ライフサイエンスコーパス: human breast cancer

1 se, resulting in prostaglandin E2 release in human breast cancer.

2 3 is upregulated in malignant and metastatic human breast cancer.

3 f BRCA1 in AR-mediated cell proliferation in human breast cancer.

4 ncreased angiogenesis, which was detected in human breast cancer.

5 ysis framework to model molecular changes in human breast cancer.

6 targets of HER2 transcriptional signaling in human breast cancer.

7 SCs) expansion is associated with aggressive human breast cancer.

8 limited metastasis in an orthotopic model of human breast cancer.

9 (PRL) in the development and progression of human breast cancer.

10 origenesis in histological investigations of human breast cancer.

11 2E3), an orphan nuclear hormone receptor, to human breast cancer.

12 y chromothripsis as a major driving event in human breast cancer.

13 factor Six2 in the metastatic progression of human breast cancer.

14 biquitylation in models of basal and luminal human breast cancer.

15 uronides to generate the parent compound, in human breast cancer.

16 echanism contributing to Myc deregulation in human breast cancer.

17 nitors, the proposed cells-of-origin of most human breast cancers.

18 iched in the basal-like molecular subtype in human breast cancers.

19 p38delta is highly expressed in all types of human breast cancers.

20 ressed in carcinoma cells in the majority of human breast cancers.

21 active SUMOlyated KAP1 is elevated widely in human breast cancers.

22 eptor 2 (HER2) is upregulated in a subset of human breast cancers.

23 sitol and is highly expressed in a subset of human breast cancers.

24 determining the transcriptional landscape of human breast cancers.

25 is mislocalized from cell-cell junctions in human breast cancers.

26 ess costs of passengers in cell lines and in human breast cancers.

27 n of HER2 has been reported in around 25% of human breast cancers.

28 AP2C in maintaining the luminal phenotype in human breast cancer and in influencing the luminal cell

29 ER2) is amplified in approximately 15-20% of human breast cancer and is important for tumor etiology

30 bB2/neu proto-oncogene is observed in 20-30% human breast cancer and is inversely correlated with the

31 acquired hormone-independent growth of ER(+) human breast cancer and is therefore a promising target

32 AB11B-AS1 is a natural lncRNA upregulated in human breast cancer and its expression is induced by hyp

33 in flies and mice and inhibits the growth of human breast cancer and leukemia xenografts, notably wit

34 d for their antiproliferative activity using human breast cancer and lung cancer cell lines.

35 nversely correlated with PHGDH expression in human breast cancer and lung cancer.

36 s an important driver of YAP/TAZ activity in human breast cancer and melanoma cells.

37 1 as a gene amplified in a large fraction of human breast cancer and overexpressed in metastatic brea

38 re associated with increased angiogenesis in human breast cancer and that inhibition of TAp73 results

39 ations in the understanding and treatment of human breast cancer and the diseases associated with mit

40 er with its high incidence of 85% in primary human breast cancers and 100% in breast cancer derived l

41 levels are detected at the invasive front of human breast cancers and independently predict metastati

42 r protein Sequestosome 1/p62 are observed in human breast cancers and significantly correlate with HE

43 )s(2)-tRNA modification, are up-regulated in human breast cancers and sustain metastasis.

44 tivating mutations in PIK3CA are frequent in human breast cancer, and phosphoinositide 3-kinase alpha

45 els of iron in preclinical murine models and human breast cancer, and used them as metabolic biomarke

46 presented in this work indicate that primary human breast cancers, and their metastases, express high

47 s coli (APC) and APC2 in the pathogenesis of human breast cancer are ill-defined, but our analysis of

48 Over 70% of human breast cancers are estrogen receptor-positive (ER(

49 somatic activating mutations within erbB2 in human breast cancers are rare.

