ライフサイエンスコーパス: MCF

1 MCF outperforms standard classifiers based on individual

2 MCF-7 cells, a human breast adenocarcinoma, were retaine

3 MCF-7 tumors, with inherently low GLS activity compared

4 The potency of 2 was evaluated against MX-1, MCF-7, ID8, L1210FR (BR+, biotin receptor overexpressed)

5 tabolites in lysates of 100, 1000, and 10000 MCF-7 breast cancer cells was carried out using a new la

6 The proliferations of Caco-2, MCF-7 and HELA cells were more inhibited when treated wi

7 cytotoxicity effect against Caco-2, HepG-2, MCF-7 and PC-3 cells in comparison with other NPs and fr

8 dges were used to enrich breast (MDA-MB-231, MCF-7) and renal (786-O, A-498) cancer cells expressing

9 uated in 3 breast cancer models: MDA-MB-231, MCF-7, and ZR-75-1.

10 tern of different cell lines (HeLa, OVCAR-5, MCF-7, and human fibroblasts), demonstrating an excellen

11 creased by 1.60 nmol (61.1 %) in 3.0 x 10(6) MCF-7 cells after 100 nM insulin stimulation.

12 es, and the in vivo efficacy of THIQ 40 in a MCF-7 human breast cancer xenograft model.

13 of tumor cell lines (HeLa, SK-MEL-28, A549, MCF-7) with effective concentrations (EC50) typically be

14 ntration of 2nM) on electrochemical activity MCF-7 cells.

15 tive response in human breast adenocarcinoma MCF-7 cells.

16 uman colon HCT116 and mammary adenocarcinoma MCF-7 cancer cells before and after simulated digestions

17 omplexes has been shown to be active against MCF-7 (human breast carcinoma), HT-29 (human colon carci

18 ainst MCF-7 and small or no activity against MCF-10A.

19 bstantial antiproliferative activity against MCF-7 and HL-60 cells with IC50 of 6.13 +/- 0.64 and 4.4

20 ct against MDA-MB-435, weak activity against MCF-7 and small or no activity against MCF-10A.

21 nstrated profound cytotoxic activity against MCF-7 cell line.

22 y showed highest inhibitory activity against MCF-7.

23 ment-dependent cellular cytotoxicity against MCF-7 and OVCAR-5 cells.

24 ptamer M17A2 generated by cell-SELEX against MCF-7R cells.

25 Low aggressive MCF-7 breast cancer cells have low endogenous PLD enzyma

26 acteristic curve [AUC] = 0.93, P < .001) and MCF (AUC = 0.92, P < .001) can be used to discriminate p

27 as observed for the viability of HCT 116 and MCF-7 cells challenged with 0.4, 4.0, and 40mug/ml nanoe

28 ge contrast agents (PCCAs) in MDA-MB-231 and MCF-7 breast cancer cells in vitro.

29 ibroblasts, NMuMG epithelial, MDA-MB-231 and MCF-7 breast cancer cells).

30 in solitary cells of GM14667, MDA-MB-231 and MCF-7 cell lines, achieving a DNA amplification efficien

31 and morphological changes of MDA-MB-231 and MCF-7 cells.

32 ail) and breast (MDA-MB-468, MDA-MB-231, and MCF-7 overexpressing Snail) cancer cells expressed lower

33 ode MEMs in different cancer models: 4T1 and MCF-7 breast carcinoma, B16F10 melanoma, WT-GBM glioma a

34 -resistant (TR) ER+ cell lines (MCF-7:5C and MCF-7:TAM1) were used for optimization, followed by vali

35 ) of breast epithelial cell lines (MCF-7 and MCF-10A) and compared it with extracellular fractions en

36 ARCaP-E and ARCaP-Neo) and breast (MCF-7 and MCF-7 Neo) cancer cells.

37 KIF20A depletion also renders MCF-7 and MCF-7Tax(R) cells more sensitive to paclitaxel-induced c

38 tectable levels of PD-L1 (SUM149, BT474, and MCF-7).

39 kemia), HepG2 (Hepatocellular carcinoma) and MCF 12A (normal epithelial breast cell line) using MTT a

40 C analysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell lines.

41 ncer cell lines A549, DLD-1, DU145, FaDu and MCF-7 using SRB assay.

