ライフサイエンスコーパス: tumor xenograft

1 nd a patient gastrointestinal adenocarcinoma tumor xenograft).

2 rformed in athymic nude mice bearing a BON-1 tumor xenograft.

3 mor cells from a lung adenocarcinoma patient tumor xenograft.

4 d photoactivated chemotherapy compounds in a tumor xenograft.

5 he regulation effects of ALKBH3 on growth of tumor xenograft.

6 colorectal cancer cells in vitro and in vivo tumor xenografts.

7 essor in KRAS(MUT) colorectal and pancreatic tumor xenografts.

8 sed cell migration and reduced the growth of tumor xenografts.

9 say to address the slowness of metastasis of tumor xenografts.

10 ed the transformed phenotype in vitro and in tumor xenografts.

11 ere performed in mice bearing B16F1 melanoma tumor xenografts.

12 nced attenuated their growth in vitro and in tumor xenografts.

13 (ER) alpha-positive breast cancer cells and tumor xenografts.

14 ancer (CRC) growth in cell culture and mouse tumor xenografts.

15 ion also significantly reduced the growth of tumor xenografts.

16 er in colonospheres, Aldefluor(+) cells, and tumor xenografts.

17 e size and neovascularization of CAG myeloma tumor xenografts.

18 ntly abrogated the growth of patient-derived tumor xenografts.

19 stigated in vivo by intravital microscopy of tumor xenografts.

20 PAI-1, and cyclin D1 in ccRCC cell lines and tumor xenografts.

21 creases cell viability and reduces growth of tumor xenografts.

22 ns and ACSS2 silencing reduced the growth of tumor xenografts.

23 ume data from MDA-MB-231-HRE-tdTomato breast tumor xenografts.

24 lar endothelial cells and human MCF-7 breast tumor xenografts.

25 quired for estrogen-dependent growth of MCF7 tumor xenografts.

26 vels dramatically reduced the growth of lung tumor xenografts.

27 or mono-drug components in cell line-derived tumor xenografts.

28 n and inhibited the growth and metastasis of tumor xenografts.

29 fbr2(flox/flox) (PKT) mice and in orthotopic tumor xenografts.

30 hibitor AZD1775 regresses H3K36me3-deficient tumor xenografts.

31 1-Foxn1(nu) mice bearing HER2-positive human tumor xenografts.

32 llular matrix nidogen-1 and laminin beta1 in tumor xenografts.

33 ponse in typically erlotinib-resistant NSCLC tumor xenografts.

34 revealing the kinetics of both processes in tumor xenografts.

35 intracranial human glioblastoma neurosphere tumor xenografts.

36 ation of the growth of spheroid cultures and tumor xenografts.

37 vels in both colorectal cancer cells and CRC tumor xenografts.

38 ucing the rate of tumor growth in s.c. mouse tumor xenografts.

39 cells both in culture and growing in vivo as tumor xenografts.

40 s to gemcitabine and delayed their growth in tumor xenografts.

41 of ovarian cancer cells to form spheroids or tumor xenografts.

42 ibution were performed on mice bearing AR42J tumor xenografts.

43 sses the growth in nude mice of human breast tumor xenografts.

44 n cell line models and suppressing growth in tumor xenografts.

45 kappaB enhanced the efficacy of docetaxel in tumor xenografts.

46 of tumor spheroids, mouse brain tissues, and tumor xenografts.

47 bits cancer cell growth both in vitro and in tumor xenografts.

48 us downregulation of these factors in animal tumor xenografts.

49 , and regional blood flow in the FME and LOX tumor xenografts.

50 metastasis of intravenous and intraprostatic tumor xenografts.

51 ditive reduction in the growth of MDA-MB-231 tumor xenografts.

52 k out tumors in nude mice bearing dual-flank tumor xenografts.

53 c cancer cells as well as impaired growth of tumor xenografts.

54 well as in HDM201-resistant patient-derived tumor xenografts.

55 from MCC cell xenografts and patient-derived tumor xenografts.

56 expression), or Calu-1 (no HER3 expression) tumor xenografts.

57 used regression of all treated A2780 ovarian tumor xenografts.

58 tumors retained abnormal SHH signaling like tumor xenografts.

59 SMA-positive CWR22Rv1 and PSMA-negative PC-3 tumor xenografts.

60 e for combinations tested in patient-derived tumor xenografts.

