotes apoptosis and inhibits pancreatic tumor growth, but its endogenous function and

174 g3beta deletion in mice drastically impaired pancreatic tumor growth, correlating with decreased angi

175 pharmacological inhibition of ILK suppressed pancreatic tumor growth, in part, by suppressing KRAS si

176 mise for therapeutic intervention to inhibit pancreatic tumor growth.

177 ptosis by SHP activation inhibits peritoneal pancreatic tumor growth.

178 hat tumor cell-derived CCN2 is important for pancreatic tumor growth.

179 ion of IKBKE and mTOR synergistically blocks pancreatic tumor growth.

180 from tumor cells is a critical regulator of pancreatic tumor growth.

181 m radiation treated invasive and preinvasive pancreatic tumors had an immune-suppressive, M2-like phe

182 tulate the functional heterogeneity of human pancreatic tumors harboring distinct cells with tumorige

183 xpressed mucins that impede drug delivery to pancreatic tumors have been therapeutically targeted, bu

184 ortantly, ATM deficiency also renders murine pancreatic tumors highly sensitive to radiation.

185 Here we studied its effect on pancreatic tumor histopathology and associated molecular

186 so observed a role for CCN2 in the growth of pancreatic tumors implanted orthotopically, with tumor v

187 tivity against xenografts of human colon and pancreatic tumors in athymic mice.

188 but not Pik3cb, prevented the development of pancreatic tumors in Kras(G12D/+);Ptf1a(Cre/+) mice.

189 emcitabine administration after resection of pancreatic tumors in mice activates NK cell-mediated ant

190 It is required for growth and metastasis of pancreatic tumors in mice and is a therapeutic target fo

191 Increased expression promotes growth of pancreatic tumors in mice and is associated with reduced

192 E inhibits the initiation and progression of pancreatic tumors in mice carrying pancreatic-specific K

193 It causes liver, testicular, and pancreatic tumors in rats.

194 orinostat treatment suppressed the growth of pancreatic tumors in vivo.

195 expression is decreased, in S100A4-deficient pancreatic tumors in vivo.

196 efficacious in treating colon, gastric, and pancreatic tumors in xenograft models in vivo.

197 Studies of patients with pancreatic tumors incidentally diagnosed demonstrate lon

198 o individuals (0.9%) in the FPC cohort had a pancreatic tumor, including one advanced PDAC and one ea

199 Pancreatic tumor initiation and progression were analyze

200 The role of GLI1 in pancreatic tumor initiation promoting the progression of

201 l compartment surrounding epithelial-derived pancreatic tumors is thought to have a key role in the a

202 or stromal cells as it affects the growth of pancreatic tumors is unknown.

203 biodistribution in vivo to detect orthotopic pancreatic tumor lesions through active targeting of the

204 ies and tumor progression of PANC-1, a human pancreatic tumor line.

205 tation group G- (FANCG-) and FANCC-deficient pancreatic tumor lines were more sensitive to the ATM in

206 iated Stat1 binding to the Duox2 promoter in pancreatic tumor lines.

207 pically implanted, luciferase-positive human pancreatic tumors (MIA PaCa-2) were subsequently (4-5 we

208 Transgenic mice with resectable pancreatic tumors might be promising tools to study adju

209 The observed alterations suggest that pancreatic tumors might originate from the newly discove

210 human pancreatic adenocarcinoma and a murine pancreatic tumor model (Pan02), that tumor cells produce

211 to image CEACAM6 expression in a xenografted pancreatic tumor model.

212 tic resonance imaging (DWI) in an orthotopic pancreatic tumor model.

213 luc-C6 prostate tumor and a human BxPc3-luc2 pancreatic tumor model.

214 NOTA-FVIIai was investigated in subcutaneous pancreatic tumor models with different levels of TF expr

215 tabine and ionizing radiation in preclinical pancreatic tumor models.

216 nguishing the TF expression level of various pancreatic tumor models.

