ライフサイエンスコーパス: breast cancer cell

1 he proliferation, migration, and invasion of breast cancer cells.

2 ing TNBC cells but not LIPG-negative luminal breast cancer cells.

3 ptotic effects on the antiestrogen-resistant breast cancer cells.

4 terized hypoxia-induced lncRNA RAB11B-AS1 in breast cancer cells.

5 ls of cell cycle regulators were examined in breast cancer cells.

6 its micronucleus formation and DNA damage in breast cancer cells.

7 RK3 reduces metastatic potential of invasive breast cancer cells.

8 pleting the subunit in breast epithelial and breast cancer cells.

9 tical role in ER stress-induced autophagy in breast cancer cells.

10 om the surface of APCs to be internalized by breast cancer cells.

11 nificantly inhibited the growth of malignant breast cancer cells.

12 hibitors of ciliogenesis in normal and basal breast cancer cells.

13 ppresses the migration and invasion of human breast cancer cells.

14 ized at the lamellipodia edges of aggressive breast cancer cells.

15 esis and multidrug resistance in prostate or breast cancer cells.

16 t this was not observed in receptor-positive breast cancer cells.

17 ecipitation-mass spectrometry for CK5 in ER+ breast cancer cells.

18 , as a critical ERBB4-interacting protein in breast cancer cells.

19 effects of altered lipid metabolism in T47D breast cancer cells.

20 y reverse the detrimental properties of CK5+ breast cancer cells.

21 icts cell growth and migration in normal and breast cancer cells.

22 immunosuppression by altering metabolism in breast cancer cells.

23 odia formation downstream of TKS4 or TKS5 in breast cancer cells.

24 the expression of matriglycan on alpha-DG in breast cancer cells.

25 ciated invasive phenotype in triple-negative breast cancer cells.

26 newal/stemness in KRAS-driven pancreatic and breast cancer cells.

27 dC-induced HEXIM1 expression in prostate and breast cancer cells.

28 sitive (TamS) and tamoxifen-resistant (TamR) breast cancer cells.

29 ectivity and cytotoxicity of triple-negative breast cancer cells.

30 onsive genes and increases the malignancy of breast cancer cells.

31 mily-TIMP2 axis in regulation of motility in breast cancer cells.

32 factor 2 alpha (eIF2alpha), in vitro and in breast cancer cells.

33 tributes to chromosome segregation errors in breast cancer cells.

34 e Kinase 4 (MLK4) to aggressive phenotype of breast cancer cells.

35 and mTOR pathways and rewired metabolism in breast cancer cells.

36 the progesterone receptor (PR) and STAT1 in breast cancer cells.

37 rin regulated the secretion of exosomes from breast cancer cells.

38 movement toward the leading edge in invasive breast cancer cells.

39 a more open chromatin state under hypoxia in breast cancer cells.

40 and further immunoregulatory checkpoints in breast cancer cells.

41 ometrial cancer cells that are distinct from breast cancer cells.

42 r estrogen-stimulated proliferation of ER(+) breast cancer cells.

43 nd the consequences for genomic stability in breast cancer cells.

44 ved from parental MDA-MB-231 triple-negative breast cancer cells.

45 N dephosphorylates and downregulates Abi1 in breast cancer cells.

46 rease in the number of mouse circulating 4T1 breast cancer cells.

47 ution with leukemic cells moving faster than breast cancer cells.

48 man GPVI, had platelet adhesion to colon and breast cancer cells.

49 ntal and spontaneous metastasis of colon and breast cancer cells.

50 and disseminating phenotypes in early lesion breast cancer cells.

51 agy, thereby promoting therapy resistance in breast cancer cells.

52 s cellular functions in both pluripotent and breast cancer cells (3) overexpression of GRP78 in breas

53 natant from the MDA-MB-134-VI FGFR-amplified breast cancer cells-activated FGFR siganalling in osteob

54 we show that elevated Aurora B expression in breast cancer cells activates AKT/GSK3beta to stabilize

55 Though breast cancer cells also express CCR2, its functions in

56 er cell-cell contact was established between breast cancer cells and antigen presenting cells (APCs),

57 ll-characterized cellular reference samples (breast cancer cells and B cells), captured either separa

58 ized a 3D co-culture model incorporating ER+ breast cancer cells and bone marrow mesenchymal stem cel

59 mplement logic gating to specifically detect breast cancer cells and execute therapeutic immunomodula

