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1 as lower in the liver tumor than that in the subcutaneous tumor.
2 r tumor was significantly higher than in the subcutaneous tumor.
3 n liver tumor was twofold lower than that in subcutaneous tumor.
4 hifted to smaller size compared with that of subcutaneous tumor.
5 ed and transfected CSCs both in vitro and in subcutaneous tumor.
6 Ab to penetrate and bind to cells within the subcutaneous tumors.
7 in the plasma of mice without tumors or with subcutaneous tumors.
8 r coincident with central necrosis, than the subcutaneous tumors.
9 skinfold chamber model was used to study the subcutaneous tumors.
10 may be different from those obtained against subcutaneous tumors.
11 ted HCC cell growth in culture and xenograft subcutaneous tumors.
12 pMMR CRC cells grown as liver metastases and subcutaneous tumors.
13 ive (PD-L1(-)) and PD-L1-positive (PD-L1(+)) subcutaneous tumors.
14 it intravital optical techniques to large or subcutaneous tumors.
15 s following intravenous injection but not of subcutaneous tumors.
16 e quantities of VEGF secreted by microscopic subcutaneous tumors (0.5-1 mm(3)) result in an elevation
17                           Biodistribution in subcutaneous tumors 1, 3, and 7 d after [(177)Lu]Lu-ofat
18                                 Mice bearing subcutaneous tumors (50 mm(3), NIH:OVCAR-3) were injecte
19                        Methods: Mice bearing subcutaneous tumors (50 mm(3), NIH:OVCAR-3) were injecte
20 y also resulted in improved local control of subcutaneous tumor after surgical resection.
21                Growth and vascularization of subcutaneous tumor allografts was enhanced in 2+tRNAi(Me
22                                              Subcutaneous tumors (amyloidomas) were induced in BALB/c
23  injected into C57BL/6 mice to establish one subcutaneous tumor and multiple lung lesions.
24                                          The subcutaneous tumors and lung metastases derived from V12
25  cells exhibited superior in vivo control of subcutaneous tumors and persistence in the blood.
26 rkitt cells reduced their ability to grow as subcutaneous tumors, and caused visible tumor necrosis i
27 ry and sufficient for mAb-induced therapy of subcutaneous tumors, and represent a new and critical fo
28  stiffness of modified collagen matrices and subcutaneous tumors, and show that LOX-induced collagen
29  however, neither ascitic nor transplantable subcutaneous tumors are predictive of activity for solid
30 ptake of (99m)Tc-HuS/Hu-VEGF (n = 10) within subcutaneous tumor as compared with (99m)Tc-HuS/Hu-P4G7
31 e growth of established preadipocyte-induced subcutaneous tumors as well as established intraperitone
32 lete eradication of injected and noninjected subcutaneous tumors, as well as melanoma tumors in the b
33 d healing, implanted gel foam fragments, and subcutaneous tumor assays, respectively.
34 of preventing tumor relapses, and eradicated subcutaneous tumors at different growth stages.
35 , were allocated to each of five groups: (a) subcutaneous tumors, (b) kidney tumors, (c) lung tumors
36 mor or intravenous injection to CT26 and 4T1 subcutaneous tumor bearing mice yielded higher antitumor
37 A conjugates were evaluated in murine B16F10 subcutaneous tumor-bearing C57BL/6 mice.
38 ficant tumor uptake and good contrast in the subcutaneous tumor-bearing mice, which agreed well with
39 and prolonged survival in established B16F10 subcutaneous tumor-bearing mice.
40 med at 5 time points after treatment of C4-2 subcutaneous tumor-bearing NSG mice.
41 cific fusion protein accumulated not only in subcutaneous tumors but also in lungs and livers affecte
42 of INP contrast (MicroCT) previously seen in subcutaneous tumors but not intracerebral gliomas, provi
43 lectively reduced the levels of PKC alpha in subcutaneous tumors but not those of protein kinase C ep
44 galovirus control and facilitated control of subcutaneous tumors but not tumor metastases in two inde
45 onist, CD4(+) and CD8(+) T cells infiltrated subcutaneous tumors, but only CD4(+) T cells infiltrated
46 as observed against 10 day, 1 cm established subcutaneous tumors, but only in combination with a boos
47 ad little effect on the formation of primary subcutaneous tumors, but when these tumors spontaneously
48        Unlike the immunity generated against subcutaneous tumors by GM-CSF, however, the effector res
49 coated microneedles suppressed the growth of subcutaneous tumors by ~57%, while a topical cream conta
50 inocytic index' of a particular cell line or subcutaneous tumor can be ascertained within 1-2 d.
51    The recombinant virus still propagated in subcutaneous tumors, causing total regression and sustai
52 c liver metastases, when compared with their subcutaneous tumor counterparts.
