ライフサイエンスコーパス: triple-negative breast cancer

1 , p53 and PTEN, are strongly associated with triple negative breast cancer.

2 plus cyclophosphamide +/- B in stage II-III triple negative breast cancer.

3 duces tumorigenesis in mouse models of human triple negative breast cancer.

4 hanisms underlying cellular heterogeneity in triple negative breast cancer.

5 gold nanoshells for photothermal therapy of triple negative breast cancer.

6 cancer, especially in patients with invasive triple negative breast cancer.

7 enesis in a mouse xenograft model of hypoxic triple negative breast cancer.

8 ce of PI3K/AKT pathway activation, including triple-negative breast cancer.

9 igate copy number evolution in patients with triple-negative breast cancer.

10 than standard therapy alone specifically in triple-negative breast cancer.

11 ho were referred for BRCA1/2 testing or with triple-negative breast cancer.

12 particularly detrimental among patients with triple-negative breast cancer.

13 at diagnosis is reported to be prognostic in triple-negative breast cancer.

14 athway that is critical for dissemination of triple-negative breast cancer.

15 d decreases tumor burden in a mouse model of triple-negative breast cancer.

16 st-line therapy for patients with metastatic triple-negative breast cancer.

17 gnancy and is a novel therapeutic target for triple-negative breast cancer.

18 results supporting AKT-targeted therapy for triple-negative breast cancer.

19 010 and HR, 0.69; P = .019, respectively) in triple-negative breast cancer.

20 herapy strategy for patients with metastatic triple-negative breast cancer.

21 anaplastic thyroid cancer, glioblastoma, and triple-negative breast cancer.

22 re basal gene expression tumors, even within triple-negative breast cancer.

23 es with malignant potential in patients with triple-negative breast cancer.

24 thway appears to be particularly relevant in triple-negative breast cancer.

25 on, including regression in PDX samples from triple-negative breast cancer.

26 second PDX line obtained from a patient with triple-negative breast cancer.

27 s further investigation for the treatment of triple-negative breast cancer.

28 uptake in a mouse orthotopic model of human triple-negative breast cancer.

29 rtib to paclitaxel as first-line therapy for triple-negative breast cancer.

30 r KDM4 inhibition as a new strategy to treat triple-negative breast cancer.

31 nce knowledge related to the pathogenesis of triple-negative breast cancer.

32 romising biomarker for the identification of triple-negative breast cancer.

33 cule in the progression of HER2 positive and triple negative breast cancers.

34 ism for cell-targeted imaging and therapy of triple negative breast cancers.

35 (hazard ratio 16.918; P = 0.0005) but not in triple-negative breast cancers.

36 and kinesin-1 are up-regulated in high-grade triple-negative breast cancers.

37 e epigenome as a novel therapeutic target in triple-negative breast cancers.

38 kinase CDK7, induces apoptotic cell death in triple-negative breast cancers.

39 PIPKIgamma is overexpressed in triple-negative breast cancers.

40 f five lesion classification tasks involving triple-negative breast cancers.

41 Results Eighteen tumors (22%) were triple-negative breast cancers.

42 ll survival of patients in a large series of triple-negative breast cancers.

43 ed on single-nucleus sequencing reports that triple-negative breast cancers acquire copy number aberr

44 cumented for models of solid tumors, such as triple negative breast cancer and colon cancer.

45 Forty-six consecutive women with triple-negative breast cancer and an indication for neoa

46 with pCR to neoadjuvant chemotherapy in non-triple-negative breast cancer and may be a promising bio

47 ith a mesenchymal phenotype, particularly in triple-negative breast cancer and non-small cell lung ca

48 ages showed a significant difference between triple-negative breast cancer and non-triple-negative br

49 In a murine cancer model of human triple-negative breast cancer and prostate cancer, CP-PT

50 endothelial antigen that is overexpressed in triple-negative breast cancer and the associated tumor v

51 those with non-pCR and between patients with triple-negative breast cancer and those with non-triple-

52 cardinal molecular features of conventional triple-negative breast cancer and underpinned by specifi

53 levels of tumor-infiltrating lymphocytes in triple-negative breast cancers and while MEK inhibition

54 treated, histologically confirmed metastatic triple-negative breast cancer, and an ECOG performance s

