ライフサイエンスコーパス: micrometastases

1 tion ability, particularly of bone and liver micrometastases.

2 ing of the metastatic soil and the growth of micrometastases.

3 melanoma, especially among those with nodal micrometastases.

4 lating tumour cells, and the destiny of some micrometastases.

5 kinase family, preferentially inhibits bone micrometastases.

6 raoperative evaluation were in patients with micrometastases.

7 n treating early-stage HER-2/neu--expressing micrometastases.

8 eading to variable classification of ITC and micrometastases.

9 f SLN, or the prognostic significance of SLN micrometastases.

10 , but transgenic mice only show low rates of micrometastases.

11 cal excision produces sufficient CTL against micrometastases.

12 than unity for saturation of both tumors and micrometastases.

13 elicit a protective immune response against micrometastases.

14 in natural killer cell-mediated clearance of micrometastases.

15 rts metastasis by increasing the survival of micrometastases.

16 be extensively evaluated for the presence of micrometastases.

17 ocity and molecular clearance of circulating micrometastases.

18 s (TUNEL)-proliferation (MIB1) ratios in the micrometastases.

19 were confined to the PC, and formed hepatic micrometastases.

20 9, and PIP) designed to detect breast cancer micrometastases.

21 the time of treatment and remain dormant as micrometastases.

22 lls during the treatment of murine pulmonary micrometastases.

23 mor regression, including regression of lung micrometastases.

24 issemination and the formation of lymph-node micrometastases.

25 rds a survival benefit by directly targeting micrometastases.

26 ument the clinical implications of molecular micrometastases.

27 urvival and inhibition of the growth of lung micrometastases.

28 duces accelerated growth of residual hepatic micrometastases.

29 g with an anticytokeratin antibody to detect micrometastases.

30 nt disease, presumably because of undetected micrometastases.

31 the neck or chest and with diffuse pulmonary micrometastases.

32 resulted in the disappearance of spontaneous micrometastases.

33 ary tumor is required for maintenance of the micrometastases.

34 that regulates the "dormancy" of AT6.1-17-4 micrometastases.

35 (177)Lu, (111)In, and (161)Tb at irradiating micrometastases.

36 ing s.c. tumor cells re-expressed it in lung micrometastases.

37 bearing PSMA+, luciferase-expressing PC3-ML micrometastases.

38 s but also in lungs and livers affected with micrometastases.

39 emboli, circulating tumor cell clusters, and micrometastases.

40 ar tools for quantitative detection of brain micrometastases.

41 cancer cells and supports their expansion to micrometastases.

42 and to rapidly test drug efficacies on bone micrometastases.

43 ysis enabled confirmation of the presence of micrometastases.

44 ing promise for treatment of prostate cancer micrometastases.

45 drives the progression from single cells to micrometastases.

46 for eradicating disseminated tumor cells and micrometastases.

47 otocytotoxicity and resolution of individual micrometastases.

48 imens were reviewed to assess CALI, TRG, and micrometastases.

49 ta) was identified around perivascular brain micrometastases.

50 to survive at secondary sites and establish micrometastases.

51 e containing both established metastases and micrometastases.

52 mor cells, and 4.39 (95% CI, 1.46-13.24) for micrometastases.

53 otes the survival and outgrowth of pulmonary micrometastases.

54 ic agent for the treatment of uveal melanoma micrometastases.

55 ary uveal melanoma and spread of its hepatic micrometastases.

56 Of those with micrometastases, 16 underwent CAD with 1 patient having

57 mined by histology, whereas the rate of OSNA-micrometastases (18%) was significantly higher than that

58 The mean signal ratios acquired with MSOT in micrometastases (2.5 +/- 0.3, n = 6) and in-transit meta

59 to the SLN was found in 48 patients (21 had micrometastases, 27 had macrometastases).

