ライフサイエンスコーパス: tumor mass

1 lso caused regression of large BCLs (> 1.5 g tumor mass).

2 xoid matrix, which can represent most of the tumor mass.

3 s to divide and become incorporated into the tumor mass.

4 epresenting between 0 and 0.04% of the total tumor mass.

5 y maintain tumor cell heterogeneity within a tumor mass.

6 ografts through necrosis of up to 90% of the tumor mass.

7 er number of CD8(+) T cells infiltrating the tumor mass.

8 hen using labeled bevacizumab to outline the tumor mass.

9 as clusters of cells distinct from the main tumor mass.

10 ount and retention of the nanoparticles in a tumor mass.

11 /AMF deficiency lost their abilities to form tumor mass.

12 traces of the molecule were detected in the tumor mass.

13 t angiogenesis is necessary for expansion of tumor mass.

14 e microvasculature with the evolution of the tumor mass.

15 witch and correlates with rapid expansion of tumor mass.

16 ells to critical stromal elements within the tumor mass.

17 re observed in their distribution within the tumor mass.

18 ccommodate the requirements of the expanding tumor mass.

19 ns at CISs in subdominant populations in the tumor mass.

20 es in the basal and superficial areas of the tumor mass.

21 distribute TRAIL protein throughout a brain tumor mass.

22 e serous cavities without a detectable solid tumor mass.

23 y exogenous stimuli after drug enrichment in tumor mass.

24 ependent of apoptosis or necrosis within the tumor mass.

25 strictly limited by the size of the resected tumor mass.

26 eratinocytes and allows dissemination of the tumor mass.

27 ensive delivery of the foreign cDNA into the tumor mass.

28 umor cells and stem cell compartments in the tumor mass.

29 rant expression of epithelial markers in the tumor mass.

30 , but by stromal cells within and around the tumor mass.

31 ty of 131I, because of uncertainty about the tumor mass.

32 ssels to form an initially well-vascularized tumor mass.

33 or distribution of the vector throughout the tumor mass.

34 ver-expressed in the cancer cells within the tumor mass.

35 was expressed in the cancer cells within the tumor mass.

36 ty in the cancer cells within the pancreatic tumor mass.

37 r cells and by hypoxic conditions inside the tumor mass.

38 g anticancer immunosurveillance and reducing tumor mass.

39 rates and more rapid emergence of a palpable tumor mass.

40 ade the tumor and can be seen throughout the tumor mass.

41 tisense had no effect on thrombin-stimulated tumor mass.

42 ew tumor foci at sites distant from the main tumor mass.

43 ructures, and non-malignant cells within the tumor mass.

44 quired for surviving cells to repopulate the tumor mass.

45 ed by stable clonal expansions that form the tumor mass.

46 effusions without an identifiable contiguous tumor mass.

47 effusions without an identifiable contiguous tumor mass.

48 fusions in the absence of a contiguous solid tumor mass.

49 fusions in the absence of a contiguous solid tumor mass.

50 ls in vivo with significant shrinkage in the tumor mass.

51 oblastic leukemia (T-ALL) efficiently reduce tumor mass.

52 erapy resistance and increased growth of the tumor mass.

53 CSCs comprised more than 30% of the tumor mass.

54 out both the multicellular spheroids and the tumor mass.

55 nder viral replication and spread within the tumor mass.

56 must be conserved to reseed a heterogeneous tumor mass.

57 ng analysis of tumor cell subsets within the tumor mass.

58 remission in 13 (72%) of 18 patients with a tumor mass.

59 e generation of differentiated proliferating tumor mass.

60 tion that marks dissemination in the primary tumor mass.

61 s they are in active myeloma, independent of tumor mass.

62 at can comprise a substantial portion of the tumor mass.

63 conjugate (P-DTX) effective in debulking the tumor mass.

64 a GRK2-specific peptide inhibitor increased tumor mass.

65 se inhibitor protein (RKIP) did not increase tumor mass.

66 type of host-derived cells infiltrating the tumor mass.