60 Therefore, we ablated K19 expression in MCF7 breast cancer cells and found that K19 was required for

61 w strategy to achieve eradication of primary breast cancer cells and inhibition of pulmonary metastas

62 FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR

63 e kinase inhibitors of BT-20 triple-negative breast cancer cells and of treatment with erlotinib of P

64 ilization of stemness and drug resistance of breast cancer cells and position mTOR inhibition as a tr

65 al a mechanism of induction of plasticity of breast cancer cells and provide a molecular basis for th

66 ontractile actin stress fibers in normal and breast cancer cells and strongly impairing breast cancer

67 latelets promote the metastasis of colon and breast cancer cells and suggests that GPVI represents a

68 the mesenchymal phenotype of triple-negative breast cancer cells and that CBFbeta-depleted cells unde

69 frequently change in ER+ endocrine-resistant breast cancer cells and that the differential interactio

70 pe cells adopt MAPK-dependent circuitries in breast cancer cells and that the kinase TTK is important

71 lay of HIFs, angiogenesis, and metabolism in breast cancer cells and the tumor microenvironment.

72 oratories, we characterised a range of human breast cancer cells and their protein-level responses to

73 at upon binding to CD80, forces generated by breast cancer cells and transmitted via CTLA-4 were suff

74 rugs and overexpressed LHRH receptors on the breast cancer cells and tumors.

75 ional coupling between collectively invading breast cancer cells and, via hemichannels, adenosine nuc

76 ression correlate with enhanced migration of breast cancer cells, and knockdown of HSATII RNA reduces

77 hat HER2 physically interacts with CB(2)R in breast cancer cells, and that the expression of these he

78 itiating cell (TIC) population (4) sGRP78(+) breast cancer cells are enriched for stemness genes and

79 is achieved and different subtypes of human breast cancer cells are successfully discriminated.

80 of metastasis, we establish that keratin-14+ breast cancer cells are vulnerable to NK cells.

81 C), and Michigan Cancer Foundation-7 (MCF-7) breast cancer cells, as well as the effect of the drugs

82 enting cells (APCs), CTLA-4 expressed on the breast cancer cells bind to CD80 expressed on the APCs,

83 , as well as head and neck metastasis of 4T1 breast cancer cells, both in early and late stages of ca

84 ast array of long noncoding RNAs (lncRNA) in breast cancer cells, but their biological functions rema

85 ctors including VEGFA and ANGPTL4 in hypoxic breast cancer cells by increasing recruitment of RNA pol

86 herapeutic outcome and long-term survival of breast cancer cells by influencing autophagy.

87 opy the PYCR1 knockdown in MCF10A H-RAS(V12) breast cancer cells by inhibiting de novo proline biosyn

88 ions as a metastasis-suppressing microRNA in breast cancer cells by limiting colony-stimulating facto

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

90 NF750) opposes the migration and invasion of breast cancer cells by repressing a prometastatic transc

91 Sfrp2 is induced in breast cancer cells by signals from lung epithelial cell

92 e notion that MCs influence the phenotype of breast cancer cells by stimulating a luminal phenotype a

93 Chronic stimulation of CD95 on breast cancer cells can increase their cancer initiating

94 transition of well-differentiated epithelial breast cancer cells characterized by estrogen and proges

95 Complementary studies using human breast cancer cell culture models revealed that siRNA-me

96 migration assays were performed for invasive breast cancer cells cultured in mechanically plastic, na

97 e of MeJA-treated Arabidopsis leaves, on the breast cancer cell cycle, is associated with Cell Divisi

98 Wnt signaling and transcriptional control in breast cancer cell dedifferentiation, EMT, and metastasi

99 haracterize effects of unacylated ghrelin on breast cancer cells, define its mechanism of action, and

100 rotein synthesis upon addition of 2 to MCF-7 breast cancer cells demonstrated 2's selectivity and upr

101 determination of signatures found in ER+/PR+ breast cancer cells derived from MCF-7 using different e

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

103 , structure and unique surface properties of breast cancer cell-derived small EVs (sEV) obtained usin

104 Ablation of PINCH-1 from breast cancer cells diminished myoferlin level and suppr

105 advance to the molecular mechanisms by which breast cancer cells disseminate from the primary tumor s

106 Breast cancer cells 'educate' lymphatic endothelial cell

107 pletion of alpha-parvin from triple-negative breast cancer cells effectively inhibits breast cancer c

