ライフサイエンスコーパス: MCF

1 MCF-0.8 exhibits a half-wave potential ( E(1/2)) of 0.89

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

3 1895 protein groups were identified from 100 MCF-7 cells (~10 ng protein content).

4 e peptides and 3069 protein groups from 1000 MCF-7 cells (~100 ng protein content), and 13 367 peptid

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

6 on four human cell lines (GM12878, MCF-10A, MCF-7 and MDA-MB-231).

7 not react with K15 deficient NEB-1, KEB-11, MCF-7 and SW13 cells expressing only exogenous K8 and K1

8 The 19 MCF laser cores operated in CW mode at 1030 nm.

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

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

11 fferent tumor cell lines (HepG2, MDA-MB-231, MCF-7 and Caco2).

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

13 imal composition Mn(0.8)(CoFe(2))(0.73)O(4) (MCF-0.8), that are effective electrocatalysts for the ox

14 nducted our research on human normal (MRC-5, MCF-10A) and tumor (A549, MCF-7) cell lines using a micr

15 (BM-MSC), and Michigan Cancer Foundation-7 (MCF-7) breast cancer cells, as well as the effect of the

16 vivo biologic specificity was assessed in a MCF-7 cell line and in mice bearing MCF-7 breast tumors.

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

18 This behavior was verified using a MCF laser model developed in-house.

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

20 ccumulated selectively in tumor cells (A549, MCF-7) and this fact contributed to the reduction of tum

21 man normal (MRC-5, MCF-10A) and tumor (A549, MCF-7) cell lines using a microfluidic system.

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

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

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

25 y showed highest inhibitory activity against MCF-7.

26 ation and antiproliferative activity against MCF-7/Dox cells.

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

28 in selective anticancer cytotoxicity against MCF-7 breast cancer cells in vitro.

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

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

31 ntiproliferative activity against Caco-2 and MCF-7 cancer cell lines (tumour cell lines of intestinal

32 three-fold and two-folds against Caco-2 and MCF-7 cell lines, respectively.

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

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

35 created isogenic cell panels (MDA-MB-231 and MCF-7) expressing five ADAM15 variants including wild-ty

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

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

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

39 forming sequences, we screened the MCF-7 and MCF-10A methylomes to map 5-methylcytosine and found the

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

41 A10 and MCF represent suitable prognostic parameters in predicti

42 CLF group with significantly reduced A10 and MCF.

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

44 es secreted by MCF-7 breast cancer cells and MCF-10A normal breast cells.

45 FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulv

46 BxPC-3 cells and MCF-7 cells were engineered to overexpress a catalytical

47 MDA-MB-468, 4T1 (triple-negative cells), and MCF-7 (estrogen receptor (ER)/progesterone receptor (PR)

48 cell lines: A549 (lung), HCT116 (colon) and MCF-7 (breast), were treated with various concentrations

49 on, we then paraxially propagate the CSD and MCF to any plane [Formula: see text].

50 st to interrogate U-indel editing in EMF and MCF life cycle stages.

51 ) fluorescence intensity ratios for HeLa and MCF-7 cancer cells in comparison to HEK-293 healthy cell

52 oderate cytotoxic activity against HepG2 and MCF-7 cell lines.

53 1R activity in mitochondrial protection, and MCF-7 cells with suppressed IGF-1R activity became highl

54 uated in the drug-resistant MCF-7-Epi(R) and MCF-7-Tax(R) compared to the parental MCF-7 breast cance

55 nt mutations in small populations of RKO and MCF-7 FFPE cell blocks.

56 thoxy substituents, through in vitro assays: MCF-7 cell proliferation and VM7Luc4E2 transactivation.

57 sed in a MCF-7 cell line and in mice bearing MCF-7 breast tumors.

58 studies were conducted in nude mice bearing MCF-7-Y1 tumours.

59 ar patterns and opposite clinical behaviors: MCF-7 that belong to the luminal A subtype connected to

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

61 ticles emitted from (223)Ra in bone for both MCF-7 and MDA-MB-231 cells.

62 nt in its ability to degrade ERalpha in both MCF-7 and CAMA-1 cell lines.

63 29b-1 and miR-29a target transcripts in both MCF-7 and LCC9 cells.

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

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

66 ty to differentiate the exosomes secreted by MCF-7 breast cancer cells and MCF-10A normal breast cell

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

68 aTC cell lines showed the highest uptake by MCF-7 cells and negligible uptake by the healthy cells (

69 strogen receptor (ER)-positive breast cancer MCF-7 cells showed that inhibitor treatment recapitulate

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

71 n of endogenous metabolites in breast cancer MCF-7 spheroids.

