ライフサイエンスコーパス: human breast cancer

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

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

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

4 origenesis in histological investigations of human breast cancer.

5 2E3), an orphan nuclear hormone receptor, to human breast cancer.

6 echanism contributing to Myc deregulation in human breast cancer.

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

8 ssays representing 319 proteins expressed in human breast cancer.

9 ecifically in the triple negative subtype of human breast cancer.

10 hich faithfully recapitulate key features of human breast cancer.

11 d to the highly aggressive "triple negative" human breast cancer.

12 use mammary tumors that parallel subtypes of human breast cancer.

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

14 3 is upregulated in malignant and metastatic human breast cancer.

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

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

17 targets of HER2 transcriptional signaling in human breast cancer.

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

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

20 determining the transcriptional landscape of human breast cancers.

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

22 olactin receptor is seen in more than 95% of human breast cancers.

23 ggressive behavior and metastatic ability in human breast cancers.

24 orrelated inversely with BRCA1 expression in human breast cancers.

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

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

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

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

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

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

31 psin B (CTSB) is frequently overexpressed in human breast cancer and correlated with a poor prognosis

32 creases in other heat shock proteins in both human breast cancer and dopaminergic neural cells, demon

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

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

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

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

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

38 nding and lysoPLD activity in stimulation of human breast cancer and mouse aortic vascular smooth mus

39 eceptor (IL4R) is expressed and activated in human breast cancer and mouse models of breast cancer.

40 1 as a gene amplified in a large fraction of human breast cancer and overexpressed in metastatic brea

41 s (PDX) that encompass the main diversity of human breast cancer and retain the major clinicopatholog

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

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

44 tablish Six2 as a regulator of metastasis in human breast cancers and demonstrate an epigenetic funct

45 biomarker and metastasis-driving oncogene in human breast cancers and determined that DP103 elevates

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

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

48 135b is up-regulated in basal or normal-like human breast cancers, and it correlates with patient sur

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

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

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

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

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

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

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

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

57 found that the frequency of Gal1(+) cells in human breast cancer biopsies correlated positively with

58 mary cancer represents an excellent model of human breast cancer, but is greatly understudied.

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

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

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

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

63 3D in vitro model to analyze organ-specific human breast cancer cell extravasation into bone- and mu

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

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

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

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

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

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

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

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

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

73 Four human breast cancer cell lines (MDA-MB-231, BT-20, Zr-75

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

75 elate with metastatic potential in mouse and human breast cancer cell lines and is elevated in metast

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

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

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

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

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

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

82 Similarly, in human breast cancer cell lines in which ErbB2 is overexp

83 3A expressing human mammary fibroblasts with human breast cancer cell lines into mouse mammary fat pa

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

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

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

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

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

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

90 peptide blocks microtubule nucleation in two human breast cancer cell lines, suggesting that this mec

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

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

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

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

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

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

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

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

99 ve and resistant to cisplatin (A2780S/R), in human breast cancer cells (MCF7) and in a nontumorigenic

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

101 Overexpression of ZNF24 in human breast cancer cells also inhibited tumor angiogene

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

103 nhibiting CT-L activity in intact MDA-MB-468 human breast cancer cells and inhibiting their survival.

104 Furthermore, both human breast cancer cells and mouse mammary epithelial t

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

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

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

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

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

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

111 sure pol-II occupancy genome-wide when MCF-7 human breast cancer cells are treated with estradiol (E2

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

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

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

115 n, and was recently shown to be repressed in human breast cancer cells by hypermethylation of regulat

116 chanisms of the reversal of MDR phenotype in human breast cancer cells by using doxorubicin-liposome-

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

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

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

120 ation to assess the tumorigenic potential of human breast cancer cells following RNA interference-med

121 cal-biomedical applications by sorting MCF-7 human breast cancer cells from nonmalignant leukocytes,

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

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

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

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

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

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

128 ckdown of IRP2 in triple-negative MDA-MB-231 human breast cancer cells increases ferritin H expressio

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

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

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

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

133 overexpression of microRNA 155 (miR-155) in human breast cancer cells reduces the levels of RAD51 an

134 nscriptome sequencing analyses of metastatic human breast cancer cells subjected to the chemotherapeu

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

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

137 Our in vitro and in vivo experiments using human breast cancer cells that do not express ATX (MDA-M

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

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

140 ntified differentially methylated regions to human breast cancer cells undergoing a gain of migratory

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

142 perimental platform was established in which human breast cancer cells were embedded in 3D aldimine c