61 accumulation of (111)In-PA-L1 in MDA-MB-231 tumor xenografts (5.7 +/- 0.9 percentage injected dose [

62 er tumor spheroids (A549), and a lung cancer tumor xenograft (A549) in nude mice.

63 fectively inhibited the growth of human lung tumor xenografts (A549) harboring aberrantly active STAT

64 5.3-fold photoacoustic signal enhancement in tumor xenografts after systemic administration.

65 raction of tumors and wounds, we developed a tumor xenograft/allograft (human head and neck squamous

66 Anticancer efficacy studies in WiDr tumor xenograft and 4T1 tumor syngraft models demonstrat

67 nti-CD20) was studied in both bulky lymphoma tumor xenograft and MRD animal models.

68 e in multiple orthotopically implanted human tumor xenograft and syngeneic murine tumor models.

69 cancer activity against the KB-3-1 cell line tumor xenograft and the tumor size was smaller after the

70 99m)Tc, was injected into mice bearing CCK2R tumor xenografts and examined by gamma scintigraphy and

71 In vivo, depletion of GDF-15 in Ras-driven tumor xenografts and in an orthotopic model of pancreati

72 nally, single-cell characterization of human tumor xenografts and in vivo CRISPR screens identified e

73 n vivo were fast, with the highest uptake in tumor xenografts and kidneys (both PSMA-specific).

74 fically toxic to PTEN mutant cancer cells in tumor xenografts and reversible by reintroduction of wil

75 analysis of genetic heterogeneity of breast tumor xenografts and shows that changes in clonal divers

76 ments of firefly luciferase-expressing Hep3B tumor xenografts and the effects of the immune response

77 of KIT in cultured cells and in human colon tumor xenografts and this contributed to the clonogenic

78 4 significantly suppressed the growth of CCA tumor xenografts and tumor metastasis while displaying l

79 ous models, including mammalian cells, mouse tumor xenograft, and Drosophila larvae.

80 oyed to accelerate spontaneous metastasis in tumor xenografts, and the anti-metastatic activity of th

81 70.8 +/- 23.7 %ID/g, respectively) in LNCaP tumor xenografts, and this peak was sustained up to 120

82 We compare mitoses and CA in patient tumors, xenografts, and tumor cell lines.

83 ineation of subcutaneous and orthotopic SCLC tumor xenografts as well as distant organ metastases wit

84 Notably, in tumor xenograft assays in mice, we documented the abilit

85 Here, we use gene transduction and human tumor xenograft assays to establish that the tumour supp

86 eration in vitro and their growth in vivo in tumor xenograft assays.

87 PC-3 tumor-xenografted BALB/c nu/nu mice were injected with e

88 ng animals as well as in KB-3-1 and COLO-205 tumor xenograft-bearing nude mice.

89 In mice harboring P493 tumor xenografts, BPTES treatment inhibited tumor cell g

90 nd XIAP in multiple cancer cell lines and in tumor xenografts, but not in healthy cells.

91 in vivo potency of TRAIL in TRAIL-resistant tumor xenografts by (1) extending the half-life of the l

92 ol treatment suppressed the growth of BxPC-3 tumor xenografts by 48% as compared to 17% when treated

93 fic monoclonal antibodies to eliminate human tumor xenografts by enhancing macrophage-mediated antibo

94 Moreover, growth of tumor xenografts by Hpa2-overexpressing cells was unaffe

95 In vivo FES uptake was measured in tumor xenografts by using small-animal positron emission

96 and little effect in a sphere analogous to a tumor xenograft compared with (64)Cu in the Cy or on the

97 ered in three doses before PDT of H460 human tumor xenografts, compared with 16% after PDT-alone.

98 nced growth as tumorspheres and intracranial tumor xenografts, compared with mock-infected human GSCs

99 In support of these results, tumor xenografts composed of prostate adenocarcinoma cel

100 overexpressed in cells derived from prostate tumor xenografts, delta-catenin gene invariably gives ri

101 icacy studies in colorectal cancer cell WiDr tumor xenograft demonstrate that candidate compounds are

102 ) in three-dimensional spheroid cultures and tumor xenografts derived from colon cancer cells.

103 Tumor-xenografts derived from orthotopic-inoculation of

104 In mouse models of tumor xenografts, DHS was efficacious against pancreatic

105 knockdown of xCT strongly impaired growth of tumor xenografts established from KRAS-transformed cells

106 experimental results from orthotopic breast tumor xenograft experiments conducted in Nod/Scidgamma m

107 Moreover, tumor xenograft experiments demonstrated that even thoug

108 , along with in vivo fluorescence imaging of tumor xenografts expressing SoNar in mice.

