ライフサイエンスコーパス: breast carcinoma

1 ), MCF-7 (breast carcinoma), and MDA-MB-436 (breast carcinoma).

2 emical inflammation (turpentine) and cancer (breast carcinoma).

3 l of human cancer cell lines (HCC, renal and breast carcinomas).

4 oxifen or no-adjuvant treatment for invasive breast carcinoma.

5 protein 15 is also suggestive of metastatic breast carcinoma.

6 obstruction secondary to metastatic lobular breast carcinoma.

7 low grade and lymph node metastasis-negative breast carcinoma.

8 r maintaining the luminal phenotype in human breast carcinoma.

9 s a noninvasive precursor lesion to invasive breast carcinoma.

10 ved docetaxel treatment after resection of a breast carcinoma.

11 ion in clinical specimens of triple-negative breast carcinoma.

12 ght be a target for therapy in patients with breast carcinoma.

13 oma) and an orthotopically xenografted human breast carcinoma.

14 of a history of melanoma, suggests a primary breast carcinoma.

15 on and invasion in an in vivo mouse model of breast carcinoma.

16 net ring cell) gastric carcinoma and lobular breast carcinoma.

17 argeted therapy in HER2-overexpressing human breast carcinoma.

18 aneous ovarian cancer, and possibly in human breast carcinoma.

19 ed underlying cancer in 2 cases: myeloma and breast carcinoma.

20 vIII expression and amplification in primary breast carcinoma.

21 of GPIT have increased expression levels in breast carcinoma.

22 previous chemotherapy, either for ovarian or breast carcinoma.

23 ent a rational strategy for treating HER2(+) breast carcinoma.

24 of melanoma, colorectal adenocarcinoma, and breast carcinoma.

25 ng as a prominent EVI1 effector mechanism in breast carcinoma.

26 in the premetastatic niche) in the models of breast carcinoma.

27 hat CD44 might be a novel target of DACH1 in breast carcinoma.

28 al samples of human spindle cell metaplastic breast carcinoma.

29 pha with CaM may be useful in the therapy of breast carcinoma.

30 Twenty-four of 50 participants had a breast carcinoma.

31 een HOXB7 and TGFbeta2 expression in primary breast carcinomas.

32 utcome in epithelial malignancies, including breast carcinomas.

33 er cells is highly overexpressed in invasive breast carcinomas.

34 constitutively activated in more than 60% of breast carcinomas.

35 /NOTCH1 axis that controls breast TICs in TN breast carcinomas.

36 eu were found to be co-expressed in invasive breast carcinomas.

37 ionally regulated by Pin1 in a proportion of breast carcinomas.

38 ognostic marker and novel therapy target for breast carcinomas.

39 ellular EphA2 in invasive cells within human breast carcinomas.

40 r and to recognize somatic KLLN deletions in breast carcinomas.

41 inactivated in many human cancers including breast carcinomas.

42 which is deleted or mutated in 27.7% of all breast carcinomas.

43 nd is amplified and/or overexpressed in many breast carcinomas.

44 ilable microarray data sets from prostate or breast carcinomas.

45 miR-221/222/181b expression in primary human breast carcinomas.

46 in approximately 80% of in situ and invasive breast carcinomas.

47 sion exhibits strong correlations in primary breast carcinomas.

48 histologically similar to human metaplastic breast carcinomas.

49 R(+)) and estrogen receptor-negative (ER(-)) breast carcinomas.

50 tively correlated with the aggressiveness of breast carcinomas.

51 dary non-Hodgkin lymphoma, 19% for secondary breast carcinoma, 15% for secondary thyroid carcinoma, a

52 -7.1]); soft-tissue sarcoma (2.8 [2.1-3.9]); breast carcinoma (2.1 [1.8-2.4]); acute myeloid leukemia

53 d and neck squamous cell carcinoma SAS/mouse breast carcinoma 4T1) wound mouse model.

54 en phthalate exposures and incident invasive breast carcinoma according to tumor estrogen receptor st

55 Rudhira/Breast Carcinoma Amplified Sequence 3 (BCAS3) is a cytos

56 Of 24 breast carcinomas analyzed, 3 (13%) have somatic KLLN he

57 o classify tumor-infiltrating lymphocytes in breast carcinoma and cutaneous melanoma.

