ライフサイエンスコーパス: metastases

1 recurrences, 63 lymph nodes, and 31 distant metastases).

2 a knife radiosurgery for uveal melanomas and metastases.

3 ent of gene and cell therapies against brain metastases.

4 ting of patients receiving therapy for liver metastases.

5 3 months of PTX therapy for recurrent liver metastases.

6 trophils, and inflammatory monocytes to lung metastases.

7 r intraindividual genomic consistency across metastases.

8 y encounter, and acquire the ability to form metastases.

9 se, 160 were detected in at least one of the metastases.

10 ients with HER2-positive breast cancer brain metastases.

11 in circulation, and angiogenesis at sites of metastases.

12 l tumour, and the side and number of hepatic metastases.

13 exit route for tumour cell dissemination and metastases.

14 )Ho radioembolization in patients with liver metastases.

15 ancer hospitalized with a diagnosis of brain metastases.

16 ession, especially in central nervous system metastases.

17 ctal cancer patient with nonresectable liver metastases.

18 ted response rates in the treatment of liver metastases.

19 CT/MRI regarding the presence and number of metastases.

20 s have a higher risk for lung and lymph node metastases.

21 tinib together with FBXL7 depletion prevents metastases.

22 m survival due to locoregional recurrence or metastases.

23 both primary tumor growth rates and distant metastases.

24 r (NSCLC) primary tumors and matched distant metastases.

25 ndently associated with an increased risk of metastases.

26 recurrence, extraocular spread, and systemic metastases.

27 s associated with a different risk for liver metastases.

28 , adjacent normal tissues, and matched liver metastases.

29 en primary colorectal tumors and their liver metastases.

30 y clones from primary tumors and/or existing metastases.

31 ially if the lesion location is atypical for metastases.

32 coming the predominant population in distant metastases.

33 ations, and 67% of them had biopsy-confirmed metastases.

34 CDR1 was sufficient to promote migration and metastases.

35 35) were independently associated with liver metastases.

36 hout distant metastatic recurrence (DMR) and metastases.

37 ografts to investigate the cell of origin of metastases.

38 ate production in breast-cancer-derived lung metastases.

39 s-free death or 3) death after appearance of metastases.

40 alignant cell migration and the formation of metastases.

41 lacked mutant BRAF in at least one of their metastases.

42 logy, both for primary gliomas and for brain metastases.

43 e status of 2, and 18% of patients had brain metastases.

44 ing untreated (n = 99) and treated (n = 100) metastases.

45 distant metastasis, and 42.9% had bone-only metastases.

46 ated with mitigated tumor growth and reduced metastases.

47 notypes from normal tissue to drug-resistant metastases.

48 tage, tumor grade, and presence of bone-only metastases.

49 osuppression is also present in extracranial metastases.

50 onsidered for subjects with isolated adrenal metastases.

51 ch show stem-like characteristics and induce metastases.

52 activity and ability to form liver and lung metastases.

53 ies for primary brain malignancies and brain metastases.

54 rimary treatment for uveal melanoma or uveal metastases.

55 NA molecules that might promote formation of metastases.

56 s in both pathways led to ACC with pulmonary metastases.

57 astases with no corresponding (18)F-FDG-avid metastases.

58 of tumor cells were significantly larger in metastases.

59 fe in selected patients with untreated brain metastases.

60 lung, lymph node, and chest wall/breast/skin metastases.

61 ipulating the tumor microenvironment in bone metastases.

62 nts with inoperable, chemorefractory hepatic metastases.

63 metastatic sites, and presence of bone-only metastases.

64 Mouse imaging analyses were used to identify metastases.

65 onectomy for primary tumors and 12 (32%) for metastases.

66 ely), whereas sensitivity was lower for lung metastases (48.3% vs. 100% and 75.9%, respectively).

67 ac (6/16, 38%) and internal iliac lymph node metastases (6/16, 38%).