42 ive phenotype on minimally invasive HeLa and MCF-7 cell lines.

43 ibroblasts) and transformed cells (LNCaP and MCF-7 cancer cells), as well as non-mammalian cells (fro

44 1R activity in mitochondrial protection, and MCF-7 cells with suppressed IGF-1R activity became highl

45 muM against HT-29 colon carcinoma as well as MCF-7 and MDA-MB-231 mammary carcinoma cells (cisplatin:

46 The binding of 4-(11)C-MBZA to B16F1, MCF-10A, and MDA-MB-231 cells was 6.41% +/- 1.28%, 1.51%

47 connections could be built not only between MCF-7R cells, but also from MCF-7R to other cells after

48 micropallet arrays in the presence of blood, MCF-7 cells were mixed into whole blood and added to sma

49 29b-1 and miR-29a target transcripts in both MCF-7 and LCC9 cells.

50 prostate (ARCaP-E and ARCaP-Neo) and breast (MCF-7 and MCF-7 Neo) cancer cells.

51 interference) function approaches in breast (MCF-7 and MDA-MB-231) and ovarian (SKOV3 and SKOV3ip) ca

52 In contrast, once taken up by MCF-7 cells, the iodide ligand is rapidly pumped out.

53 ctroscopy the response of live breast cancer MCF-7 and mammary breast adenocarcinoma MDA-MB 231 cell

54 injections in mice with human breast cancer MCF-7 cells depleted for SMAR1 showed increased CD44 var

55 tudies were conducted on human breast cancer MCF-7 cells to investigate both cellular uptake and cyto

56 quantification of pY in human breast cancer MCF-7 cells, indicating that pY increased by 1.60 nmol (

57 Here, we show that in breast cancer MCF-7 cells, TLE3, a co-repressor of the Groucho/Grg/TLE

58 cer activity against HeLa (cervical cancer), MCF-7 (breast cancer), HL-60 (Human promyelocytic leukem

59 CTP by short hairpin RNA in breast carcinoma MCF-7 cells leads to the declined repair efficiency for

60 CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copper chelator, inhi

61 state carcinoma), HCT-116 (colon carcinoma), MCF-7 (breast carcinoma) and NCI-H460 (lung carcinoma) b

62 mean channel fluorescence (MCF), and CD107a MCF to detect biallelic mutations were 59.5%, 96.6%, and

63 r NK-cell cytotoxicity, perforin MCF, CD107a MCF, and combined perforin and CD107a MCFs were 0.690, 0

64 CD107a MCF, and combined perforin and CD107a MCFs were 0.690, 0.971, 0.860, and 0.838.

65 SKBR3, MDA-MB-468) than normal breast cells (MCF-10A) or cell lines derived from other tumor types.

66 468, BT20, MDA-MB-231); normal breast cells (MCF-10A); and cell lines derived from colon (HT29), ovar

67 Human breast cancer cells (MCF-7) grown on serum protein-coated gold sensors were p

68 analysis of normal mammary epithelial cells (MCF-12A) under oxygen gradients revealed 70% mortality a

69 was performed using B16F1 (melanoma cells), MCF-10A (breast epithelial cells), and MDA-MB 231 (breas

70 argeting of p38delta in breast cancer cells, MCF-7 and MDA-MB-231 resulted in a reduced rate of cell

71 e blood cells, DU-145 prostate cancer cells, MCF-7 breast cancer cells, and LU-HNSCC-25 head and neck

72 cal ionization of both methyl chloroformate (MCF) and methoxime-trimethylsilyl (MO-TMS) derivatives o

73 -carrier DP-16QAM system over 800 km 19-core MCF to validate the digital compensation of inter-core X

74 (n = 20) and healthy women (n = 7) decreased MCF-7 (hormone-sensitive) and MDA-MB-231 (hormone-insens

75 as 0.5 mg/kg dose in the estrogen-dependent MCF-7 xenograft model, where this effect was accompanied

76 Conclusion Cardiovascular MR-derived MCF and LAS serve as reliable diagnostic and prognostic

77 elial line MCF-10A and its mutant descendant MCF-10A-H1047R.

78 AS) targets in organotypic three-dimensional MCF-10A cell cultures that mimic a context relevant to b

79 nanoparticle in breast cancer cell line i.e. MCF-7.