58 determine the effects of TIGAR expression on breast carcinoma and fibroblast glycolytic phenotype and

59 Infection of transformed breast carcinoma and glioma stem cells similarly inhibit

60 We used MDA-MB-231 breast carcinoma and HT1080 fibrosarcoma as cell models.

61 lation analysis of public databases of human breast carcinoma and IHC analysis of mice xenograft tumo

62 mulated data and the gene expression data in breast carcinoma and lung adenocarcinoma from The Cancer

63 ssed gene clusters but also novel targets in breast carcinoma and lung adenocarcinoma.

64 rotein 1 (Drp1) expression in human invasive breast carcinoma and metastases to lymph nodes.

65 only in glioblastoma but in triple-negative breast carcinoma and normal keratinocytes as well.

66 ed ENO-1 protein levels were found in ductal breast carcinoma and on the cell surface of highly metas

67 III, including one patient with inflammatory breast carcinoma and one with metaplastic chondrosarcoma

68 Here we use mouse models of breast carcinoma and other solid tumours to show that se

69 s revealed ANTXR1 amplification in medullary breast carcinoma and overexpression in estrogen receptor

70 growth and metastasis in established murine breast carcinoma and sarcoma tumor models.

71 , M2-related TAM subset was present in human breast carcinomas and bone metastases after chemotherapy

72 and protein expression was elevated in human breast carcinomas and cell lines derived from breast car

73 ere coexpressed in invasive human basal-like breast carcinomas and corresponding cell lines, where th

74 LIFR is downregulated in human breast carcinomas and inversely correlates with metastas

75 in 2) is overexpressed in non-cultured human breast carcinomas and is negatively correlated with PTEN

76 n the GNAO1 (Galphao) gene was identified in breast carcinomas and shown to promote oncogenic transfo

77 We found that TLR5 was highly expressed in breast carcinomas and that TLR5 signaling pathway is ove

78 m resulted in development of highly invasive breast carcinomas and the formation of whole chromosomes

79 arcinoma), HCT-116 (colon carcinoma), MCF-7 (breast carcinoma) and NCI-H460 (lung carcinoma) by 4-34%

80 carcinoma), KB (epidermal carcinoma), MCF-7 (breast carcinoma), and MDA-MB-436 (breast carcinoma).

81 er, but still evident on HLA-A2(+) melanoma, breast carcinoma, and lymphoblastoid cells.

82 trong antitumor activity in murine melanoma, breast carcinoma, and lymphoma models and against human

83 for the transition from in situ to invasive breast carcinoma, and, accordingly, high EPN3 levels are

84 breast tissues, 17 noninvasive, 151 invasive breast carcinomas, and 6 cell lines by in-house-develope

85 LC) accounts for approximately 10% to 15% of breast carcinomas, and although it responds poorly to ne

86 USP7 was overexpressed in breast carcinomas, and the level of expression positivel

87 R expression was found in 30% of 751 primary breast carcinomas, and was associated with larger tumors

88 hanisms for the anti-tumor roles of DACH1 in breast carcinoma are still lack of extensive understandi

89 shed that more than one-fifth of ovarian and breast carcinomas are associated with inherited risk.

90 carcinomas, which faithfully represent human breast carcinomas at the molecular level, provide indisp

91 Ms in different cancer models: 4T1 and MCF-7 breast carcinoma, B16F10 melanoma, WT-GBM glioma and MKN

92 llagen fibers in cases diagnosed as invasive breast carcinoma (BC) of histological special types (IBC

93 In breast carcinoma-bearing mice that were immunocompetent,

94 activation is a frequent event in basal-like breast carcinomas (BLC).

95 ce of EVI1 overexpression in triple-negative breast carcinoma but not in the HER2-positive breast car

96 herin promotes metastasis of invasive ductal breast carcinoma by enhancing the survival of tumor cell

97 ntibodies (mAbs) to detect MGA expression in breast carcinoma by immunohistochemistry.

98 y investigated the role of integrin beta5 in breast carcinomas by depleting integrin beta5 using RNA

99 ression of NRF2 and SRXN1 was studied in 373 breast carcinomas by immunohistochemistry.

100 ters (menopausal status, personal history of breast carcinoma) by means of univariate and then multiv

101 Breast carcinomas can be stratified into different entit

102 ocarcinoma, lung squamous cell carcinoma and breast carcinoma cancer cells.

103 ur device, we performed tests on 76 invasive breast carcinoma cases expressing various levels of HER2

104 between December 2002 and February 2008, 39 breast carcinoma cases were identified.

105 gulation of MLK4 occurred in 23% of invasive breast carcinoma cases.