55 in vivo in murine model systems of melanoma, triple-negative breast cancer, and patient-derived ortho

56 rbors the complex genomic landscape of usual triple-negative breast cancer, and the salivary gland-li

57 ly, which includes nonobligate precursors of triple-negative breast cancer, and, despite being low-gr

58 is expressed at higher levels in basal-like triple-negative breast cancers, and its overexpression i

59 herin localization to the plasma membrane in triple-negative breast cancers, and to suppress cellular

60 In fact, most triple-negative breast cancers are poor-prognosis tumors

61 ermal growth factor receptor 2-positive, and triple-negative breast cancers-are necessary.

62 d good performance for the identification of triple-negative breast cancer (area under the receiver o

63 ied genes potentially regulated by miRNAs in Triple Negative Breast Cancer, as well as miRNA-gene rel

64 risk, nor any patient with HER2-positive or triple-negative breast cancer, because of the lack of de

65 s presenting with early-onset breast cancer, triple-negative breast cancer, bilateral breast cancer,

66 Important elements of triple-negative breast cancer biology include high proli

67 y cannot be combined into a unified model of triple-negative breast cancer biology.

68 py has a role in the treatment of metastatic triple-negative breast cancer but its full potential has

69 s from melanoma, head and neck, bladder, and triple-negative breast cancers but showed no response to

70 dministration in vivo fostered the growth of triple-negative breast cancer by promoting proliferation

71 st cancers are distinguished from ER+ve and 'triple-negative' breast cancers by harbouring not only t

72 of FoxQ1 protein was significantly higher in triple-negative breast cancer cases compared with normal

73 morspheres and in a panel of mouse and human triple negative breast cancer cell-derived tumorspheres.

74 induced Pin1 ablation also potently inhibits triple-negative breast cancer cell growth in human cells

75 ock three AHR-dependent biologic activities: triple-negative breast cancer cell invasion or migration

76 (R9-cc-caPeptide) exhibits cytotoxicity in a triple-negative breast cancer cell line, MDA-MB-436, whi

77 in tumor cell migration and invasion in two triple-negative breast cancer cell lines was observed wi

78 Overexpression of CSTF3 was common in triple-negative breast cancer cell lines, and elevated C

79 inhibitor provided enhanced cell killing in triple-negative breast cancer cell lines, suggesting tha

80 Endothelial cells promote triple-negative breast cancer cell metastasis via PAI-1

81 increased cisplatin inhibition of MDA-MB-231 triple-negative breast cancer cell proliferation and tum

82 ic reticulum homeostasis and is critical for triple-negative breast cancer cell survival.

83 se tissue and estrogen receptor-positive and triple-negative breast cancer cell types.

84 This action is essential for the survival of triple negative breast cancer cells in vitro and in vivo

85 aster than DOX are more effective at killing triple negative breast cancer cells in vitro.

86 types, we used next generation sequencing of triple negative breast cancer cells in which the isoform

87 reases HIF-1alpha, and triggers apoptosis of triple negative breast cancer cells only under hypoxic c

88 ce the steady state level of PAK4 protein in triple negative breast cancer cells.

89 Notably, triple-negative breast cancer cells and non-small cell l

90 PAF production could be abrogated in triple-negative breast cancer cells by inhibition of cal

91 In triple-negative breast cancer cells, IL30 boosted a broa

92 icient inhibitor of growth and metastasis of triple-negative breast cancer cells, paving the way for

93 substantially lower level than Akt3/+S472 in triple-negative breast cancer cells, specific ablation o

94 itabine sensitization or resistance in human triple-negative breast cancer cells, we identified NIMA

95 sesses intrinsic inhibitory activity against triple-negative breast cancer cells.

96 which drives the growth of therapy-resistant triple-negative breast cancer cells.