80 l-cell adhesion protein, E-cadherin, enables MCF-10A cells to slide on narrower micropatterns; meanwh

81 with non-tumorigenic human breast epithelial MCF-10A and MCF7 cells revealed that NO2-OA more selecti

82 MARCA4 knockdown in human mammary epithelial MCF-10A cells resulted in 176 up-regulated genes, includ

83 rial extrusion of non-tumorigenic epithelial MCF-10A cells through filters with different pore sizes.

84 riminate with minimized classification error MCF-7 promoter and enhancer transcription response subcl

85 -IIB-GFP-, and 19% of NM-IIC1-GFP-expressing MCF-7 cells show multiple bleb formation, compared with

86 Multicopper ferroxidases (MCFs) play an important role in cellular iron homeostasi

87 n, AlHV-1 induces malignant catarrhal fever (MCF), a fatal lymphoproliferative disease of ruminants,

88 xing (SDM), incorporating multi-core fibers (MCFs), has been demonstrated for effectively maximizing

89 We report on the use of a multi-core fibre (MCF) comprising strongly-coupled cores for accurate stra

90 munoassay platform, the Microcapillary Film (MCF).

91 dic chip, called a microfluidic cold finger (MCF).

92 unction, perforin mean channel fluorescence (MCF), and CD107a MCF to detect biallelic mutations were

93 nsparency and flat geometry of fluoropolymer MCF allowed quantitation of PSA in the range 0.9 to 60 n

94 45-fold for MDA-MB-231 cells and 7-fold for MCF-7 cells, relative to untargeted PCCAs.

95 (Ea = 2.1 +/- 0.1 and 0.80 +/- 0.19 kPa for MCF-7 and MDA-MB-231 cells).

96 ntargeted mass-spectroscopy metabolomics for MCF-7 cells.

97 ppressor in lumA-michigan cancer foundation (MCF)-7 and triple negative-MD Anderson (MDA) metastatic

98 ed with control (Michigan Cancer Foundation; MCF-10A) and malignant (M.D. Anderson-metastatic breast;

99 ER tumors, eight MDA-MB-231 tumors, and four MCF-7 ER-positive tumors).

100 Myocardial contraction fraction (MCF) was calculated by dividing left ventricular (LV) st

101 e the sequences of N-glycans on Gal-3BP from MCF-7 and MDA-MB-231 cells, especially the sequences wit

102 NOTCH3 and PBX1 ChIP-seq data acquired from MCF-7 breast cancer cells.

103 not only between MCF-7R cells, but also from MCF-7R to other cells after co-culture.

104 s our approach on existing GRO-seq data from MCF-7 breast cancer cells.

105 A case study on data from MCF-7 cell-line reveals that PEDAL can identify successf

106 ata and RNA polymerase II ChIA-PET data from MCF-7 cells did not suggest remote effects of the enhanc

107 ide population (NSP or main population) from MCF-7 cell line, and evaluated the impact of CCN5 on the

108 Compared with that from MCF-7, the Gal-3BP from MDA-MB-231 cells had fewer tetra

109 aving PTEN promoter methylated (as in, e.g., MCF-7 cell line).

110 on affects breast cancer cells, we generated MCF-7 cells stably overexpressing StARD3-green fluoresce

111 and MSSA and cytotoxicity against NCI-H460, MCF-7 and HeLa.

112 tested, including telomerase-positive (HeLa, MCF-7, HCT-116, and HEK293T) and telomerase-negative cel

113 Human MCF-7 cells lacking functional FADS2-mediated Delta6-des

114 bilical vascular endothelial cells and human MCF-7 breast tumor xenografts.

115 Here, we demonstrate that treatment of human MCF-7 breast cancer cells with pro-inflammatory cytokine

116 primary human macrophages (MPhi) with human MCF-7 breast carcinoma cells, which caused cell death of

117 Importantly, MCF-7 cell-derived exosomes that are caspase-3-deficient

118 In MCF-10A, this mutation induces an extensive cellular reo

119 In MCF-7 and ZR75.1 breast cancer cells, IGF-1 induces pero

120 In MCF-7 cells and xenograft tumors, MnO2 /DVDMS is reduced

121 In MCF-7 cells Oct-1 binds the iNOS promoter, recruits RNA

122 ression to be basally repressed by Nkx3-1 in MCF-7 cells and TOT treatment appeared to elevate Nkx3-1

123 currence of open compartments on chr16-22 in MCF-7 cells.