108 In breast cancer cells, ER genomic binding is enabled by FO

109 LECs co-cultured with breast cancer cells exhibited cell-line dependent altere

110 Injected human leukemic and breast cancer cells exhibited cell-type specific pattern

111 ficient delivery of AQP5-targeting miRNAs to breast cancer cells, exosomes expressing both miRNAs and

112 Here, we found that melanoma and lung and breast cancer cells experiencing stress from oncogene in

113 Collectively invading breast cancer cells express the gap junction protein con

114 er administration, MDA-MB-231 or MCF-7 human breast cancer cells expressing luciferase were injected

115 Methods: ER+, PR+ T47D breast cancer cells expressing wild-type (WT) ER or an a

116 as used to enrich CoCl(2) treated MDA-MB 231 breast cancer cells from an untreated population.

117 reased nucleotides metabolism which protects breast cancer cells from chemotherapeutic-induced DNA da

118 controlling both stability and integrity of breast cancer cell genomes.

119 MDA-MB231 and SKBR3 breast cancer cells grown in 3D downregulated the prolif

120 ive breast cancer cells effectively inhibits breast cancer cell growth, migration, and invasion in vi

121 In MDA-MB-231-derived human triple-negative breast cancer cells implanted as orthotopic xenografts,

122 nsLTP1 suppressed the growth of MCF-7 human breast cancer cells in a dose-dependent manner with an I

123 compounds reduced extravasation of invasive breast cancer cells in a zebrafish model.

124 h in 3D co-cultures and a mouse model of ER+ breast cancer cells in bone marrow.

125 d examined their functional interaction with breast cancer cells in culture and in mice.

126 nd that GLI1 is activated in triple-negative breast cancer cells in response to ionizing radiation (I

127 Here we reveal how the behaviour of indolent breast cancer cells in the lung is determined by their i

128 study the cellular environment of metastatic breast cancer cells in the lung.

129 AZP-531 also suppresses the growth of breast cancer cells in vitro and in xenografts, and may

130 of IFNbeta and IFN-stimulated genes (ISG) in breast cancer cells in vitro and tumors in vivo.

131 When cocultured with breast cancer cells in vitro, MCs hindered activation of

132 nteractions, uptake and cytotoxic effects in breast cancer cells in vitro.

133 knocked down JAG1 in hybrid E/M SUM149 human breast cancer cells in vitro.

134 inhibit migration and invasion of 4T1 murine breast cancer cells in vitro.

135 ective anticancer cytotoxicity against MCF-7 breast cancer cells in vitro.

136 tasis formation by invasive murine and human breast cancer cells in vivo.

137 the metastatic cascade of both melanoma and breast cancer cells in vivo.

138 ng high GLS levels, we verified that several breast cancer cells (including TN cells) express endogen

139 Overexpression of WT NCS1 in MDA-MB231 breast cancer cells increased Ca(2+) signaling and survi

140 Inducing expression of CEP135(full) in breast cancer cells increases the frequency of CA, multi

141 diated down-regulation of VAV3 expression in breast cancer cells indicated that active VAV3 is involv

142 the disseminating phenotypes in early lesion breast cancer cells; inhibition of Tpl2 enhances early d

143 Neurofibromin-deficient ER(+) breast cancer cells initially retain sensitivity to sele

144 Pi-mediated growth control in BRCA1/2-intact breast cancer cells involving rDNA transcription and rib

145 t the plasticity of at least some metastatic breast cancer cells is dependent on the transcriptional

146 Here we show that collective invasion of breast cancer cells is regulated by the energetic status

147 rs distinct features to ER-negative DCIS.com breast cancer cells, leading to populations enriched wit

148 cancer cells (3) overexpression of GRP78 in breast cancer cells leads to an induction of a CD24(-)/C

149 he molecular level, knockdown of TMPRSS13 in breast cancer cells led to increased protein levels of t

150 re established from a triple-negative murine breast cancer cell line (4T1), electric currents and pot

151 odel by monitoring tumor growth from a mouse breast cancer cell line (AT-3, Gpr81-negative) implanted

152 ar uptake experiments performed on the MCF-7 breast cancer cell line (ER-positive and HER(2)-negative

153 and a high ABCB1 expressing triple-negative breast cancer cell line (MDA-MB-231-luc) were treated wi

154 ivity by growth inhibition in the MDA-MB-231 breast cancer cell line and low IC(50) (225.18 +/- 0.61

155 rformed whole-genome sequencing of the SKBR3 breast cancer cell line and patient-derived tumor and no

156 stem states, respectively, in the basal-like breast cancer cell line MCF10CA1a.

