ライフサイエンスコーパス: micrometastases

1 environment in mouse xenograft breast cancer micrometastases.

2 to survive at secondary sites and establish micrometastases.

3 e containing both established metastases and micrometastases.

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

5 otes the survival and outgrowth of pulmonary micrometastases.

6 ic agent for the treatment of uveal melanoma micrometastases.

7 ary uveal melanoma and spread of its hepatic micrometastases.

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

9 melanoma, especially among those with nodal micrometastases.

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

11 ed on the specific physiology of a patient's micrometastases.

12 raoperative evaluation were in patients with micrometastases.

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

14 eading to variable classification of ITC and micrometastases.

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

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

17 cal excision produces sufficient CTL against micrometastases.

18 than unity for saturation of both tumors and micrometastases.

19 elicit a protective immune response against micrometastases.

20 in natural killer cell-mediated clearance of micrometastases.

21 rts metastasis by increasing the survival of micrometastases.

22 be extensively evaluated for the presence of micrometastases.

23 ocity and molecular clearance of circulating micrometastases.

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

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

26 9, and PIP) designed to detect breast cancer micrometastases.

27 the time of treatment and remain dormant as micrometastases.

28 lls during the treatment of murine pulmonary micrometastases.

29 mor regression, including regression of lung micrometastases.

30 issemination and the formation of lymph-node micrometastases.

31 ument the clinical implications of molecular micrometastases.

32 urvival and inhibition of the growth of lung micrometastases.

33 duces accelerated growth of residual hepatic micrometastases.

34 g with an anticytokeratin antibody to detect micrometastases.

35 nt disease, presumably because of undetected micrometastases.

36 the neck or chest and with diffuse pulmonary micrometastases.

37 astases, compared to mammary tumors or brain micrometastases.

38 resulted in the disappearance of spontaneous micrometastases.

39 hysiology and nanoparticle delivery of 1,301 micrometastases.

40 ary tumor is required for maintenance of the micrometastases.

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

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

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

44 h may be particularly effective to eliminate micrometastases.

45 path, particularly to single tumor cells and micrometastases.

46 self-organization prohibits the outgrowth of micrometastases.

47 t have disseminated to the lungs expand into micrometastases.

48 g tumor cells, disseminated tumor cells, and micrometastases.

49 Its timing coincides with the seeding of micrometastases.

50 tion ability, particularly of bone and liver micrometastases.

51 t KLK3 ectopic expression is associated with micrometastases.

52 g tumor cells, disseminated tumor cells, and micrometastases.

53 ows effective treatment of local lesions and micrometastases.

54 and to rapidly test drug efficacies on bone micrometastases.

55 kinase family, preferentially inhibits bone micrometastases.

56 rds a survival benefit by directly targeting micrometastases.

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

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

59 emboli, circulating tumor cell clusters, and micrometastases.

60 ar tools for quantitative detection of brain micrometastases.

61 cancer cells and supports their expansion to micrometastases.

62 ysis enabled confirmation of the presence of micrometastases.

63 ing promise for treatment of prostate cancer micrometastases.

64 drives the progression from single cells to micrometastases.

65 for eradicating disseminated tumor cells and micrometastases.

66 otocytotoxicity and resolution of individual micrometastases.

67 undetected LNMs were either PSMA-negative or micrometastases.

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

69 ta) was identified around perivascular brain micrometastases.

70 Among 160 patients with SN micrometastases, 126 received inguinofemoral radiotherap

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

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

73 dard of care (IFL), whereas patients with SN micrometastases ( 2 mm) continued to receive inguinofemo

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

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

76 icles access a higher proportion of cells in micrometastases (50% nanoparticle-positive cells) compar

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

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

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

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

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

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

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

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

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

86 earchers to measure nanoparticle delivery to micrometastases and highlights an opportunity to target

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

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

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

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

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

92 ter adherence and early treatment of distant micrometastases and may increase pathological complete r

93 Subsequent micrometastases and metastases were visualized by GFP fl

94 lution programs before surgery may eliminate micrometastases and reduce tumor recurrence.

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

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

97 t facilitate the progression of pre-existing micrometastases and the initiation of new metastases, wh

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

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

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

101 313 patients with stage III disease, 81% had micrometastases, and 19% had clinically detectable macro

102 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

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

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

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

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

107 s motility pathway genes were upregulated in micrometastases, and stress response signaling was upreg

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

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

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

111 Micrometastases are dependent on angiogenesis, suggestin

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

113 prognosis for malignant INS is poor, because micrometastases are frequently missed during surgery.

114 and strategies to optimize penetration into micrometastases are important for RPT therapy with carri

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

116 tastases is difficult to investigate because micrometastases are small in size and lie deep within ti

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

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

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

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

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

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

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

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

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

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

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

128 predict nanoparticle delivery to individual micrometastases based on their physiology.