68 nts who recurred, 62% presented with distant metastases (63% of pN0 and 62% of pN1, P = 0.553), 24% w

69 eoperative chemotherapy for colorectal liver metastases (70%, 82%, 89%, P < 0.001) and median operati

70 nt group, in which 68% recurred with distant metastases (76% of pN0 and 64% of pN1, P = 0.326) and 18

71 vs. 69.7% and 89.4%, respectively) and liver metastases (97.3% vs. 92.1% and 94.8%, respectively), wh

72 patients with nonresectable colorectal liver metastases a 5-year overall survival comparable to other

73 ay of treatment for many patients with brain metastases, a growing number of systemic options are now

74 le treatment options for patients with brain metastases, a multidisciplinary approach is strongly rec

75 Metastases account for most cancer-related deaths, yet t

76 Metastases account for the majority of cancer deaths.

77 rtant to detect and monitor response in bone metastases accurately.

78 ic breast cancer, including those with brain metastases, adding tucatinib to trastuzumab and capecita

79 ately 3% of patients hospitalized with brain metastases also had a diagnosis of ICH, which was signif

80 nt metastases without (18)F-FES-avid distant metastases, although in one patient liver metastases wer

81 ignancy and 1-5 metastatic lesions, with all metastases amenable to stereotactic ablative radiotherap

82 Metastasis-derived cell lines in vitro and metastases analyzed ex vivo from an autochthonous lung c

83 emical shift SI index did not differ between metastases and adenomas (P = .748).

84 set of bounding box predictions encompassing metastases and associated detection confidences.

85 CDR1as or CDR1 significantly inhibited LUSC metastases and CDR1 was sufficient to promote migration

86 8)Ga-PSMA-11 PET for osseous prostate cancer metastases and improve bone uptake interpretation using

87 l carcinoma with measurable disease and bone metastases and is generally well tolerated.

88 he presence of lymph node as well as distant metastases and is specifically up-regulated in CMS4 tumo

89 ast tumours with elevated risk of developing metastases and may require more aggressive therapies.

90 ntitumor immunity, leading to increased lung metastases and mortality.

91 Although treatment of bone metastases and myeloma bone disease is rarely curative,

92 patients with bone-only urothelial carcinoma metastases and patients with rare histologies of the gen

93 atment and management of patients with brain metastases and provide speculation on future research di

94 osis proteins (IAPs), eliminated early-stage metastases and reduced progression of advanced BC metast

95 faster rate, than KC mice, and had more lung metastases and significantly shorter average survival ti

96 ling in the promotion of breast cancer brain metastases and support the prognostic and therapeutic cl

97 that somatic alterations contribute to brain metastases and that genomic sequencing of a sufficient n

98 escribed improvements in the imaging of bone metastases and their response to therapy have led to ado

99 analysis, (18)F-FDG PET, G3 tumor, >=2 liver metastases, and >=2 prior therapies were independent pro

100 Nine were alive and well, 1 was alive with metastases, and 6 had died of metastatic disease (includ

101 (no bone metastases [M0], equivocal for bone metastases, and bone metastases present [M1]) and on a d

102 ity in detecting primary tumors, soft-tissue metastases, and bone or bone-marrow metastases was 72%,

103 ity in detecting primary tumors, soft-tissue metastases, and bone or bone-marrow metastases was 83%,

104 3%) patients, in 63 (29%) CT/MRI showed more metastases, and in 16 (7%) CT/MRI showed fewer metastase

105 ied by previous platinum use, history of CNS metastases, and oestrogen and progesterone receptor stat

106 ) after controlling for CTR, number of liver metastases, and preoperative extrahepatic disease.

107 nd the combination to inhibit lung and liver metastases, and prolong host survival without toxicity.

108 results in overall lower LN yields, lower LN metastases, and significant downstaging of tumors.

109 ents one of the most common sites of distant metastases, and spinal bone metastasis is the most commo

110 nd bone-only disease; patients with visceral metastases; and patients aged up to 40 years.

111 Brain metastases are a very common manifestation of cancer tha

112 Lymphatic metastases are closely associated with tumor relapse and

113 Bone metastases are common, especially in more prevalent mali

114 In contrast, metastases are enriched for key endoderm and lung-specif

115 Bone metastases are frequently the only source for obtaining

116 Although UM metastases are less responsive than cutaneous melanoma t

117 data reveals that downregulated pathways in metastases are mainly immune-related.