50 It is not known whether ER/PR-negative human breast cancer arises from an ER/PR-negative cell o

51 frequently overexpressed in both murine and human breast cancer as well as in prostate cancers, and

52 e we analysed AZD1775 response in a panel of human breast cancer (BC) cell lines by global proteome/t

53 have investigated the metabolic profiles of human breast cancer (BC) cell lines carrying BRCA1 patho

54 In multiple murine xenograft models of human breast cancer, BETd-246 and a further optimized an

55 stribution of giant obscurins are altered in human breast cancer biopsies compared with matched norma

56 BMPs are overexpressed in human breast cancers, but loss of BMP signaling in mamma

57 d and overexpressed in a large proportion of human breast cancers, but the signaling pathways that co

58 oach in an athymic mouse model of metastatic human breast cancer by targeting epidermal growth factor

59 MA) stimulation was demonstrated using T-47D human breast cancer carcinoma cell model.

60 Complementary studies using human breast cancer cell culture models revealed that si

61 3D in vitro model to analyze organ-specific human breast cancer cell extravasation into bone- and mu

62 perimental results from the ERalpha-positive human breast cancer cell line (MCF-7) treated with 17-be

63 For in vivo studies, a human breast cancer cell line (MDA-231) was implanted in

64 sion of 800 miRNAs in the estrogen-dependent human breast cancer cell line MCF7 and its estrogen-inde

65 opment of field based 3D-QSAR model based on human breast cancer cell line MCF7 in vitro anticancer a

66 vant betaAR subtype in the highly metastatic human breast cancer cell line MDA-MB-231HM.

67 In MCF7 cells, a human breast cancer cell line, MSNBA competitively inhib

68 as well as differences in the mechanotype of human breast cancer cell lines (Ea = 2.1 +/- 0.1 and 0.8

69 allows us to discriminate between normal and human breast cancer cell lines (fibrocystic and metastat

70 he positive control vinblastine, and against human breast cancer cell lines (IC50=9.6 mug/ml).

71 Enforced expression of SERPINE2 and SLPI in human breast cancer cell lines also programmed them for

72 In human breast cancer cell lines and 4T1 mouse mammary tum

73 ro and in vivo activity against a variety of human breast cancer cell lines and patient derived xenog

74 LSD1 proteins were positively correlated in human breast cancer cell lines and tissue specimens of p

75 CaSR signaling promoted the proliferation of human breast cancer cell lines and tumor cells cultured

76 nally, we find defective KDM3A expression in human breast cancer cell lines and tumors.

77 We find that in human breast cancer cell lines containing amplified 17q2

78 Functional expression of this receptor in human breast cancer cell lines decreases cyclic AMP prod

79 ADAM17-expressing human breast cancer cell lines MCF-7 and MDA-MB-453 also

80 epigenomes (using ChIP-seq) of 11 different human breast cancer cell lines representing five major m

81 ng capability and cell toxicity to image two human breast cancer cell lines T47D and MDA-MB-231 are a

82 960 breast invasive tumors and 56 human breast cancer cell lines were assessed for OR gene

83 cellular vesicles from metastatic murine and human breast cancer cell lines, and miR-200 levels were

84 ndicate that RNF168 deficiency, including in human breast cancer cell lines, confers resistance to th

85 wo miRNAs, miR-221 and miR-17, are tested in human breast cancer cell lines, demonstrating the 70 app

86 (MSCs) and MDA-MB231 (OPN+) and MCF7 (OPN-) human breast cancer cell lines, we demonstrate that OPN

87 Using genetic mouse models and human breast cancer cell lines, we show that deletion or

88 ymorphism (SNP) discrimination in cDNAs from human breast cancer cell lines, which makes such platfor

89 In this preclinical study, we used eight human breast cancer cell lines, which represent the majo

90 lly, and seven of these exhibited synergy in human breast cancer cell lines.

91 ted at high levels in a subset of tumors and human breast cancer cell lines.

92 nd proteomic profiling data sets measured in human breast cancer cell lines.

93 Here, using human breast cancer cell models, we identified a pathway

94 NA-based apoptosis screen in a PIK3CA mutant human breast cancer cell.

95 Human breast cancer cells (MCF-7) grown on serum protein

96 cells, i.e., mouse macrophages (RAW 264.7), human breast cancer cells (T47D and Hs578T), and mouse p

97 n characterized and incubated with MCF-7/ADR human breast cancer cells and followed by US exposure.

98 verexpression of KLF8 and EPSTI1 in invasive human breast cancer cells and patient tumors.