157 the glycan type profile of proteins from the breast cancer cell line MCF7, and we quantitatively reve

158 Conversely, in a breast cancer cell line MDA-MB-231 NMDAR blockade result

159 Here, we demonstrate that in the metastatic breast cancer cell line MDA-MB-231, retromer regulates t

160 ntly immunized mice against challenge with a breast cancer cell line that expresses the same immunodo

161 o small EV sub-populations from a metastatic breast cancer cell line, with biochemical features consi

162 and proinflammatory cytokines in the SUM159 breast cancer cell line.

163 rval) was 15.6 days versus 210 days, for the breast cancer cell line.

164 c, phospho-proteomic and fluxomics data in a breast cancer cell-line (MCF7) across three different gr

165 ell as Young's modulus using AFM, across two breast cancer cell-line populations dosed with three dif

166 uantification of exosomes derived from three breast cancer cell lines (MCF7, MDA-MB-231 and SKBR3).

167 line PC-3 (PC3) along with STAT3-proficient breast cancer cell lines (MDA-MB-231, SUM149) revealed t

168 In human breast cancer cell lines and 4T1 mouse mammary tumor cel

169 nase-targeted therapy in a subset of HER2(+) breast cancer cell lines and allow cancer cells to proli

170 ate ImageAEOT on chromatin images of various breast cancer cell lines and human tissue samples, there

171 binding with its promoter region in luminal breast cancer cell lines and indirectly through a distal

172 and gene expression in large collections of breast cancer cell lines and patient tumors to identify

173 Compound 1 was cytotoxic for both breast cancer cell lines and the majority of cells died

174 nd apoptosis, was induced in seven of the 31 breast cancer cell lines by hypoxia.

175 mass spectrometry (UPLC-MS/MS) on MDA-MB-231 breast cancer cell lines constructed with siRNA and CRIS

176 Cadaverine treatment of breast cancer cell lines corresponding to its serum refe

177 HER2 inhibitor-sensitive (HER2iS) and HER2iR breast cancer cell lines exhibit high sensitivity to THZ

178 que gene expression patterns of 31 different breast cancer cell lines exposed to hypoxic conditions.

179 Additionally, various breast cancer cell lines growing in adherent, two-dimens

180 2, but not mesenchymal-like, triple-negative breast cancer cell lines have increased epigen expressio

181 xpression renders aggressive triple-negative breast cancer cell lines highly responsive to chemothera

182 SNHG7 regulates proliferation of breast cancer cell lines in a dose-dependent manner, and

183 ely, knockdown of RAD51AP1 (RADP51AP1 KD) in breast cancer cell lines reduced tumor growth.

184 rough CK5 knockout and overexpression in ER+ breast cancer cell lines that CK5 is important for tumor

185 CA12 is transcriptionally silenced in basal breast cancer cell lines through histone deacetylation a

186 -culture with MCF-7, MDA-MB-231, and SK-BR-3 breast cancer cell lines using [Formula: see text] nucle

187 potent cytotoxic cell death in luminal (ER+) breast cancer cell lines which fail to upregulate A20 ex

188 the CEP135(full:mini) ratio) is increased in breast cancer cell lines with high CA.

189 itors of AKT and HER2 was conducted in HER2+ breast cancer cell lines with or without PIK3CA mutation

190 Using patient breast tumor specimens, breast cancer cell lines, and a patient-derived xenograf

191 methylated in normal breast tissue and some breast cancer cell lines, and could be reversed by treat

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

193 d across a series of increasingly metastatic breast cancer cell lines.

194 istance to single-agent anti-HER2 therapy in breast cancer cell lines.

195 et genes in six human mammary epithelial and breast cancer cell lines.

196 one H3 acetylation to compare non-cancer and breast cancer cell lines.

197 ific uptake of the probe into the cytosol in breast cancer cell lines.

198 ir requirement for cell growth in a panel of breast cancer cell lines.

199 we overexpressed several of its isoforms in breast cancer cell lines.

200 t anti-HER2 treatment in PIK3CA-mutant HER2+ breast cancer cell lines.

201 NA templates and validated with DNA from two breast cancer cell-lines and two patient tumour tissue s

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

203 erum or 0.024 wt % of the total protein from breast cancer cell lysates.

204 Here, we show that breast cancer cells maintained in hypoxia release small

205 ntangle the role played by water dynamics in breast cancer cells (MCF-7) after treatment with a chemo

206 an intriguing potency in the triple-negative breast cancer cells MDA-MB-231.

