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 metastasis of intravenous and intraprostatic tumor xenografts.

5 stigated in vivo by intravital microscopy of tumor xenografts.

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

7 creases cell viability and reduces growth of tumor xenografts.

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

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

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

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

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

13 vels dramatically reduced the growth of lung tumor xenografts.

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

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

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

17 hibitor AZD1775 regresses H3K36me3-deficient tumor xenografts.

18 1-Foxn1(nu) mice bearing HER2-positive human tumor xenografts.

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

20 used regression of all treated A2780 ovarian tumor xenografts.

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

22 ponse in typically erlotinib-resistant NSCLC tumor xenografts.

23 revealing the kinetics of both processes in tumor xenografts.

24 intracranial human glioblastoma neurosphere tumor xenografts.

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

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

27 tumors retained abnormal SHH signaling like tumor xenografts.

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

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

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

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

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

33 ibution were performed on mice bearing AR42J tumor xenografts.

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

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

36 he caspase-3 activity in doxorubicin-treated tumor xenografts.

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

38 4)Sc-cm09 allowed excellent visualization of tumor xenografts.

39 and serine biosynthesis in cancer cells and tumor xenografts.

40 ented luciferase signals in HEK293TNKS mouse tumor xenografts.

41 ere performed on HER2-positive and -negative tumor xenografts.

42 tion suppressed the growth of BRG1-deficient tumor xenografts.

43 3-dimensional (3D) spheroid cultures and in tumor xenografts.

44 R) spectroscopy and its application to mouse tumor xenografts.

45 OFMSCs) and is capable of generating OF-like tumor xenografts.

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

47 titumor effect against trastuzumab-resistant tumor xenografts.

48 nst PlGF, showed antitumor activity in human tumor xenografts.

49 wth and resistance to radiation treatment in tumor xenografts.

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

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

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

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

54 ere performed in mice bearing B16F1 melanoma tumor xenografts.

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

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

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

58 ion also significantly reduced the growth of tumor xenografts.

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

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

61 e size and neovascularization of CAG myeloma tumor xenografts.

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

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

64 28 to athymic nude mice implanted with human tumor xenografts afforded significant and dose-dependent

65 5.3-fold photoacoustic signal enhancement in tumor xenografts after systemic administration.

66 OXB13-expressing ER+ breast cancer cells and tumor xenografts, alone or in combination with TAM.

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 addition, data from tumor xenografts and human cancer specimens indicate tha

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

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

74 herapeutic agents on BCSC-derived orthotopic tumor xenografts and promoted metastatic progression bot

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

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

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 We also analyzed Tff1(-/-) mice, growth of tumor xenografts, and human tissues.

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

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 The same result is seen in vivo with tumor xenograft-bearing mice, in control tumors and foll

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

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

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

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

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

94 ugates were further evaluated in vivo in PC3 tumor xenografts by biodistribution and PET imaging stud

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

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

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

98 In vivo tumor xenografts carrying p21-3H also showed increased l

99 ed cell lines, and B7-H4 was lost rapidly by tumor xenograft cells after short-term in vitro culture.

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

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

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

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

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

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

106 Tumor-xenografts derived from orthotopic-inoculation of

107 ficacious, whereas ARv7-expressing LuCap23.1 tumor xenografts displayed docetaxel resistance.

108 In ARv567-expressing LuCap86.2 tumor xenografts, docetaxel treatment was highly efficac

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

110 1A12 was efficacious in tumor xenografts expressing Hsp90(alpha)/p23 reporters r

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

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

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

114 In tumor xenografts generated from carcinoma cells that wer

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

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

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

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

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

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

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

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

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

124 romoted an epithelial phenotype and impaired tumor xenograft growth.

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

126 dose-dependent inhibition of multiple human tumor xenografts growth in mice.

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

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

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

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

131 ression of HIF-2alpha promotes the growth of tumor xenografts in association with enhanced CDCP1 expr

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

133 ular tumor spheroids and in vivo using human tumor xenografts in athymic mice.

134 increased apoptosis and decreased growth of tumor xenografts in athymic nude mice.

135 Growth of PLC5 tumor xenografts in BALB/c nude mice was inhibited by da

136 hree-dimensional extracellular matrix and as tumor xenografts in contrast to conventional monolayer c

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

138 extravasation, and delayed the outgrowth of tumor xenografts in immune-deficient mice.

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

140 ox nanoassembly-treated MiaPaCa-2 pancreatic tumor xenografts in mice decreased by 95% compared with

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

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

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

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

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

146 ulting in a remarkable increase in uptake in tumor xenografts in mice.

147 neoplastic B cells in culture and growth as tumor xenografts in mice.

148 and abolished growth of lung adenocarcinoma tumor xenografts in mice.

