ライフサイエンスコーパス: breast cancer cell line

1 rogen receptor alpha activation in the MCF-7 breast cancer cell line.

2 ted the findings with growth inhibition in a breast cancer cell line.

3 chorage-independent colony formation of MCF7 breast cancer cell line.

4 nt in the PTEN gene in the Basal-like SUM149 breast cancer cell line.

5 rom the NA12878 human genome and the HCC1954 breast cancer cell line.

6 ty during a time course of a hypoxia-exposed breast cancer cell line.

7 yrosine 537, in the estrogen-responsive MCF7 breast cancer cell line.

8 a subset of high MELK-expressing basal-like breast cancer cell lines.

9 signature for metastasis for a cohort of 10 breast cancer cell lines.

10 ation study with HER2-positive and -negative breast cancer cell lines.

11 utant p53 transcriptional target in multiple breast cancer cell lines.

12 nation of 1100 primary breast tumors and six breast cancer cell lines.

13 fic cytotoxicity against MDA-MB-231 and T47D breast cancer cell lines.

14 cancer activity against ErbB2-overexpressing breast cancer cell lines.

15 phorylation state of CDCP1 across a panel of breast cancer cell lines.

16 tive of sensitivity to PI3K inhibitors among breast cancer cell lines.

17 gulated at the mature miRNA level in luminal breast cancer cell lines.

18 ll cycle arrest, and cell death in sensitive breast cancer cell lines.

19 ysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell lines.

20 ER3 stimulated MLK3 kinase activity in HER2+ breast cancer cell lines.

21 ifically reduced the growth of 20q amplified breast cancer cell lines.

22 TOR results in feedback activation of AKT in breast cancer cell lines.

23 high levels in a subset of tumors and human breast cancer cell lines.

24 teomic profiling data sets measured in human breast cancer cell lines.

25 and/or the PI3K inhibitor BKM120 in 3 ER(+) breast cancer cell lines.

26 M 8) subchallenge: time course prediction in breast cancer cell lines.

27 ilitates ERalpha-stimulated proliferation in breast cancer cell lines.

28 this pattern was observed in 13 established breast cancer cell lines.

29 trant response was measured in a panel of 20 breast cancer cell lines.

30 e show that SOD2 itself is down-regulated in breast cancer cell lines.

31 signaling is activated in TICs isolated from breast cancer cell lines.

32 GPR161 impairs proliferation of human basal breast cancer cell lines.

33 which are enriched in MCSCs from established breast cancer cell lines.

34 lls induced to undergo EMT- and CSC-enriched breast cancer cell lines.

35 cells (HMECs) and estrogen receptor-positive breast cancer cell lines.

36 reatest inhibitory effects observed in ER+ve breast cancer cell lines.

37 R1 deficit in colorectal, ovarian, renal and breast cancer cell lines.

38 oach to globally profile CARM1 substrates in breast cancer cell lines.

39 with low expression of miR-9-3p in different breast cancer cell lines.

40 regulated in most primary breast tumours and breast cancer cell lines.

41 ts of PI3K blockade in trastuzumab-resistant breast cancer cell lines.

42 ect sequencing (ChIP-seq) for TFAP2C in four breast cancer cell lines.

43 with sensitivity to PI3K inhibitors in these breast cancer cell lines.

44 tent stem cells with conditioned medium from breast cancer cell lines.

45 ive (E198A) mutant version of MMP-8 in human breast cancer cell lines.

46 n and selectively kills cancer stem cells in breast cancer cell lines.

47 ported by gene set enrichment analyses in 51 breast cancer cell lines.

48 nd seven of these exhibited synergy in human breast cancer cell lines.

49 ncreased apoptosis in a panel of ER-positive breast cancer cell lines.

50 liparib and radiation on metabolism in three breast cancer cell lines.

51 icantly altered metformin sensitivity in two breast cancer cell lines.

52 hairpin RNA (shRNA) "dropout screens" on 77 breast cancer cell lines.

53 and multiple additional estrogen-independent breast cancer cell lines.

54 d greater growth-inhibitory activity against breast cancer cell lines.

55 predicted lncRNAs could be validated in both breast cancer cell lines.

56 enriched after PARP inhibition in all three breast cancer cell lines.

57 nhanced Dox treatment efficacy in a panel of breast cancer cell lines.

58 tic cancer tissues as well as pancreatic and breast cancer cell lines.

59 reported to modulate the binding of FOXA1 in breast cancer cell lines.