118 Background Brain metastases are manually identified during stereotactic r

119 tions for VTE treatment; patients with brain metastases are now addressed in the VTE treatment sectio

120 Metastases are the cause of the vast majority of cancer

121 Brain metastases are the most common intracranial tumors in ad

122 stration-resistant prostate cancer and liver metastases assigned to (177)Lu-PSMA alone (n = 31) or in

123 Here we show that IL33 is upregulated in metastases-associated fibroblasts in mouse models of spo

124 in primary tumors, lymph nodes, and distant metastases at 1 h after injection, with an SUV(max) of m

125 bone, lymph node, and chest wall/breast/skin metastases at baseline was observed.

126 ded because of unequivocal evidence of liver metastases at baseline whole-body MRI, two participants

127 ined sensitivity to 100% for detecting nodal metastases at ePLND.

128 rrelated with absence of axillary lymph node metastases at final pathology (ypN0) in patients treated

129 ired for outgrowth for primary melanomas and metastases at secondary sites.

130 s with ROS1 fusion-positive NSCLC have brain metastases at the diagnosis of advanced disease.

131 as more challenging to trace migrations from metastases back to primary tumors.

132 lmost perfect except for judgment of distant metastases based on the PSMA Reporting and Data System (

133 oma on the lobar distribution of its hepatic metastases based on the streamline hypothesis.

134 Breast cancer brain metastases (BCBM) have a 5-20 year latency and account f

135 r 2 (HER2)-positive breast cancer with brain metastases (BMs) showed statistically significant improv

136 Up to 50% of patients develop distant metastases, but current systemic therapies have limited

137 e discovered that breast-cancer-derived lung metastases, but not the corresponding primary breast tum

138 t give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2-)

139 rtion of breast cancer patients develop bone metastases, but the mechanisms regulating tumor cell dis

140 Metastases cause a vast majority of cancer morbidity and

141 iologist 1 and radiologist 2) were higher in metastases compared with adenomas when assessed by both

142 erentially mutated or copy-number altered in metastases compared with the paired primary tumors from

143 as significantly higher in luminal/ER+ tumor metastases compared with their primaries.

144 However, many metastases continue to express E-cadherin, and a full EM

145 Furthermore, decitabine reduces metastases derived from prostate and pancreatic cancer c

146 ary outcome measure was freedom from distant metastases, designed with 80% power to detect an improve

147 20, and >20 ng/mL) and the incidence of bone metastases detected by total-body (68)Ga-prostate-specif

148 ancer patients with nonresectable liver-only metastases determined by computed tomography (CT)/magnet

149 Thus, lymph node and distant metastases develop through fundamentally different evolu

150 In vivo, lung metastases developing from orthotopic MDA-MB-231 tumors

151 rivate 'driver' mutations, whereas untreated metastases did not, suggesting that treatment promotes c

152 astasis at diagnosis of DP-NET, 50 developed metastases during follow-up, and 69 died.

153 -five per cent (n = 5) of patients presented metastases during follow-up.

154 ng treatment options for patients with brain metastases, enrolment in clinical trials is essential to

155 lesions lacking avidity, and 2 had solitary metastases exhibiting very low avidity.

156 was performed in which the ability to detect metastases for CNN- and gaussian-filtered bone scans wit

157 pilot case of prostate cancer with multiple metastases for genetic analyses.

158 The 10 metastases for which treatment failed were managed furth

159 ors, lymph node metastases (LNMs), and liver metastases from 10 CRC patients.

160 The lobar distribution of hepatic metastases from colorectal adenocarcinoma may not be ass

161 T2-weighted heterogeneity can differentiate metastases from lipid-poor adenomas.

162 Brain metastases from lung adenocarcinoma (BM-LUAD) frequently

163 Pembrolizumab has activity in brain metastases from NSCLC with PD-L1 expression at least 1%

164 t known proportions, created from two clonal metastases from the same patient.