60 and 96% for patients younger than 40 y with micrometastases, 70% and 65% for patients older than 40

61 ore than 2 mm) was better than for detecting micrometastases, 73 versus 25%, respectively (P = 0.059)

62 sing proliferative programs in breast cancer micrometastases, a reaction that is partially dependent

63 icantly improved survival in mice bearing PC micrometastases after systemic administration.

64 A decrease in micrometastases, an increase in target-specific cytolysi

65 e regressions of established pulmonary 3-day micrometastases and 7-day macrometastases as well as est

66 /R) injury of the liver stimulates growth of micrometastases and adhesion of tumor cells, the clinica

67 ffers prospects for catching early recurrent micrometastases and for treating occult disease.

68 nal (3D) model representing adherent ovarian micrometastases and high-throughput quantitative imaging

69 ing modality for the detection of lymph node micrometastases and in-transit metastases from melanoma

70 SOT enabled detection of melanoma lymph node micrometastases and in-transit metastases undetectable w

71 in the SN more accurately reflects melanoma micrometastases and is also a more powerful predictor of

72 following: size-based discrimination between micrometastases and isolated tumor cells; identifiers to

73 maging, we show a widespread distribution of micrometastases and macrometastases in the brain, recapi

74 Subsequent micrometastases and metastases were visualized by GFP fl

75 ting lymph node involvement, (d) identifying micrometastases and residual microscopic disease, and (e

76 rief note about the escalating role of nodal micrometastases and sentinel node biopsy in the definiti

77 ents with T1 breast cancer, individuals with micrometastases and those with negative nodes have simil

78 rch and innovation for detection of systemic micrometastases and treatment of metastatic disease are

79 reatment is recommended in patients with SLN micrometastases and unfavorable tumor characteristics.

80 313 patients with stage III disease, 81% had micrometastases, and 19% had clinically detectable macro

81 54.7) and 44.9% (34.2-55.9) in patients with micrometastases, and 62.7% (56.5-68.6) and 65.7% (59.4-7

82 tiparameter assays, detection of bone marrow micrometastases, and circulating tumor cells.

83 istant tissues, the formation of new foci of micrometastases, and finally the growth of micrometastas

84 he growth of otherwise-indolent tumor cells, micrometastases, and human tumor surgical specimens loca

85 was 63%; it was 67% for patients with nodal micrometastases, and it was 43% for those with nodal mac

86 argins, to identify residual tumor cells and micrometastases, and to determine if the tumor has been

87 iganglioside antibodies prevent outgrowth of micrometastases, and we use this model to establish some

88 Here we demonstrate that micrometastases are associated with instigation of astro

89 Micrometastases are dependent on angiogenesis, suggestin

90 y whole-body imaging, and macrometastases or micrometastases are detected by intravital imaging or fl

91 complete surgical resection, suggesting that micrometastases are present even in localized disease an

92 t setting, where circulating tumor cells and micrometastases are the primary targets.

93 As such, micrometastases are usually missed and most patients cli

94 and effective tool to noninvasively identify micrometastases as an alternate to sentinal node biopsy

95 de-negative disease, isolated tumor cells or micrometastases as final nodal status.

96 detection and characterisation of lymph-node micrometastases, as well as potential microenvironmental

97 al; extravasation; growth and progression to micrometastases; as well as tumor microenvironment of me

98 at patients in dormancy have between 1 and 5 micrometastases at 10 years postresection, when they esc

99 sociated with increased formation of hepatic micrometastases at 48 hours and gross metastatic disease

100 Carboplatin alone did not eradicate ovarian micrometastases at a dose of 400 mg/m2, leaving survivin

101 6) and 65.7% (59.4-71.5) in patients without micrometastases at presentation (p<0.001).