67 attached or co-administered payload into the tumor mass.

68 hy, pre-existing vessels, thus bypassing the tumor mass.

69 antibodies from the vascular space into the tumor mass.

70 ed but distinct subclones compete within the tumor mass.

71 nner associated with a dramatic reduction in tumor mass.

72 system can effectively eliminate even large tumor masses.

73 , however, often in the presence of residual tumor masses.

74 d LMO1 developed pre-T LBL with large thymic tumor masses.

75 ty of immune cells present in and around the tumor masses.

76 s tumor-expressed albumin from in vivo grown tumor masses.

77 e critical to maintenance of even very small tumor masses.

78 enetration of scFv from the vasculature into tumor masses.

79 all (11 of 11) patients with rapidly growing tumor masses.

80 bital carcinoid tumors appear as nonspecific tumor masses.

81 ite-specific delivery of anticancer drugs to tumor masses.

82 fluorescence within cells and throughout the tumor masses.

83 se stabilization in the presence of residual tumor masses.

84 morphic cells that occupied up to 75% of the tumor masses.

85 and increased CD8-to-Treg cell ratios inside tumor masses.

86 s possessed hypoxic gradients throughout the tumor mass (0.1-6% pO2).

87 Tumor mass (1.6+/-0.2 g) and volume (131+/-15 mm(3), 12

88 ice developed large breast tumors with total tumor mass 3.5 +/- 0.5 g and volume 265 +/- 36 mm(3) (SE

89 nfiltration and CD68 immunoreactivity in the tumor mass; (3) decreases astrogliosis in peritumoral ar

90 -F delivers 3.5 times more boron to the main tumor mass [99 +/- 36 microg/g tissue (mean +/- SD)] tha

91 ctive at rapidly debulking directly injected tumor masses, achieving complete eradication of establis

92 ric nanoparticle provides information on the tumor mass across various size scales in vivo, from mill

93 ealed a 90.4 and a 46% decrease in the final tumor mass after 3 days of treatment.

94 The various types of cells that comprise the tumor mass all carry molecular markers that are not expr

95 ion of treatment in the presence of residual tumor mass almost inevitably leads to tumor progression.

96 The tumor masses also infiltrated the surrounding tissue.

97 ogeneous distribution of (186)Re-HEDP in the tumor mass: Although the "soft-tissue" component showed

98 otoxin resulted in regression of the primary tumor mass and a decrease in the incidence of lymph node

99 umors resulted in a significant reduction in tumor mass and a prolonged life span compared to control

100 mic VEGF levels might quantitatively reflect tumor mass and angiogenic activity.

101 ating adenovirus would spread throughout the tumor mass and cause direct oncolysis of tumor cells.

102 There was only a weak correlation between tumor mass and circulating PCs, suggesting that the appe

103 umor growth, increased tumor numbers, larger tumor mass and decreased survival rates compared with mi

104 relevant disease state of tissue within the tumor mass and examination of the resection cavity walls

105 cause tumor cell detachment from the primary tumor mass and facilitate escape of the tumor cells from

106 rating macrophages isolated from the primary tumor mass and in TAMs isolated from lung containing met

107 iostatic therapy was associated with reduced tumor mass and increased survival in a rat 9L gliosarcom

108 of variable values, unbounded growth of the tumor mass and invasion of the environment are observed

109 We observed 3-fold increases in tumor mass and levels of angiogenesis markers in animals

110 infiltration beyond the margins of the main tumor mass and local recurrence after surgery.

111 r both tracers correlated significantly with tumor mass and Met expression and was not affected by th

112 ng progression from single cancer cells to a tumor mass and metastases, tumor cells send signals that

113 cells in DRS xenografts resulted in restored tumor mass and microvessel density.

114 thermore, this combinatorial therapy reduces tumor mass and prevents relapse much more effectively th

115 Tumor doses were inversely related to the tumor mass and ranged between 2 and 218 cGy/mCi.

116 nomas with doxorubicin led to a reduction in tumor mass and resulted in down-regulation of uMUC-1.