97 Triple-negative breast cancer, compared with non-TNBC, l

98 For some patients, especially those with triple-negative breast cancer, current treatments contin

99 Of relevance, triple negative breast cancer currently lacks good bioma

100 term outcomes was strongest in patients with triple-negative breast cancer (EFS: HR 0.24, 95% CI 0.18

101 erty of triple-negative breast cancers: most triple-negative breast cancers express aberrant DNA hype

102 In patients with triple-negative breast cancer, expression of these 7 gen

103 atase PIPP/INPP5J, frequently inactivated in triple-negative breast cancers, functions as a tumor sup

104 Different subgroups of triple-negative breast cancer have been identified on th

105 Triple-negative breast cancers have increased expression

106 ontrast enhancement in aggressive MDA-MB-231 triple negative breast cancer in mice at a low dose (1.7

107 The increased risk of triple-negative breast cancer in African American women

108 Triple-negative breast cancers (including basal-like and

109 Among these subtypes, triple negative breast cancer is particularly difficult

110 Triple-negative breast cancer is a heterogeneous disease

111 Recognition that triple-negative breast cancer is an operational term and

112 Triple-negative breast cancer is viewed clinically as an

113 resence of tumor-infiltrating lymphocytes in triple-negative breast cancers is correlated with improv

114 A pivotal phase II trial (METRIC [Metastatic Triple-Negative Breast Cancer]) is underway.

115 was able to identify patients with sporadic triple-negative breast cancer lacking a BRCA1/2 mutation

116 Progression to high-grade triple-negative breast cancer likely occurs in both subg

117 D mice harboring xenografts of MDA-MB-231, a triple-negative breast cancer line constitutively expres

118 significant anti-proliferative effects in a triple-negative breast cancer MDA-MB-231 xenograft model

119 Among them, triple-negative breast cancer MDA-MB-231, which has the

120 ance in several of the cell lines, including triple-negative breast cancer (MDA-MB231) and androgen r

121 ably detect a model EpCAM(low) cell line for triple negative breast cancer, MDA-MB-231, with a recove

122 d/receptor pair Jagged1/Notch1 that sustains triple-negative breast cancer migration and invasion.

123 90% tumor reduction is achieved in vivo in a triple-negative breast cancer model following 80% MRP1 s

124 DK4/6 blocks breast tumour metastasis in the triple-negative breast cancer model, without affecting t

125 nhancement is consistently observed in other triple negative breast cancer models, but not in low-ris

126 d a novel fundamental biological property of triple-negative breast cancers: most triple-negative bre

127 rinkage two weeks post-gel implantation in a triple-negative breast cancer mouse model.

128 e identification of patients with metastatic triple-negative breast cancer (mTNBC) who are expected t

129 urvival benefit for patients with metastatic triple-negative breast cancer (mTNBC), with no standard

130 there are no established targeted agents for triple-negative breast cancer (negative ER, progesterone

131 The triple-negative breast cancer, or basal breast cancer, i

132 etween triple-negative breast cancer and non-triple-negative breast cancer (P = .009, .003, and .001,

133 < .01), Ashkenazi Jewish ancestry (P < .01), triple-negative breast cancer (P = .01), and family hist

134 was independently associated with pCR in non-triple-negative breast cancer (P = .033).

135 both EGFR and PTEN were especially common in triple-negative breast cancer patients and rarely were s

136 y impact drug sensitivity, as exemplified by triple-negative breast cancer patients with diminished S

137 been demonstrated to improve the survival of triple-negative breast cancer patients; however, such th

138 , inoperable, locally advanced or metastatic triple-negative breast cancer previously untreated with

139 s the enzymes of FAD biosynthetic pathway in triple-negative breast cancers, reflecting the significa

140 lated cancers, its value in the treatment of triple-negative breast cancers remains to be demonstrate

141 trogen receptor alpha (ERalpha)-positive and triple-negative breast cancers, respectively.

142 In archived triple-negative breast cancer samples, we show a strong

143 nd EGFR expressions were correlated in human triple-negative breast cancer specimens.

144 This study investigates, in the triple-negative breast cancer subtype, the prognostic re

145 Rab25 is also frequently silenced in triple-negative breast cancer, suggesting its ability to

146 In triple-negative breast cancers, tGIV and cytoplasmic pYG

147 Caucasian and African-American patients with triple-negative breast cancer that might help explain di

148 us breast cancer subtypes revealed that more triple-negative breast cancers, the most aggressive brea

149 t KPT-9274 is a novel therapeutic option for triple negative breast cancer therapy.

150 Triple negative breast cancer (TNBC) accounts for 10-15%

151 of NPs in MDA-MB-468, an EFGR-overexpressing triple negative breast cancer (TNBC) cell line.

