ライフサイエンスコーパス: metastatic breast cancer

1 in the placebo group (sepsis, pneumonia, and metastatic breast cancer).

2 sured immunohistochemically in patients with metastatic breast cancer.

3 t PLD2 as a potential therapeutic target for metastatic breast cancer.

4 ase overall survival in a xenograft model of metastatic breast cancer.

5 response assessment with (18)F-FDG PET/CT in metastatic breast cancer.

6 or benefit in hormone receptor (HR)-positive metastatic breast cancer.

7 inhibitor (AI) therapy in patients with ER+ metastatic breast cancer.

8 nemia in patients receiving chemotherapy for metastatic breast cancer.

9 the 12 relapses seen, 2 were due to distant metastatic breast cancer.

10 iR-31) has been shown to be overexpressed in metastatic breast cancer.

11 an individual's predilection for developing metastatic breast cancer.

12 es in clinical and translational research in metastatic breast cancer.

13 reported in the literature for patients with metastatic breast cancer.

14 nt CTC as a clinically relevant biomarker in metastatic breast cancer.

15 as a strategy to treat solid tumors such as metastatic breast cancer.

16 ith previously treated, locally recurrent or metastatic breast cancer.

17 d the landscape of therapy for patients with metastatic breast cancer.

18 s of metastatic disease in a murine model of metastatic breast cancer.

19 al concern in the treatment of HER2-positive metastatic breast cancer.

20 50 postmenopausal women who later developed metastatic breast cancer.

21 hed in the peripheral blood of patients with metastatic breast cancer.

22 taxel in unresectable, locally recurrent, or metastatic breast cancer.

23 f trastuzumab in patients with HER2-positive metastatic breast cancer.

24 n-ABY-025 for determining the HER2 status in metastatic breast cancer.

25 s middle T oncoprotein (PyMT) mouse model of metastatic breast cancer.

26 s from 170 patients with locally relapsed or metastatic breast cancer.

27 tients with hormonal therapy-resistant (HTR) metastatic breast cancer.

28 target in the treatment of Nanog-expressing metastatic breast cancer.

29 be used to detect CTCs in a murine model of metastatic breast cancer.

30 mprovements have been achieved with relapsed metastatic breast cancer.

31 burden and treatment response in women with metastatic breast cancer.

32 rs, we enrolled 11 patients with ER-positive metastatic breast cancer.

33 icant therapeutic impact against primary and metastatic breast cancer.

34 nografts of disseminated leukemia, lung, and metastatic breast cancer.

35 longed the survival of mice with established metastatic breast cancer.

36 ent skeletal-related events in patients with metastatic breast cancer.

37 uce morbidity and mortality in patients with metastatic breast cancer.

38 ed NK-92 cells to the brain using a model of metastatic breast cancer.

39 oping miR-708 as a therapeutic agent against metastatic breast cancer.

40 docrine therapy in patients with ER-positive metastatic breast cancer.

41 ich may be used for clinical interference of metastatic breast cancer.

42 uently, as a potential therapeutic target in metastatic breast cancer.

43 or complex 2-induced H3K27 trimethylation in metastatic breast cancer.

44 ising ER antagonist for locally advanced and metastatic breast cancer.

45 specific, and highly sensitive biomarker of metastatic breast cancer.

46 el in patients with HER2-positive first-line metastatic breast cancer.

47 on of distant metastases in a mouse model of metastatic breast cancer.

48 tasis in a spontaneous animal model of human metastatic breast cancer.

49 all survival in chemonaive patients with non-metastatic breast cancer.

50 , phase 3 equivalence study in patients with metastatic breast cancer.

51 ease; its loss is a prognostic signature for metastatic breast cancer.

52 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer.

53 s the outcome in patients with HER2-positive metastatic breast cancer.

54 patients with hormone-receptor (HR)-positive metastatic breast cancer.

55 crine-refractory, estrogen receptor-positive metastatic breast cancer.

56 genic effect of WAT progenitors on local and metastatic breast cancer.

57 e receptor-negative, HER2-negative recurrent metastatic breast cancer.

58 ights into a better understanding of distant metastatic breast cancer.

59 (mTOR) are currently used to treat advanced metastatic breast cancer.

60 and opportunities for precision treatment of metastatic breast cancer.