124 r and apoptosis-inducing potentials of 9f in MCF-7 and HL-60 cells via intrinsic pathway.

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

126 actor)-mediated activation of ERK and AKT in MCF-7 cells.

127 nhances UVC irradiation-induced apoptosis in MCF-7 cells, and causes sensitization to DNA-damaging dr

128 nize beta-estradiol in a functional assay in MCF-7 human breast cancer cells and they have no E/Z iso

129 significantly reduce breast cancer burden in MCF-7 xenograft mouse model.

130 e cellular uptake of the monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.

131 significantly in TNBC, but did not change in MCF-7 tumors.

132 otably, Oct-4 levels were highly elevated in MCF-7-tam(r) cells, and appeared critical for their TOT

133 e show that FOXM1 SUMOylation is enhanced in MCF-7 breast cancer cells in response to treatment with

134 level is low but inducible by epirubicin in MCF-7 cells.

135 ere achieved for the detection of ERalpha in MCF-7 cell lysate.

136 antagonize the activity of beta-estradiol in MCF-7 human breast cancer cells.

137 s candidates for regulation were examined in MCF-7 cells.

138 mitotic arrest resulting from WA exposure in MCF-7, SUM159, and SK-BR-3 cells was associated with a m

139 nce of the genes differentially expressed in MCF-10A-H1047R cells and the established protein and RNA

140 hIP-BIT as being differentially expressed in MCF-7 cells.

141 wnregulated ERalpha and ERbeta expression in MCF-7 breast cancer cells.

142 human miR-125, we validated our findings in MCF-7 and MDA-MB-231 breast cancer cell lines, which har

143 uronic acid nanoparticle (NP) formulation in MCF-7 and MDA-MB-231, two cell lines representative of d

144 ha1,2- and alpha1,3 fucose linkages found in MCF-7 cells.

145 ulted in an increase in turnover of FOXM1 in MCF-7 cells treated with the protein synthesis inhibitor

146 Overexpression of FoxQ1 in MCF-7 and SUM159 cells increased ALDH1 activity and the

147 Lastly, the reported effect is greater in MCF-7 than in MDA-MB-231 breast cancer cells, which coul

148 cription factor Sp1 and coactivator GRIP1 in MCF-7 human breast and HepG2 liver cancer cell lines.

149 (ATP) and guanosine-5'-triphosphate (GTP) in MCF-7 breast cancer cells by using graphene oxide nanosh

150 sphorylation of HER1, HER2, HER3 and HER4 in MCF-7 cells, indicative of activation of these proteins.

151 thylated in MCF7 cells but hypomethylated in MCF/CEACAM1 cells, ID4 expression was induced in MCF7 ce

152 ading to increased migration and invasion in MCF-7 cells.

153 activity and thus increased miR-221 level in MCF-7 cells.

154 enhancement of FOXA1 promoter methylation in MCF-7 breast cancer cells, whereas the reconstitution of

155 nts indicated that the effects of 3-OST3A in MCF-7 cells were mediated by altered interactions betwee

156 A and increased with OTUB1 overexpression in MCF-7 cells, arguing that OTUB1 positively regulates FOX

157 ic expression of functionally active PAR1 in MCF-7 cells induced a hormone-refractory, invasive pheno

158 ere screened for cytoprotective potential in MCF-7 cells, including the mitochondrial membrane potent

159 RB inactivation increases IL-6 production in MCF-7 cells appeared to involve fatty acid oxidation (FA

160 both, or absence of any such protrusions in MCF-7 cells.

161 miR-29b-1/a did not drive TAM-resistance in MCF-7 breast cancer cells.

162 of miR-873 reversed tamoxifen resistance in MCF-7/TamR cells.

163 the genome at near-nucleotide resolution in MCF-7 cells.

164 C50 values of 38 and 19 nM, respectively, in MCF-7 breast cancer cells, inhibited the polymerization

165 knockdown of p62 by small interfering RNA in MCF-7 cells abrogates Vps34-dependent tumor growth.