207 role in cell migration, we here investigated breast cancer cell (MDA-MB-231) migration by video micro

208 DOX-loaded MONs coated with 4T1 breast cancer cell membranes (CM@MON@DOX) show greater a

209 cells and patient-derived primary metastatic breast cancer cells, mesothelioma cells, and lung cancer

210 n studies revealed that RAB11B-AS1 increased breast cancer cell migration and invasion in vitro and p

211 forming growth factor beta (TGFbeta)-induced breast cancer cell migration and invasion.

212 argeting miRNAs and examine their effects on breast cancer cell migration through exosome-mediated de

213 ation, our results imply that Atox1 mediates breast cancer cell migration via coordinated copper tran

214 ich could be exploited for the inhibition of breast cancer cell migration via the exosome-mediated de

215 Aquaporin-5 (AQP5) plays a role in breast cancer cell migration.

216 vents and 41 splicing factors regulated in a breast cancer cell model of acquired resistance to doxor

217 Here, using human breast cancer cell models, we identified a pathway in wh

218 hibition of RSK2-mediated autophagy rendered breast cancer cells more sensitive to paclitaxel, a chem

219 FGFR TKIs in the bone microenvironment where breast cancer cells most frequently metastasize and also

220 d breast cancer cells and strongly impairing breast cancer cell motility and invasion.

221 W264.7 or THP-1) were cultured alone or with breast cancer cells (mouse polyoma-middle T virus or pri

222 We report that in breast cancer cells NANOG, SNAIL and NODAL transcripts m

223 ignificance of O-GlcNAcylation in a panel of breast cancer cells of different phenotypes.

224 of NAT1 N-acetylation activity in MDA-MB-231 breast cancer cells on global cellular metabolism and to

225 While the majority of injected breast cancer cells predominantly adhered to nearby vasc

226 cogenic while BRD4-L is tumor-suppressive in breast cancer cell proliferation and migration, as well

227 ls diminished myoferlin level and suppressed breast cancer cell proliferation, migration, and endothe

228 ASB13 knockout in breast cancer cells promoted cell migration and decrease

229 ZMYND8 knockout (KO) in breast cancer cells promoted infiltration of CD4(+) and

230 itioned media from RAB11B-AS1-overexpressing breast cancer cells promoted tube formation of human umb

231 HER2- and p95HER2- mediated miRNA changes in breast cancer cells, provides novel mechanistic insight

232 PRR11-amplified breast cancer cells rely on PIK3CA and are highly sensit

233 y, but its intrinsic regulatory mechanism in breast cancer cells remains poorly understood.

234 Therefore, sEVs released by hypoxic breast cancer cells reprogram mitochondrial dynamics and

235 and converging on ECT2, that participate to breast cancer cell resistance to doxorubicin.

236 ptosis in long-term estrogen deprived (LTED) breast cancer cells resistant to antiestrogens.

237 ic, but not non-macropinocytic, pancreas and breast cancer cells resistant to these treatments.

238 icinal plant Arabidopsis thaliana with human breast cancer cells, selectively suppresses cancer cell

239 appear to be a subset of TICs (5) sGRP78(+) breast cancer cells show an enhanced ability to seed met

240 To overcome this, breast cancer cells stably overexpressing BC200 and vari

241 ta that, upon engagement of its receptors in breast cancer cells, suppressed the abundance of the tra

242 el comprising a central high-density mass of breast cancer cells surrounded by collagen type-1 and we

243 We showed comparable potency in reduction of breast cancer cell survival in vitro and in growth restr

244 An RNAi loss-of-function screen in breast cancer cells targeting all DUBs identified USP11

245 solate, fluorescently immunolabel, and count breast cancer cells that are positive for human epiderma

246 Pulsed magnetic field exposure of human breast cancer cells that express a sialic-acid rich glyc

247 We previously demonstrated that breast cancer cells that had undergone an oncogenic EMT

248 that sGRP78 marks a stem-like population in breast cancer cells that has increased metastatic potent

249 We show that VEGF-C, secreted by breast cancer cells that have undergone an EMT, promotes

250 Herein, we identify exosomes from autologous breast cancer cells that show effective lung targeting a

251 lammatory TAMs promoted a metabolic state in breast cancer cells that supported various protumorigeni

252 panel of cell lines derived from MDA-MB-231 breast cancer cells that vary in their metastatic potent

253 We also demonstrated that in MDA-MB-231 breast cancer cells, the cell-surface transporter densit

254 se bioactive factors induced triple-negative breast cancer cell (TNBC) death in vitro and reduced tum

255 unctional DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3B-mediated mutations and double

256 rteporfin resensitized ZNF367-overexpressing breast cancer cells to anoikis and abrogated metastasis.