106 o inhibit both A549 lung carcinoma and MCF-7 breast carcinoma cell growth in micromolar concentration

107 lating the ability of trastuzumab to inhibit breast carcinoma cell growth.

108 We show that Nck advances breast carcinoma cell invasion by regulating actin dynam

109 s, cleavage-prone EphA2-D359I mutant shifted breast carcinoma cell invasion from collective to rounde

110 KT and ERK activation resulting in increased breast carcinoma cell invasion.

111 regulator of RhoA-dependent, MMP14-mediated breast carcinoma cell invasion.

112 omising cytotoxic activity of (+)-T7 against breast carcinoma cell line MCF-7.

113 ated XylNapOH- and XylNap-primed GAGs from a breast carcinoma cell line, HCC70, and a breast fibrobla

114 (LCC) cells from early stage human lung and breast carcinoma cell lines and defined the mechanisms t

115 atinib-mediated autophagy in Her2-expressing breast carcinoma cell lines and in Beclin-1 signaling in

116 that signaling via the HER2/HER3 pathway in breast carcinoma cell lines may lead to enhanced NKG2D-M

117 otent stromal cells (MSCs) and two different breast carcinoma cell lines, MDA-MB-231 (MDA) and MA11.

118 ical microtubule capture and ErbB2-dependent breast carcinoma cell migration.

119 cell motility factors such as RHOJ regulated breast carcinoma cell migration.

120 in tropic, HER2-transfected MDA-MB-231 human breast carcinoma cells (231-BR-HER2).

121 We study the dynamics of human breast carcinoma cells (MDA-MB-231) in these microstruct

122 ciferase-based assay using recombinant human breast carcinoma cells (VM7Luc4E2, ERalpha-positive).

123 at TRIM21 enhances the proliferation of MCF7 breast carcinoma cells and counteracts the decrease in c

124 es were performed on HER2-expressing BT474M1 breast carcinoma cells and in mice with BT474M1 subcutan

125 ys were performed on HER2-expressing BT474M1 breast carcinoma cells and in paired-label tissue distri

126 tegrin beta5 in the tumorigenic potential of breast carcinoma cells and therapeutic targeting of inte

127 n these anisotropic constructs, we find that breast carcinoma cells are acutely sensitive to the dire

128 nhibited the migration and invasion of human breast carcinoma cells at 0.4 muM.

129 wn that BLM selectively targeted MCF-7 human breast carcinoma cells but not the "normal" breast cell

130 s critical for induction of proliferation of breast carcinoma cells by activated epidermal growth fac

131 We investigated QSOX1 cDNA derived from T47D breast carcinoma cells by RT-PCR and 3'-RACE PCR and ide

132 Our measurements show that breast carcinoma cells cultured in collagen gels generat

133 We demonstrate that breast carcinoma cells exposed to radiation shed TMPs co

134 Breast carcinoma cells express high levels of integrin b

135 dothelial growth factor A (VEGFA) in MDA-231 breast carcinoma cells expressing constitutively-active

136 We computed forces of MDA-MB-231 breast carcinoma cells from the measured network deforma

137 ctors involved in beta4-mediated invasion of breast carcinoma cells identified SPARC, or secreted pro

138 t and retracting rear of polarised migrating breast carcinoma cells in both two-dimentional (2D) and

139 oteasome inhibition, and cytotoxicity toward breast carcinoma cells in comparison with nontargeting d

140 CTLs pre-cultured with TMPs from irradiated breast carcinoma cells increases tumor growth rates in m

141 t to increase MRTF-A activity in MCF-7 human breast carcinoma cells independently of external growth

142 Knockdown of TFAP2C in luminal breast carcinoma cells induced epithelial-mesenchymal tr

143 sms of trastuzumab resistance that emerge in breast carcinoma cells is clinically important.

144 that the speed of single, mechanically soft breast carcinoma cells is dramatically enhanced by surro

145 Dissemination of breast carcinoma cells is mediated by membrane type 1-ma

146 pletion of integrin beta5 in triple-negative breast carcinoma cells markedly reduced tumor take, grow

147 ude mice orthotopically implanted with human breast carcinoma cells of the types MCF-7 and 4T1-Luc.