61 s without prior treatment for ERBB2-positive metastatic breast cancer.

62 the role of bone-modifying agents (BMAs) in metastatic breast cancer.

63 curement; and redesign of clinical trials in metastatic breast cancer.

64 ical activity in patients with HER2-positive metastatic breast cancer.

65 th or without pertuzumab in US patients with metastatic breast cancer.

66 py may be a promising treatment strategy for metastatic breast cancer.

67 n of this enzyme as a therapeutic target for metastatic breast cancer.

68 ormone receptor-positive locally advanced or metastatic breast cancer.

69 nce is crucial for treatment optimisation in metastatic breast cancer.

70 lyzed lesions affects response assessment in metastatic breast cancer.

71 resistance is a key therapeutic challenge in metastatic breast cancer.

72 relbine for such patients with HER2-positive metastatic breast cancer.

73 vasation, and metastasis in a mouse model of metastatic breast cancer.

74 ubtype and outcome in first-line HR-positive metastatic breast cancer.

75 as a therapeutic approach for patients with metastatic breast cancer.

76 wth factor receptor 2 (HER2) -overexpressing metastatic breast cancer.

77 th fulvestrant plus placebo in patients with metastatic breast cancer.

78 f eliminating ERalpha expression in advanced metastatic breast cancers.

79 as an effective target for the treatment of metastatic breast cancers.

80 e mutations in aromatase inhibitor-resistant metastatic breast cancers.

81 erapeutic opportunity to limit the spread of metastatic breast cancers.

82 at target GFR signals to treat p120-negative metastatic breast cancers.

83 oncogene is overexpressed in 25% of invasive/metastatic breast cancers.

84 s, CTCs were isolated from 181 patients with metastatic breast cancer, 102 of which were successfully

85 tcome in patients with ERBB2 (HER2)-positive metastatic breast cancer; a clinically effective biosimi

86 t in Hormone Receptor-Positive HER2-Negative Metastatic Breast Cancer After Endocrine Failure) trial,

87 In January 2016, the Metastatic Breast Cancer Alliance (the Alliance) convene

88 efficacy in estrogen receptor (ER)-positive metastatic breast cancer, although their cytostatic effe

89 mising potential as an effective therapy for metastatic breast cancer and a broader patient populatio

90 nown to promote the progression of local and metastatic breast cancer and angiogenesis.

91 Patients with metastatic breast cancer and HER2 non-amplified primary

92 Seven patients with metastatic breast cancer and HER2-positive (n = 5) or -n

93 However, the molecular basis of metastatic breast cancer and its therapeutic vulnerabili

94 In this study, we used mouse models of metastatic breast cancer and melanoma to investigate the

95 ht women with biopsy-confirmed HER2-positive metastatic breast cancer and no anti-HER2 therapy for 4

96 herapy improves progression-free survival in metastatic breast cancer and pathological complete respo

97 vestigate the effects of age at diagnosis on metastatic breast cancer and patients' prognosis, we col

98 various mechanisms that shape the genome of metastatic breast cancer and the value of studying advan

99 Understanding the etiology of recurrent or metastatic breast cancer and underlying mechanisms is cr

100 ecause Fra-1 often is overexpressed in human metastatic breast cancers and has been shown to control

101 h estrogen receptor alpha (ERalpha)-positive metastatic breast cancer, and is attributed to various m

102 n Csf1r+ myeloid cells associated with human metastatic breast cancer, and levels of these miRs in CD

103 emcitabine had shown significant activity in metastatic breast cancer, and there was evidence of a fa

104 n the placebo group; most deaths were due to metastatic breast cancer, and two were considered treatm

105 genomic profiles in a group of patients with metastatic breast cancer based on an analysis with next-

106 Capecitabine is an active drug in metastatic breast cancer (BC).

107 evolution in a patient (index patient) with metastatic breast cancer bearing an activating PIK3CA (p

108 umour cells correlate with poor prognosis in metastatic breast cancer, but there are few data describ

109 circulating tumour cell (CTC) line, MCF-7, a metastatic breast cancer by targeting epithelial cellula

110 ication for prognostication of patients with metastatic breast cancer by undertaking a pooled analysi

111 In culture, murine and human metastatic breast cancer cell extracellular vesicles tra

112 investigate whether intrinsic properties of metastatic breast cancer cell growth can be regulated th

113 We found that the human metastatic breast cancer cell line MDA-MB-231 secretes a

114 carcinoma and on the cell surface of highly metastatic breast cancer cell line MDA-MB-231.