166 nism of cytotoxicity of SeChry and SePQue in MCF-7 human mammary cancer cells demonstrated their capa

167 Using GRO-seq in MCF-7 cells, we defined the immediate transcriptional ef

168 Chromatin Immunoprecipitation sequencing in MCF-7 breast cancer cells to map Pol II pausing across t

169 Structure-function analyses of SgK269 in MCF-10A mammary epithelial cells demonstrated a critical

170 we found that CXCR3-B-mediated signaling in MCF-7 and T47D breast cancer cells induced apoptotic cel

171 by blockade of beta-adrenergic signaling in MCF-7 cells, indicating that catecholamines were the res

172 iple ceramide and dihydroceramide species in MCF-7 cells treated with TNFalpha occurred by up-regulat

173 Inhibition of FAK or Src in MCF-10A cells plated at low cell density prevented the a

174 tro, disrupted the microtubular structure in MCF-7 cells as visualized by confocal microscopy, and ca

175 n, to displace FOXM1 from genomic targets in MCF-7 breast cancer cells, and induce concomitant transc

176 bility maintenance of Rad51 requires TCTP in MCF-7 cells under normal cell culture conditions.

177 K signaling to support junctional tension in MCF-7 cells.

178 to characterize the lncRNA transcriptome in MCF-7 human breast cancer cells, including >700 previous

179 mechanisms of regulated lactate transport in MCF-7 human breast cancer cells.

180 on reduced upon genotoxic agent treatment in MCF-7 cells, but remained relatively constant in resista

181 toxicity and enhance accumulation of ZnPc in MCF-7 cells, improving apoptotic cell death upon irradia

182 al Kerr effects, intra- and inter-core XT in MCFs.

183 ated on various cancer cell lines including, MCF-7 breast, HL-60 leukemia, MIA PaCa-2 pancreatic, DU1

184 the survival predictive power of individual MCF pathways strongly correlates with their power in pre

185 Here, we investigate MCF-7 cells that are adapted to grow in acidic condition

186 ectivity toward cancer cell lines (HeLa, KB, MCF-7, Hep-G2, and U87) relative to HDF normal cells tha

187 up-to -11.56 dB of inter-core XT over 800 km MCF, offering flexibility to fabricate dense core struct

188 carcinoma cell lines, but not to normal-like MCF-10a breast cells, dramatically reduces cancer cell v

189 xposed the human breast epithelial cell line MCF-10A to fractionated doses of X-rays and examined the

190 of the human breast adenocarcinoma cell line MCF-7 obtained directly from a cell bank that are invisi

191 -intact luminal-type breast cancer cell line MCF-7 promoted a positive feed forward loop between IL-6

192 xel effectiveness on breast cancer cell line MCF-7.

193 otoxicity to GM2-expressing cancer cell line MCF-7.

194 cell lines: the human breast epithelial line MCF-10A and its mutant descendant MCF-10A-H1047R.

195 rigenic normal mammary epithelial cell line (MCF-10A) was markedly more resistant to mitotic arrest b

196 lpha-positive human breast cancer cell line (MCF-7) treated with 17-beta-estradiol or vehicle control

197 evant human breast adenocarcinoma cell line (MCF-7/FLV1), exploits the overexpression of ABCG2 transp

198 in the parent endocrine-dependent cell line (MCF-7:WS8), in 2D and 3D cultures, using ERalpha in-cell

199 rom real samples of breast cancer cell line, MCF-7.

200 a model circulating tumour cell (CTC) line, MCF-7, a metastatic breast cancer by targeting epithelia

201 17-expressing human breast cancer cell lines MCF-7 and MDA-MB-453 also degraded recombinant IFN-gamma

202 g events to STn-expressing cancer cell lines MCF-7 and OVCAR-5.

203 (19-60 nt) of breast epithelial cell lines (MCF-7 and MCF-10A) and compared it with extracellular fr

204 ug resistant (MDR) breast cancer cell lines (MCF-7/ADR).

205 Treatment-resistant (TR) ER+ cell lines (MCF-7:5C and MCF-7:TAM1) were used for optimization, fol

206 were studied in two breast tumor cell lines, MCF-7 and MDA-MB-231.

207 n bone marrow, multiple leukemia cell lines, MCF-7 cells, and subjects after GM-CSF treatment but not

208 at MaBiDZ sensor can be internalized in live MCF-7 breast cancer cells and activated by a magnetic fi

209 n distal non-tumor tissue and low-metastatic MCF-7 cells, respectively.