152 growth factor receptor 2 (HER2) positive and triple negative breast cancer (TNBC) cells after treatme

153 , (1) is highly enriched at the enhancers of triple negative breast cancer (TNBC) cells, (2) acts as

154 inase library containing 704 kinases against triple negative breast cancer (TNBC) cells.

155 Triple negative breast cancer (TNBC) is a highly heterog

156 Using in vivo lineage tracing and triple negative breast cancer (TNBC) patient derived xen

157 Triple negative breast cancer (TNBC) remains a serious u

158 Triple negative breast cancer (TNBC) represents an anoma

159 hibitor in a murine based xenograft model of triple negative breast cancer (TNBC) resulted in tumor g

160 Hypoxia enables progression of triple negative breast cancer (TNBC), the most aggressiv

161 ify the microbial signatures associated with triple negative breast cancer (TNBC).

162 as suggest increased copy number of PRKCE in triple negative breast cancer (TNBC).

163 cetaxel (DTX) to overcome drug resistance of triple negative breast cancer (TNBC).

164 regimens for several malignancies, including triple negative breast cancer (TNBC).

165 Triple negative breast cancers (TNBC) are aggressive tum

166 Triple negative breast cancers (TNBC) are among the most

167 ent survival, but there are no therapies for triple negative breast cancers (TNBC) that lack expressi

168 hological features similar to those of human triple-negative breast cancer (TNBC) (for example, pushi

169 Triple-negative breast cancer (TNBC) accounts for 20% of

170 One third of patients with triple-negative breast cancer (TNBC) achieve pathologic

171 Enriched only in triple-negative breast cancer (TNBC) and in ovarian, end

172 Triple-negative breast cancer (TNBC) and other molecular

173 New treatments for triple-negative breast cancer (TNBC) are urgently needed

174 CCN5/WISP-2 represents a promising target in triple-negative breast cancer (TNBC) because treatment o

175 Interestingly, triple-negative breast cancer (TNBC) cell lines did not

176 d reduced the survival of several metastatic triple-negative breast cancer (TNBC) cell lines.

177 es CSCs in a dose-dependent fashion in human triple-negative breast cancer (TNBC) cell lines.

178 one (Dex, a synthetic GC)-regulated genes in triple-negative breast cancer (TNBC) cells are associate

179 factor beta (TGF-beta)-induced migration of triple-negative breast cancer (TNBC) cells is dependent

180 to enable stratification of mesenchymal-like triple-negative breast cancer (TNBC) cells that differ f

181 in pre-metastatic niches, are conditioned by triple-negative breast cancer (TNBC) cells to accelerate

182 pression is upregulated widely in aggressive triple-negative breast cancer (TNBC) cells, both in prim

183 CL-1) is a major cause of drug resistance in triple-negative breast cancer (TNBC) cells.

184 a given class of drug response phenotype in triple-negative breast cancer (TNBC) cells.

185 Triple-negative breast cancer (TNBC) classified by trans

186 Triple-negative breast cancer (TNBC) comprises approxima

187 Triple-negative breast cancer (TNBC) has high rates of l

188 ion, and chemotherapeutic approaches against triple-negative breast cancer (TNBC) has not been invest

189 Triple-negative breast cancer (TNBC) has poor prognostic

190 Triple-negative breast cancer (TNBC) has the worst progn

191 Triple-negative breast cancer (TNBC) has the worst progn

192 Patients with triple-negative breast cancer (TNBC) have a high inciden

193 Patients with triple-negative breast cancer (TNBC) have poor outcome w

194 ntibodies associated with the development of triple-negative breast cancer (TNBC) in the before diagn