165 y feared complication in patients with brain metastases given the potential for significant morbidity

166 Metastases had higher T2-weighted SI ratio than adenomas

167 biology and molecular underpinnings of brain metastases has greatly improved, resulting in more sophi

168 The incidence of brain metastases has markedly increased in the past 20 years o

169 While molecular imaging of metastases has witnessed substantial progress as an area

170 In clinical specimens, brain metastases have elevated HIF1A protein expression, compa

171 atio, 18.7; P < .0001), formation of distant metastases (hazard ratio, 32.1; P < .0001), and shorter

172 ry breast tumors, and in patients with brain metastases, hypoxic signaling within CTCs predicts decre

173 ect on measured PSMA activity in small nodal metastases, impacting the miPSMA score.

174 Astrocyte reactivity associated with brain metastases impaired cerebrovascular responses to stimuli

175 US failed to suggest metastases in 10 patients.

176 as fully consistent with CT/MRI in detecting metastases in 113 (53%) patients, in 63 (29%) CT/MRI sho

177 of 4 previously unknown lung and lymph node metastases in 2 patients.

178 rs agreed on the number and location of bone metastases in 205 (93.6%) patients.

179 nodes were detected in 23 patients and bone metastases in 5 on (68)Ga-PSMA-11 PET/MRI.

180 -FDG PET/CT detected previously unidentified metastases in 8 (38%) of 21 patients, resulting in upsta

181 e the role of PSMA PET/CT in detecting nodal metastases in a large cohort of men and compare imaging

182 way to assess the treatment response of bone metastases in clinical trials.

183 bated with PGE(2) formed more liver and lung metastases in mice than control LS174T cells.

184 lity of pancreatic cancer cells to form lung metastases in mice.

185 rably with (18)F-FDG PET/CT for detection of metastases in patients with metastatic ILC.

186 n (18)F-NaF PET/CT for the detection of bone metastases in patients with PCa was very high among trai

187 a sensitive screening modality in detecting metastases in patients with primary uveal melanoma, if c

188 oride (NaF) PET/CT for the detection of bone metastases in patients with prostate cancer (PCa).

189 -stroma interactions that favor formation of metastases in the liver.

190 intravenously administered erythrocytes with metastases in the lungs, we show that treatment with che

191 s with both regressive and progressive liver metastases in the same patient (best vs. worst respondin

192 sympathetic neuroblasts, and drives distant metastases in vivo.

193 ((89)Zr)-pertuzumab can depict HER2-positive metastases in women with HER2-negative primary breast ca

194 CT was successful in detecting HER2-positive metastases in women with HER2-negative primary breast ca

195 Lymph node metastases, in contrast, display high levels of inter-le

196 gnaling pathway to suppress tumor growth and metastases, in part, by limiting ROS activity.

197 rmal prostate epithelium to localized PCa to metastases-in specimens derived from human tissue.

198 ys were preferentially mutated or altered in metastases, including mTOR, CDK/RB, cAMP/PKA, WNT, HKMT,

199 imization factors: bone metastases; visceral metastases; investigational site; and prior abiraterone

200 th recurrences to develop lung or lymph node metastases is eightfold (p = 0.056).

201 Presence of leptomeningeal metastases is indicative of poor prognosis.

202 Genetic diversity among metastases is poorly understood but contains important i

203 Metastases largely rely on hematogenous dissemination of

204 Undetected lymph node metastases (LNMs) underwent immunohistochemical PSMA sta

205 les, covering the primary tumors, lymph node metastases (LNMs), and liver metastases from 10 CRC pati

206 of 12 months or less; patients with de-novo metastases, lobular histology, and bone-only disease; pa

207 -L1 status, and presence or absence of liver metastases, lung metastases, or both.

208 ient level using a 3-category scale (no bone metastases [M0], equivocal for bone metastases, and bone

209 n PET/CT, localized disease, and any distant metastases (M1) were 20%, 43%, and 37%, respectively.

210 a) were detected in 31.4% (217/691) and bone metastases (M1b) in 16.8% (116/691).