53 nversion rates (k(pl)) and lactate signal in subcutaneous tumors derived from high L/A tumor cells, c
54 te 13-acetate (PMA), inhibited the growth of subcutaneous tumors derived from PAM212 (mouse SCC) and
55                                    A visible subcutaneous tumor developed in 10-14 days.
56  subgroup of patients who received TILs from subcutaneous tumors, eight of 15 patients receiving unse
57 D scid gamma-(NSG) mice were inoculated with subcutaneous tumors engineered to either be constitutive
58                               Mice harboring subcutaneous tumors exhibited elevated levels of DNA dam
59                                              Subcutaneous tumors expressed less activated Smad-1/5 an
60 FHBG) was performed in mice with established subcutaneous tumors, expressing wild-type HSV1-tk and it
61 Akt activation, cell growth in soft agar, or subcutaneous tumor formation in nude mice.
62 migration and invasion in vitro and enhanced subcutaneous tumor formation in vivo, transforming the m
63                              Finally, serial subcutaneous tumor formation using late passage transfor
64                 In limiting dilution assays, subcutaneous tumor formation was inhibited by ST6Gal-I k
65                                In nude mice, subcutaneous tumors from antisense transfectants showed
66 ferred an advantage for lung metastasis from subcutaneous tumors (fs120/164 vs. fs188/WT); fs120 cell
67 o single agents when tested in mice carrying subcutaneous tumors generated by transplantation of FGFR
68                                              Subcutaneous tumors generated in nude mice by implanting
69 tiology characterized by multiple, recurring subcutaneous tumors, gingival hypertrophy, joint contrac
70 ter RF ablation, coagulation diameter in the subcutaneous tumor groups was the same (mean, 9.8 mm +/-
71 ively determine the oxygen distribution in a subcutaneous tumor growing in rats.
72 nd prodrug activation assays in vitro and in subcutaneous tumors grown from the corresponding cell li
73 resulted in: inhibition of MV4-11 (FLT3-ITD) subcutaneous tumor growth and complete suppression of AM
74 gand Sonic Hh (SHH) in these cells decreased subcutaneous tumor growth and decreased stromal cell pro
75                          B20-4.1.1 inhibited subcutaneous tumor growth and decreased vascular density
76 ice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 ce
77 umorsphere-derived cells delayed established subcutaneous tumor growth and strongly impaired pulmonar
78 uggesting that host-expressed Cav-2 promotes subcutaneous tumor growth and tumor-induced neovasculari
79 st HCT-116 cells and significantly inhibited subcutaneous tumor growth in mice compared with 5-FU.
80 +/-) and KPC/Cdh11(-/-) mice only or reduced subcutaneous tumor growth in mT3 engrafted Cdh11(+/+) mi
81 o assess tumor cell-induced angiogenesis and subcutaneous tumor growth in nude mice using mouse Lewis
82                                              Subcutaneous tumor growth in nude mice who received intr
83 tered cell cycle progression, and suppressed subcutaneous tumor growth in nude mice.
84 ast, A6 or cisplatin (CDDP) alone suppressed subcutaneous tumor growth in vivo by 48% and 53%, respec
85 in vitro and increases dissemination but not subcutaneous tumor growth in vivo, thus supporting its s
86 cogenic and transforms melanocytes, enabling subcutaneous tumor growth in vivo.
87 ell proliferation and migration in vitro and subcutaneous tumor growth in vivo.
88            Previously it has been shown that subcutaneous tumor growth is enhanced in mice lacking se
89 lation of normal liver can stimulate distant subcutaneous tumor growth mediated by HGF/c-Met pathway
90 s the expression of AGS1/RASD1 inhibited the subcutaneous tumor growth of A549 cells in athymic nude
91 oxic doses in mice resulted in inhibition of subcutaneous tumor growth of cells derived from various
92 lly, exogenous expression of JMJD2B enhanced subcutaneous tumor growth of colon cancer cells in a p53
93  contribution of stromal SPARC, we evaluated subcutaneous tumor growth of TRAMP cell lines in syngene
94                        The protocol leads to subcutaneous tumor growth usually within 1-3 weeks of ce
95                                              Subcutaneous tumor growth was also prevented from cells
96 ition with HTS01037 suppressed syngeneic KPC subcutaneous tumor growth with reduction of EMT and stem
97  pharmacologic or genetic, leads to enhanced subcutaneous tumor growth, similar to the phenotype obse
98 (+/-) mice had increased bone metastatic and subcutaneous tumor growth, suggesting that increased Hh
99 utively active RalB(G23V) exhibited enhanced subcutaneous tumor growth, whereas those transfected wit
100 cle-treated animals, but it had no effect on subcutaneous tumor growth.
101 tastatic colonies in lungs without affecting subcutaneous tumor growth.
102 lation of S100A8 and S100A9 had no effect on subcutaneous tumor growth.
