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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
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
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
38 ficant tumor uptake and good contrast in the subcutaneous tumor-bearing mice, which agreed well with
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
49 coated microneedles suppressed the growth of subcutaneous tumors by ~57%, while a topical cream conta
51 The recombinant virus still propagated in subcutaneous tumors, causing total regression and sustai
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
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
60 FHBG) was performed in mice with established subcutaneous tumors, expressing wild-type HSV1-tk and it
62 migration and invasion in vitro and enhanced subcutaneous tumor formation in vivo, transforming the m
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
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 +/-
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
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
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
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
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
107 be less efficient in cranial tumors than in subcutaneous tumors, (ii) delivery may be reduced during
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
113 rm colonies in soft agar and highly invasive subcutaneous tumors in both immunodeficient and immunoco
115 s expressing core3 O-glycans barely produced subcutaneous tumors in contrast to robust tumor formatio
118 l in vitro but formed fewer and much smaller subcutaneous tumors in mice compared with tumors formed
124 mor cells (experimental metastasis) and from subcutaneous tumors in nude mice (spontaneous metastasis
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
134 demonstrate that this model is applicable to subcutaneous tumors, lung metastases, and intracranial t
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
141 rther verified by in vivo evaluations in the subcutaneous tumor model and orthotopic breast tumor mod
145 as observed at 3-4 d after injection for the subcutaneous tumor model, in contrast to approximately 7
153 us hyperthermia (42 degrees C for 25 min) in subcutaneous tumor models, based on tumor growth inhibit
157 by the inaccuracy of caliper measurement of subcutaneous tumors, of counting lung nodules in metasta
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.
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
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
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
183 g in vivo models in which intraperitoneal or subcutaneous tumors were induced in immunodeficient mice
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.
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
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