195 Triple-negative breast cancer (TNBC) includes basal-like

196 Triple-negative breast cancer (TNBC) is a breast cancer

197 Triple-negative breast cancer (TNBC) is a heterogeneous

198 Triple-negative breast cancer (TNBC) is a highly aggress

199 Triple-negative breast cancer (TNBC) is a highly aggress

200 Triple-negative breast cancer (TNBC) is a highly aggress

201 Triple-negative breast cancer (TNBC) is a highly aggress

202 Triple-negative breast cancer (TNBC) is a highly heterog

203 Triple-negative breast cancer (TNBC) is a molecularly he

204 Triple-negative breast cancer (TNBC) is a subtype of bre

205 Triple-negative breast cancer (TNBC) is an aggressive an

206 Triple-negative breast cancer (TNBC) is an aggressive cl

207 Triple-negative breast cancer (TNBC) is an aggressive di

208 Triple-negative breast cancer (TNBC) is an aggressive di

209 Triple-negative breast cancer (TNBC) is an aggressive su

210 Triple-negative breast cancer (TNBC) is an aggressive su

211 Triple-negative breast cancer (TNBC) is considered an ea

212 Triple-negative breast cancer (TNBC) is currently the on

213 Triple-negative breast cancer (TNBC) is notoriously aggr

214 Triple-negative breast cancer (TNBC) is one of the most

215 proxies for stem cell function in vitro, in triple-negative breast cancer (TNBC) lines and dissociat

216 er, the involvement of ECs in the process of triple-negative breast cancer (TNBC) metastasis has not

217 t inhibitors in mouse models of melanoma and triple-negative breast cancer (TNBC) metastasis.

218 ombination with radioiodine in an orthotopic triple-negative breast cancer (TNBC) murine model.

219 Despite its aggressive nature, triple-negative breast cancer (TNBC) often exhibits leuc

220 Triple-negative breast cancer (TNBC) patients commonly e

221 Triple-negative breast cancer (TNBC) patients have the h

222 ts prognostic value within racially distinct triple-negative breast cancer (TNBC) patients is unknown

223 nd angiogenesis, and is also associated with triple-negative breast cancer (TNBC) phenotype, which ma

224 Triple-negative breast cancer (TNBC) remains an aggressi

225 Triple-negative breast cancer (TNBC) represents a highly

226 Triple-negative breast cancer (TNBC) represents a subtyp

227 71 estrogen receptor-positive (ER(+)) and 25 triple-negative breast cancer (TNBC) samples.

228 st cancer patients, those diagnosed with the triple-negative breast cancer (TNBC) subtype have the wo

229 lead 4ab showed an in vivo efficacy in mouse triple-negative breast cancer (TNBC) syngeneic models wi

230 y, who are more likely to have basal-like or triple-negative breast cancer (TNBC) than are women of E

231 nd BRCA2, in a large cohort of patients with triple-negative breast cancer (TNBC) unselected for fami

232 ted in cancer progression, but their role in triple-negative breast cancer (TNBC), a subtype of letha

233 se 2 (SHP2), on cell migration in metastatic triple-negative breast cancer (TNBC), an aggressive dise

234 r all patients, 17.9 weeks for patients with triple-negative breast cancer (TNBC), and 18.0 weeks for

235 of 28) versus 0% (0 of 11) in patients with triple-negative breast cancer (TNBC), and 40% (four of 1

236 factor MYC is disproportionately elevated in triple-negative breast cancer (TNBC), as compared to est

237 ently been reported to be a driving force in triple-negative breast cancer (TNBC), contributing to th

238 ter understating of the genetic landmarks in triple-negative breast cancer (TNBC), functional validat

239 Triple-negative breast cancer (TNBC), in which cells lac

240 Although IMP3 is expressed preferentially in triple-negative breast cancer (TNBC), its function is po

241 In estrogen receptor-negative (ER(-)) and triple-negative breast cancer (TNBC), nitric oxide synth

242 In triple-negative breast cancer (TNBC), PDGFRbeta has been

243 Triple-negative breast cancer (TNBC), the deadliest form

244 Indeed, in triple-negative breast cancer (TNBC), there is recurrent

245 rticoid receptor (GR) is highly expressed in triple-negative breast cancer (TNBC), we investigated cr

246 in a subset of breast cancers, in particular triple-negative breast cancer (TNBC), where it acts to d

247 transmembrane mucin MUC1 are upregulated in triple-negative breast cancer (TNBC), where they contrib

248 Triple-negative breast cancer (TNBC)--a form of breast c

249 s, and JNK is highly activated in basal-like triple-negative breast cancer (TNBC).

250 improves survival outcomes of patients with triple-negative breast cancer (TNBC).

251 idence support the study of immunotherapy in triple-negative breast cancer (TNBC).