99 growth, migration and invasion of MDA-MB-231 human breast cancer cells and Py8119 mouse mammary carci

100 ct laboratories, we characterised a range of human breast cancer cells and their protein-level respon

101 eta-estradiol in a functional assay in MCF-7 human breast cancer cells and they have no E/Z isomers,

102 (PAF) content and PAF receptor expression in human breast cancer cells and tissue.

103 Herein we report that BRCA-1-defective human breast cancer cells are more sensitive than wild-t

104 In CXM, human breast cancer cells are orthotopically implanted i

105 ficity is achieved and different subtypes of human breast cancer cells are successfully discriminated

106 find that specific tRNAs are upregulated in human breast cancer cells as they gain metastatic activi

107 silencing the expression of the GFP gene in human breast cancer cells at concentrations of 5mug/mL,

108 Lentiviral silencing of CBS in human breast cancer cells attenuated GSH/GSSG, total GSH

109 d its binding affinity toward native CD44 on human breast cancer cells by nearly 200-fold.

110 Knockdown of TRIM37 in human breast cancer cells containing amplified 17q23 sub

111 Moreover, MDA-MB-231 human breast cancer cells could be separated from human

112 on in MMTV- Wnt1 tumor cells or knockdown in human breast cancer cells decreased the number of functi

113 We compared across an isogenic panel of human breast cancer cells derived from MDA-MB-231 cells.

114 rs after administration, MDA-MB-231 or MCF-7 human breast cancer cells expressing luciferase were inj

115 ce lattice-light sheet imaging of MDA-MB-231 human breast cancer cells genetically engineered to brig

116 Finally, Ltv1 knockdown in human breast cancer cells impaired apoptosis induced by

117 3 interfered with estrogen's actions on T47D human breast cancer cells in 3D differently at different

118 fennel nsLTP1 suppressed the growth of MCF-7 human breast cancer cells in a dose-dependent manner wit

119 x 10(-7) M) effectively reduced invasion of human breast cancer cells in three-dimensional cultures

120 ant (Withania somnifera), inhibits growth of human breast cancer cells in vitro and in vivo and preve

121 s, we knocked down JAG1 in hybrid E/M SUM149 human breast cancer cells in vitro.

122 metastasis formation by invasive murine and human breast cancer cells in vivo.

123 Here, we used triple-negative human breast cancer cells in which AMPK activity had bee

124 ormal breast epithelial cells and a panel of human breast cancer cells including estrogen receptor (E

125 Here, we show that single human breast cancer cells loaded with mesoporous silica

126 Three-dimensional cultures of human breast cancer cells on Matrigel revealed an altere

127 In our experiments, human breast cancer cells primarily assimilated ammonia

128 Finally, ATM-depletion in human breast cancer cells reduced lung tumors in a mouse

129 NgBR knockdown in human breast cancer cells reduces Ras membrane localizat

130 Moreover, in human breast cancer cells that become progressively more

131 ear IRF1 and the autophagy regulator ATG7 in human breast cancer cells that directly affects their ce

132 Pulsed magnetic field exposure of human breast cancer cells that express a sialic-acid ric

133 easure the adhesion strength and kinetics of human breast cancer cells to extracellular matrix such a

134 sis demonstrates that COX7AR is required for human breast cancer cells to maintain higher rates of pr

135 Exposure of MCF-7 and SUM159 human breast cancer cells to pharmacological concentrati

136 Staining of the complexes into living human breast cancer cells was observed.

137 r, t1/2 8.02 d), and their activity in MCF-7 human breast cancer cells was studied.

138 nuclear translocation of LASP-1.Treatment of human breast cancer cells with CXCL12, EGF and HRG, and

139 ne (DMDD) remarkably inhibited the growth of human breast cancer cells with little toxicity.