72 tro regarding binding to human breast cancer MCF-7-Y1 cells and slices of tumour xenografts.

73 Using a human breast cancer (MCF-7 xenograft) model in nude mice, EO-33 blocked 90% o

74 more, a synergistic effect on breast cancer (MCF-7) and melanoma (SK-MEL-5) was proven.

75 om 1.5 x 10(2) to 7.5 x 10(6) breast cancer (MCF-7) cells and the limit of detection was calculated a

76 of adherent colon (HT-29) and breast cancer (MCF-7) cells from the interphase through mitosis and the

77 ial interferents, such as the breast cancer (MCF-7), human embryonic kidney (HEK293), and leukemia (H

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

79 breast epithelial, MCF-10A or breast cancer, MCF-7 cells that do not harbor constitutively active STA

80 s used to specifically recognize and capture MCF-7 cells.

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

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

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

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

85 nd C15 linked) for their effects on BC cell (MCF-7, tamoxifen-resistant MCF-7, mouse mammary carcinom

86 nd MDA-MB-231 and of breast epithelial cells MCF-10A with BAPOs and UV irradiation induces apoptosis.

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

88 468, BT20, MDA-MB-231); normal breast cells (MCF-10A); and cell lines derived from colon (HT29), ovar

89 ed by water dynamics in breast cancer cells (MCF-7) after treatment with a chemotherapy drug.

90 15 and sheep red blood cells), cancer cells (MCF-7, MDA-435 and CD34(+)), yeast cells (saccharomyces

91 strain) in normal mammary epithelial cells (MCF-10A cells) was sufficient to cause rupture of the nu

92 Importantly, normal breast epithelial cells (MCF-10A) that do not express miR-515 are not affected by

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

94 ble cytotoxicity against noncancerous cells (MCF-10A and peripheral blood mononuclear cells).

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

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

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

98 thy and tumorigenic breast epithelial cells, MCF-10A cells and BT474 cells, respectively.

99 In contrast, MCF-7 cells had 7- and 65-day growth delays in the 50 an

100 n experiment, using a cladding-pumped 7-core MCF amplifier as an integrated parallel amplifier array

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

102 probes between wild-type and lamin-depleted MCF-10A cells revealed that lamin A/C, but not lamin B2,

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

104 CS to sort three different cell lines (i.e., MCF-7, MDA-231, and human-induced pluripotent stem-cell-

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

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

107 mal nuclear shape in human breast epithelial MCF-10A cells.

108 mplex disruption in human mammary epithelial MCF-10A cells and canine kidney epithelial MDCK II cells

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

110 weaker effects on normal breast epithelial, MCF-10A or breast cancer, MCF-7 cells that do not harbor

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

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

113 rationally designed Mn-doped cobalt ferrite (MCF) spinel nanocrystals, with an optimal composition Mn

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

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

116 strongly coupled asymmetric multicore fiber (MCF) fusion spliced at 180 degrees with respect to each

117 network of injection-locked multicore fiber (MCF) lasers.

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

119 ussian beams emitted from a multicore fibre (MCF) amplifier.

120 tion microendoscopy using a multicore fibre (MCF) with an adiabatic multimode-to-single-mode "photoni

121 ctic acid (PLA) and micro cellulose fibrils (MCF).

122 ents, in that none in the cohort arm (FibTEM-MCF, >=7 mm) demonstrated clinically significant early p

123 The corresponding FibTEM-MCF values were as follows: pre-dose, 5.3 mm (1.9); post

124 d intraoperative measured and desired FibTEM-MCF.

125 mboelastometry maximum clot firmness (FibTEM-MCF; fibrinogen contribution to clot firmness).

126 If FibTEM-MCF >=7 mm, patients entered the monitoring cohort.

127 If FibTEM-MCF <=6 mm, patients were randomized to receive FC/place

128 5 minutes post-FC administration were FibTEM-MCF (desired range, 8-13 mm) and fibrinogen levels (desi

129 Maximum clot firmness (MCF) was significantly divergent between both patient gr

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

131 45-fold for MDA-MB-231 cells and 7-fold for MCF-7 cells, relative to untargeted PCCAs.

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

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

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

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

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

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

138 in ER+/PR+ breast cancer cells derived from MCF-7 using different extraction solvents including: A,

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

140 ensity (CSD) and mutual coherence functions (MCFs) for twisted space-frequency and space-time Gaussia

141 nanoNOMe) on four human cell lines (GM12878, MCF-10A, MCF-7 and MDA-MB-231).