148 Therefore, TIGAR expression in breast carcinoma cells promotes metabolic compartmentali

149 t, overexpression of matriptase in 4T1 mouse breast carcinoma cells resulted in visible changes in mo

150 Doxorubicin treatment of MCF-7 breast carcinoma cells results in FOXO3a nuclear relocat

151 We demonstrate that in Her2-expressing breast carcinoma cells that do not succumb to lapatinib,

152 In MDA-231 breast carcinoma cells that express elevated levels of C

153 ically expressing these genes in MCF-7 human breast carcinoma cells that produce undetectable levels

154 In MDA-MB-231 human breast carcinoma cells the only noted consequence of mat

155 a reveal that expression of IRS-2 sensitizes breast carcinoma cells to apoptosis in response to treat

156 o-temporal mechanical response of MDA-MB-231 breast carcinoma cells to the inhibition of Syk protein

157 Breast carcinoma cells use specialized, actin-rich protr

158 When breast carcinoma cells were seeded into the fibroblast-f

159 CR4 mediates breast cancer metastasis, MCF-7 breast carcinoma cells were transduced to express wild-t

160 in migratory and invasive sub-populations of breast carcinoma cells, and is involved in tumor cell in

161 ing, and RhoA activation in MDA-MB-231 human breast carcinoma cells, but not HeLa cells.

162 on lateral protrusions from immobile SUM159 breast carcinoma cells, gene-edited to express AP2-EGFP.

163 hibits HIF-1-dependent VEGF transcription in breast carcinoma cells, it does not prevent HIF-1alpha s

164 tion of tTG to the leading edges of MDAMB231 breast carcinoma cells, where it also plays an essential

165 ely up-regulated and coexpressed in invasive breast carcinoma cells, where, upon physical interaction

166 ry human macrophages (MPhi) with human MCF-7 breast carcinoma cells, which caused cell death of cance

167 production of lysyl oxidase (LOX) from human breast carcinoma cells, which is sufficient to enhance t

168 ionally leads to attenuated proliferation in breast carcinoma cells.

169 and mitochondrial DNA (mtDNA) in MDA-MB-231 breast carcinoma cells.

170 and AMF secretion were inversely related in breast carcinoma cells.

171 II and CRMP-2 at the cell periphery in human breast carcinoma cells.

172 her influence oncogenesis and progression of breast carcinoma cells.

173 T1-MMP-containing late endosomes in invasive breast carcinoma cells.

174 examined the effect of low pH (6.7) on human breast carcinoma cells.

175 ZEB1, human lung carcinoma cells, and human breast carcinoma cells.

176 optosis resistance in mammary epithelial and breast carcinoma cells.

177 contributes to the migration and invasion of breast carcinoma cells.

178 fect on constitutive ERK activity in HER2(+) breast carcinoma cells.

179 rescued by estrogen supplementation in ER(+) breast carcinoma cells.

180 her influence oncogenesis and progression of breast carcinoma cells.Oncogene advance online publicati

181 several independent cohorts of patients with breast carcinoma characterized by poor prognosis.

182 Basal-like breast carcinomas, characterized by unfavorable prognosi

183 ion is statistically down-regulated in human breast carcinoma compared with normal breast tissue.

184 sion was significantly increased in invasive breast carcinoma compared with normal breast tissues.

185 Melanoma and breast carcinoma comprised 96.8% of all cutaneous metast

186 tified at the tumor invasion front in ductal breast carcinomas correlates with increased lymphovascul

187 s suggest that early inactivation of HIC1 in breast carcinomas could predispose to stress-induced met

188 we did not find any variation in HRs across breast carcinomas defined by their estrogen receptor or

189 HER2-enriched breast carcinomas display evidence of elevated levels of

190 In human breast carcinomas, epithelial-to-mesenchymal transition

191 ed with a doubling of the risk of developing breast carcinoma, even though its role in carcinogenesis

192 P4 and phospho-p38 levels in 69% of invasive breast carcinomas examined, consistent with the function

193 n breast tumors, and high-grade or recurrent breast carcinomas exhibit lower VPS4B expression.

194 orm the basis for intervention in aggressive breast carcinomas expressing 14-3-3sigma.

195 nts for up to half of the mutational load in breast carcinomas expressing this enzyme.

196 yme in multiple cancer cell types, including breast carcinoma, fibrosarcoma, and melanoma.

197 n the National Cancer Database with invasive breast carcinoma from 2012-2016 that underwent upfront l

198 unohistochemistry is needed to differentiate breast carcinoma from other carcinomas.

199 Differentiating metastatic breast carcinoma from primary gastric adenocarcinoma can

200 ncing data are available, and on an invasive breast carcinoma genome that we sequenced using the same

201 ne (95% CI, 34.8% to 87.8%) women with prior breast carcinoma had a recurrent carcinoma with a second

202 carcinomas, which histologically match human breast carcinomas, harbor extensive genomic aberrations,

203 k is a tyrosine kinase and its expression in breast carcinoma has been linked to tumor progression.