217 In a pancreatic tumor mouse model, MDB5 containing nanopartic

218 uptake were characterized in a subcutaneous pancreatic tumor mouse model.

219 small duodenal tumor; less frequently had a pancreatic tumor, multiple tumors, or developed a new le

220 ydroxy guanosine (8-OHG) and MUC4 in primary pancreatic tumors (n=25).

221 oncogenic plasmids, mice developed a single pancreatic tumor nodule with histopathologic features of

222 only CD4(+) T cells infiltrated spontaneous pancreatic tumors (not CD8(+) T cells).

223 In pancreatic tumors of mice, loss of P53 function activate

224 s without conferring a specific phenotype to pancreatic tumors or changing the status of the tumor su

225 ved more frequently in breast tumors than in pancreatic tumors or normal controls failed to detect a

226 We re-evaluated all resections due to a pancreatic tumor over a period of 15 years.

227 EGFR2 expression was significantly higher in pancreatic tumors (P < .001; mean fluorescent intensity,

228 -driven breast cancer model and in syngeneic pancreatic tumor (Pan02) xenografts.

229 s study supports the clinical use of DWI for pancreatic tumor patients for early assessment of drug e

230 wide search for target genes associated with pancreatic tumor progression and demonstrated that PLAC8

231 neoangiogenesis and lymphangiogenesis during pancreatic tumor progression and metastasis.

232 novel pathway regulated by GLI1 controlling pancreatic tumor progression and provide a new theoretic

233 he potential role of p53 loss of function in pancreatic tumor progression, demonstrate the feasibilit

234 cted PDAC and it plays an inhibitory role in pancreatic tumor progression.

235 lated gene that is thought to play a role in pancreatic tumor progression.

236 of human pancreatic stellate cells (HPSC) on pancreatic tumor progression.

237 ld be a novel approach for the inhibition of pancreatic tumor progression.

238 at mAb16D10 holds great potential to prevent pancreatic tumor proliferation by apoptotic cell death,

239 tus can predict the metastatic propensity of pancreatic tumors, providing valuable guidance for perso

240 To induce localized inertial cavitation in pancreatic tumors, pulsed high-intensity focused ultraso

241 les, which resulted in significantly greater pancreatic tumor reduction than either treatment alone.

242 mechanisms that regulate this activation in pancreatic tumors remain elusive.

243 gp130 were expressed, in mice that developed pancreatic tumors resulting from expression of activated

244 ctional TCR-I T cells intensively infiltrate pancreatic tumors, resulting in increased survival of RI

245 asured protein levels in HCC, colorectal and pancreatic tumor samples from patients.

246 Pancreatic tumor samples have increased levels of nuclea

247 d IVS14+1G>A) were also detected in separate pancreatic tumor samples.

248 o, MSN-UPA particles demonstrated orthotopic pancreatic tumor specific accumulation compared to liver

249 We obtained frozen pancreatic tumor specimens from patients and measured le

250 dly overexpressed in both PDA cell lines and pancreatic tumor specimens, and the expression of Met co

251 In human pancreatic tumors, STAT3 phosphorylation correlated with

252 ently developed approaches for reshaping the pancreatic tumor stroma and discuss how these might impr

253 activation of STAT3 and modification of the pancreatic tumor stroma in patients and mice.

254 pancreatic stellate cells, which produce the pancreatic tumor stroma.

255 , breast, urinary bladder, kidney, lung, and pancreatic tumors studied.