60 in inhibiting growth of tamoxifen-resistant breast cancer cell lines.

61 rowth and signaling activity in prostate and breast cancer cell lines.

62 antiviral interferon-stimulated response in breast cancer cell lines.

63 ng siRNA screening, followed by MTS assay in breast cancer cell lines.

64 uppresses BMP4-induced signaling in multiple breast cancer cell lines.

65 y the method to predict the drug response of breast cancer cell lines.

66 ancreatic neuroendocrine tumour (panNET) and breast cancer cell lines.

67 ith the FGF10 and MRPS30 promoter regions in breast cancer cell lines.

68 d invasion and induced apoptosis in multiple breast cancer cell lines.

69 A luciferase-transfected breast cancer cell line (2LMP-Luc) in combination with p

70 ical CTC phenotype more lysis-resistant than breast cancer cell lines, a capacity to report protein e

71 inoside (Er), and arbutin (Ab), on two human breast cancer cell lines: Adriamycin-resistant MCF-7/Adr

72 The cytotoxic effect of resveratrol on a breast cancer cell line also displays a progressive patt

73 ell line, an ovarian cancer cell line, and a breast cancer cell line also showed that Net-RSTQ estima

74 GABRP expression in breast cancer cell lines also demonstrates a significant

75 Here, we show that human and mouse breast cancer cell lines also express myoferlin at vario

76 ced expression of SERPINE2 and SLPI in human breast cancer cell lines also programmed them for vascul

77 ctively blocks NFkappaB activity in multiple breast cancer cell lines and abrogates NFkappaB-dependen

78 ngs are validated in therapy-resistant basal breast cancer cell lines and animal models, where inhibi

79 ell-derived EVs promoted brain metastasis of breast cancer cell lines and are preferentially incorpor

80 In human breast cancer cell lines and breast cancer samples, expr

81 We inhibited autophagy in a panel of breast cancer cell lines and found that some of them are

82 receptor-alpha (ERalpha) in ERalpha-positive breast cancer cell lines and high-level expression of PN

83 d expression of RUNX3 is frequently found in breast cancer cell lines and human breast cancer samples

84 Expression of Rap2B was examined in breast cancer cell lines and human normal breast cell li

85 n total RNA (RNAt) extracted from metastatic breast cancer cell lines and human tissues.

86 K inhibitor GDC-0941 from parental PTEN-null breast cancer cell lines and identified a novel PIK3CB D

87 we generated a panel of Wnt reporting human breast cancer cell lines and identified a previously unr

88 l on exome sequencing data generated from 16 breast cancer cell lines and identified both novel and k

89 ysis in i) normal colon cells, ii) colon and breast cancer cell lines and iii) cancer stem-like cell

90 evated in metastatic liver, lung, colon, and breast cancer cell lines and in high-grade tumors and th

91 3 signals constitutively in a panel of basal breast cancer cell lines and in more than one third of b

92 direct transcriptional target of HIF in many breast cancer cell lines and in solid tumors.

93 with metastatic potential in mouse and human breast cancer cell lines and is elevated in metastatic l

94 types, observed from both NTMT1 knockdown in breast cancer cell lines and knockout mouse models, sugg

95 We apply CCAST on single cell data from both breast cancer cell lines and normal human bone marrow.

96 dent MDA-MB-435 and estrogen dependent MCF-7 breast cancer cell lines and one non-cancerous breast li

97 Knockdown of ANO1 in ANO1-amplified breast cancer cell lines and other cancers bearing 11q13

98 in vivo activity against a variety of human breast cancer cell lines and patient derived xenografts,

99 vercome these resistance phenotypes, both in breast cancer cell lines and patient-derived xenograft m

100 at ANO1 is amplified and highly expressed in breast cancer cell lines and primary tumors.

101 a locus associated with cancer metastasis in breast cancer cell lines and serum-derived samples.

102 me analysis' (IMAHP) method to a panel of 41 breast cancer cell lines and show that deviations of the

103 Investigations in endocrine-resistant breast cancer cell lines and SRC-1(-/-)/PyMT mice confir

104 1 (ARF1) is overexpressed in highly invasive breast cancer cell lines and that epidermal growth facto

105 how that PLD expression is increased in four breast cancer cell lines and that hypoxia, cell overcrow

106 proteins were positively correlated in human breast cancer cell lines and tissue specimens of primary

107 ignaling promoted the proliferation of human breast cancer cell lines and tumor cells cultured from M

108 lator Id4 This signature drove clustering of breast cancer cell lines and tumors into the common subt

109 we find defective KDM3A expression in human breast cancer cell lines and tumors.