109 onel and abiraterone inhibited the growth of tumor xenografts expressing the clinically relevant muta

110 Tumor xenografts expressing Y537S-ER (mean percentage in

111 SHMT1/2 knockout blocks HCT-116 colon cancer tumor xenograft formation.

112 ate carcinoma cells in a hydrogel or excised tumor xenografts from mice were placed into primary tumo

113 In tumor xenografts generated from carcinoma cells that wer

114 Notably, tumor xenografts generated from FGFR1-dependent lung can

115 hemosensitivity was confirmed in MC38 murine tumor xenografts generated from PD-L1-knockout vs. paren

116 bioluminescence imaging in a human prostate tumor xenograft growing in a rat.

117 In this paper, breast tumor xenografts grown from MDA-MB-231-HRE-tdTomato cell

118 ion during an oxygen challenge in H1299 lung tumor xenografts grown in a murine model as independentl

119 (18)F-FES uptake was measured in tumor xenografts grown in female athymic nude mice by sm

120 ls armed with anti-PSCA-DAP12 caused delayed tumor xenograft growth and resulted in complete tumor er

121 lls and inhibits mutant p53-associated colon tumor xenograft growth in a p73-dependent manner in vivo

122 n, colony formation, 3D spheroid growth, and tumor xenograft growth in mice.

123 Finally, C-B or C-I inhibited tumor xenograft growth in nude mice and decreased the ex

124 clonogenic capacity in vitro, and suppressed tumor xenograft growth in severe combined immunodeficien

125 and blocked cell proliferation in vitro and tumor xenograft growth in vivo Mechanistically, GON4L in

126 -Cas9 system to identify genes affecting the tumor xenograft growth of human mutant KRAS (KRAS(MUT))

127 Tumor xenograft growth was delayed but not suppressed in

128 d EGFR resulted in significant inhibition of tumor xenograft growth, further supporting the significa

129 ession and cell survival in vitro as well as tumor xenograft growth.

130 ent anti-leukemic activity in cell lines and tumor xenografts harboring NOTCH3 activating mutations.

131 g data acquired from eight orthotopic breast tumor xenografts (i.e. a tumor 'ensemble').

132 with mice bearing either U87MG or MDA-MB-435 tumor xenografts immediately before and after PDT at dif

133 Human macrophages infiltrated a human tumor xenograft in MITRG and MISTRG mice in a manner res

134 eover 7-[(18)F]FTrp accumulated in different tumor xenografts in a chick embryo CAM model.

135 n Dll4 inhibited the growth of several human tumor xenografts in association with the formation of no

136 SCC-47 and UM-SCC-22B, respectively) to grow tumor xenografts in athymic nude mice and demonstrated t

137 ts in vitro and in vivo on PSMA-positive PC3 tumor xenografts in cytotoxicity and survival curves (P

138 ies, as well as growth rates of BCSC-derived tumor xenografts in immunodeficient mice.

139 Based on immunohistochemical staining, the tumor xenografts in mice treated with 29dL showed time-d

140 adiated nanoparticles was evaluated in human tumor xenografts in mice using 2-deoxy-2-[F-18]fluoro-D-

141 nts with human tumor cell lines, fresh human tumor xenografts in mice, and fresh human breast specime

142 When injected into tumor xenografts in mice, cancer-selective NPs were reta

143 In tumor xenografts in mice, treatment with either BGJ398 o

144 zed SLC7A11 and led to growth suppression of tumor xenografts in mice, which was associated with redu

145 ting in potent activity in cell cultures and tumor xenografts in mice.

146 ckdown inhibited the growth of C4-2 prostate tumor xenografts in mice.

147 nabled specific delivery of siRNA species to tumor xenografts in mice.

148 defects, and inhibits SRC phosphorylation in tumor xenografts in mice.

149 ro-Leu) in B1R-positive (B1R+) HEK293T::hB1R tumor xenografts in mice.

150 proliferation using human tissue samples and tumor xenografts in mice.

151 necessary and sufficient for growth of human tumor xenografts in mice.

152 ressed growth of WT and mutant ER-expressing tumor xenografts in NOD/SCID-gamma mice after oral or su

153 noma can contribute to enhanced lethality of tumor xenografts in nude mice.

154 n addition, ACEE reduced the growth of human tumor xenografts in nude mice.