117 e astrocytes, inducing their exodus from the tumor mass and the resultant encapsulation of noninvasiv

118 viruses to spread effectively throughout the tumor mass and thereby increase the extent of viral repl

119 from host stroma was readily detected in the tumor mass and treatment with a newly developed anti-VEG

120 ed large numbers of circulating DCs into the tumor mass and, in the case of CT26 tumors, led to compl

121 dendritic cells (pDCs) highly populate lung tumor masses and are strictly correlated to bad prognosi

122 mas had an abnormal EUS: eight with discrete tumor masses and eight with gastric wall infiltration (s

123 f solid tumors include poor penetration into tumor masses and the immune response to the toxin compon

124 ogenesis is the prevailing process, then the tumor mass (and volume) will grow as a cubic power of ti

125 ffector T cells able to reduce/eliminate the tumor mass, and (b) long-lasting tumor-specific memory T

126 ently drive accelerated growth of the entire tumor mass, and thereby actively maintain tumor cell het

127 he vasculature while ignoring changes in the tumor mass, and those that predict tumor expansion in th

128 at distinct subpopulations of cells within a tumor mass are capable of driving tumorigenesis.

129 ture of glioma cells that escape the primary tumor mass are key impediments to the eradication of tum

130 tween initial mutation and a fully developed tumor mass are particularly poorly understood in glioma.

131 It is unclear which cells within the tumor mass are responsible for tumor initiation and main

132 macrophages, constituting a major portion of tumor mass, are involved in several pro-tumorigenic mech

133 We examined the tumor mass as a potential site of activation after adopt

134 an angiogenic response within the developing tumor mass, as demonstrated by immunostaining and microv

135 ivity of 4o, which significantly reduced the tumor mass at a dose thirty times lower than that requir

136 ive imaging that LRC are leaving the primary tumor mass at a very early stage and disseminate to peri

137 mor activity which significantly reduced the tumor mass at doses ten times lower than that required f

138 ic gemcitabine yielded a 40%-50% decrease in tumor mass at the end of treatment as compared with cont

139 ed in the cancer cells within the pancreatic tumor mass but were even more abundant in the acinar and

140 ity to chemotherapy directed not only at the tumor mass, but also invading glioblastoma cells.

141 (<20nm in diameter) penetrate well into the tumor mass, but are limited by their rapid systemic elim

142 maining tumor cells, which comprise 99.9% of tumor mass, but paradoxically have a poor tumor-initiati

143 Deletion of Rap1A, but not of Rap1B, reduced tumor mass by >70% relative to control.

144 fering RNA treatment of ALDH+ tumors reduced tumor mass by 91%.

145 ion of PTLD (defined as disappearance of the tumor mass by physical examination or computed tomograph

146 Tumor masses can contain regulatory lymphocytes, myeloid

147 The different subpopulations with a tumor mass communicate with each other and influence the

148 23)I-MIP-1072 was proportional to changes in tumor mass: decreased by paclitaxel treatment and increa

149 n for the existence of significant prostatic tumor mass despite a low-serum PSA.

150 Hence, the complete regression of tumor mass driven by inactivation of the MYC oncogene re

151 moral injection of Ad-MyD88 into established tumor masses enhanced adaptive immune responses and inhi

152 ells, such that only 50%-60% of cells in the tumor mass exhibited somatic NF1 loss.

153 The T cells infiltrating the tumor mass expressed the activation marker CD25 within 2

154 e inefficient spread of virus throughout the tumor mass following intratumoral injection.

155 ons occurring in the absence of a contiguous tumor mass for their clinical, morphologic, immunophenot

156 an unexpected redox-controlled link between tumor mass formation and metastatic capacity.

157 us and usually grow in body cavities without tumor mass formation.

158 ow that sustained activation of ARF6 reduces tumor mass growth but significantly enhances the invasiv

159 patients with a bulky lymphoma (at least one tumor mass >/=7 cm in diameter).