110 d between FoxQ1 and DACH1 gene expression in breast cancer cell lines and tumors.

111 vity against estrogen receptor (ER)-positive breast cancer cell lines and xenografts, alone and with

112 med with MCF7, an estrogen receptor positive breast cancer cell line, and MCF10A, a nontumorigenic im

113 E2 regulated in ILC cell lines versus other breast cancer cell lines, and a subset of these genes we

114 ssion of CSTF3 was common in triple-negative breast cancer cell lines, and elevated CSTF3 levels were

115 express higher A2BR than luminal and Her2(+) breast cancer cell lines, and high expression of A2BR is

116 enced in human primary breast tumor tissues, breast cancer cell lines, and in tumor tissues of three

117 tional repressor BCL6 is highly expressed in breast cancer cell lines, and its locus is amplified in

118 ar vesicles from metastatic murine and human breast cancer cell lines, and miR-200 levels were increa

119 GT promoters in AR-positive/ERalpha-negative breast cancer cell lines, androgen treatment did not inf

120 Using two breast cancer cell lines as a comparative model, we foun

121 Using three breast cancer cell lines as murine syngeneic immunocompe

122 ed accumulation of Rad17 in various types of breast cancer cell lines as well as human breast cancer

123 ys were assessed in a number of prostate and breast cancer cell lines as well as in normal prostate e

124 virions produced by some teratocarcinoma and breast cancer cell lines, as well as by peripheral blood

125 tion and induces apoptosis in the MDA-MB-231 breast cancer cell line at subnanomolar concentrations i

126 CTLs specific for p373-382 also killed human breast cancer cell lines at higher levels than did CTLs

127 Knocking down PI5P4Kalpha and beta in a breast cancer cell line bearing an amplification of the

128 onapristone treatment of multiple unmodified breast cancer cell lines blocked estradiol-mediated CTSD

129 r CIP2A reduces the tumorigenic potential of breast cancer cell lines both in vitro and in vivo.

130 ied specific and nonspecific uptake in three breast cancer cell lines: BT-474, SK-BR-3, and MDA-MB-23

131 a membrane of breast cancer tissue cells and breast cancer cell lines BT474 and SK-BR3.

132 etermined that EPO was induced by hypoxia in breast cancer cell lines, but not in human mammary epith

133 icated these findings by silencing Rictor in breast cancer cell lines, but not silencing the mTORC1 c

134 s shown on CD44 positive cells in the SUM159 breast cancer cell line by incubating the cells sequenti

135 rough the reprogramming of a triple-negative breast cancer cell line by the GATA3 transcription facto

136 rbon monoxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting CBS.

137 ng antioxidant enzyme expression in multiple breast cancer cell lines caused ATP reduction and compro

138 ore, altering hTERT levels in four different breast cancer cell lines caused minimal and discordant e

139 included genetically RRM1-modified lung and breast cancer cell lines, cell lines with gemcitabine-in

140 t BCL6 regulates a unique cohort of genes in breast cancer cell lines compared with B-cell lymphomas.

141 The SOX7 promoter is hypermethylated in breast cancer cell lines compared with nontumorigenic ce

142 is absent, or significantly reduced in 7/10 breast cancer cell lines compared with normal HMECs.

143 Elafin is downregulated in the majority of breast cancer cell lines compared with normal human mamm

144 e that RNF168 deficiency, including in human breast cancer cell lines, confers resistance to the anti

145 We find that in human breast cancer cell lines containing amplified 17q23, TRI

146 On the SUM159 breast cancer cell line data, CCAST indicates at least f

147 n of TieDIE to The Cancer Genome Atlas and a breast cancer cell line dataset identified key signaling

148 ctional expression of this receptor in human breast cancer cell lines decreases cyclic AMP production

149 multicellular RNA-Seq data for the MD-MB231 breast cancer cell-line delineated variant heterogeneity

150 NAs, miR-221 and miR-17, are tested in human breast cancer cell lines, demonstrating the 70 approxima

151 Using breast cancer cell lines derived from low and intermedia

152 We generated MCF7 breast cancer cell line-derived DPH gene knockout (ko) c

153 1 in total RNA extracted from human lung and breast cancer cell lines, discriminating between the can

154 nation therapy because they are essential in breast cancer cell lines, druggable, enriched in stem-li

155 l as differences in the mechanotype of human breast cancer cell lines (Ea = 2.1 +/- 0.1 and 0.80 +/-

156 ce cell death in two tumor cell lines, mouse breast cancer cell line EMT-6 and human melanoma cell li

157 ry subunit of HIF-1 (HIF-1alpha) in a murine breast cancer cell line, EMT6.