102 atients already harbor dormant, undetectable micrometastases at the time of cancer diagnosis (Hensel

103 h for more sensitive in vivo detection of LN micrometastases, based on the use of ultrasound-guided s

104 alpha-Particles are suitable to treat cancer micrometastases because of their short range and very hi

105 with an increased likelihood of subclinical micrometastases before treatment or with posttreatment t

106 The numbers of micrometastases between the two groups are equivalent; t

107 ses) in sentinel lymph nodes and bone marrow micrometastases (BMM) were independently described as pr

108 urden not by preventing the establishment of micrometastases but rather by preventing vascularization

109 significantly higher local invasion and lung micrometastases but, unexpectedly, lower proliferation t

110 sensitive method for detection of lymph-node micrometastases, but accurate quantitative assessment ha

111 broblast growth factor (FGF) 1 have frequent micrometastases, but macrometastases are not observed.

112 reduced the numbers of MLL lung colonies and micrometastases by 40- to >100-fold, whereas Ac-HSPNC-NH

113 by preventing vascularization and growth of micrometastases by 55% and 43%, respectively.

114 potential of specific mRNA markers to detect micrometastases by reverse-transcriptase polymerase chai

115 c value as mRNA markers for the detection of micrometastases by the RT-PCR assay because they are exp

116 to assess the sensitivity of CK-20 to detect micrometastases by the RT-PCR assay in the blood and fro

117 tes show that extravasation and formation of micrometastases by TRCs are more efficient than by the c

118 Breast cancer bone micrometastases can remain asymptomatic for years before

119 We found that nearly all lgl micrometastases co-express the neuronal cell marker, ELA

120 status, and vascular invasion, the effect of micrometastases decreased and was no longer significant,

121 Micrometastases detected by immunohistochemistry are spe

122 invasive lobular and ductal cancers had node micrometastases, detected by haematoxylin and eosin, com

123 membrane antigen (PSMA) for the treatment of micrometastases due to prostate cancer (PC).

124 cannot effectively reach residual disease or micrometastases, especially within the lymphatic system.

125 atients with axillary node-negative or nodal micrometastases, estrogen receptor-positive, and human e

126 Mice with preexisting wild-type pulmonary micrometastases exhibit prolonged survival and an increa

127 By contrast, most of the brat micrometastases expressed neither marker.

128 7)Ga is a promising radionuclide for killing micrometastases, for high-density target antigens, but m

129 arrest, transendothelial migration and early micrometastases formation.

130 s, circulating tumor cell clusters, and lung micrometastases frequently expressed the epithelial cyto

131 We examined micrometastases from a murine model of ovarian carcinoma

132 be necessary in patients with sentinel node micrometastases from T1/T2 lesions, or in patients with

133 osomes are effective in treating early-stage micrometastases, giving median survival times similar to

134 15 of these 16 patients with evidence of micrometastases had the highest cytokeratin 19 transcrip

135 Bone-marrow micrometastases have been found in patients with primary

136 for evaluating the effect of chemotherapy on micrometastases; however, knowledge of such a response p

137 orectal cancer cells led to the formation of micrometastases; however, loss of PTEN is required for s

138 We detected micrometastases in 15% of ovarioles from wild type host

139 We detected micrometastases in 15.8% of ovarioles from wild type hos

140 CK-IHC and RT-PCR identified occult micrometastases in 53% of patients whose SNs were negati

141 melanoma growth and the formation of hepatic micrometastases in a dose-dependent manner.

142 -labetuzumab-IRDye800CW can detect pulmonary micrometastases in a mouse model.

143 otect the disseminated prostate cancer liver micrometastases in a proliferation-independent manner, a

144 valid surrogates for the detection of occult micrometastases in ALN.

145 .4) completely eradicated breast cancer lung micrometastases in approximately 67% of HER-2/neu transg

146 otential to prevent the development of brain micrometastases in breast cancer patients.