115 east epithelial cell line MCF10A, moderately metastatic breast cancer cell line MDA-MB-468 and 143B c

116 rget miRs in total RNA (RNAt) extracted from metastatic breast cancer cell lines and human tissues.

117 tor (EGF)-mediated chemotaxis and CIL guides metastatic breast cancer cell motility, whereby cells be

118 Our results demonstrate that metastatic breast cancer cells (MDA-MB-231) exhibit more

119 icin gradient across a population of motile, metastatic breast cancer cells (MDA-MB-231).

120 e failure of producing E-cadherin protein in metastatic breast cancer cells after overexpressing E-ca

121 hich these procedures reduce the presence of metastatic breast cancer cells among the isolated follic

122 by facilitating the re-epithelialization of metastatic breast cancer cells and downmodulating the cy

123 also inhibits the Rac activity of MDA-MB-231 metastatic breast cancer cells and reduces Rac-directed

124 ction of regulating the metastatic growth of metastatic breast cancer cells and reducing the activati

125 hibit both the early colonization of bone by metastatic breast cancer cells and the initiation of the

126 s where Runx2 is not detected, and absent in metastatic breast cancer cells and tissue biopsies that

127 se-like 2 (hLOXL2) is highly up-regulated in metastatic breast cancer cells and tissues and induces e

128 Furthermore, in metastatic breast cancer cells but not in normal mammary

129 ostaglandin E2 release could be abrogated in metastatic breast cancer cells by inhibition of iPLA2.

130 es to identify miRs that were upregulated in metastatic breast cancer cells by TGF-beta.

131 s simulations of the active cytoskeleton, on metastatic breast cancer cells embedded in a three-dimen

132 t al. now show that two tRNAs upregulated in metastatic breast cancer cells enhance stability and tra

133 We found that brain metastatic breast cancer cells evolved the ability to su

134 In suspended cell culture conditions, metastatic breast cancer cells exhibited high alpha-tubu

135 ressor isoform of Ovol2 is able to reprogram metastatic breast cancer cells from a mesenchymal to an

136 tream of the HER2 driver oncogene in SUM-225 metastatic breast cancer cells from dynamic gene express

137 Moreover, we found that GIT1 depletion in metastatic breast cancer cells greatly reduced alpha5bet

138 Moreover, inhibiting BORG expression in metastatic breast cancer cells impedes their metastatic

139 of mice after injection of metastatic or non-metastatic breast cancer cells in 4T1.2 BALB/cJ and MDA-

140 n summary, NT-3 appears to promote growth of metastatic breast cancer cells in the brain by facilitat

141 The restoration of miR-203 in highly metastatic breast cancer cells inhibited tumor cell inva

142 ained uPA expression is achieved in invasive/metastatic breast cancer cells is unknown.

143 Using the HIF-1alpha-positive and metastatic breast cancer cells MDA-MB-231, we show that

144 ore importantly, increased NT-3 secretion in metastatic breast cancer cells results in a reversion of

145 ning of naive mice with exosomes from highly metastatic breast cancer cells revealed the accumulation

146 s, mitochondria also were more fragmented in metastatic breast cancer cells that express higher level

147 y reduce plasma membrane PI(4,5)P2 levels in metastatic breast cancer cells through two independent m

148 etastasis showing increased ability of brain metastatic breast cancer cells to counteract oxidative s

149 MDA-MB-231 human metastatic breast cancer cells transduced with BRMS1(NLS

150 l heterogeneity, with generation of invasive/metastatic breast cancer cells within populations of non

151 ion attenuated the mesenchymal attributes of metastatic breast cancer cells, accompanied by distinctl

152 These genes are upregulated in highly metastatic breast cancer cells, and their increased expr

153 In estrogen receptor negative (ER-) metastatic breast cancer cells, equol induced elevated l

154 in vivo in controlling multiple myelomas and metastatic breast cancer cells, in the latter case also

155 characteristically expressed and secreted by metastatic breast cancer cells, is a potent regulator of

156 Compared with non-metastatic breast cancer cells, mitochondria also were m

157 GA2 gene and protein are highly expressed in metastatic breast cancer cells.

158 sary for maintaining tumorigenic activity in metastatic breast cancer cells.