103  decreased bone metastasis without affecting subcutaneous tumor growth.
104 o inhibit in vitro angiogenesis and suppress subcutaneous tumor growth.
105 integrin in hemostasis, bone resorption, and subcutaneous tumor growth.
106 inhibited bone metastasis but did not affect subcutaneous tumor growth.
107  be less efficient in cranial tumors than in subcutaneous tumors, (ii) delivery may be reduced during
108 eplication (U373MG) was adapted to grow as a subcutaneous tumor in nude mice.
109 h knockdown lasting approximately 10 days in subcutaneous tumors in A/J mice and 3-4 weeks in the non
110 erated Moloney murine sarcoma virus, induced subcutaneous tumors in about 14% of infected mice but di
111 R7Delta447, induced brain lesions as well as subcutaneous tumors in all injected mice.
112 ell lines give rise to progressively growing subcutaneous tumors in athymic mice.
113 rm colonies in soft agar and highly invasive subcutaneous tumors in both immunodeficient and immunoco
114 atically reduced, as was the ability to form subcutaneous tumors in CD1 nu/nu mice.
115 s expressing core3 O-glycans barely produced subcutaneous tumors in contrast to robust tumor formatio
116 (-/-) cultures retained the capacity to form subcutaneous tumors in immunocompromised mice.
117                        Pbrm1 deficient Renca subcutaneous tumors in mice are more resistance to ICB,
118 l in vitro but formed fewer and much smaller subcutaneous tumors in mice compared with tumors formed
119                                   Imaging of subcutaneous tumors in mice was performed by using an ex
120            Our in vivo results indicate that subcutaneous tumors in mice were regressed after VP trea
121 ngle cell level and in connecting tissues of subcutaneous tumors in mice.
122 act and damaged targeting agents for imaging subcutaneous tumors in mice.
123 lted in a complete regression of established subcutaneous tumors in most animals.
124 mor cells (experimental metastasis) and from subcutaneous tumors in nude mice (spontaneous metastasis
125                    Furthermore, treatment of subcutaneous tumors in nude mice with 2-5A-anti-hTR sign
126  FGFR-1 cDNAs into human melanomas, grown as subcutaneous tumors in nude mice.
127 and the sphere-forming CSC-like cells formed subcutaneous tumors in nude mice.
128                                    Bilateral subcutaneous tumors in rats were treated with either int
129 mulated NK proliferation in vitro and formed subcutaneous tumors in severe combined immunodeficiency/
130 s in nude mice bearing VLA-4-positive B16F10 subcutaneous tumors in the flank were conducted to valid
131 proved the efficacy of paclitaxel to regress subcutaneous tumors in vivo.
132 inistering anti-asialo GM1 antibodies before subcutaneous tumor injection.
133                 Using a mouse model with two subcutaneous tumors, it was demonstrated that MRgHIFU en
134 demonstrate that this model is applicable to subcutaneous tumors, lung metastases, and intracranial t
135               A sixth group comprised larger subcutaneous tumors (mean diameter, 46 mm +/- 4) that we
136 ctive T cells into mice bearing a variety of subcutaneous tumors mediated limited antitumor effects a
137      In addition, on generation of a primary subcutaneous tumor, metastasis to regional lymph nodes w
138 am (%ID/g) at 30 min after injection for the subcutaneous tumor model and greater than 1.5 %ID/g for
139    In vivo testing was conducted in a murine subcutaneous tumor model and in the canine prostate.
140          We then describe in more detail the subcutaneous tumor model and key steps needed to establi
141 rther verified by in vivo evaluations in the subcutaneous tumor model and orthotopic breast tumor mod
142 ted regimen of alpha-radioimmunotherapy in a subcutaneous tumor model in mice.
143 imizes proteasome cleavage and survival in a subcutaneous tumor model in mice.
144                                         In a subcutaneous tumor model, GZ17-6.02 decreased tumor volu
145 as observed at 3-4 d after injection for the subcutaneous tumor model, in contrast to approximately 7
146                                       In the subcutaneous tumor model, the combined therapy resulted
147                                         In a subcutaneous tumor model, the combined treatment resulte
148 in the metastasis model and no effect in the subcutaneous tumor model.
149 ficantly increased therapeutic effect in the subcutaneous tumor model.
150 gin growing beneath the skin of a mouse: the subcutaneous tumor model.
151 lan's efficacy and cytotoxicity in vivo in a subcutaneous tumor model.
152                 In established pulmonary and subcutaneous tumor models, anti-CD137 synergistically en
153 us hyperthermia (42 degrees C for 25 min) in subcutaneous tumor models, based on tumor growth inhibit
154  and human PD-L1 expressing cancer cells and subcutaneous tumor models.
155  for optimal CD8(+) T cell activation in two subcutaneous tumor models.