211 ollowing estrogen-deprivation, and ER-mutant metastases may respond to immunotherapies due to elevate

212 In mouse models of pulmonary metastases, MDSCs are key factors in the formation of th

213 For metastases measuring at least 6 mm, sensitivity was 98%

214 hat D9 plus MK-2206 blocked formation of new metastases more effectively than tamoxifen.

215 stinct MRI appearance compared to lymph node metastases (mrLNMs).

216 l seeding was common in untreated lymph node metastases (n = 17 out of 29, 59%) and distant metastase

217 tastases (n = 17 out of 29, 59%) and distant metastases (n = 20 out of 70, 29%), but less frequent in

218 , 29%), but less frequent in treated distant metastases (n = 9 out of 94, 10%).

219 vage) occurs in 25% of patients, and distant metastases occur in 10% of patients.

220 In 9 patients (3.2%), nodal metastases occurred in the Virchow node.

221 Bone metastases occurred most frequently in restaging M1, fol

222 index: 18.5 kg/m) with neuroendocrine liver metastases of a digestive origin underwent hybrid liver

223 on therapy (SIRT) for the treatment of liver metastases of castration-resistant prostate cancer.

224 d diffuse subtypes of gastric cancer (and in metastases of these subtypes), and often displays altere

225 Treated metastases often harbored private 'driver' mutations, wh

226 e of detection of the primary malignancy and metastases on (18)F-FDG PET/CT, Mayo stage after (18)F-F

227 A small number of metastases on imaging could represent different clinical

228 All patients without suspected LN metastases on PSMA PET/CT were considered candidates for

229 h colorectal adenocarcinoma, who had hepatic metastases on the initial diagnostic stage or on the fol

230 resence or absence of liver metastases, lung metastases, or both.

231 without prior anti-PD-(L)1 treatment, liver metastases, or upper-tract disease.

232 de status were significantly associated with metastases outside the prostatic fossa.

233 staging and response assessment of skeletal metastases over standard imaging methods, being able to

234 r positive lymph nodes (P = .04) and distant metastases (P = .01), and had lower odds of an FN findin

235 Dom) was significantly associated with fewer metastases (P = 0.01), lower stage at presentation (P =

236 Plectin knock-down inhibited number of metastases per organ, as well as decreased overall metas

237 the same patient (best vs. worst responding metastases per patient: -35% vs. +63% diameter change; P

238 iclonal mixtures form large solid peritoneal metastases, populated almost entirely by CL31, suggestin

239 By contrast, intense PSMA-ligand uptake in metastases predicted both treatment response (P = 0.0030

240 M0], equivocal for bone metastases, and bone metastases present [M1]) and on a dichotomous scale (M0/

241 Prostate cancer metastases primarily localize in the bone where they ind

242 ion to the surgical cavity of resected brain metastases results in low rates of local failure.

243 ed analysis of 77 primary tumors with paired metastases revealed that the FGFR4-induced signature was

244 terval [CI]: 1.2, 2.4; P = .002) and osseous metastases (RR: 1.9; 95% CI: 1.6, 2.3; P = .02); RB1 mut

245 rough whole-genome sequencing of 13 melanoma metastases sampled at autopsy from a treatment naive pat

246 acilitated development of liver but not lung metastases, suggesting that ANGPT2 and CXCR4 are importa

247 perience less oxidative stress and form more metastases than melanoma cells in blood.

248 iled to demonstrate higher uptake by hepatic metastases than patients who received intravenous admini

249 tastases, and in 16 (7%) CT/MRI showed fewer metastases than US.

250 ch3-MMP-3 axis in human prostate cancer bone metastases that contributes to osteoblastic lesion forma

251 Lymph node metastases that occur frequently provide sites of tumor

252 ot detector models detected nearly all brain metastases that were 6 mm or larger with limited false-p

253 al an miRNA/circRNA axis that regulates LUSC metastases through a previously unstudied protein, CDR1.