210 actually inhibited it in the non-metastatic MCF-7 cancer cells or in normal cells.

211 tandem effect between the acidic Al modified MCF-17 and the Pt metal.

212 rphyrazines with EC50 values as low as 5 nM (MCF-7 cells) for the best compound; this activity was se

213 In luminal nonmetastatic MCF-7 breast cancer cells, HuR silencing was sufficient

214 iber-like dimensions, whereas nontransformed MCF-10A mammary epithelial cells require much wider micr

215 rd MDA-MB-231 breast cancer cells and normal MCF-10A breast epithelial cells.

216 Of note, MCF-7 cells with acquired resistance to an IGF-1 recepto

217 enome-wide target gene profiling analysis of MCF-7 breast cancer cell populations that were sensitive

218 ork reports the impedance characteristics of MCF-7 cell lines treated with anticancer drug ZD6474 to

219 9f caused arrest of cell cycle of MCF-7 and HL-60 cells at G0/G1 phase.

220 The deformability of MCF-7 breast cancer cells was characterized based on the

221 formance for the ultrasensitive detection of MCF-7 cells and quantification of cell surface glycan.

222 Exposure of MCF-7 and SUM159 human breast cancer cells to pharmacolo

223 eckpoint activation following IR exposure of MCF-7 breast cancer cells is dependent on the activation

224 s to running wheels showed reduced growth of MCF-7 (-36%, P < 0.05) and MDA-MB-231 (-66%, P < 0.01) t

225 The motility of MCF-7 cells increases following expression of a human PM

226 of MAGEA1 on migration and proliferation of MCF-7 and MDA-MB-231 cells.

227 Proliferation of MCF-7 and SK-BR-3 cells was evaluated by MTT assays.

228 anterior pituitary, or the proliferation of MCF-7a breast cancer cell xenografts.

229 t features in the electrochemical readout of MCF-7 breast cancer cells versus MCF-10A mammary epithel

230 Different sizes of MCF-7 breast cancer cells (8 to 15 mum) were used in thi

231 protein that overexpressed on the surface of MCF-7 cells, the aptamer conjugated MBs showed a predomi

232 nation to inhibit the growth and survival of MCF-7 and MDA-MB-231 breast cancer cells.

233 However, the role of MCFs in renal metabolism remains unclear.

234 Cp) knockout (KO) mice to study the roles of MCFs in the kidney.

235 cancer cells, we performed Hi-C analysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell

236 echanistic studies of 9f were carried out on MCF-7 and HL-60 cell lines.

237 D. Anderson-metastatic breast; MDA-MB-231 or MCF-7) human epithelial breast cells revealed that MAD-2

238 Our MCF interferometers were used for sensing strain.

239 Our MCF is designed to mode match a standard single mode opt

240 An important advantage of our MCF interferometers is their capability to operate at ve

241 In addition, a packaged MCF interferometer was transferred into field trials to

242 AUCs for NK-cell cytotoxicity, perforin MCF, CD107a MCF, and combined perforin and CD107a MCFs w

243 THFD1 translocates to the nucleus in S-phase MCF-7 and HeLa cells.

244 st cancer xenografts compared to ER-positive MCF-7 xenografts with or without VEGF overexpression tha

245 ib sensitivity in estrogen receptor-positive MCF-7 breast cancer cells.

246 1 T), but not in oestrogen receptor-positive MCF-7 tumours.

247 duced tumorigenesis by 50% when preincubated MCF-7 breast cancer cells were inoculated into NMRI-Foxn

248 Here we present MCF (Metabolic classifier and feature generator), which

249 KIF20A depletion also renders MCF-7 and MCF-7Tax(R) cells more sensitive to paclitaxel

250 is overexpressed in the epirubicin-resistant MCF-7Epi(R) cells and its expression level is low but in

251 lpha in tamoxifen- and fulvestrant-resistant MCF-7 cells, with pharmacologic inhibition of ERRalpha s

252 at of doxorubicin in the multidrug resistant MCF-7/ADR xenografted nude mice.

253 and deregulated in the paclitaxel-resistant MCF-7Tax(R) cells.