160 etwork of Organ Sharing criteria (those with tumor mass >3 cm, transperitoneal tumor biopsy, or metas

161 deed, retention of the labeled ligand in the tumor mass has a good tumor/background ratio, and a sign

162 sion coefficients and fluorescent signals in tumor masses immediately after the treatments.

163 d lower ERalpha protein levels and a reduced tumor mass, implying a tumor-suppressive-like function o

164 Further, TMEPAI knockdown decreased breast tumor mass in a mouse xenograft model in a manner associ

165 d intramuscularly exhibited markedly smaller tumor mass in a syngeneic host compared to a hybridoma p

166 uclear phagocyte lineage that constitute the tumor mass in dt-GCT.

167 lls comprise a substantial proportion of the tumor mass in human nonsmall cell lung cancers (NSCLC),

168 can account for as much as 50% of the total tumor mass in invasive breast carcinomas.

169 ral bone as well as co-localization with the tumor mass in marrow.

170 ine was significantly reduced as compared to tumor mass in mice provided with standard diet and injec

171 Tumor mass in mice that were provided with 333 or 500 mg

172 cells in a syngeneic mouse model and reduced tumor mass in mice with fully developed disease.

173 BRCA1a also significantly inhibited tumor mass in nude mice bearing human CAL-51 TN breast c

174 imulated cell proliferation, markedly reduce tumor mass in nude mice bearing human MCF-7 breast cance

175 HD demonstrated dose-dependent reduction in tumor mass in response to SGN-30 therapy.

176 accumulation was observed away from the main tumor mass in small clusters of neoplastic cells (47 +/-

177 An accumulation of DCs within solid tumor masses in situ has been associated indirectly with

178 esions were observed adjacent to plasma cell tumor masses in the bone marrow, indicating early stages

179 iral vector encoding FasL rapidly eliminated tumor masses in the Fas+ Renca tumor by inducing cell de

180 represent up to one half of the cells of the tumor mass, including both infiltrating macrophages and

181 V-PyVT)(634Mul) parent, but accumulated less tumor mass, indicating a net decrease in tumor growth.

182 nt tumor cells that migrate from the primary tumor mass into adjacent tissue(s) or circulate in the b

183 s/macrophages, which can be found within the tumor mass (intratumoral) or surrounding the tumor (peri

184 f the head showed right cerebral hemispheric tumor masses involving parasagittal, temporal and pariet

185 The heterogeneity of a tumor mass is an old concept that has lately become both

186 an glioma xenografts when 95 to 97.5% of the tumor mass is composed of bystander cells.

187 During tumor progression, an increase in tumor mass is concomitant with serum deprivation prior t

188 The final tumor mass is not affected in these animals, providing f

189 to pituitary tumors, but, unexpectedly, the tumor mass is not derived from the Sox2(+) mutation-sust

190 Tumor mass is remarkably decreased in animals injected w

191 ls to migrate great distances from a primary tumor mass is the primary cause of tumor recurrence.

192 Local radiation of tumor masses is an established modality for the therapy

193 exploratory laparotomy and resection of all tumor masses larger than 2 cm.

194 d ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and lowering o

195 ve monocyte/macrophage infiltration into the tumor mass, leading to its destruction within a few days

196 tment strategies are based on the removal of tumor mass mainly by surgery.

197 eading of a therapeutic agent throughout the tumor mass may be a useful adjunct to local therapy for

198 The boron-10 concentration in the main tumor mass (MTM) was approximately twice that of the inf

199 h bilateral involvement (n = 27 of 55; 47%), tumor masses (n = 27 of 36; 75%), and involvement of the

200 In the tumor mass, nuclear S100A4 expression by cholangiocarcin

201 Like a rapidly expanding tumor mass, obese adipose tissue becomes hypoxic due to

202 nhibitor, resulted in a dramatic decrease in tumor mass of the main forms of basal-like carcinomas.

203 Tumor masses of 10, 20, and 40 g were used in each model

204 s with stage III ovarian cancer and residual tumor masses of 2 cm or less.

205 sting that the T cells could eliminate large tumor masses once immune responses were induced.