204 situ (DCIS) and its progression to invasive breast carcinoma have not been defined.

205 detected by immunohistochemistry, in primary breast carcinomas have been associated with better disea

206 Two subgroups of invasive breast carcinomas have been identified with a poor progn

207 In human breast carcinoma, high Skp2 and low Tpl2 expression are

208 e and luminal-type cancer in comparison with breast carcinoma, high-grade and basal-like tumors respe

209 been shown to be active against MCF-7 (human breast carcinoma), HT-29 (human colon carcinoma), A2780

210 into 3D matrices, and conversion from ductal breast carcinoma in situ to invasive carcinoma in mouse

211 XCR4 signaling axis in a triple-negative 4T1 breast carcinoma in syngeneic mice.

212 n, we cultured epithelium from primary human breast carcinomas in different ECM gels.

213 oat cells from women with a prior history of breast carcinomas in situ (CIS) and in healthy controls.

214 Of 452 breast carcinomas in The Cancer Genome Atlas project, 93

215 NGAL was detected in 42.2% of the breast carcinomas in the cytoplasm.

216 In breast carcinomas, increased levels of insulin-like grow

217 In mice with orthotopic mammary breast carcinoma, intravenous injections of well-tolerat

218 Metaplastic breast carcinoma is an aggressive form of invasive breas

219 Breast carcinoma is the leading cause of cancer-related

220 oidy reduction and morphological reversal to breast carcinoma-like morphological characteristics, whi

221 Metaplastic breast carcinoma (MBC) is a highly aggressive form of tr

222 Metaplastic breast carcinoma (MBC) is a rare histological breast can

223 erved in Mycoplasma hyorhinis-infected human breast carcinoma MCF-7 cell cultures (MCF-7.Hyor), depen

224 , in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of

225 Silencing TCTP by short hairpin RNA in breast carcinoma MCF-7 cells leads to the declined repai

226 Using CoCl2-induced EMT of human breast carcinoma MCF-7 cells, we found that TEPA, a copp

227 were evaluated in human promyelocytic HL-60, breast carcinoma MCF-7, and neuroblastoma Kelly cell lin

228 and suppresses mesenchymal motility in human breast carcinoma (MDA-MB-231).

229 ted within the past 6 months for early-stage breast carcinoma, men undergoing surveillance after test

230 reast carcinomas and cell lines derived from breast carcinoma metastases.

231 -ETP 2 and meso-ETP 2 in a fully established breast carcinoma model by intravital microscopy.

232 rowth and metastasis burden in an aggressive breast carcinoma model in vivo Our work reveals a distin

233 In addition, in the late stages of the breast carcinoma model, NETosis occurs concomitant with

234 aken forward into the orthotopic MDA-MB-231 (breast carcinoma) model in mice.

235 c and antitumor activities in both colon and breast carcinoma models.

236 Treatment of human breast carcinoma MX-1 xenograft-bearing nude mice with c

237 In clinical breast carcinomas, Myo10 was predominantly expressed at

238 ed features of Treg cells in untreated human breast carcinomas, normal mammary gland, and peripheral

239 In cell lines and breast carcinoma NuMA prevents 53BP1 accumulation at DNA

240 ion was characterized by the predominance of breast carcinomas observed in 79% of the females, and ST

241 m 99 patients with IBC-ST and 21 of invasive breast carcinoma of no special type (IBC-NST) were submi

242 a median 85 months from surgery for invasive breast carcinoma or ductal carcinoma in situ.

243 ll other organs that typically house primary breast carcinoma or tumor metastasis.

244 In light of the critical role of ER-alpha in breast carcinoma, our data suggest that small molecules

245 Because MSCs migrate and localize to breast carcinoma, our findings indicate that formation o

246 5 (95% CI, 8.2% to 32.8%) with no history of breast carcinoma (P = .007, Fisher's exact test).

247 Analyzing a tissue microarray of 608 breast carcinoma patient specimens, we documented EVI1 o

248 he expression of cyclin E and p-CDK2 in 1676 breast carcinoma patients by immunohistochemistry.

249 enes among three sub-populations of invasive breast carcinoma patients.

250 s clear survival advantages in HER2-positive breast carcinoma patients.