254 , 66 years +/- 10 [standard deviation]) with metastases to 23 patients (mean age, 60 years +/- 15) wi

255 multi-institutional experience with adrenal metastases to describe survival outcomes and identify su

256 cer (NSCLC) or melanoma with untreated brain metastases to determine the activity of PD-1 blockade in

257 III trial enrolled adult patients with brain metastases to HA-WBRT plus memantine or WBRT plus memant

258 critical component of metastatic niches, in metastases to the brain, lungs, liver, and bone marrow,

259 mab emtansine, who had or did not have brain metastases, to receive either tucatinib or placebo, in c

260 patients with uveal melanomas or intraocular metastases treated primarily with gamma knife radiosurge

261 ques provide high-resolution images of small metastases, tumor inflammation, perfusion, oxygenation,

262 women, three had biopsy-proven HER2-positive metastases, two had pathologic findings that demonstrate

263 Electron microscopy of metastases uncovered irregular mitochondria with bridgin

264 rmed GIST and unresectable primary lesion or metastases undergoing an extended protocol for detailed

265 Traditional factors such as size of metastases, uni versus bilobar involvement, and liver-fi

266 ional status was correlated with location of metastases using the chi(2) or Fisher exact test.

267 y innocuous tumor subpopulations can promote metastases via "hit-and-run" commensal interactions.

268 t allocation used minimization factors: bone metastases; visceral metastases; investigational site; a

269 Progression of liver metastases warranted further therapy and temozolomide-ca

270 t-tissue metastases, and bone or bone-marrow metastases was 72%, 33%, and 38%, respectively, for (123

271 etecting soft-tissue and bone or bone-marrow metastases was 77% and 86%, respectively-significantly h

272 t-tissue metastases, and bone or bone-marrow metastases was 83%, 50%, and 92%, respectively, for (123

273 etecting soft-tissue and bone or bone-marrow metastases was 86% and 99%, respectively-significantly h

274 The presence of lymph node metastases was determined by an experienced reader indep

275 A final diagnosis of bone metastases was made for 211 of 219 patients.

276 Conclusion: SLND of pelvic nodal metastases was often not complete according to PSMA PET.

277 uencing of 100 castration-resistant prostate metastases, we discovered alterations affecting driver g

278 A total of 481 metastases were counted on CT from 22 right-sided and 64

279 nt metastases, although in one patient liver metastases were evident on (18)F-FDG but not on (18)F-FE

280 al post-treatment changes and information on metastases were extracted from the follow-up.

281 cular subtypes with differing risks of liver metastases were identified.

282 , and (18)F-FDG PET, G3 tumor, and >=3 liver metastases were independent prognostic factors for PFS.

283 itro and in vivo mechanisms involved in PDAC metastases were investigated following treatment with P-

284 seven cases with recurrence and all distant metastases were of MSFs, (iii) recurrence-free survival

285 Surprisingly, we found that lung metastases were predominantly derived from the epithelia

286 Results: Lymph node metastases were present in 18 patients (31.0%) and were

287 Lymph node metastases were present in the pelvis in 42% of patients

288 Further, 99% of the mutations shared by all metastases were present in the plasma.

289 primary tumors and numbers of liver and lung metastases were quantified and analyzed by histology.

290 jected into the tail veins of mice, and lung metastases were quantified.

291 foci that were suspicious for HER2-positive metastases were tissue sampled and examined by pathologi

292 ients with uveal melanoma and 34 intraocular metastases, were eligible for systematic review.

293 ng micrometastases and the initiation of new metastases, while simultaneously jeopardizing immune con

294 Patients with primary liver cancer or liver metastases who underwent radioembolization with glass mi

295 One patient had (18)F-FES-avid metastases with no corresponding (18)F-FDG-avid metastas

296 l of 37.3% (41 of 110) of the studies showed metastases, with diverse FDG PET findings throughout the

297 ported with partial hepatectomy for solitary metastases, with percutaneous hepatic perfusion with mel

298 of treating uveal melanomas and intraocular metastases, with reliable tumour control rates.

299 were no patients with (18)F-FDG-avid distant metastases without (18)F-FES-avid distant metastases, al

300 rmation of both spontaneous and experimental metastases, without limiting primary or metastatic tumor