155 R1 mutation, Y537S-ER, were used to generate tumor xenografts in ovariectomized female immunodeficien

156 In vivo efficacy of C1 was seen toward H460 tumor xenografts in severe-combined immunodeficient mice

157 99mTc-anti-CD56 mAb in SCID mice bearing ARO tumor xenografts in the right thigh, 24 h after being re

158 es were maintained in subsequent passages of tumor xenografts in vivo and in cell lines ex vivo.

159 Moreover, RgA was capable of inhibiting tumor xenografts in vivo without obvious side effects.

160 e used to examine EGFR-GFP behavior in mouse tumor xenografts in vivo.

161 and blocked growth of bevacizumab-resistant tumor xenografts in vivo.

162 ls in vitro and enhanced clearance of PD-L1+ tumor xenografts in vivo.

163 oliferation in vitro and inhibited growth of tumor xenografts in vivo.

164 od vessels in the tumor was determined using tumor xenografts in which tumor cells were integrin alph

165 All tumor xenografts in zebrafish retained the histological

166 specific and high-contrasted images of B1R+ tumors xenografted in mice.

167 ed intratumoral chemo-radio therapy in mouse tumor xenografts (in terms of tumor response and mouse s

168 1 silencing delayed the growth of irradiated tumor xenografts, in a manner that was associated with r

169 of orthotopic primary triple-negative breast tumor xenografts, including a patient-derived xenograft.

170 Similar efficacy was seen in primary human tumor xenografts, including with cells from patients wit

171 udies were conducted in rat AR42J pancreatic tumor xenograft mice to determine whether (188)Re-P2045

172 o, biodistribution studies were performed in tumor-xenografted mice to determine the optimal dose for

173 r, targeting Lin28A/Lin28B in cell lines and tumor xenografts mimicked the effects of ESE3/EHF and re

174 is further demonstrated on a chicken embryo tumor xenograft model and a chicken brain, showing both

175 In a tumor xenograft model in severe combined immunodeficienc

176 amine-CD3 PET probe was assessed in a murine tumor xenograft model of anti-cytotoxic T-lymphocyte ant

177 Similar findings were made in a human tumor xenograft model using a narrow range of doses of a

178 f KOX/PEGbPHF systemically administered to a tumor xenograft model was significantly higher than that

179 ion of WNT pathway activity in a solid human tumor xenograft model with evidence for tumor growth inh

180 In the human tumor xenograft model, detectable tumors were rejected u

181 transgenic cancer model and a DLC1-positive tumor xenograft model, due to reactivation of the tumor

182 In a tumor xenograft model, GUS inhibition prevents intestina

183 ha2 acts as a tumor suppressor in the HCT116 tumor xenograft model, HNF4alpha8 does not.

184 Using an orthotopic tumor xenograft model, we demonstrated that ectopic expr

185 olite can be imaged by MALDI-MSI in a breast tumor xenograft model.

186 nto biomarker modulation in an in vivo human tumor xenograft model.

187 ndent manner, both in vitro and in vivo in a tumor xenograft model.

188 wth in the mouse PTEN-deficient PC3 prostate tumor xenograft model.

189 ced cellular invasion in vivo in a zebrafish tumor xenograft model.

190 bited tumor growth in the HPAF-II pancreatic tumor xenograft model.

191 rmation assay, transwell invasion assay, and tumor xenograft model.

192 VII alpha 1 chain) genes, and in an in vivo tumor xenograft model.

193 ificantly lower IFP in three different human tumor xenograft models (Colo205, MiaPaca-2 and a patient

194 ison with (11)C-choline in 2 prostate cancer tumor xenograft models (DU-145 and PC-3).

195 ablished approximately 1,000 patient-derived tumor xenograft models (PDXs) with a diverse set of driv

196 Targeting MUC1-C in CTCL tumor xenograft models demonstrated significant decrease

197 s to evaluating antitumor agents using human tumor xenograft models have generally used cohorts of 8

198 To illustrate VERDICT, we used two tumor xenograft models of colorectal cancer with differe

199 s proautophagic function, as demonstrated in tumor xenograft models of human cancer and through use o

200 In this study, we evaluated in human tumor xenograft models the proinflammatory properties of

201 and tumor regression in NSCLC cell lines and tumor xenograft models, both as monotherapy and in combi

202 Moreover, in two distinct tumor xenograft models, combined delivery of ICOVIR-15K-

203 In ovarian tumor xenograft models, Dll4 was expressed specifically

204 ibited tumor growth in human patient-derived tumor xenograft models, either as single agents or in co

205 In tumor xenograft models, the development of resistance fo

206 induced vascular regression and necrosis in tumor xenograft models, with highly glycolytic tumors be

207 rubicin (Doxil) in HER2-overexpressing BT474 tumor xenograft models.