140 e, we analyzed the intravasation of invasive human breast cancer cells within a tissue-engineered mic

141 In human breast cancer cells, alphavbeta3 was necessary and

142 Osteopontin was highly secreted by mouse and human breast cancer cells, and tumor cell-secreted osteo

143 In human breast cancer cells, EVI1 silencing reduced prolif

144 In human breast cancer cells, GLS protein levels and sensit

145 the genomic distribution of H1.0 and H1X in human breast cancer cells, in which we previously observ

146 aracterize the lncRNA transcriptome in MCF-7 human breast cancer cells, including >700 previously una

147 ed, they are highly cytocidal toward several human breast cancer cells, including hormone-independent

148 In human breast cancer cells, MEDICA treatment attenuated s

149 ncRNAs increased the metastatic potential of human breast cancer cells, possibly by increasing the ab

150 Here we demonstrate that in human breast cancer cells, SDHAF2/SDH5 is dispensable fo

151 on-medicinal plant Arabidopsis thaliana with human breast cancer cells, selectively suppresses cancer

152 In human breast cancer cells, simultaneous knockdown of Rb

153 Here we report that in human breast cancer cells, the acute 17beta-estradiol-de

154 polyribosome profiling of tumor tissues and human breast cancer cells, we observe an intrinsic resis

155 correlated with the tumorigenic activity of human breast cancer cells.

156 f FGFR/RTK signaling in ErbB2-overexpressing human breast cancer cells.

157 with higher efficiency than anti-miR-221 in human breast cancer cells.

158 inst therapy-sensitive and therapy-resistant human breast cancer cells.

159 resulting in a decrease in proliferation of human breast cancer cells.

160 with the adhesion and invasion properties of human breast cancer cells.

161 brain, heart, liver, and aggressive forms of human breast cancer cells.

162 temness markers and self-renewal capacity in human breast cancer cells.

163 ansgenic mouse model of breast cancer and in human breast cancer cells.

164 nize the activity of beta-estradiol in MCF-7 human breast cancer cells.

165 ly active PLD enhanced expression of EGFR in human breast cancer cells.

166 isms of regulated lactate transport in MCF-7 human breast cancer cells.

167 invasion and anchorage-independent growth of human breast cancer cells.

168 ell survival and antiapoptotic signaling, in human breast cancer cells.

169 LK1 suppresses the migration and invasion of human breast cancer cells.

170 A is required for autophagosome clearance in human breast cancer cells.

171 e used a mouse xenograft model of metastatic human breast cancer combining CXCR4+ breast cancer cells

172 Formalin-fixed human breast cancer core-needle biopsy specimens, were e

173 on of TFAP2B and the RANK inhibitor, OPG, in human breast cancer correlate and are associated with re

174 Aberrant expression of CXCR4 in human breast cancer correlates with metastasis to tissue

175 Analysis of human breast cancer data reveal that autophagy gene expr

176 Here, we analyzed human breast cancer data to identify transcriptional pro

177 Analysis of human breast cancer datasets and additional experiments

178 hibition was associated with poor outcome in human breast cancer datasets, consistent with a tumor-su

179 Examination of human breast cancers demonstrated elevated IL26 transcri

180 ts supports the relevance of this pathway in human breast cancer, demonstrating that VEGF-C strongly

181 f NAD(P)H-rich EVs is highly correlated with human breast cancer diagnosis, which emphasizes the impo

182 double minute chromosomes, and about 20% of human breast cancer display genomic amplification and pr

183 We show that human breast cancers display active BMP signaling, which

184 In human breast cancer E2F2, status was also correlated wit

185 In clinical specimens of human breast cancer, elevated levels of the mammalian pa

186 Using human breast cancer explants, in vitro cell lines, mouse

187 In human breast cancer, expression of IL12A and cytotoxic e

188 study, an analysis of chromothripsis in 252 human breast cancers from two patient cohorts (149 metas

189 t with brc-1 and brd-1, the orthologs of the human breast cancer genes BRCA1 and BARD1, respectively.

190 s been established as a prognostic factor in human breast cancer, however, its role in the establishm

191 (MYC) oncoprotein is often overexpressed in human breast cancer; however, its role in driving diseas

192 esence of physiologic levels of estradiol in human breast cancer in nude mice and in murine breast ca

193 serial propagation of primary and metastatic human breast cancers in immunodeficient mice.

194 oles of miR-34a are maintained in a model of human breast cancer, in which chronic expression of miR-

195 EYA1 is known to be overexpressed in human breast cancer, in which the Myc protein is also ac

196 The majority of human breast cancer is estrogen receptor alpha (ER) posi

197 ts of human TERT (hTERT) on Wnt signaling in human breast cancer lines and HeLa cells.

198 nts in poorly and highly metastatic isogenic human breast cancer lines.

