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 y but combines with oncogenic Ras to produce pancreatic tumors.

4 tions have been identified in resected human pancreatic tumors.

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

6 tivated form of KRAS and develop spontaneous pancreatic tumors.

7 lished in the index journals were related to pancreatic tumors.

8 tic devices that are implanted directly onto pancreatic tumors.

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

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

11 atures of infiltrating immune cells in human pancreatic tumors.

12 tent antimetastatic agents for Vav1-positive pancreatic tumors.

13 efficiently enhance chemotherapy delivery to pancreatic tumors.

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

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

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

17 dentification of strategies to target CIN in pancreatic tumors.

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

19 his specific Vav is ectopically expressed in pancreatic tumors.

20 entified in various tumors, including cystic pancreatic tumors.

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

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

23 tains CSCs and contributes to development of pancreatic tumors.

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

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

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

27 y led to the development of undifferentiated pancreatic tumors.

28 ghts into designing novel therapies to treat pancreatic tumors.

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

30 al signal to activated T cells) in mice with pancreatic tumors.

31 n was differentially regulated in metastatic pancreatic tumors.

32 tion and is upregulated in tumors, including pancreatic tumors.

33 regulator Yap in maintenance of Kras-mutant pancreatic tumors.

34 ession both in cultured cell lines and human pancreatic tumors.

35 n advanced, poorly differentiated p53-mutant pancreatic tumors.

36 mice did not develop precancerous lesions or pancreatic tumors.

37 the maintenance of amino acid levels within pancreatic tumors.

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

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

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

41 Pancreatic tumor 3D clusters recapitulated mutant KRAS d

42 We optimized the culture of pancreatic tumor 3D clusters that utilized Matrigel as a

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

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

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

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

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

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

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

50 We collected eleven pancreatic tumors and identified three shared and five p

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

52 ion of T-regulatory and exhausted T cells in pancreatic tumors and increases numbers of memory CD4+ a

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

54 is of KS expression was performed on primary pancreatic tumors and metastatic tissues.

55 We compared levels of messenger RNAs in pancreatic tumors and normal pancreas in The Cancer Geno

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

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

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

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

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

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

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

63 -);Rosa26(EYFP/+) (PKCY) mice, which develop pancreatic tumors, and PKCY mice with disruption of IL22

64 Pancreatic tumors appear to evade the immune response by

65 Pancreatic tumors are poorly vascularized and severely h

66 Pancreatic tumors are renowned for their extremely hypox

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

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

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

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

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

74 Treatment of orthotopic pancreatic tumor-bearing mice with gemcitabine alone or

75 Pancreatic tumor-bearing mice with luciferase-transduced

76 NPs at the dose of 20 mg/kg into orthotopic pancreatic tumor-bearing NSG mice every alternate day re

77 onents require complete understanding of the pancreatic tumor biology to better understand the therap

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

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

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

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

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

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

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

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

86 has shown that a GM-CSF-secreting allogenic pancreatic tumor cell vaccine (GVAX) may prime the tumor

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

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

89 -3beta positively affected p53 expression in pancreatic tumor cells after mAb16D10 binding.

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

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

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

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

94 10 inhibited the proliferation of only human pancreatic tumor cells expressing 16D10 plasma membrane

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

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

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

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

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

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

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

102 Pancreatic tumor cells release small extracellular vesic

103 We show that EVs derived from more invasive pancreatic tumor cells that express high levels of tumor

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

105 orm to identify novel therapeutics to target pancreatic tumor cells using PDOs.

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

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

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

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

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

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

112 ed signaling has proproliferative effects on pancreatic tumor cells.

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

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

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

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

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

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

119 ormation, matrix remodeling, and invasion by pancreatic tumor cells.

120 d with greater-than-additive cell killing of pancreatic tumor cells.

121 s both mutant K-RAS and YAP function to kill pancreatic tumor cells.

122 d infiltration of lymphocytes throughout the pancreatic tumor compared to untreated animals.

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

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

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

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

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

128 Adult patients with left-sided pancreatic tumors confined to the pancreas without vascu

129 In patients with left-sided pancreatic tumors confined to the pancreas, MIDP reduces

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

131 antitative RT-PCR studies of human colon and pancreatic tumors demonstrating significantly higher DUO

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

133 d in human pancreatic tumor specimens, human pancreatic tumor-derived organoids, and organoids derive

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

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

136 IL22 to be increased during pancreatitis and pancreatic tumor development and to be required for tumo

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

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

139 0 fused-type protein, is highly expressed on pancreatic tumor endothelium in a vascular endothelial g

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

141 Pancreatic tumors exhibit enhanced autophagy as compared

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

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

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

145 of the autophagy related 5 (Atg5) protein on pancreatic tumor formation and progression.

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

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

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

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

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

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

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

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

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

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

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

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

158 In murine orthotopic PDAC models, pancreatic tumor growth was delayed when iNOS inhibition

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

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

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

162 mise for therapeutic intervention to inhibit pancreatic tumor growth.

163 ptosis by SHP activation inhibits peritoneal pancreatic tumor growth.