256 n vivo model was the metastatic human Hs766T pancreatic tumor that, upon IP injection, produced widel

257 Pancreatic tumors that expressed myrAkt2 infiltrated the

258 ell as the use of this approach to visualize pancreatic tumor tissue in vivo as early as 1 h postinje

259 we found increased CCN2 staining in clinical pancreatic tumor tissue relative to stromal cells surrou

260 Increased expression of KLF4alpha in pancreatic tumor tissue was inversely correlated with ov

261 rthotopic transplantation of patient-derived pancreatic tumor tissue, BPTES nanoparticle monotherapy

262 in clinical specimens such as colorectal and pancreatic tumor tissues as well as in premalignant panc

263 at mAb16D10 specifically discriminates human pancreatic tumor tissues from other cancer and nontumor

264 Human primary and metastatic pancreatic tumor tissues stained strongly for cancer cel

265 Higher levels of CD44v6 mRNA in human pancreatic tumor tissues were associated with increased

266 C4, alpha7nAChR and pSTAT3 expression in the pancreatic tumor tissues.

267 aggressive pancreatic cancer cells and human pancreatic tumor tissues.

268 ysis of the mathematical model indicates the pancreatic tumors to be mostly resistant to Gemcitabine

269 the anti-CEA CAR T cells reduced the size of pancreatic tumors to below the limit of detection in all

270 ppaB, resulting in the chemosensitization of pancreatic tumors to conventional therapeutics.

271 ppaB, resulting in the chemosensitization of pancreatic tumors to conventional therapeutics.

272 To understand the resistance of pancreatic tumors to Fas death receptor-induced apoptosi

273 1-MMP could be a novel approach to sensitize pancreatic tumors to gemcitabine.

274 and pharmacologic blockade of IGF sensitized pancreatic tumors to gemcitabine.

275 women; mean age, 64 years) with 23 solitary pancreatic tumors underwent dual-energy CT.

276 s receptor CD63 in metastasis of early-stage pancreatic tumors using mice and human cell lines and ti

277 ression clones were performed and effects on pancreatic tumor volumes and hepatic and pulmonary metas

278 The growth of mouse pancreatic tumors was inhibited by genetic ablation of t

279 In addition, imaging of orthotopic pancreatic tumors was performed using (64)Cu-NOTA-FVIIai

280 lung, breast, stomach, prostate, colon, and pancreatic tumors, we identified a solid cancer miRNA si

281 ence of p53 mutations in PanIN 3 lesions and pancreatic tumors, we interrogated the comparative abili

282 studies showed a marked increase in the mean pancreatic tumor weight (low dose (100 mg/m(3) total sus

283 ng, elevated levels of HIF-1alpha and SHH in pancreatic tumors were determined to be markers of decre

284 Salivary exosomes from mice with PDAC where pancreatic tumors were engineered to suppress exosome bi

285 Mice with pancreatic tumors were given gemcitabine and a Janus kin

286 r, the data indicate that pHIFU treatment of pancreatic tumors when resulting in high and sustained c

287 GOT2 K159 acetylation is increased in human pancreatic tumors, which correlates with reduced SIRT3 e

288 activity through 60 days in the prostate and pancreatic tumors with no appreciable radioactive accumu

289 In vivo investigations of pancreatic tumors with restored SLIT2 expression demonst

290 man pancreatic cancer, 2/79 (2.5%) developed pancreatic tumors, with both tumors arising in fish inje

291 lequinones was also tested in the MIA PaCa-2 pancreatic tumor xenograft in nude mice, and lead indole

292 Studies were conducted in rat AR42J pancreatic tumor xenograft mice to determine whether (18

293 scence signal was present in TLR2 expressing pancreatic tumor xenografts 24 h after injection of 13,

294 served colocalization of CCN2 and hypoxia in pancreatic tumor xenografts and clinical pancreatic aden

295 over, cucurbitacin B decreased the volume of pancreatic tumor xenografts in athymic nude mice by 69.2

296 SQ-Dox nanoassembly-treated MiaPaCa-2 pancreatic tumor xenografts in mice decreased by 95% com

297 overexpressing cFLIP and (b) growth of human pancreatic tumor xenografts in vivo.

298 Treatment of pancreatic tumor xenografts with MIT and TA produced dos

299 with established heterotopic and orthotopic pancreatic tumor xenografts, pharmacologic ascorbate com

300 tumor suppressor in KRAS(MUT) colorectal and pancreatic tumor xenografts.