158 interfering RNA libraries were screened in a breast cancer cell line engineered to report Notch.

159 K-ras mutant breast cancer cell line enriched for CSCs was resistant

160 A1 is also consistently expressed in luminal breast cancer cell lines even in the absence of ER.

161 addition, some of RB-intact basal-like type breast cancer cell lines exhibited a similar phenotype f

162 By using a bi-inducible MDA-MB-231 breast cancer cell line expressing PRA and/or PRB, we an

163 To investigate this question, we developed breast cancer cell lines expressing an inducible, consti

164 ble source of DNA C-to-U editing activity in breast cancer cell-line extracts.

165 us to discriminate between normal and human breast cancer cell lines (fibrocystic and metastatic sta

166 We selected lung and breast cancer cell lines for the ability to infiltrate a

167 ict signaling protein activity in a panel of breast cancer cell lines for which gene expression and d

168 cer datasets and additional experiments with breast cancer cell lines further suggest the relevance o

169 Using paired-end RNA-Seq data from breast cancer cell lines, FusionQ detected both the prev

170 on real and simulated data from the CRL-2324 breast cancer cell line genotyped on the Illumina 370K a

171 red protein activities and drug responses in breast cancer cell lines grouped several drugs that are

172 The MB-231 triple-negative breast cancer cell line has been extensively characteriz

173 t and anchorage-dependent growth of multiple breast cancer cell lines having increased pStat3 or tota

174 In breast cancer cell lines having low Cav1 expression (des

175 ome and transcriptome sequencing data from a breast cancer cell line (HCC1395) and matched lymphoblas

176 MCF7 cells, an ERalpha positive breast cancer cell line homozygous for the wild-type all

177 As a model system, cells from the breast cancer cell line HS578T, SKBR3 and MCF7 were used

178 tracellular detection of ZnO nanoparticle in breast cancer cell line i.e. MCF-7.

179 itive control vinblastine, and against human breast cancer cell lines (IC50=9.6 mug/ml).

180 hibited selective activity against the MCF-7 breast cancer cell line in the micromolar range.

181 liferation of several esophageal, liver, and breast cancer cell lines in a dose-dependent manner.

182 ive, and metastatic capabilities of lung and breast cancer cell lines in vitro and reduced metastasis

183 Similarly, in human breast cancer cell lines in which ErbB2 is overexpressed

184 Kindlin-3 overexpression in a breast cancer cell line increased primary tumor growth a

185 In breast cancer cell lines, increased levels of centrosome

186 taNp63-CYGB axis is also present in lung and breast cancer cell lines, indicating that CYGB-mediated

187 ressing human mammary fibroblasts with human breast cancer cell lines into mouse mammary fat pads, we

188 Their efficacy on breast cancer cell lines is higher than that of free DOX

189 at expression of Enpp1 was elevated in human breast cancer cell lines known to produce bone metastasi

190 o than paclitaxel in the multidrug resistant breast cancer cell line LCC6-MDR.

191 in this isogenic setting or a panel of eight breast cancer cell lines leads to activation of the ster

192 RB inactivation in an RB-intact luminal-type breast cancer cell line MCF-7 promoted a positive feed f

193 e delineated in unique CCH derived cells and breast cancer cell line MCF-7 suggesting anti-proliferat

194 distinct ERalpha phosphorylation site in the breast cancer cell line MCF-7 using a phospho-T(594)-spe

195 n evaluating the paclitaxel effectiveness on breast cancer cell line MCF-7.

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

197 ntal results from the ERalpha-positive human breast cancer cell line (MCF-7) treated with 17-beta-est

198 s of serum-free conditioned media from three breast cancer cell lines (MCF-7, SK-BR-3, and MDA-MB-231

199 ug efflux by model multidrug resistant (MDR) breast cancer cell lines (MCF-7/ADR).

200 le as well as detection from real samples of breast cancer cell line, MCF-7.

201 tification of an SSEA-4-binding protein in a breast cancer cell line, MCF-7.

202 counterpart population from non-tumorigenic breast cancer cell line, MCF10A.