199 d that vessel co-option is also prevalent in human breast cancer liver metastases, a setting in which

200 In human breast cancer, low PRKAR1A/high SRC expression def

201 e mitochondrial COX subunit that facilitates human breast cancer malignancy.

202 addition, tail-vein injections in mice with human breast cancer MCF-7 cells depleted for SMAR1 showe

203 vitro photodynamic studies were conducted on human breast cancer MCF-7 cells to investigate both cell

204 lied to the absolute quantification of pY in human breast cancer MCF-7 cells, indicating that pY incr

205 characterised in vitro regarding binding to human breast cancer MCF-7-Y1 cells and slices of tumour

206 Using a human breast cancer (MCF-7 xenograft) model in nude mice

207 Human breast cancer MCF10DCIS.com cells were delivered i

208 egulating sGCalpha1 and -beta1 expression in human breast cancer MDA-MB-231 and MDA-MB-468 cell lines

209 red to display IC50 less than 10 muM against human breast cancer MDA-MB-231 cells at 24 h of treatmen

210 tiinvasive effects against highly metastatic human breast cancer MDA-MB-231 cells via aberration of M

211 en each of these miRNAs was transfected into human breast cancer MDA-MB-231 cells.

212 phosphonate drug, inhibited the migration of human breast cancer MDA-MB-231 cells.

213 on therapy in two orthotopic mouse models of human breast cancer, MDA-MB-231 and T-47D, which morphol

214 phosphorylation and DNA-binding activity in human breast cancer, MDA-MB-231 or MDA-MB-468 cells.

215 e detected an increase in SNX9 expression in human breast cancer metastases compared with primary tum

216 these genes, Fgf13, is associated with early human breast cancer metastasis in a clinical dataset.

217 In the MDA-MB-231.LM2-4 human breast cancer model, adjuvant sunitinib was ineffe

218 Here, we use mouse and human breast cancer models to identify a collective sign

219 fficacy of this delivery strategy in HER2(+) human breast cancer models.

220 ed tumor growth and metastasis in animal and human breast cancer models.

221 vivo tumor samples, sections of snap frozen human breast cancer murine xenografts were subjected to

222 In cell models of human breast cancer or in a cyclin D1-deficient model, w

223 inical significance of VGLL dysregulation in human breast cancer pathogenesis remains unknown.

224 ession is significantly higher in high-grade human breast cancer patient samples, whereas depletion o

225 athway are evident in xenografts in mice and human breast cancer patient samples.

226 nd performance assessment in anticipation of human breast cancer patient studies.

227 We then analyzed gene expression profiles of human breast cancer patients and patient-derived xenogra

228 ically, we showed that brain metastases from human breast cancer patients expressed higher levels of

229 ex with MCT1 and MCT4 in tissue samples from human breast cancer patients, but not healthy breast tis

230 Furthermore, in human breast cancer patients, FBXW7 expression in periph

231 targeting the TGF-beta signaling pathway in human breast cancer patients.

232 lin correlates with poor clinical outcome in human breast cancer patients.

233 tween Nanog expression and poor prognosis of human breast cancer patients.

234 ic signatures are predictive of survival for human breast cancer patients.

235 ells and correlate with metastatic status in human breast cancer patients.

236 hat upregulation of Mad1, which is common in human breast cancer, prevents stress-induced stabilizati

237 egulation of this pathway is associated with human breast cancer progression and patient survival out

238 ary adenocarcinoma mouse model and models of human breast cancer progression, we identified two TAp63

239 e identity of metastasis-initiating cells in human breast cancer remains elusive, and whether metasta

240 isomer, CDK11(p110), in the tumorigenesis of human breast cancer remains unclear.

241 Elucidating the molecular drivers of human breast cancers requires a strategy that is capable

242 Extension to HER2-positive (HER2+) human breast cancer revealed a number of HER2+ subtypes

243 TCGA analyses of human breast cancers revealed that NS is co-enriched pos

244 teinase matrix metalloproteinase 9 (MMP9) in human breast cancer samples and in cancer cells.

245 Human breast cancer samples display an inverse correlati

246 In human breast cancer samples, activation of this pathway

247 In human breast cancer samples, PR-positive tumors exhibite

248 Importantly, in IL8(high) human breast cancer samples, we also observed similar al

249 levels of canonical SREBP targets in primary human breast cancer samples.