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

130 benzylguanidine, is ineffective at targeting micrometastases because of the low-linear-energy-transfe

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

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

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

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

135 pression and activities specifically in bone micrometastases (BMMs), leading to endocrine resistance.

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

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

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

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

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

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

142 nd reduced the formation of spontaneous lung micrometastases by PDX tumors in mice.

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

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

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

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

147 Breast cancer bone micrometastases can remain asymptomatic for years before

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

149 tioxidant programs were induced in pulmonary micrometastases, compared to mammary tumors or brain mic

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

151 Micrometastases detected by immunohistochemistry are spe

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

153 We find that both primary tumours and micrometastases display transcriptional heterogeneity bu

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

155 ma, (131)I-MIBG, is ineffective at targeting micrometastases due to the low linear energy transfer (L

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

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

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

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

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

161 arrest, transendothelial migration and early micrometastases formation.

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

163 We examined micrometastases from a murine model of ovarian carcinoma

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

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

166 15 of these 16 patients with evidence of micrometastases had the highest cytokeratin 19 transcrip

167 es display transcriptional heterogeneity but micrometastases harbour a distinct transcriptome program

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

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

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

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

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

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

174 These interactions may arrest the growth of micrometastases in a dormant state and prevent newly arr

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

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

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

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

179 s system enabled visualization of peritoneal micrometastases in an immune-competent environment.

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

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

182 site led to increased apoptosis and limited micrometastases in combination with paclitaxel treatment

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

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

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

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

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

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

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

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

191 Importantly, MRI could detect micrometastases in lung tissue comprised on the order of

192 h resolutions and able to detect spontaneous micrometastases in lungs of mice provides a useful tool

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

194 proresolving autacoid mediators, eliminated micrometastases in multiple tumor-resection models, resu

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

196 to discover personalized strategies against micrometastases in non-metastatic NSCLC patients.

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

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

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

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

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

202 uation can miss clinically relevant melanoma micrometastases in SLNs.

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

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

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

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

207 231-BR clones produced comparable numbers of micrometastases in the brain as control transfectants; h

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

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

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

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

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

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

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

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

216 horylation as the top pathway upregulated in micrometastases, in contrast to higher levels of glycoly

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

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

219 fficulties in identifying tumor boundary and micrometastases intraoperatively.

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

221 However, nanoparticle delivery to micrometastases is difficult to investigate because micr

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

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

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

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

226 Undetected LNMs either were micrometastases located in the lymph node border or were

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

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

229 T) cells, similar to cells derived from lung micrometastases (LUNG).

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

231 Nodal micrometastases may not be detected with current standar

232 Micrometastases (microscopic vascular or biliary invasio

233 therapy to eradicate tumor cell clusters and micrometastases might offer cure.

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

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

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

237 s with low disease burden sentinel node (SN) micrometastases, namely, American Joint Committee on Can

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

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

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

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

242 At POM 5 micrometastases occurred in bones and lungs, which were

243 Micrometastases of colorectal cancer can remain dormant

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

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

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

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

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

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

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

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

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

253 Micrometastases significantly impacted prognosis assessm

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

255 44s protein expression was conserved in lung micrometastases suggesting that it may have been necessa

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

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

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

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

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

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

262 Drug-resistant micrometastases that escape standard therapies often go

263 heterogeneity with variable PSMA expression, micrometastases that may not absorb sufficient radiation

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

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

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

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

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

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

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

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

272 4 loss prevents tumor formation, it promotes micrometastases to distant organs in this melanoma-prone

273 tumor sites and determines the transition of micrometastases to macrometastases.

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

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

276 is essential for the progression of dormant micrometastases to rapidly growing and clinically overt

277 tors involved in predicting the responses of micrometastases to targeted (225)Ac-based therapies and

278 32 patients with non-IM in-transit nodes had micrometastases to these in-transit nodes.

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

280 Targeting micrometastases using nanoparticles could offer a way to

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

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

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

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

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

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

287 Hepatic micrometastases were enumerated.

288 The micrometastases were evaluated for apoptosis and prolife

289 Micrometastases were identified in SLNs of 16 of the 106

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

291 Subsequent micrometastases were visualized by GFP fluorescence in t

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

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

294 (<10 mum), making them suitable for treating micrometastases while sparing normal tissues.

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

296 ases and highlights an opportunity to target micrometastases with nanoparticles.

297 d image analysis to assess the physiology of micrometastases with single-cell resolution and quantify

298 safe alternative for IFL in patients with SN micrometastases, with minimal morbidity.

299 s) can explain a broad range of behaviors of micrometastases, without the need for complex molecular-

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