159 dimensional extracellular matrix invasion in metastatic breast cancer cells.

160 3 was significantly down-regulated in highly metastatic breast cancer cells.

161 nvironment alter migration and morphology of metastatic breast cancer cells.

162 ytes in the bone marrow of 6/8 patients with metastatic breast cancer compared with age- and gender-m

163 improves clinical outcomes in patients with metastatic breast cancer compared with docetaxel treatme

164 ivation of PKCzeta signaling in invasive and metastatic breast cancers compared to non-invasive disea

165 and docetaxel in patients with HER2-positive metastatic breast cancer, compared with placebo, trastuz

166 hally irradiated MMTV-PyVmT mice (a model of metastatic breast cancer) decreased tumor growth and alt

167 fulvestrant for the treatment of HR-positive metastatic breast cancer, despite the use of a dose of f

168 ed tumor cells (CSFTC) from 15 patients with metastatic breast cancer diagnosed with leptomeningeal c

169 is an organ specific molecular biomarker for metastatic breast cancer diagnosis.

170 ormone-receptor-positive locally advanced or metastatic breast cancer did not improve outcomes.

171 ce to a class I PI3K inhibitor in a model of metastatic breast cancer driven by PI3K and MYC was asso

172 imes and the four markers mainly involved in metastatic breast cancer (EPCAM, CD47, CD44 and MET).

173 ab)/Docetaxel in Patients With HER2-Positive Metastatic Breast Cancer] evaluated first-line bevacizum

174 tients with previously treated HER2-positive metastatic breast cancer even in the presence of crossov

175 the brain, with 15% to 20% of patients with metastatic breast cancer eventually developing brain met

176 For patients with metastatic breast cancer, expanding therapeutic options

177 r whether bone regions typically targeted by metastatic breast cancer feature distinct HA materials p

178 eptor-positive, or both, locally advanced or metastatic breast cancer from 113 academic hospitals and

179 Currently, antiangiogenic strategies in metastatic breast cancer have demonstrated modest improv

180 more HER2-directed regimens for recurrent or metastatic breast cancer have few effective therapeutic

181 rns of genomic evolution between primary and metastatic breast cancer have not been studied in large

182 died in large numbers, despite patients with metastatic breast cancer having dismal survival.

183 MM-302/trastuzumab therapy for HER2-positive metastatic breast cancer in a randomized phase II clinic

184 10 positively correlated with progression of metastatic breast cancer in clinical patient tumour samp

185 g the 4T1 model of aggressive, spontaneously metastatic breast cancer in immunologically intact mice,

186 bevacizumab to treat postsurgical, advanced metastatic breast cancer in mice.

187 th stage-dependent targeting in mice bearing metastatic breast cancer in the bone, and carried out st

188 ld be an attractive therapeutic strategy for metastatic breast cancer in the future.

189 ficacy in MDA-MB-231 and 4T1 mouse models of metastatic breast cancer, including functional cures in

190 Metastatic breast cancer is the second leading cause of

191 d HER2 heterogeneity during the evolution of metastatic breast cancer is unknown.

192 ation of markers and therapeutic targets for metastatic breast cancers is imperative.

193 eceptor 2 (HER2) -positive locally recurrent/metastatic breast cancer (LR/MBC).

194 anslated to improve the clinical outcome for metastatic breast cancer management.

195 the combination of PANVAC with docetaxel in metastatic breast cancer may provide a clinical benefit.

196 es in patients with pretreated HER2-positive metastatic breast cancer (MBC) and has demonstrated supe

197 ptimal frequency of monitoring patients with metastatic breast cancer (MBC) is unknown; however, data

198 gen receptor alpha (ESR1) mutations found in metastatic breast cancer (MBC) promote ligand-independen

199 Metastatic breast cancer (MBC) remains an incurable illn

200 y survival endpoints in 4 separate phase III metastatic breast cancer (MBC) trials, either alone or w

201 tion markers to predict survival outcomes in metastatic breast cancer (MBC) using a new quantitative

202 al growth factor receptor 2 (HER2)-positive, metastatic breast cancer (MBC) who previously received t

203 al growth factor receptor 2 (HER2) -positive metastatic breast cancer (MBC) whose disease had progres

204 omponent for several malignancies, including metastatic breast cancer (MBC), ovarian cancer, and adva

205 itabine in patients with locally advanced or metastatic breast cancer (MBC).