203 f 800 miRNAs in the estrogen-dependent human breast cancer cell line MCF7 and its estrogen-independen

204 of field based 3D-QSAR model based on human breast cancer cell line MCF7 in vitro anticancer activit

205 To do this, we used the breast cancer cell line MCF7, which expresses a function

206 senescence and apoptosis are induced in the breast cancer cell line MCF7.

207 cancer cell line MDA-MB-231 and the luminal breast cancer cell line MCF7: a) a 3D collagen embedded

208 This cytotoxicity has been observed in other breast cancer cell lines (MCF7 and HCC1937) and other fo

209 fold more potent at inhibiting the growth of breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D,

210 e initial cell line panel to now include the breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D,

211 ion (AGO2-IP) and microarray analyses in two breast cancer cell lines, MCF7 and MDA-MB-231, represent

212 Enpp1 expression was stably increased in the breast cancer cell line MDA-MB-231 and the ability to co

213 o models employing the triple-negative basal breast cancer cell line MDA-MB-231 and the luminal breas

214 We found that the human metastatic breast cancer cell line MDA-MB-231 secretes activity tha

215 28-39), which has femtomolar activity in the breast cancer cell line MDA-MB-231, has significant dose

216 tion for several cancer cell lines including breast cancer cell line MDA-MB-231, lung cancer cell lin

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

218 to inhibit the viability of the claudin-low breast cancer cell line MDA-MB-231.

219 ole in the migration and invasiveness of the breast cancer cell line MDA-MB-231.

220 etaAR subtype in the highly metastatic human breast cancer cell line MDA-MB-231HM.

221 lial cell line MCF10A, moderately metastatic breast cancer cell line MDA-MB-468 and 143B cells.

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

223 Four human breast cancer cell lines (MDA-MB-231, BT-20, Zr-75-1 and

224 ) exhibits cytotoxicity in a triple-negative breast cancer cell line, MDA-MB-436, while having less o

225 d macrophages induced apoptosis in the human breast cancer cell line, MDA-MB-468.

226 The highly invasive breast cancer cell lines, MDA-MB-231 and 4T1, express ve

227 ssing expression of ROR1 in metastasis-prone breast cancer cell lines, MDA-MB-231, HS-578T, or BT549,

228 of EPCAM expression in human pancreatic and breast cancer cell lines, mediated through direct bindin

229 In breast cancer cell line models, depletion of XBP1 inhibi

230 erexpressed in Endo-R derivatives of several breast cancer cell line models.

231 l genomic annotation using data derived from breast cancer cell-line models indicates that these SNPs

232 Using breast cancer cell lines, mouse xenograft models and mat

233 In MCF7 cells, a human breast cancer cell line, MSNBA competitively inhibited G

234 in vitro cytotoxicity against the MDA-MB-231 breast cancer cell line of most of these derivatives are

235 t 3-OST3A is epigenetically repressed in all breast cancer cell lines of a panel representative of di

236 R/Cas9 has no effect on the fitness of basal breast cancer cell lines or cell lines from six other ca

237 Overexpression of TRIM28 in breast cancer cell line promotes cell migration and inva

238 a-nuclear accumulation of the PRMT5/WDR77 in breast cancer cell lines relative to immortalized breast

239 etrix gene expression microarray data for 30 breast cancer cell lines representing different breast t

240 nomes (using ChIP-seq) of 11 different human breast cancer cell lines representing five major molecul

241 In contrast, breast cancer cell lines representing the basal subtype

242 ir potential effect on gene expression in 30 breast cancer cell lines representing three molecular ph

243 rtantly, depletion of RB in osteosarcoma and breast cancer cell lines results in sensitivity to DNA-d

244 Transgene overexpression of MACROD2 in breast cancer cell lines results in tamoxifen resistance

245 RNA and protein analysis of a panel of breast cancer cell lines revealed that BRCA1 deficiency

246 yte differentiation, whereas less aggressive breast cancer cell lines secrete less of this activity.

247 es ('methylomes') with Cav1 expression in 30 breast cancer cell lines showed that differential methyl

248 A validation study on 21 breast cancer cell lines showed that our prediction agre

249 In breast cancer cell lines, shRNA-mediated knockdown of GR

250 Loss of p120 in anchorage-dependent breast cancer cell lines strongly promoted anoikis resis

251 18)F-FASu demonstrated tumor uptake in all 3 breast cancer cell lines studied.