208 ure and a significantly improved response in tumor xenograft models.

209 ith the extent of tumor growth inhibition in tumor xenograft models.

210 tumor-initiating capability of spheroids in tumor xenograft models.

211 t in HDI-resistant NSCLC- or patient-derived tumor xenograft models.

212 ing and imaging-guided cancer therapy in two tumor xenograft models.

213 analogs exhibited dose-dependent efficacy in tumor xenograft models.

214 97 in both cell lines and in patient-derived tumor xenograft models.

215 efficacy, and tumor accumulation in multiple tumor xenograft models.

216 y in cell-based assays, as well as in murine tumor xenograft models.

217 tumor growth was investigated in mouse s.c. tumor xenograft models.

218 on, which was confirmed experimentally in 13 tumor xenograft models.

219 nduced senescence both in vitro and in human tumor xenograft models.

220 anti-tumor activity in both liquid and solid tumor xenograft models.

221 We confirmed using a human-derived tumor xenograft mouse model that bicalutamide pre-treatm

222 Using tumor xenograft mouse model, knocking down endogenous DA

223 Using a TNBC tumor xenograft mouse model, we found that DSF/BKM in co

224 emission tomography (PET) imaging using U87 tumor xenograft mouse model.

225 In two solid tumor xenograft mouse models, a single infusion of human

226 essed tumor growth in vivo in multiple human tumor xenograft mouse models.

227 Tumor xenografts of melanoma cell populations that were

228 ve for syngeneic murine tumors and for human tumor xenografts of prostate cancer (PC-3) and pancreati

229 Tumor xenografts originating from Spry1 knockdown MDA-MB

230 ressed the growth of intraperitoneal ovarian tumor xenografts outperforming their nontargeted counter

231 n of 4 mg/kg BOL significantly inhibited CRC tumor xenografts [p < 0.001], but no effect was observed

232 ltaG4Rs) in 22 breast cancer patient-derived tumor xenograft (PDTX) models.

233 plying this approach to patient-derived lung tumor xenografts (PDTX), we show that the liver supplies

234 collection of breast cancer patient-derived tumor xenografts (PDTXs), in which the morphological and

235 h elevated MYC expression in patient-derived tumor xenograft (PDX) and MYC-driven transgenic mouse mo

236 Patient-derived tumor xenograft (PDX) models are frequently used to stud

237 ll apoptosis in vitro and in patient-derived tumor xenograft (PDX) models, resulting in tumor regress

238 Patient-derived tumor xenograft (PDX) mouse models are a versatile oncol

239 Patient-derived tumor xenografts (PDX) have emerged as a powerful techno

240 Patient-derived tumor xenografts (PDX) have emerged as reliable preclini

241 e, by studying 52 colorectal patient-derived tumor xenografts (PDX), we examined key molecular altera

242 ltured ex vivo or in vivo as patient-derived tumor xenografts (PDX).

243 provided by transplantable, patient-derived tumor xenografts (PDX).

244 using patient-derived primary and metastatic tumor xenografts (PDX).

245 GEM sensitive and resistant patient-derived tumor xenografts (PDXs) indicate that PGM3 expression is

246 BRAF oncogene (BRAF(amp)) in patient-derived tumor xenografts (PDXs) that were treated with a direct

247 lished heterotopic and orthotopic pancreatic tumor xenografts, pharmacologic ascorbate combined with

248 ers of human regulatory T lymphocytes in the tumor xenografts, possibly explaining the efficacy of th

249 heparanase inhibitors restrain the growth of tumor xenografts produced by lymphoma cell lines.

250 ells lack intrinsic heparanase activity, but tumor xenografts produced by this cell line exhibit typi

251 and prevented HK1(-)HK2(+) multiple myeloma tumor xenograft progression.

252 c lethality in culture and for inhibition of tumor xenograft progression.