149 cy and induces the regression of established tumor xenografts in mice.

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

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

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

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

154 ented increase in radiolabel accumulation in tumor xenografts in mice; this increase might translate

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

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

157 te efficiently inhibits the growth of breast tumor xenografts in nude mice.

158 ssion significantly suppressed the growth of tumor xenografts in nude mice.

159 as highly active against subcutaneous B-cell tumor xenografts in severe combined immunodeficient mice

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

161 In this study, we used a model of s.c. human tumor xenografts in severely immunodeficient mice to ass

162 99mTc-anti-CD56 mAb in SCID mice bearing ARO tumor xenografts in the right thigh, 24 h after being re

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

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

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

166 ed cell proliferation in vitro and growth of tumor xenografts in vivo.

167 ed sensitivity to bortezomib in vitro and in tumor xenografts in vivo.

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

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

170 All tumor xenografts in zebrafish retained the histological

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

172 1 silencing delayed the growth of irradiated tumor xenografts, in a manner that was associated with r

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

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

175 ylation of endogenously produced antibodies, tumor xenograft membranes, and neutrophil adhesion glyca

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

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

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

179 ficacy when dosed orally in an A2780 ovarian tumor xenograft model (TGI of 97% was observed on day 17

180 h in a c-Met amplified (GTL-16) subcutaneous tumor xenograft model and may have an advantage over ina

181 In a tumor xenograft model in severe combined immunodeficienc

182 In a separate tumor xenograft model in which mouse HCC cells (Hepa1-6)

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

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

185 In a tumor xenograft model using SCID mice inoculated with Hu

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

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

188 emonstrates antitumor activity in a prostate tumor xenograft model with limited host toxicity.

189 endent inhibition of MPS1 in an HCT116 human tumor xenograft model, and is an attractive tool compoun

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

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

192 tics of an agonistic DR5 antibody in a brain tumor xenograft model, we utilized a noninvasive imaging

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

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

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

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

197 d in vivo pharmacodynamic effects in a human tumor xenograft model.

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

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

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

201 bited in-vivo colon cancer growth in a mouse tumor xenografts model.

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

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

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

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

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

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

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

209 Herein, cell and human tumor xenograft models of prostate cancer were utilized

210 In tumor xenograft models of several drug-resistant human c

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

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

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

214 In ovarian tumor xenograft models, Dll4 was expressed specifically

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

216 In tumor xenograft models, the development of resistance fo

217 In human tumor xenograft models, we confirmed the greater antitum

218 al antibody, both in vitro and in orthotopic tumor xenograft models, where an increased median surviv

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

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

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

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

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

224 97 in both cell lines and in patient-derived tumor xenograft models.

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

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

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

228 agent and in various combinations in myeloma tumor xenograft models.

229 s, and it displayed single-agent efficacy in tumor xenograft models.

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

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

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

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

234 Using tumor xenograft mouse model, knocking down endogenous DA

235 1 (breast) and MIA PaCa-2 (pancreatic) human tumor xenograft mouse models with insignificant toxicity

236 namic PET imaging demonstrated uptake in EL4 tumor xenografts of approximately 6 percentage injected

237 d with the trimeric aptamer, animals bearing tumor xenografts of human gastric origin reflected reduc

238 Tumor xenografts of melanoma cell populations that were

239 Analyses of primary tumor xenografts of patient-derived lung and pancreatic

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

241 Tumor xenografts originating from Spry1 knockdown MDA-MB

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 Correlative immunohistochemistry on tumor xenograft sections confirmed in vivo results.

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

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

260 owest effective antitumor dose against human tumor xenografts showed an improved therapeutic range (a

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

264 326 showed tumor suppressor (TS) activity in tumor xenograft studies.

265 antimetastatic activity in orthotopic human tumor xenografts, syngeneic tumors, and a genetic model

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

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

268 Tumor xenografts that initially responded to VEGF-A inhi

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

270 In NSCLC tumor xenografts, the expression of a tyrosine phosphomi

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

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

273 in 3-BrPA-resistant cancer cells sensitizes tumor xenografts to 3-BrPA treatment in vivo.

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

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

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

280 sion in triple negative breast cancer (TNBC) tumor xenografts using near infrared imaging and (111)In

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

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

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

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

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

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

287 Tumor xenografts were clearly detectable by small-animal

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

289 Scintillation-camera imaging showed that tumor xenografts were the only sites with prominent accu

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

291 Subcutaneous and lung tumor xenografts were used to compare lesion detectabili

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 t human prostate, breast, bladder, and colon tumor xenografts, where its efficacy could be further en

295 A tumor xenograft with Mel-18 knockdown MCF-7 cells consis

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

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

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

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

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