257 e direction, with loss of ARID1A sensitizing breast cancer cells to bromodomain and extraterminal dom

258 lung and moderately impaired the ability of breast cancer cells to colonize the lung when delivered

259 Hypoxia sensitizes breast cancer cells to EGFR inhibitors in an HIF1alpha-

260 nockdown of RSK2 enhanced the sensitivity of breast cancer cells to ER stress both in vitro and in vi

261 tenance of genome stability by ZMYND8 causes breast cancer cells to evade cytotoxic T-lymphocyte surv

262 the adhesion strength and kinetics of human breast cancer cells to extracellular matrix such as fibr

263 regulates tumor dormancy and the response of breast cancer cells to hormone and chemotherapy.

264 e have employed varying EMT models of murine breast cancer cells to identify the key players establis

265 f CBFbeta inhibits the ability of metastatic breast cancer cells to invade bone cell cultures and sup

266 (B16F10), and orthotopic injection of E0771 breast cancer cells to show that alternative forms incre

267 ation of autophagy increased the response of breast cancer cells to tamoxifen on soft substrata.

268 of 7 inhibited 14,15-EET production in T47D breast cancer cells transfected with CYP4Z1.

269 P followed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the proteasome inhibito

270 LHRH receptors serve as binding sites on the breast cancer cells/tumor and the LHRH-conjugated drugs

271 In MYC-amplified, and p53-mutant breast cancer cells, UBR5 has an important role in suppr

272 In breast cancer cells under normoxia, CHD4 enrichment at H

273 (IC(50)) of these samples on triple-negative breast cancer cells using the MTT assays.

274 gnaling by kinases Akt and ERK revealed that breast cancer cells utilized oxidative phosphorylation a

275 tion and to characterize lipid metabolism in breast cancer cells via quantitative kinetic models and

276 Investigating the behavior of breast cancer cells via reaction kinetics may help unrav

277 ation, migration, and invasion of epithelial breast cancer cells, via non-canonical activation of GLI

278 indicated that 8a decreases triple-negative breast cancer cell viability, and immunoblotting reveale

279 2beta-PE detected in breast tumors, altering breast cancer cell viability, proliferation, and migrati

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

281 nd 3D chemotaxis assays on single metastatic breast cancer cells, we investigate the links among thes

282 and matched non-invading SUM149 inflammatory breast cancer cells were enriched using this device and

283 educed drug responsiveness was observed when breast cancer cells were maintained in 3D under fluid fl

284 nvironments reminiscent of metastatic sites, breast cancer cells were more resistant to the estrogen

285 kin-4 receptor, which is highly expressed in breast cancer cells, were bioengineered and their inhibi

286 h p53 and PTEN activated MEOX1 expression in breast cancer cells, whereas individual knockdowns of ei

287 uggests paracrine signaling between LECs and breast cancer cells which could have a pro-metastatic ro

288 hibited higher cytotoxicity against TNBC and breast cancer cells which present high intracellular lev

289 Furthermore, treatment of breast cancer cells with 7e, 7f, 7g, or 9k inhibited via

290 of MDA-MB-231 and MDA-MB-453 triple-negative breast cancer cells with a newly developed thienopyridin

291 SPANXB1 overexpressing breast cancer cells with an enhanced SPANXB1:SH3GL2 rati

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

293 Treatment of breast cancer cells with bis-indole-derived NR4A1 antago

294 Breast cancer cells with CRISPR-Cas9-edited ER (D538G, Y

295 akdown and concomitant drug release, when in breast cancer cells with increased levels of reducing ag

296 found that disulfiram is capable of killing breast cancer cells with simultaneous formaldehyde accum

297 pressed MYC-mediated apoptosis in p53-mutant breast cancer cells with UBR5/MYC coamplification.

298 this study, we reconstituted PTEN-deficient breast cancer cells with wild-type and mutant PTEN, demo

299 nhibitor, MK-2206, preferentially eliminated breast cancer cells without altering viability of bone m

300 not reveal lactate shuttling into LECs from breast cancer cells, yet showed other [Formula: see text