147 s (25%), and CK-IHC of SNs identified occult micrometastases in four patients (10%) whose SNs were ne

148 Additional processing revealed occult micrometastases in four patients (three in sentinel node

149 led a significantly reduced presence of lung micrometastases in HIF-1alpha(flox/flox)/LysMcre mice tr

150 RT)-PCR for detecting clinically significant micrometastases in histopathologically normal archival p

151 y and clinically significant prostate cancer micrometastases in histopathologically normal PLN, RT-PC

152 analogous approach may be effective against micrometastases in human patients, including tumors whos

153 pletely prevented the formation of pulmonary micrometastases in Lewis lung carcinoma (P = 0.0001).

154 ere not required for aggressive outgrowth of micrometastases in livers treated with surgery.

155 avenous injection, these materials can image micrometastases in multiple organs with spatiotemporal r

156 oup patients with clinically relevant occult micrometastases in N0-PLN, who may benefit from addition

157 The presence of bone-marrow micrometastases in patients with primary breast cancer i

158 to be an accurate method for detecting nodal micrometastases in previously untreated patients with ea

159 Quantitative analyses of pulmonary micrometastases in primary tumor-bearing mice indicated

160 lecular detection of isolated tumor cells or micrometastases in regional lymph nodes indicates high r

161 Detection of micrometastases in sentinel lymph nodes (SLNs) is import

162 uation can miss clinically relevant melanoma micrometastases in SLNs.

163 designed to determine the survival impact of micrometastases in SNs of patients with invasive breast

164 treatment and facilitated identification of micrometastases in solid organs at autopsy.

165 ti-carbohydrate Abs reduced the outgrowth of micrometastases in the 4T1 spontaneous tumor model, sign

166 Moreover, there were fewer lung micrometastases in the 5C4 animals.

167 231-BR clones produced comparable numbers of micrometastases in the brain as control transfectants; h

168 bes that are capable of imaging tiny (<1 mm) micrometastases in the liver, lung, pancreas, kidneys, a

169 nsitions were frequently observed among lung micrometastases in the organ parenchyma and immediately

170 Detection of micrometastases in the regional tumor-draining lymph nod

171 cancer patients with isolated tumor cells or micrometastases in the sentinel node (SLN).

172 ) has led to an increase in the detection of micrometastases in the sentinel node (SN).

173 isolated tumor cells, and 1028 patients with micrometastases in the SLN were included.

174 of intrahepatic NK cells associated with the micrometastases in treated groups.

175 infiltrates (SNTI; isolated tumor cells and micrometastases) in sentinel lymph nodes and bone marrow

176 None of the patients with micrometastases, including those without CAD, has eviden

177 The last of these involves the growth of micrometastases into macroscopic tumors.

178 ming axillary treatment in patients with SLN micrometastases is associated with an increased 5-year r

179 Furthermore, treatment of micrometastases is impeded by several biobarriers, inclu

180 distant disease; however, in the presence of micrometastases, it represents a marker of distant relap

181 mited by tumor vascular permeability, and in micrometastases, limited by diffusion.

182 In the absence of micrometastases, local recurrence would be a determinant

183 In larger micrometastases (</= 100 mum in diameter), the activity

184 is improved detection of both bone and liver micrometastases (<2 mm) with excellent tumor-to-normal c

185 understanding the survival and outgrowth of micrometastases may hold greater promise to combat metas

186 Nodal micrometastases may not be detected with current standar

187 Micrometastases (microscopic vascular or biliary invasio

188 to determine the prognostic significance of micrometastases (MM) and isolated tumor cells (ITCs) in

189 el node (SN) biopsy indicate a 29.6% rate of micrometastases (MM) identified by immunohistochemical s

190 tage II CRC having > or =12 LNs negative for micrometastases (N0i-) are likely cured by surgery alone

191 NGS: For women with isolated tumour cells or micrometastases [nodal deposit(s) >0.2-2 mm] in one or m

192 es (SNs) draining a primary CRC could detect micrometastases not detected by conventional histopathol

193 s; thus, PCR for CgA can be used to identify micrometastases not evident by light microscopy or IHC a

194 sis demonstrated that in patients with nodal micrometastases, number of tumor-containing lymph nodes,

195 astatic tumours and enables the detection of micrometastases of size <0.5 mm, extending the detection

196 riable, potentially due to undetected occult micrometastases (OM).