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

143 In vitro assays on HeLa, MCF-7, and HCT-116 cells confirmed higher photoactivity

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

145 tively active MNK1 (caMNK1)-expressing human MCF-10A-derived DCIS cell lines, which were orthotopical

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

147 alyzed the transcriptional response of human MCF-7 cells to retinoic acid and TGF-beta, applied indiv

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

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

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

151 In MCF-7 cells, ADAM15E was the principal variant inducing

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

153 electivity of C(3)-ZIF(MCF) to accumulate in MCF-7 tumor cells.

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

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

156 inhibited the metastasis of breast cancer in MCF-7 and 4T1-bearing mice by altering the expression of

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

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

159 quencing was performed on pS118-ER and ER in MCF-7 cells treated with estrogen.

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

161 S1P pathway and is normally not expressed in MCF-7 cells.

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

163 the binding of key transcription factors in MCF-7 cells.

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

165 was transiently overexpressed (~5.4-fold) in MCF-7 cells for whole genome miRNA profiling (miRNA-seq)

166 ROS formation in MCF-7 cells and three-dimensional (3D) spheroids was pro

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

168 on of cell proliferation than fulvestrant in MCF-7 cells.

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

170 owed energy production pathways to be key in MCF-7 cell lines.

171 fectively reduced the PRMT5 protein level in MCF-7 cells.

172 n degradation) values of 0.17 and 0.43 nM in MCF-7 and T47D ER+ breast cancer cell lines, respectivel

173 The cytotoxic effect of pcm in MCF-7 cells was potentiated under H(2)O(2)-induced oxida

174 27 was more potent in MCF-7:CFR cells than six BET inhibitors in clinical tria

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

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

177 ficantly elevate FGF20 protein production in MCF-7 cells, between two- and four-fold.

178 tatively similar changes in miRNA profile in MCF-7 breast cancer cells, a subset of changes are disti

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

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

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

182 ocytes, and modulated DNA damage response in MCF-7 cells.

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

184 Using an ORF kinome screen in MCF-7 cells treated with the CDK4/6 inhibitor ribociclib

185 nd ChIP followed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the proteasome in

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

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

188 We show that in MCF-7 mammary gland cells, AGO1 associates with transcri

189 adiol, and TNFalpha combination treatment in MCF-7.

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

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

192 a multi-core Yb-doped phosphate fiber laser (MCF).

193 ing MYB in the ER(+) breast cancer cell line MCF-7 led to increased DNA damage accumulation, as marke

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

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

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

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

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

199 ce viability of the breast cancer cell lines MCF-7 and BT-474, further underlining the biological rel

200 at treatment of the breast cancer cell lines MCF-7 and MDA-MB-231 and of breast epithelial cells MCF-

201 r activity against breast cancer cell lines (MCF-7 and MDA-MB-231) was assessed by 3-(4,5-Dimethylthi

202 e kinds of EpCAM positive cancer cell lines (MCF-7 breast cancer, SW480 colon cancer, and PC3 prostat

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

204 clitaxel resistant breast cancer cell lines, MCF-7 and 4T1 by continuous exposure to paclitaxel for s

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

206 ective T cells, we challenged peptide-loaded MCF-7 breast cancer cells with antigen-specific CD8(+) T

207 ergy efficiency of the foams was best at low MCF fractions.

208 orce of cancer cells representing malignant (MCF-7 cells and MDA-MB-231 cells) and nonmalignant (MCF-

209 eckpoints in epimastigote (EMF), metacyclic (MCF), and BSF.

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

211 ern by individually exciting the single-mode MCF cores, and that these patterns are highly stable to

212 Moreover, MCF-0.8 exhibits remarkable durability (Delta E(1/2) = 0

213 distribution of ER-positive, HER(2)-negative MCF-7 breast cancer models showed a specific uptake of a

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

215 ells and MDA-MB-231 cells) and nonmalignant (MCF-10A cells) states.

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

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

218 ited proliferation and promoted apoptosis of MCF-7 cells dose- and time-dependently.

219 lular lactate production and the capacity of MCF-7 cells for anchorage independent growth in soft aga

220 ned tumor-stromal assay (muTSA) comprised of MCF-7 breast cancer cells and bone marrow stromal cells

221 9f caused arrest of cell cycle of MCF-7 and HL-60 cells at G0/G1 phase.

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

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

224 significantly suppressed the development of MCF-7 tumor cells (P < 0.01) as compared with an untreat

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

226 ng of fennel nsLTP1 suppressed the growth of MCF-7 human breast cancer cells in a dose-dependent mann

227 90% has been achieved, and the isolation of MCF-7 tumor cells from spiked human blood samples has al

228 Super-resolution microscopy of MCF-7 cells treated with the targeted MOF system reveals

229 tify ~20,000 phosphopeptides from 100 mug of MCF-7 cell lysate.