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

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

166 We found that a pancreatic tumor has minimal to moderate infiltration of

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

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

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

170 e effects of ATM inhibition and radiation on pancreatic tumor immunogenicity.

171 Results were compared with pancreatic tumor implants (control group).

172 ze with gemcitabine to eradicate established pancreatic tumors in a syngeneic, Kras(G12D)-driven, PDA

173 Compared with pancreatic tumors in KPC/Cdh11(+/+) mice, tumors of KPC/

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

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

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

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

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

179 of interleukin (IL) 22 in the development of pancreatic tumors in mice.

180 PRLR signaling contributes to the growth of pancreatic tumors in mice.

181 ied the roles of HIF1A in the development of pancreatic tumors in mice.

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

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

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

185 Studies of patients with pancreatic tumors incidentally diagnosed demonstrate lon

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

187 lly recapitulate the epithelial component of pancreatic tumors, including previously described molecu

188 e pancreatic tumor stroma, reduces growth of pancreatic tumors, increases their response to gemcitabi

189 Pancreatic tumor initiation and progression were analyze

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

191 t loss of cell identity is rate limiting for pancreatic tumor initiation.

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

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

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

195 In patient pancreatic tumors, low ATM expression inversely correlat

196 ned by Yap, Myc, Sox2, and p53 that dictates pancreatic tumor metabolism, growth, survival, and diffe

197 bine leads to extensive reprogramming of the pancreatic tumor microenvironment and that patients who

198 CD1d(hi)CD5(+) B(reg) differentiation in the pancreatic tumor microenvironment.

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

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

201 ier and improve nanodrug delivery in a human pancreatic tumor model and it may also be applied to oth

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

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

204 to naked oAd/RLX or oAd/RLX-treated hMSC in pancreatic tumor model.

205 ion approaches to show that squamous-subtype pancreatic tumor models become enriched with neutrophils

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

207 ed tumor growth rates in vivo in established pancreatic tumor models, inducing regressions in one mod

208 t only induced regressions in colorectal and pancreatic tumor models, it also exhibited at least 5-fo

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

210 tabine and ionizing radiation in preclinical pancreatic tumor models.

211 In a pancreatic tumor mouse model, MDB5 containing nanopartic

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

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

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

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

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

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

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

219 and sequential drug screens on human-derived pancreatic tumor organoids.

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

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

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

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

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

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

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

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

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

229 A total of 70 KPC mice with autochthonous pancreatic tumors received oral FG-4592 or vehicle contr

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

231 otential radiologic and serologic markers of pancreatic tumor response to therapy, using pathologic m

232 cing of Pik3ca in KrasG12D/Trp53R172H-driven pancreatic tumors resulted in infiltration of T cells, c

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

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

235 Pancreatic tumor samples have increased levels of nuclea

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

237 t show that LINC00346 is highly expressed in pancreatic tumor specimens as compared to normal pancrea

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

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

240 F5A were increased and co-localized in human pancreatic tumor specimens, human pancreatic tumor-deriv

241 In human pancreatic tumors, STAT3 phosphorylation correlated with

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

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

244 of CDH11, which is expressed by CAFs in the pancreatic tumor stroma, reduces growth of pancreatic tu

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

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

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

248 emerged as an intriguing option for treating pancreatic tumors that are addicted to mutant KRAS, thus

249 Pancreatic tumors that expressed myrAkt2 infiltrated the

250 oth were overexpressed in brain, gastric and pancreatic tumors that implies MDFIC to also promote tum

251 In one pancreatic tumor, there were many more L1 insertions in

252 ng also showed distinct tumor specificity to pancreatic tumor tissue in relation to normal pancreatic

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

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

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

256 Levels of KDM3A were increased in human pancreatic tumor tissues and cell lines, compared with a

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

258 We analyzed pancreatic tumor tissues from mice and pancreatic cancer

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

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

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

262 Human pancreatic tumor tissues were implanted into interscapul

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

264 aggressive pancreatic cancer cells and human pancreatic tumor tissues.

265 Additionally, treatment with DON sensitized pancreatic tumors to anti-PD1 therapy, resulting in tumo

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

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

268 his pathway might help mediate resistance of pancreatic tumors to chemotherapeutic agents.

269 wn of PAF1 reduces the ability of orthotopic pancreatic tumors to develop and progress in mice and th

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

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

272 1-MMP could be a novel approach to sensitize pancreatic tumors to gemcitabine.

273 ese sEVs promote metastasis of xenograft and pancreatic tumors to lung in mice.

274 expression and increased the sensitivity of pancreatic tumors to PD-L1-blocking antibody in associat

275 Pancreatic tumors undergo rapid growth and progression,

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

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

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

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

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

281 multimodal intersection analysis to primary pancreatic tumors, we find that subpopulations of ductal

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

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

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

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

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

287 Nude mice with orthotopic pancreatic tumors were randomly assigned into 3 groups r

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

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

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

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

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

293 po pathway was deregulated in BAP1-deficient pancreatic tumors, with the tumor suppressor LATS exhibi

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

295 cantly inhibited tumor growth in the HPAF-II pancreatic tumor xenograft model.

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

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

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.