143 Cultured MDA-MB-231 human breast cancer cells were treated with different co

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

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

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

147 In human breast cancer cells, 19-phenyl BQAs induced growth

148 In human breast cancer cells, alphavbeta3 was necessary and

149 tain Hsp90 and growth-inhibitory activity in human breast cancer cells, although with diminished pote

150 nt hTERT interaction with the Wnt pathway in human breast cancer cells, and any detectable influence

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

152 In human breast cancer cells, EVI1 silencing reduced prolif

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

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

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

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

157 During invadopodium formation in MDA-MB-231 human breast cancer cells, increased association of SNAP

158 In human breast cancer cells, MEDICA treatment attenuated s

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

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

161 In human breast cancer cells, simultaneous knockdown of Rb

162 ens for autophagy-regulating phosphatases in human breast cancer cells, we identify CIP2A (cancerous

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

164 ction of the Slug-Puma axis was confirmed in human breast cancer cells, where Slug knockdown increase

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

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

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

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

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

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

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

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

173 ar calcium signal in the induction of EMT in human breast cancer cells.

174 ient increase in cytosolic calcium levels in human breast cancer cells.

175 e the genomic localization of PELP1 in MCF-7 human breast cancer cells.

176 novel target of WA-mediated growth arrest in human breast cancer cells.

177 the anticancer activities of 1,25(OH)2D3 in human breast cancer cells.

178 in cellular transformation and the growth of human breast cancer cells.

179 inhibited the growth of the ERalpha-positive human breast cancer cells.

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

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

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

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

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

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

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

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

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

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

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

191 Analysis of human breast cancer datasets and additional experiments

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

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

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

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

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

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

198 e (i) significantly upregulated in recurrent human breast cancers; (ii) differentially expressed acro

199 by studying NAMPT expression and function in human breast cancer in vivo and in vitro.

200 eighted MRI (DW-MRI) in a xenograft model of human breast cancer in which daily administration of sor

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

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

203 novel KLF8 to MMP14 signaling that promotes human breast cancer invasion and metastasis.

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

205 low and high metastatic lines derived from a human breast cancer line, we have identified miR-149 to

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

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

208 s in the invasiveness of two closely matched human breast cancer lines.

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

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

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

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

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

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

215 Human breast cancer MCF10DCIS.com cells were delivered i

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

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

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

219 are capable of delivering Notch-1 shRNA into human breast cancer MDA-MB-231 cells with high efficienc

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

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

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

223 In silico analysis of human breast cancer microarray and reverse-phase protein

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

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

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

227 yperactivation of BMP signaling is common in human breast cancers, most notably in the basal molecula

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

229 Finally, in primary human breast cancer, NDY1/KDM2B expression correlates ne

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

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

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

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

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

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

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

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

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

239 nd is elevated in metastatic lung lesions in human breast cancer patients.

240 ly correlated with metastatic progression in human breast cancer patients.

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

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

243 y studied and characterized, but its role in human breast cancer remains elusive.

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

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

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

247 In human breast cancer samples, elevated phosphorylation of

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 is further supported by clinical analysis of human breast cancer samples.

252 inal and myoepithelial cells and are rare in human breast cancer, seem to lack genomic abnormalities.

253 Analyses of human breast cancer showed inverse correlations between

254 this study, expression profiling of Pfn1 in human breast cancer specimens correlates lower Pfn1 expr

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

256 Interestingly, human breast cancer specimens expressed the same pattern

257 Analysis of human breast cancer specimens revealed an association be

258 correlated inversely with CDH1 expression in human breast cancer specimens, corroborating the disease

259 In human breast cancer specimens, we found that immunohisto

260 tivated TGF-beta signaling and metastasis in human breast cancer specimens.

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

262 that miR-142 and miR-150 are upregulated in human breast cancer stem cells (BCSCs) as compared to th

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

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

265 n the tumorigenicity and progression of this human breast cancer subtype.

266 + cells led collective invasion in the major human breast cancer subtypes.

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

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

269 Human breast cancers that exhibit high proportions of im

270 Human breast cancers that have HER2 amplification/overex

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

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

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

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

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

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

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

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

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

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

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

282 Human breast cancer tumors grown in mice were subjected

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

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

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

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

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

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

289 Using genomic information of human breast cancer, we have discovered that the orphan

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

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

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

293 Human breast cancer xenoengraftment is used as a means o

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

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

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

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

298 In contrast, DIM did not protect human breast cancer xenograft tumors against radiation u

299 tor 11d displayed good in vivo efficacy in a human breast cancer xenograft.

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