252 Tie2 pathway, in a mouse model of resectable triple-negative breast cancer (TNBC).

253 n women to be obese and to be diagnosed with triple-negative breast cancer (TNBC).

254 the target genes conveying BETi activity in triple-negative breast cancer (TNBC).

255 tes the growth of certain cancers, including triple-negative breast cancer (TNBC).

256 Aurora A signaling is highly correlated with triple-negative breast cancer (TNBC).

257 , and locoregional management of, women with triple-negative breast cancer (TNBC).

258 ohorts, MEL-18 was markedly downregulated in triple-negative breast cancer (TNBC).

259 nase protein kinase D3 (PKD3) is elevated in triple-negative breast cancer (TNBC).

260 (DFS) and overall survival (OS) in operable triple-negative breast cancer (TNBC).

261 olved in oncogenesis and is overexpressed in triple-negative breast cancer (TNBC).

262 athway, is highly up-regulated in basal-like triple-negative breast cancer (TNBC).

263 mplete response (pCR) rates in patients with triple-negative breast cancer (TNBC).

264 th particular enrichment among patients with triple-negative breast cancer (TNBC; OR = 3.56, 95% CI =

265 y and is associated with BRCA1-deficient and triple-negative breast cancers (TNBC) and with resistanc

266 Basal-type triple-negative breast cancers (TNBC) are aggressive and

267 Patients with triple-negative breast cancers (TNBC) are at high risk f

268 Triple-negative breast cancers (TNBC) are highly aggress

269 Here we show how the efficacy of PARPi in triple-negative breast cancers (TNBC) can be expanded by

270 Triple-negative breast cancers (TNBC) exhibit higher rat

271 y clinical trials indicate that up to 50% of triple-negative breast cancers (TNBC) express androgen r

272 Approximately 30% of triple-negative breast cancers (TNBC) harbor molecular a

273 Triple-negative breast cancers (TNBC) remain clinically

274 In triple-negative breast cancers (TNBC), elevated levels o

275 dapted by many aggressive cancers, including triple-negative breast cancers (TNBC), to utilize glutam

276 ssion is associated with a poor prognosis in triple-negative breast cancers (TNBC).

277 We show that, in triple-negative-breast cancer (TNBC) cells enriched with

278 receptor, progesterone receptor, and ERBB2 (triple-negative breast cancer [TNBC]).

279 Triple negative breast cancers (TNBCs) have a high morta

280 Triple-negative breast cancers (TNBCs) are a heterogeneo

281 Basal-like/triple-negative breast cancers (TNBCs) are among the mos

282 Triple-negative breast cancers (TNBCs) are more common a

283 Why some triple-negative breast cancers (TNBCs) have high and oth

284 Triple-negative breast cancers (TNBCs) have poor prognos

285 Purpose Trop-2, expressed in most triple-negative breast cancers (TNBCs), may be a potenti

286 y resistance and high therapeutic failure of triple-negative breast cancers (TNBCs).

287 ssue, and plays critical roles in aggressive Triple-Negative breast cancers (TNBCs).

288 to subtype, longer TTC caused patients with triple-negative breast cancer to have worse overall surv

289 e implications for improving the response of triple-negative breast cancers to cytotoxic chemotherapy

290 metastatic cell line MDA-MB-231 and primary triple-negative breast cancer tumor cells, the repressor

291 ve cPKC were observed in the more aggressive triple negative breast cancer tumors as compared to the

292 -negative breast cancer and one patient with triple negative breast cancer underwent rapid autopsy as

293 With regard to triple-negative breast cancer, veliparib-carboplatin had

294 Triple-negative breast cancer was associated with younge

295 FAK complex, tumorigenesis and metastasis in triple-negative breast cancer were markedly reduced.

296 with normal tissue, including in aggressive triple-negative breast cancers where BMX overexpression

297 th factor 2-neu (HER2) resistance, targeting triple-negative breast cancers (which do not express the

298 ight be a potential therapeutic strategy for triple-negative breast cancers, which currently lack an

299 trates that PRL can influence this subset of triple-negative breast cancers, which may have been obsc

300 tivity in the MV4;11 leukemia and MDA-MB-231 triple-negative breast cancer xenograft models in mice.