206 epidermal growth factor receptor 2-positive metastatic breast cancer (MBC).

207 d pertuzumab, in patients with HER2-positive metastatic breast cancer (MBC).

208 blood) are associated with poor prognosis in metastatic breast cancer (MBC).

209 actor receptor 2 (HER2) status in women with metastatic breast cancer (MBC).

210 al growth factor receptor 2 (HER2) -positive metastatic breast cancer (MBC).

211 likely contributes to hormone resistance in metastatic breast cancer (mBC).

212 to confer survival benefits in patients with metastatic breast cancer (mBC).

213 Patients (n = 1822) with metastatic breast cancer, metastatic prostate cancer, or

214 n, but patients with luminal A/HER2-negative metastatic breast cancer might be good candidates for le

215 We used the 4T1 metastatic breast cancer model and B7x knockout (B7x (-/

216 nd that stable SDPR overexpression in highly metastatic breast cancer model cell lines inhibited pros

217 Metastatic breast cancer mouse models were used to gener

218 Data from 13 trials (5,480 patients with metastatic breast cancer, non-small-cell lung cancer, or

219 zed clinical trial enrolled 48 patients with metastatic breast cancer of all subtypes, without limita

220 ally, our investigations in the 4T1 model of metastatic breast cancer of the V-ATPase inhibitor archa

221 (OS) using a tissue microarray with 149 non-metastatic breast cancer patient samples.

222 C expressing vimentin and TF in the blood of metastatic breast cancer patients consistent with our ob

223 We finally identified 4932 eligible metastatic breast cancer patients diagnosed between 2010

224 Treatment of stage IV metastatic breast cancer patients is limited to palliati

225 e assayed in clinical trial samples from ER+ metastatic breast cancer patients randomized either to t

226 onal study of 102 postmenopausal, HR + HER2- metastatic breast cancer patients treated with everolimu

227 Metastatic breast cancer patients were identified in the

228 pes and liver metastasis on the prognosis of metastatic breast cancer patients who received combined

229 n metastases occur in more than one-third of metastatic breast cancer patients whose tumors overexpre

230 one metastases occur in approximately 70% of metastatic breast cancer patients, often leading to skel

231 e cells is present in the bone marrow of non-metastatic breast cancer patients, only part of which ar

232 available evidence should be discussed with metastatic breast cancer patients.

233 about nonpalliative primary tumor surgery in metastatic breast cancer patients.

234 sis was an independent prognostic factor for metastatic breast cancer patients.

235 act of primary tumor surgery on mortality in metastatic breast cancer patients.

236 mes of 63 single cells isolated from six non-metastatic breast cancer patients.

237 inical efficacy of docetaxel and thiotepa on metastatic breast cancer patients; and metastatic sites

238 om 70% (14/20) of primary and 70% (21/30) of metastatic breast cancer patients; none were captured fr

239 ountries, patients with locally recurrent or metastatic breast cancer previously treated with an anth

240 rmone-receptor-positive, locally advanced or metastatic breast cancer previously treated with endocri

241 2-positive unresectable, locally advanced or metastatic breast cancer previously treated with trastuz

242 the treatment of patients with HER2-positive metastatic breast cancer previously treated with trastuz

243 n, intratumor vascularization, and local and metastatic breast cancer progression.

244 such it exemplifies epigenetic regulation of metastatic breast cancer progression.

245 fic DNA in peripheral blood of patients with metastatic breast cancer provides the opportunity to det

246 al growth factor receptor 2 (HER2) -positive metastatic breast cancer, raising interest in evaluating

247 n of outcomes in patients with HER2-positive metastatic breast cancer randomized to an antibody-based

248 epidermal growth factor receptor 2-positive metastatic breast cancer receiving lapatinib-capecitabin

249 Among women with ERBB2-positive metastatic breast cancer receiving taxanes, the use of a

250 asive tool for discriminating HER2 status in metastatic breast cancer, regardless of ongoing HER2-tar

251 currently being used to treat HER2-positive metastatic breast cancer, relapsed or refractory Hodgkin

252 Metastatic breast cancer remains challenging to treat, a

253 t of the primary tumor site in patients with metastatic breast cancer remains controversial.