253 this hypothesis, analysis of patient-derived tumor xenografts propagated in immune-deficient mice sho

254 Inhibiting HER2 expression in bone tumor xenografts reduced proliferation and RANK expressi

255 apeutic inhibition of AXL signaling in ccRCC tumor xenografts reduced tumor vessel density and growth

256 We also established a tumor xenograft rejection model in these hPBMCs immune s

257 ed human desmoplastic cancers and orthotopic tumor xenografts revealed that traditional maximum-toler

258 domimetics in mice bearing receptor-positive tumor xenografts revealed up to 4-fold increased tumor u

259 were further confirmed by immunostaining of tumor-xenograft sections with collagen-I, fibronectin (m

260 Immunohistochemical staining of PANC-1 tumor xenografts showed a marked decrease in STAT3 in th

261 SN12 tumor xenografts showed decreased growth when treated wi

262 tumor ECM preparation (Matrigel) and breast tumor xenograft slices ex vivo.

263 Tumor xenograft studies confirmed this effect, and it wa

264 Finally, in vivo anti-tumor xenograft studies demonstrated high anti-tumour ef

265 326 showed tumor suppressor (TS) activity in tumor xenograft studies.

266 an cancer cells enhances the growth of mouse tumor xenografts, suggesting that RBM10 acts as a tumor

267 d DDR1 inhibitor caused greater shrinkage of tumor xenografts than either agent alone.

268 rovide higher accumulation of radiometals in tumor xenografts than in the kidneys.

269 Tumor xenografts that initially responded to VEGF-A inhi

270 ystem, we found in cells and patient-derived tumor xenografts that STAT3 is constitutively acetylated

271 d every 3 d for 16 d to nude mice with AR42J tumor xenografts that were approximately 20 mm(3) at stu

272 Against SK-OV-3 tumor xenografts, the rGel/4D5 construct with excellent

273 observed with clear cell-cell variations in tumor xenograft tissues, neuronal culture, and mouse bra

274 odel of estrogen receptor (ERalpha(+)) MCF-7 tumor xenografts to demonstrate how altering light/dark

275 enerated cell lines from anti-VEGF-resistant tumor xenografts to investigate the mechanisms by which

276 of animals bearing NCI-H929 multiple myeloma tumor xenografts treated with 800 muCi of anti-CD38 pret

277 g human brain (U251) and breast (MDA-MB-468) tumor xenografts treated with a single dose (0.5 mg) of

278 Tumor xenografts treated with combination PIT showed sig

279 n of senescence is validated in mice bearing tumor xenografts treated with senescence-inducing chemot

280 In NSCLC tumor xenografts, tumor growth was markedly inhibited an

281 In s.c. tumor xenografts, tumors dominated by stromal markers we

282 reater amount of AON is delivered to ovarian tumor xenografts using the ternary copolymer-stabilized

283 In vivo, tumor xenografts vascularized with EGF-silenced endothel

284 he therapeutic efficacy on p21-3H-expressing tumor xenografts was assessed by daily administration wi

285 aving observed complete eradication of solid tumor xenografts, we conclude that targeted alpha-therap

286 aving observed complete eradication of solid tumor xenografts, we conclude that targeted alpha-therap

287 er, including HGF-dependent and -independent tumor xenografts, we determined that the ADCC-enhanced a

288 Tumor xenografts were clearly detectable by small-animal

289 At 1 h after injection, HT-29 tumor xenografts were clearly visualized in PET images w

290 aring CA20948 somatostatin receptor-positive tumor xenografts were treated with (177)Lu-DOTATATE or s

291 egy of MMAE and IR, PANC-1 or HCT-116 murine tumor xenografts were treated with nontargeted free MMAE

292 onment of a range of human cancers and mouse tumor xenografts where its activation inhibits tumor gro

293 lls isolated from metastatic patient-derived tumor xenografts, where HIF2A levels could be reduced by

294 three human pancreatic ductal adenocarcinoma tumor xenografts with differing physiologic and metaboli

295 rties of (64)Cu-L19K-FDNB in VEGF-expressing tumor xenografts with its noncovalent binding analogs, (

296 estrogen receptor (ER)-positive human breast tumor xenografts with or without VEGF overexpression.

297 of mice harboring platinum-resistant ovarian tumor xenografts with pHLIP-PNA constructs suppressed HO

298 igh target-selective uptake in PSMA+ PC3 PIP tumor xenografts, with tumor-to-kidney ratios of >1 by 4

299 ity of doxorubicin released locally in liver tumor xenografts without inducing any adverse effect.

300 one inhibited the growth and angiogenesis of tumor xenografts without significant secondary adverse e