206 sponse, including regressions of bulky liver tumor masses, ongoing beyond 7 y following adoptive TIL

207 e lesion, which may not represent the larger tumor mass or other sites of disease.

208 of therapeutic and imaging agents to either tumor masses or sites of inflammation.

209 sion of cortical parenchyma near the growing tumor mass, or from tumor cell invasion directly into th

210 ity may be correlated with changes in viable tumor mass over time.

211 howed that PPTT was capable of improving the tumor mass penetration of HPMA copolymers.

212 environmental pH to values that characterize tumor masses (pH 6-6.5) was sufficient to establish an a

213 Tumor masses presented a higher percentage of pDCs than

214 0 mg) and large (250-400 mg) xenografts with tumor mass reductions in all 10 models.

215 mice show a significant decrease in prostate tumor mass relative to TRAMP mice containing functional

216 ls that have the ability to migrate into the tumor mass, relatively extensive anatomic and temporal e

217 ell data, we find that samples from the same tumor mass share genomic and expression signatures, wher

218 h initially beneficial as judged with actual tumor mass shrinkage, this therapy invariably fails and

219 For example, in measurements of tumor mass, some individuals may exhibit no tumors; in m

220 Hostile microenvironmental conditions within tumor masses, such as nutrient deprivation, oxygen limit

221 y correlated with renalase expression in the tumor mass, suggesting a pathogenic role for renalase.

222 ls, but not vascular endothelium, within the tumor mass, suggesting that vascular endothelial BCA-1 e

223 ogous to cells isolated from the fluorescent tumor mass (T).

224 We used grossly dissected tumor masses that included tumor, blood vessels, connect

225 Moreover, clonally related tumor masses that showed distinct expression profiles we

226 available in clinical practice to treat such tumor masses, these therapeutic modalities are always as

227 Although PALs present as solid tumor masses, they are otherwise similar to BCBLs in tha

228 ed at restoring O2 delivery to the expanding tumor masses through the activation of a transcriptional

229 MTF-1 enhances the ability of the developing tumor mass to evade fibrosis and scarring of the tumor,

230 uantitative fashion describe the increase in tumor mass/volume over time.

231 Reduction of the tumor mass was accompanied by attenuation of angiogenesi

232 The tumor mass was demarcated well on narrow-band imaging, a

233 A 66% reduction in tumor mass was observed in the nude mice.

234 e distribution of Lip/Gd/DiI-DS covering the tumor mass was well defined and monitored with MRI.

235 tissue proximal to, but clearly outside the tumor mass, was also increased.

236 sduction and distribution of adenovirus in a tumor mass, we generated an adenovirus to selectively re

237 ly shown that the endothelial cell regulates tumor mass, we hypothesized that normal adult organ mass

238 CT acquisitions at multiple time points, and tumor masses were delineated from corresponding CT scans

239 of GCV (10 mg per kg) for 6 d, the residual tumor masses were excised and the animals challenged wit

240 Abdominal tumor masses were prominent in 63 cases (33 B-ALL and 30

241 rs was more localized and uniform across the tumor mass when compared to other methods of heating.

242 ributing nanoparticles throughout the entire tumor mass where they remain for an extended period (sev

243 ferent cancer stem cell populations within a tumor mass, where the tumor initiation and metastasis pr

244 an ovarian carcinomas, particularly in solid tumor masses, where they represent the majority of Treg.

245 asts to produce matrix within and around the tumor mass, whereas control tumors showed less stroma an

246 within a tumor to selectively irradiate the tumor mass while minimizing systemic toxicity.

247 ulogenesis is the dominant process, then the tumor mass will be characterized by a linear growth in t

248 arge numbers of the E1-deleted ad within the tumor mass will increase the transduction efficiency.

249 ess aggressive phenotypes in a heterogeneous tumor mass with smooth, noninvasive margins.

250 resulting in complete eradication of sizable tumor mass, with no recurrence of tumor growth.

251 selectively replicated throughout the solid tumor mass without apparent hepatotoxicity, caused tumor