251 OR transcript abundance in a large invasive breast carcinoma population and identified two OR genes,

252 As the majority of patients with basal-like breast carcinoma present with invasive, metastatic disea

253 By identifying Nck as an important driver of breast carcinoma progression and metastasis, these resul

254 en >= 50 years of age with low-risk invasive breast carcinoma (pT1-2 pN0) were randomly assigned to 5

255 -ERK5 pathway in the progression of clinical breast carcinoma remains poorly understood.

256 es samples including The Cancer Genome Atlas breast carcinoma samples and liver samples exposed to ge

257 In human breast carcinoma samples, stromal Sdc1 expression correl

258 n total, 20 women with primary or metastatic breast carcinoma (score of 2+ or 3+ on HER2 immunohistoc

259 Immunohistochemical analysis of breast carcinomas showed significant correlation between

260 comine database revealed that 52 of 53 human breast carcinomas showed substantial upregulation of WNT

261 Further immunohistochemical analysis on 42 breast carcinoma specimens showed that MHG1152 and MGD78

262 hemical staining of a cohort of 100 invasive breast carcinoma specimens.

263 vimentin in the cancer cell lines and human breast carcinoma specimens.

264 ssion was observed in stage III and IV human breast carcinoma specimens.

265 reast carcinoma but not in the HER2-positive breast carcinoma subset.

266 Brk is overexpressed in 60% of breast carcinomas, suggesting that this facilitates cell

267 In addition, FBXO44 expression pattern in breast carcinomas suggests that SCF(FBXO44)-mediated BRC

268 on levels of TARBP2, APP and ZNF395 in human breast carcinomas support their experimentally uncovered

269 range, 40-75 y) with metastatic prostate or breast carcinoma suspected either on imaging or because

270 notype representative of advanced basal-like breast carcinoma that readily formed metastatic lesions

271 In invasive breast carcinoma, there is a positive relationship betwe

272 s or tissue microarrays (TMAs) from invasive breast carcinoma tissue were tested by both IHC and ISH

273 tric tetra-antennary N-glycan found in human breast carcinoma tissue, which represents the most compl

274 tion in the G-protein alpha subunit GNAO1 in breast carcinoma tissue.

275 Evaluation of breast carcinoma tissues from patients revealed that cel

276 (low)p-Hsp27(low), which also exist in human breast carcinoma tissues.

277 xpression is associated with triple-negative breast carcinomas (TNBCs), which are aggressive tumors a

278 e with recently diagnosed metastatic lobular breast carcinoma to skin was referred to gastroenterolog

279 sification) estrogen receptor (ER) -positive breast carcinoma treated by lumpectomy were randomly ass

280 es were injected orthotopically to establish breast carcinoma tumors in immunodeficient and immunocom

281 arrier status and a prior history of lobular breast carcinoma underwent prophylactic total gastrectom

282 In the 3 pigmented lesions (all metastatic breast carcinoma), various melanocytic patterns were obs

283 st infiltrative tumor (MDA-MB-231 metastatic breast carcinoma) was the softest.

284 Within a subset of invasive primary breast carcinoma, we observed relatively abundant expres

285 trial cohort including in total 564 invasive breast carcinomas, we examined TGFBR2 expression (n=252)

286 m line susceptibility genes in patients with breast carcinoma were developed to identify carriers of

287 Eleven women with invasive breast carcinoma were imaged with DOS tomography prior t

288 Seventy-four consecutive women with invasive breast carcinoma were recruited to undergo preoperative

289 d expression of mir-423, and triple-negative breast carcinomas were most distinct from other tumor su

290 myeloid leukemia, but is also detectable in breast carcinoma where its contributions are unexplored.

291 is especially attractive for triple-negative breast carcinomas, which are refractory to most of the c

292 ere, we define KLLN as a tumor suppressor in breast carcinomas, which inhibits tumor growth and invas

293 of the hDMP1 locus was found in 42% of human breast carcinomas, while that of INK4a/ARF and p53 were

294 R2-positive, trastuzumab-resistant, advanced breast carcinoma who had previously received taxane ther

295 Women older than 70 years with breast carcinoma, who had undergone neoadjuvant endocrin

296 godendroglioma, astrocytoma, solid papillary breast carcinoma with reverse polarity, sinonasal undiff

297 HER2-positive breast carcinomas with a PIK3CA mutation are less likely

298 nce of tumour size in patients with invasive breast carcinoma, with an emphasis on Breast Imaging Rep

299 emic decorin on a triple-negative orthotopic breast carcinoma xenograft model.

300 ystemic delivery of decorin for treatment of breast carcinoma xenografts induces paternally expressed