254 d to be downregulated in tamoxifen-resistant MCF-7/TamR cells, while CDK3 is overexpressed in these c

255 and cell proliferation of the TOT-resistant MCF-7-tam(r) breast cancer cells.

256 downregulated by paclitaxel in the sensitive MCF-7 breast cancer cells and deregulated in the paclita

257 This allows us to fabricate simple MCF interferometers whose interrogation is carried out w

258 level effects of 17beta-estradiol on single MCF-7 cells using Fourier transform infrared imaging spe

259 ed at a basal level in mice with early stage MCF-7 tumors, and jumped to 23.9% and 28.2% when tumor g

260 e-cell-imaging probe and efficiently stained MCF-7 breast cancer cell lineages.

261 Attachment of serum-starved MCF-10A cells to fibronectin, but not poly-d-lysine or l

262 icial chromosome (BAC) that is used to study MCF.

263 e the NP accumulated more in MDA-MB-231 than MCF-7 potentially due to binding of hyaluronic acid to C

264 rnalization at MI=1.0, 79.5% at MI=1.5) than MCF-7 cells (42.4% internalization at MI=1.0, 35.7% at M

265 lines as a comparative model, we found that MCF-7 express iNOS upon cytokine stimulation while MDA-M

266 yelogenous leukemia cell line as well as the MCF-7 breast cancer cell line with chromatin interaction

267 allowing for the discrimination between the MCF-7 (less aggressive) and MDA-MB-231 (more aggressive)

268 -MB-231 (-66%, P < 0.01) tumors and, for the MCF-7 tumor, increased regulation of the Hippo signaling

269 ) using an enriched phosphoproteome from the MCF-10A cell line.

270 on to PacBio data and Illumina data from the MCF-7 breast cancer cells.

271 ; telomeric and sub-telomeric regions in the MCF-10A cells display more frequent interactions than ar

272 ter-chromosomal interaction frequency in the MCF-10A epithelial cells.

273 33-regulatory region, but was present in the MCF-7 and primary ER+ tumor cells.

274 om estrogen receptor alpha activation in the MCF-7 breast cancer cell line.

275 -rich chromosomes chr16 through chr22 in the MCF-7 breast cancer genome display decreased interaction

276 equent interactions than are observed in the MCF-7 cells.

277 Use of the MCF device, along with a temperature-controlled setup, p

278 Pathway analysis of the MCF-7 up-regulated genes located in altered compartment

279 lar adhesion molecule (EpCAM) present on the MCF-7 cell membrane.

280 Reassuringly, the MCF pathways identified lead to metabolites known to be

281 Our results suggest that the MCF strain sensors here proposed are likely to reach the

282 We also used the MCF to demonstrate the basal-plane affinity of several I

283 Using the MCF, we show that the fluorescence signal of IBPs conjug

284 It subsequently interacted with the MCF-7 cell layer, distributed in the lung, heart and fat

285 Aggregating gene expression through MCF pathways leads to markedly better predictions of bre

286 molecules were also found to be non-toxic to MCF 12A cells.

287 eads to kidney iron deposition and toxicity, MCFs could protect kidney against a damage from iron exc

288 m nanoparticles were loaded onto traditional MCF-17, the catalyst showed very low activity toward iso

289 of multiple PKC isoforms in non-transformed MCF-10A human breast cells.

290 nd -3 activities were observed in 9f-treated MCF-7 and HL-60 cells.

291 intensive in normal NHDF cells than in tumor MCF cells.

292 8b, 11a, and 11b were tested on tumorigenic MCF-7 and A2058 cells expressing high levels of sigma2 a

293 To investigate this, we used MCF-7 cells, in which EGF-induced transient ERK activati

294 Using MCF 10A cell line cells as an example, we demonstrated h

295 Using MCF-10A mammary epithelial cells, we show that exposure

296 Using MCF-7 cells as in vitro model for anti-cancer mechanisti

297 readout of MCF-7 breast cancer cells versus MCF-10A mammary epithelial cells, when subjected to indi

298 predictive composite pathways identified via MCF are hence more likely to capture key metabolic alter

299 tracer uptake (P = 0.0058 when compared with MCF-7; P < 0.0001 when compared with ZR-75-1).

300 es are then characterized and incubated with MCF-7/ADR human breast cancer cells and followed by US e