230 distribution was shown for the EI output of MCF-7 cells.

231 First structurally, the presence of MCF led to an initial increase followed by a decrease of

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

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

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

235 Such segments of MCF are sandwiched between standard single mode fibers.

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

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

238 Here, we found that IGF-1 treatment of MCF-7 cells induced rapid ERalpha methylation by the arg

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

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

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

242 24 hours after administration, MDA-MB-231 or MCF-7 human breast cancer cells expressing luciferase we

243 ounced, impacts on either ERalpha binding or MCF-7 cell proliferation.

244 Our MCF interferometers were used for sensing strain.

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

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

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

248 R) and MCF-7-Tax(R) compared to the parental MCF-7 breast cancer cells.

249 tions of PERK inhibitor compared to parental MCF-7 cells.

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

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

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

253 1 T), but not in oestrogen receptor-positive MCF-7 tumours.

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

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

256 ansient overexpression of HNRNPA2/B1 reduced MCF-7 sensitivity to 4-hydroxytamoxifen and fulvestrant,

257 pression is attenuated in the drug-resistant MCF-7-Epi(R) and MCF-7-Tax(R) compared to the parental M

258 or their actions against tamoxifen-resistant MCF-7 cells and a patient-derived xenograft triple-negat

259 C4 and C5 inhibited tamoxifen-resistant MCF-7 cells with equal potency (IC(50) = 4-8 muM) and ef

260 fects on BC cell (MCF-7, tamoxifen-resistant MCF-7, mouse mammary carcinoma, MDA-MB-231, and BT-549)

261 growth inhibition in fulvestrant-resistant (MCF-7:CFR) cells was confirmed in endocrine-resistant, p

262 as compared to parental, tamoxifen-sensitive MCF-7 cells.

263 herefore hypothesized that 2 could sensitize MCF-7 cells to anti-HER2 therapies.

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

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

266 d Scanning Electron Microscopy revealed that MCF decreased the glass transition of PLA allowing for a

267 The results showed that MCF had a concentration dependent impact on the foams.

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

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

270 33-regulatory region, but was present in the MCF-7 and primary ER+ tumor cells.

271 ction inside breast cancer live cells of the MCF-7 lineage as an efficient catalyst for cross-couplin

272 Cellular uptake experiments performed on the MCF-7 breast cancer cell line (ER-positive and HER(2)-ne

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

274 d i-motif forming sequences, we screened the MCF-7 and MCF-10A methylomes to map 5-methylcytosine and

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

276 l neoprotein synthesis upon addition of 2 to MCF-7 breast cancer cells demonstrated 2's selectivity a

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

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

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

280 lasin B treated and N-Ethylmaleimide treated MCF-7 breast cancer cells demonstrate the ability of our

281 the superior performance of the trimetallic MCF-0.8 originates from the synergistic catalytic effect

282 8b, 11a, and 11b were tested on tumorigenic MCF-7 and A2058 cells expressing high levels of sigma2 a

283 th human breast carcinoma cells of the types MCF-7 and 4T1-Luc.

284 This unique MCF laser can be useful for applications of coherent, co

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

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

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

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

289 -fold repression in the EGFP expression when MCF-7 were transfected with C(3)-ZIF(HELA).

290 ion in the EGFP expression was observed when MCF-7 were transfected with C(3)-ZIF(MCF) compared to 1-

291 g for a decrease in cell wall thickness when MCF was added.

292 brils and undergo cellular senescence, while MCF-7 do not exhibit these behaviors.

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

294 d metabolites inside LECs in co-culture with MCF-7, MDA-MB-231, and SK-BR-3 breast cancer cell lines

295 hanical performance initially increased with MCF and then decreased.

296 Incubation of C(3)-ZIF(MCF) with MCF-7, HeLa, HDFn, and aTC cell lines showed the highest

297 e interaction of Mt-HSA NCs/PGE surface with MCF-7 cells.

298 5% was obtained for the PLA foam with 3 wt.% MCF when expressed as a fractional percentage of the pur

299 ed when MCF-7 were transfected with C(3)-ZIF(MCF) compared to 1-fold repression in the EGFP expressio

300 esting confirmed the selectivity of C(3)-ZIF(MCF) to accumulate in MCF-7 tumor cells.

301 Incubation of C(3)-ZIF(MCF) with MCF-7, HeLa, HDFn, and aTC cell lines showed t