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 ng as a prominent EVI1 effector mechanism in breast carcinoma.

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

5 oma) and an orthotopically xenografted human breast carcinoma.

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

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

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

9 argeted therapy in HER2-overexpressing human breast carcinoma.

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

11 vIII expression and amplification in primary breast carcinoma.

12 of GPIT have increased expression levels in breast carcinoma.

13 previous chemotherapy, either for ovarian or breast carcinoma.

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

15 al samples of human spindle cell metaplastic breast carcinoma.

16 rived from the PBMC of a single patient with breast carcinoma.

17 Abs (TCRm), reduce tumor growth in models of breast carcinoma.

18 mportant prognostic and predictive marker in breast carcinoma.

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

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

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

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

23 protein 15 is also suggestive of metastatic breast carcinoma.

24 obstruction secondary to metastatic lobular breast carcinoma.

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

26 r maintaining the luminal phenotype in human breast carcinoma.

27 s a noninvasive precursor lesion to invasive breast carcinoma.

28 ved docetaxel treatment after resection of a breast carcinoma.

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

30 utcome in epithelial malignancies, including breast carcinomas.

31 er cells is highly overexpressed in invasive breast carcinomas.

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

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

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

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

36 ognostic marker and novel therapy target for breast carcinomas.

37 histologically similar to human metaplastic breast carcinomas.

38 ellular EphA2 in invasive cells within human breast carcinomas.

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

40 inactivated in many human cancers including breast carcinomas.

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

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

43 ilable microarray data sets from prostate or breast carcinomas.

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

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

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

47 f phospho-BRCA1 (Ser1423) in 39% of invasive breast carcinomas.

48 f BRCA1 tumor suppressor protein in invasive breast carcinomas.

49 ssociated with the development of basal-type breast carcinomas.

50 phospho-Akt-1 (Ser(473)) in 21% of invasive breast carcinomas.

51 sion exhibits strong correlations in primary breast carcinomas.

52 tively correlated with the aggressiveness of breast carcinomas.

53 een HOXB7 and TGFbeta2 expression in primary breast carcinomas.

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

55 -7.1]); soft-tissue sarcoma (2.8 [2.1-3.9]); breast carcinoma (2.1 [1.8-2.4]); acute myeloid leukemia

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

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

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

59 ected genes in unrelated non-migratory MCF-7 breast carcinoma and highly migratory U251 glioma cells.

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

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

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

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

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

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

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

72 on states and genotypic alterations in human breast carcinomas and evaluated diversity with ecologica

73 sed in high amounts in the majority of human breast carcinomas and in mammary epithelial cells only d

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 tic alterations in PIK3CA have been invasive breast carcinomas and the frequency of PIK3CA mutations

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

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

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

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

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 four leukemias, five thyroid carcinomas, six breast carcinomas, and four sarcomas.

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

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

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

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 In breast carcinoma-bearing mice that were immunocompetent,

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

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

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

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

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

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

99 Breast carcinomas can be stratified into different entit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 in ERalpha-positive but not ERalpha-negative breast carcinoma cell lines, suggesting that ERbeta1 rep

116 ling in ERalpha-transfected ERalpha-negative breast carcinoma cell lines, the MDA-MB-468 and the MDA-

117 ion in endocrine sensitive but not resistant breast carcinoma cell lines.

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

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

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

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

125 y two different human cancer cells, MDAMB231 breast carcinoma cells and U87 glioma cells, are capable

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

127 Most ductal breast carcinoma cells are weakly invasive in vitro and

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 Breast carcinoma cells express high levels of integrin b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 Breast carcinoma cells use specialized, actin-rich protr

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

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

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

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

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

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

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

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

163 (64)Cu-NO2A-TFpep bound to human MDA-MB-435 breast carcinoma cells, whereas almost no binding was ob

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

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

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

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

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

169 her influence oncogenesis and progression of breast carcinoma cells.

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

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

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

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

174 sponsible for the enhanced attachment of the breast carcinoma cells.

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

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

177 ionally leads to attenuated proliferation in breast carcinoma cells.

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

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

180 Basal-like breast carcinomas, characterized by unfavorable prognosi

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

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

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

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

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

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

187 ecturally abnormal ECM that is permissive to breast carcinoma directional migration and invasion.

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

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

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

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

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

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

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

195 el concentration and apoptosis in irradiated breast carcinomas for up to 3 weeks.

196 e the molecular basis of how early events in breast carcinoma formation are regulated by GnT-V, we st

197 Stromal fibroblasts of breast carcinomas frequently express the cell surface pr

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

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

209 Inflammatory breast carcinoma (IBC) is characterized by exaggerated l

210 MO7 is upregulated in the stroma of invasive breast carcinoma in a manner that correlates with the in

211 ed women with clinical T1 to T2N0M0 invasive breast carcinoma in a prospective observational study.

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

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

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

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

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

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

218 ke subgroup in a set of 297 primary invasive breast carcinomas in which the staining profile for the

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

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

221 Breast carcinoma invasion is associated with prominent a

222 Metaplastic breast carcinoma is an aggressive form of invasive breas

223 Breast carcinoma is the leading cause of cancer-related

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

225 Using a breast carcinoma line (MDA-MB-231) we also observed cell

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

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

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

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

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

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

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

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

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

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

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

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

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

239 nts classified as NP developed contralateral breast carcinoma more often but had better 10-year overa

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

241 In clinical breast carcinomas, Myo10 was predominantly expressed at

242 eatment of ER-positive, estrogen-independent breast carcinomas needing improved clinical management.

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

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

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

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

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

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

249 5 (95% CI, 8.2% to 32.8%) with no history of breast carcinoma (P = .007, Fisher's exact test).

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

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

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

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

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

255 e and human in vivo models of HER2-amplified breast carcinoma relied critically on this HER2-IL-6-Sta

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

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

258 In human breast carcinoma samples, stromal Sdc1 expression correl

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

260 Immunohistochemical analysis of breast carcinomas showed significant correlation between

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

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

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 and NF were isolated from six primary human breast carcinoma specimens.

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

267 observations suggest that Sdc1 expression in breast carcinoma stromal fibroblasts promotes the assemb

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

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

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

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

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

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

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

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

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

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

278 Evaluation of breast carcinoma tissues from patients revealed that cel

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

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

281 nant breast specimens as well as 314 primary breast carcinomas to assess its association with subcell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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