250 ER/PR/PELP1 complexes were also detected in human breast cancer samples.

251 Analyses of human breast cancer showed inverse correlations between

252 Treatment of mice with disseminated ER+ human breast cancer showed that D9 plus MK-2206 blocked

253 We showed human breast cancer signals, at both expression and muta

254 we report increased expression of Ly6K/E in human breast cancer specimens correlates with poor overa

255 Interestingly, human breast cancer specimens expressed the same pattern

256 Analysis of human breast cancer specimens revealed an association be

257 In human breast cancer specimens, we found that immunohisto

258 the HER2 receptor on membrane protrusions in human breast cancer specimens.

259 Glycosphingolipid expression differs between human breast cancer stem cells (CSC) and cancer non-stem

260 normal murine mammary gland homeostasis and human breast cancer still remains under debate.

261 Here we identify clonal human breast cancer subpopulations that display differen

262 We report that PAK4 is overexpressed in all human breast cancer subtypes and associated with poor pa

263 We use human breast cancer T47D cell lines that stably overexpr

264 re we show that liver and lung metastases of human breast cancers tend to be highly fibrotic, and unl

265 as VEGFR1) labels a subset of macrophages in human breast cancers that are significantly enriched in

266 Human breast cancers that exhibit high proportions of im

267 Human breast cancers that have HER2 amplification/overex

268 overexpressed in a significant proportion of human breast cancers that integrates signals from upstre

269 biquitin ligase RNF31 is highly expressed in human breast cancer, the most frequent neoplastic lethal

270 In a mouse xenograft model of human breast cancer, there was an association in the cor

271 asets to identify conserved roles of E2F2 in human breast cancer through the TCGA breast cancer, Canc

272 Using a human breast cancer tissue array, we confirmed elevation

273 Using data mining and human breast cancer tissue microarrays, we found that Ct

274 is finding is further confirmed from data in human breast cancer tissues showing that CNNM3 levels co

275 In human breast cancer tissues, the levels of p54(nrb) and

276 not mRNA, is significantly overexpressed in human breast cancer tissues.

277 d K19-cyclin D co-expression was observed in human breast cancer tissues.

278 In this study, we used ErbB2 mouse models of human breast cancer to investigate FIP1C function in tum

279 of the most frequent mutations occurring in human breast cancer, to induce multipotency during tumor

280 might be a potential therapeutic target for human breast cancer treatment and prevention.

281 Human breast cancer tumors grown in mice were subjected

282 ved in human TNBC and additional subtypes of human breast cancer tumors linked to a high metastatic r

283 induced angiogenesis and growth of mouse and human breast cancer tumors, where the miR-467 pathway wa

284 earing subcutaneous EGFR-positive MDA-MB-468 human breast cancer tumors.

285 periments, in independent cohorts of primary human breast cancers, upregulated endosialin expression

286 sets, we found that high LDLR expression in human breast cancers was associated with decreased recur

287 lls from patient-derived xenograft models of human breast cancer, we developed a highly sensitive flu

288 and is overexpressed in approximately 10% of human breast cancers, whereas MRPS30 plays a key role in

289 Human breast cancers with high levels of HIF-1alpha cont

290 Finally, human breast cancers with high p27pT157 differentially e

291 Pathologically, human breast cancers with Snail1(+) CAF tended to exhibi

292 thripsis affects a substantial proportion of human breast cancers, with a prevalence over 60% in a co

293 tive phenotype is the most prevalent form of human breast cancer worldwide and is characterized by po

294 Human breast cancer xenoengraftment is used as a means o

295 sitive xenograft results from the MDA-MB-468 human breast cancer xenograft model for compound 18 supp

296 poptosis in vivo during the progression of a human breast cancer xenograft model was guided by a bi-p

297 In a human breast cancer xenograft model, miR-221-overexpress

298 d the in vivo efficacy of THIQ 40 in a MCF-7 human breast cancer xenograft model.

299 mice bearing estrogen-independent MDA-MB-231 human breast cancer xenografts.

300 pidermal growth factor receptor 2-expressing human breast cancer xenografts.