254 Metastatic breast cancer remains the chief cause of canc

255 evidence of activity in treatment-resistant metastatic breast cancer requires confirmation, such as

256 The management of metastatic breast cancer requires monitoring of the tumo

257 In patient-derived metastatic breast cancer samples, only ER-ve mammosphere

258 and plasma samples in a single patient with metastatic breast cancer shows that circulating tumour D

259 ression of HSPA1A, which is overexpressed in metastatic breast cancer stem cells.

260 yaluronan synthase 2 (HAS2) occurs in highly metastatic breast cancer stem-like cells (CSC) defined b

261 lood from healthy donors and from women with metastatic breast cancer stored under ambient conditions

262 therapy and lack of curative treatments for metastatic breast cancer suggest that current therapies

263 ults point to a new therapeutic strategy for metastatic breast cancers targeted to the mitochondrial

264 ith hormone-receptor-positive, HER2-negative metastatic breast cancer that had progressed on previous

265 ent hormone-receptor-positive, HER2-negative metastatic breast cancer that has progressed on previous

266 ledronic acid every 4 weeks in patients with metastatic breast cancer that involved the bone who had

267 In patients with metastatic breast cancer that is positive for human epid

268 In patients with HER2-positive metastatic breast cancer, the addition of pertuzumab to

269 h primary mammary tumors in a mouse model of metastatic breast cancer, the polyoma middle T antigen (

270 avenous zoledronic acid for the treatment of metastatic breast cancer to bone.

271 ntries and randomized 652 with HER2-positive metastatic breast cancer to receive trastuzumab or lapat

272 nal control for selected patients with early metastatic breast cancer treated with breast-conserving

273 ) among women with hormone receptor-positive metastatic breast cancer treated with fulvestrant.

274 Mouse models of metastatic breast cancer typically feature mutated oncop

275 for patients with estrogen receptor-positive metastatic breast cancer unless improvement is medically

276 insic subtyping in hormone receptor-positive metastatic breast cancer warrants further investigation,

277 Samples of 13 patients with metastatic breast cancer were analyzed for mutations in

278 Patients with ER-positive metastatic breast cancer were eligible for the study, ir

279 Six patients with HER2-positive metastatic breast cancer were enrolled and administered

280 Eight patients with metastatic breast cancer were included.

281 Overall, 16,247 women with metastatic breast cancer were included.

282 iving first- or second-line chemotherapy for metastatic breast cancer, were randomly assigned to EPO

283 C count also improves the prognostication of metastatic breast cancer when added to full clinicopatho

284 HEXIM1 expression is decreased in human metastatic breast cancers when compared with matched pri

285 on of mammary hyperplasias into invasive and metastatic breast cancers, which are often associated wi

286 estrogen receptor-positive, locally advanced/metastatic breast cancer who had no previous therapy for

287 We randomly assigned patients with metastatic breast cancer who had not received previous c

288 Patients with HER2-positive metastatic breast cancer who had not received previous c

289 with HR-positive, HER2-negative recurrent or metastatic breast cancer who had not received previous s

290 the treatment of patients with HER2-positive metastatic breast cancer who had previously received tra

291 led female patients with HER2-overexpressing metastatic breast cancer who had progressed on or follow

292 nt of choice for patients with HER2-positive metastatic breast cancer who had progressed on trastuzum

293 ormone receptor-positive locally advanced or metastatic breast cancer who have not received previous

294 anonymised data for individual patients with metastatic breast cancer who participated in studies bet

295 and circulating tumor cells in 30 women with metastatic breast cancer who were receiving systemic the

296 positive, HER2-negative, locally advanced or metastatic breast cancer, who had relapsed on or after e

297 ER2)-negative inoperable locally advanced or metastatic breast cancer whose disease had progressed on

298 for the treatment of locally advanced and/or metastatic breast cancer with germline BRCA1/2 deleterio

299 Cu-DOTA-trastuzumab visualizes HER2-positive metastatic breast cancer with high sensitivity and is ef

300 Conclusion In endocrine-refractory metastatic breast cancer, Z-endoxifen provides substanti