252 atidylinositol 3-kinase (PI3K) inhibitors in breast cancer cell lines, suggesting that clinical evalu

253 ded enhanced cell killing in triple-negative breast cancer cell lines, suggesting that combination th

254 e blocks microtubule nucleation in two human breast cancer cell lines, suggesting that this mechanism

255 Two heterogeneous breast cancer cell lines (SUM-149 and SUM-159) were succ

256 e mesenchymal characteristics of claudin-low breast cancer cell lines (SUM159 and MDA-MB-231).

257 when miR-290 upregulation in two independent breast cancer cell lines suppressed both primary tumor a

258 NQO1 knockdown in human colorectal and breast cancer cell lines suppresses HIF-1 signalling and

259 ns were detectable in the ERalpha-expressing breast cancer cell line T47D and corresponded to undetec

260 ability and cell toxicity to image two human breast cancer cell lines T47D and MDA-MB-231 are also ev

261 on 11 of 19 ovarian cancer (OC) and 8 of 14 breast cancer cell lines tested.

262 duced cytotoxic effects and apoptosis in all breast cancer cell lines tested.

263 Furthermore, we discovered two breast cancer cell lines that retain wild-type p53 but e

264 l as the SEAP reporter assay system in MCF-7 breast cancer cell-line; the anti-platelet activity was

265 We used a panel of normal and breast cancer cell lines to assess Wnt pathway gene and

266 a focused small interfering RNA screen in 14 breast cancer cell lines to define genes that were patho

267 defects by direct and indirect assays in 12 breast cancer cell lines to estimate the spontaneous occ

268 e investigated the sensitivity of a panel of breast cancer cell lines to treatment with various types

269 st-231 cells, a prototypical highly invasive breast cancer cell line, to degrade the extracellular ma

270 an extensive gene expression analysis in ER+ breast cancer cell lines, to reveal the targets of miR-5

271 r2 transgenic mouse tumor cell lines and two breast cancer cell lines transfected with HOXB7, whereas

272 rigenesis, we knocked out CARM1 from several breast cancer cell lines using Zinc-Finger Nuclease tech

273 orced expression of Cks1 in an MTX-resistant breast cancer cell line was found to restore drug sensit

274 Reduced expression of BAP1 in breast cancer cell lines was associated with mitotic abn

275 Tumor genomic DNA from 94 patients and 2 breast cancer cell lines was labeled and hybridized to t

276 igration and invasion in two triple-negative breast cancer cell lines was observed with compound 17.

277 A panel of breast cancer cell lines was treated with increasing con

278 Using a panel of breast cancer cell lines, we confirm that CSF1R expressi

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

280 Here, using human and mouse breast cancer cell lines, we found that oncogene forkhea

281 Using high-throughput validation assays in breast cancer cell lines, we show that our integrative a

282 Using siRNAs in breast cancer cell lines, we showed that the 17q21.3 amp

283 Peptide measurements in breast cancer cell lines were able to discriminate among

284 Lapatinib-resistant ERBB2-amplified breast cancer cell lines were screened, in the presence

285 oxicity assays, IFN-gamma ELISPOT, and human breast cancer cell lines were used to assess the proteol

286 croarray, and quantitative flow cytometry in breast cancer cell lines were used to validate observed

287 Pi and platinum resistance in the SUM1315MO2 breast cancer cell line, which harbors a hemizygous BRCA

288 f 485 single nuclei to 424 single cells in a breast cancer cell line, which shows a high concordance

289 lidated our findings in MCF-7 and MDA-MB-231 breast cancer cell lines, which harbor lower hsa-miR-125

290 ism (SNP) discrimination in cDNAs from human breast cancer cell lines, which makes such platforms exc

291 this preclinical study, we used eight human breast cancer cell lines, which represent the major mole

292 nous leukemia cell line as well as the MCF-7 breast cancer cell line with chromatin interactions.

293 Ex vivo treatment of different breast cancer cell lines with anti-CD73 AD2 mAb before i

294 Importantly, breast cancer cell lines with high activity of the modul

295 In breast cancer cell lines with loss of DIRAS3 imprinting,

296 In this study, we report that breast cancer cell lines with more stem-like properties

297 eatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion an

298 h GSK1016790A reduced viability of two basal breast cancer cell lines with pronounced endogenous over

299 Treatment of breast cancer cell lines with the putative antimetastasi

300 /kg/day for 14 days and caused regression of breast cancer cell line xenografts in nude mice.