197 thological tumor regression grade (TRG), and micrometastases on long-term prognosis in patients under

198 prognostic factors as well as the effect of micrometastases on relapse-free survival and overall sur

199 owever, an insensitive technique to identify micrometastases or delineate subpopulations of NE cells.

200 allowed imaging of physiologically relevant micrometastases originating in an orthotopically implant

201 We find that bone micrometastases predominantly reside in a niche that exh

202 ls in BICA maintain features of in vivo bone micrometastases regarding the microenvironmental niche,

203 This indicates that the micrometastases result from continued seeding from the p

204 Micrometastases significantly impacted prognosis assessm

205 iates patients with T1 tumors and lymph node micrometastases (stage IB) from patients with T1 tumors

206 44s protein expression was conserved in lung micrometastases suggesting that it may have been necessa

207 stion arises as to whether clinically occult micrometastases survive in a state of balanced prolifera

208 ld more active against established pulmonary micrometastases than cultured unfractionated TDLN, and >

209 ntibodies may be more suitable for targeting micrometastases than vascularized tumors.

210 we evaluated the malignant character of lung micrometastases that emerge in such models after orthoto

211 umors seed at most an average of 6 dangerous micrometastases that escape from growth restriction with

212 o be maintained by small numbers of sizeable micrometastases that escape from growth restriction with

213 Drug-resistant micrometastases that escape standard therapies often go

214 ing procedures are needed to identify occult micrometastases that spawn BCR.

215 it still resulted in complete eradication of micrometastases that were established at that time point

216 LN3, were used as a model of prevascularized micrometastases; their response to an anti-PSMA antibody

217 routing of sinusoidal endothelial cells into micrometastases, thereby supporting early metastatic ang

218 creasing their recruitment to vasculature of micrometastases, thereby supporting progression to macro

219 ever, TF also supported the early success of micrometastases through an additional mechanism independ

220 atients with trunk melanomas, 4 patients had micrometastases to axillary SLNs (AxSLNs).

221 ls, and immune cells isolated from mice with micrometastases to determine which cell type is producin

222 effective strategy to prevent progression of micrometastases to macroscopic disease.

223 Thus, failure of micrometastases to proliferate was not due to inhibitory

224 32 patients with non-IM in-transit nodes had micrometastases to these in-transit nodes.

225 with macrometastases or older patients with micrometastases treated at GR and MSKCC, respectively (P

226 cyclopamine-treated mice developed pulmonary micrometastases versus seven of seven mice with multiple

227 The incidence of sentinel-node micrometastases was 16.0% (122 of 764 patients), and the

228 after inoculation, and the number of hepatic micrometastases was histologically determined.

229 nificant quantitative reduction in pulmonary micrometastases was observed in fibrinogen-deficient mic

230 Lymphatic and pulmonary micrometastases were detected as deposits of X-gal-stain

231 opsy with immediate lymphadenectomy if nodal micrometastases were detected on biopsy.

232 Hepatic micrometastases were enumerated.

233 The micrometastases were evaluated for apoptosis and prolife

234 Micrometastases were identified in SLNs of 16 of the 106

235 lap over the chest wall, while contralateral micrometastases were imaged through the corresponding sk

236 Subsequent micrometastases were visualized by GFP fluorescence in t

237 ill need to eliminate these small numbers of micrometastases, which may be preangiogenic and nonvascu

238 t range, offering the potential for treating micrometastases while sparing normal tissues.

239 (<10 mum), making them suitable for treating micrometastases while sparing normal tissues.

240 ize tumor boundaries and successfully detect micrometastases with diameters <1 mm.

241 means to reduce circulating tumor cells and micrometastases would be an advantage in cancer vaccine