156                  In vivo, the development of subcutaneous tumor nodules with reduced 6-O-sulfation is
157  by the inaccuracy of caliper measurement of subcutaneous tumors, of counting lung nodules in metasta
158 he tail vein or directly administered to the subcutaneous tumor on 3 or 4 alternating days.
159  CDH11 reduced growth of pre-established mT3 subcutaneous tumors only if T and B cells were present i
160 nificantly reduced the growth of established subcutaneous tumors relative to either treatment alone.
161      In vivo, injection of AdMIP-3alpha into subcutaneous tumors resulted in local expression of the
162 A-7 in p53-wild-type A549 and p53-null H1299 subcutaneous tumors resulted in significant tumor growth
163 ified DCs (CD40L-DCs) to established (day 8) subcutaneous tumors resulted in sustained tumor regressi
164  as multiple palpable soft pliable nontender subcutaneous tumors scattered over the chest, abdomen, a
165 rmacokinetic and pharmacodynamic analysis in subcutaneous tumors showed that a single administration
166 MAE selectively accumulated in HER2-positive subcutaneous tumors, significantly reducing the tumor gr
167 l adhesion to extracellular matrix proteins, subcutaneous tumor size in nude mice, and invasive behav
168    In mice, overexpression of HAS2 increased subcutaneous tumor size.
169 -to-background contrast, clearly delineating subcutaneous tumor stem cell-derived xenografts from sur
170 epleted for purine intermediates relative to subcutaneous tumors, suggesting decreased purine synthes
171 he induction of partial regressions of large subcutaneous tumors that exceeded more than 5% of the bo
172 ablished subcutaneously in nude mice and the subcutaneous tumor tissue was then orthotopically implan
173 in both healthy nude mice and nude mice with subcutaneous tumor to validate the contrast effects and
174 on of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy
175 ress high levels of PTN and metastasize from subcutaneous tumors to the lungs of experimental animals
176 lial lesions precede the onset of peripheral subcutaneous tumors, tumorigenesis progresses through ea
177 gh polarity and proximity to immune cells in subcutaneous tumors versus a diffuse spatial pattern in
178                               A mouse with a subcutaneous tumor was injected with (18)F-FDG and image
179 Recruitment of monocytes into orthotopic and subcutaneous tumors was significantly increased in these
180 ense and scrambled S-oligodeoxynucleotide in subcutaneous tumors were 2 microM after 21 daily doses o
181                                              Subcutaneous tumors were established from a triple-negat
182                                              Subcutaneous tumors were established in groups of hamste
183 g in vivo models in which intraperitoneal or subcutaneous tumors were induced in immunodeficient mice
184                                        These subcutaneous tumors were metastatic to regional lymph no
185           Mice bearing U87-MG and MDA-MB-231 subcutaneous tumors were treated with axitinib (25 mg/kg
186 elomere reserve, cells derived from the ALT+ subcutaneous tumors were unable to generate lung metasta
187 ony-stimulating factor (mM-CSF) never formed subcutaneous tumors when implanted into Fischer rats, wh
188 ged the survival time of mice bearing B16F10 subcutaneous tumors with negligible adverse effects.
189 c cells in SCID mice can engraft and grow as subcutaneous tumors with subsequent dissemination to dis
190 e characterized in vitro and in mice bearing subcutaneous tumors with varying levels of EGFR expressi
191 11 of 16 patients with B-lineage ALL grew as subcutaneous tumors, with a significant number subsequen
192 ded the growth of both U87-MG and MDA-MB-231 subcutaneous tumors, with significant differences in tum
193 ced durable and complete remissions of large subcutaneous tumors without detectable side effects.
194                               Orthotopic and subcutaneous tumor xenograft approaches were then used t
195 248 was investigated in 2 FLT3-ITD models: a subcutaneous tumor xenograft model and a bone marrow eng
196 f tumor growth in a c-Met amplified (GTL-16) subcutaneous tumor xenograft model and may have an advan
197 ramatically regresses FLT3-ITD tumors in the subcutaneous tumor xenograft model and prolongs survival
198 ion had no effect on cell growth in vitro or subcutaneous tumor xenograft-growth in vivo.
199 tic effects against cultured tumor cells and subcutaneous tumor xenografts established in athymic mic
200 ke were examined in CD1 athymic mice bearing subcutaneous tumor xenografts that expressed HER2, HER3,
201 partially delayed progression of established subcutaneous tumor xenografts, whereas combined treatmen
202 iodistribution were assessed using PSMA-high subcutaneous tumor xenografts.
203 IN or human pancreatic cancer cells grown as subcutaneous tumor xenografts.
204 , n = 12; control group, n = 14) with U87 MG subcutaneous tumor xenografts.
205                     Infection of Her2/neu(+) subcutaneous tumors yielded >10-fold more virus on days

 
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