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

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

2 nhibits growth and spontaneous metastasis of triple-negative breast cancer.

3 eatment of women aged 70 years or older with triple-negative breast cancer.

4 KRAS-driven non-small cell lung cancer, and triple-negative breast cancer.

5 y for the first-line treatment of metastatic triple-negative breast cancer.

6 al among patients with pretreated metastatic triple-negative breast cancer.

7 s and is associated with brain metastasis in triple-negative breast cancer.

8 m a patient-derived xenograft mouse model of triple-negative breast cancer.

9 tin chemotherapy in patients with metastatic triple-negative breast cancer.

10 ylase Sirtuin 1 (SIRT1) is down-regulated in triple-negative breast cancer.

11 previous anticancer therapies for metastatic triple-negative breast cancer.

12 patients with heavily pretreated metastatic triple-negative breast cancer.

13 t suppresses tumorigenesis and metastasis of triple-negative breast cancer.

14 erapeutic option for patients afflicted with triple-negative breast cancer.

15 checkpoint inhibitors using mouse models of triple-negative breast cancer.

16 a nucleoside analog used in chemotherapy for triple-negative breast cancer.

17 of chemotherapy in patients with metastatic triple-negative breast cancer.

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

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

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

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

22 as a key BRD4-S coregulator, particularly in triple-negative breast cancer.

23 unresectable, locally advanced or metastatic triple-negative breast cancer.

24 increased relapse and distant metastasis in triple-negative breast cancer.

25 out druggable mutations and in patients with triple-negative breast cancer.

26 rapy on overall survival in older women with triple-negative breast cancer.

27 anageable safety in patients with metastatic triple-negative breast cancer.

28 ated in brain metastases from ER-positive or triple-negative breast cancer.

29 expression in prostate cancer cell lines and triple negative breast cancers.

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

31 velop BCBM and enriched in HER2-enriched and triple-negative breast cancers.

32 recombination DNA repair, compared to early triple-negative breast cancers (7% versus 2%).

33 ard-approved prospective study, a woman with triple-negative breast cancer (age, 49 years) underwent

34 el the immunosuppressive microenvironment of triple negative breast cancer and facilitate the checkpo

35 matin looping genome-wide in Notch-dependent triple-negative breast cancer and B cell lymphoma, we sh

36 dataset analysis revealed that patients with triple-negative breast cancer and basal type harbored a

37 ith anti-PD-1 in a syngeneic mouse model for triple-negative breast cancer and highlights the clinica

38 expression was correlated with occurrence of triple-negative breast cancer and metastatic tumors.

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

40 renal cell carcinoma; one (<1%) patient had triple-negative breast cancer and one (<1%) had bladder

41 Methods: Triple-negative breast cancer and receptor-positive xeno

42 ical gene expression signature of basal-like triple-negative breast cancer and that combination treat

43 anced antitumor immunity in PD-L1-expressing triple-negative breast cancer and thus represent a novel

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

45 y documented, locally advanced or metastatic triple-negative breast cancer, and Eastern Cooperative O

46 of breast cancer, including human and mouse triple-negative breast cancer, and in melanoma.

47 h a PALB2 mutation, the BRCA1-deficient MX-1 triple-negative breast cancer, and the BRCA2-deficient D

48 expression signature that defines basal-like triple-negative breast cancer, and there are no targeted

49 , including lung squamous cell carcinoma and triple-negative breast cancers, and we find evidence for

50 Ovarian cancer and triple-negative breast cancer are among the most lethal

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

52 d age at least 18 years, centrally confirmed triple-negative breast cancer; at least one measurable l

53 s with PD-L1 immune cell-positive metastatic triple-negative breast cancer, atezolizumab plus nab-pac

54 ctive models performed better for women with triple negative breast cancer (AUC 0.74 to 0.80) than fo

55 alyzed data from 140 patients diagnosed with triple-negative breast cancer between January 2007 and D

56 the thermal characteristics of the subject's triple negative breast cancer by calibrating the model t

57 Treatment with 6 suppressed MDA-MB231 triple negative breast cancer cell growth and induced ap

58 f 340 nM measured against the drug-resistant triple negative breast cancer cell line MDA-MB-468, whil

59 pecifically, these bioactive factors induced triple-negative breast cancer cell (TNBC) death in vitro

60 unknown if different reovirus types lead to triple-negative breast cancer cell death.

61 f DNA-damaging agents enhances infection and triple-negative breast cancer cell killing by reovirus.

62 oblastoma (T98G) and a high ABCB1 expressing triple-negative breast cancer cell line (MDA-MB-231-luc)

63 G, and decreased the stem cell population in triple-negative breast cancer cell lines (TNBC).

64 from basal-like 2, but not mesenchymal-like, triple-negative breast cancer cell lines have increased

65 eting TMPRSS13 expression renders aggressive triple-negative breast cancer cell lines highly responsi

66 al violet assays indicated that 8a decreases triple-negative breast cancer cell viability, and immuno

67 Rs (67 nm x 33 nm, length x width) uptake in triple negative breast cancer cells (MDA-MB-231).

68 the detection and photomechanical killing of triple negative breast cancer cells that are resistant t

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

70 rus serotypes differentially infect and kill triple-negative breast cancer cells and if reovirus-indu

71 ifferent tyrosine kinase inhibitors of BT-20 triple-negative breast cancer cells and of treatment wit

72 ial to maintain the mesenchymal phenotype of triple-negative breast cancer cells and that CBFbeta-dep

73 The depletion of alpha-parvin from triple-negative breast cancer cells effectively inhibits

74 In MDA-MB-231-derived human triple-negative breast cancer cells implanted as orthoto

75 We found that GLI1 is activated in triple-negative breast cancer cells in response to ioniz

76 vatives exhibit an intriguing potency in the triple-negative breast cancer cells MDA-MB-231.

77 c inhibitor of CDK12/13, SR-4835, sensitizes triple-negative breast cancer cells to PARP inhibitors a

78 erative effects (IC(50)) of these samples on triple-negative breast cancer cells using the MTT assays

79 after treatment of MDA-MB-231 and MDA-MB-453 triple-negative breast cancer cells with a newly develop

80 employed 143B osteosarcoma cells and HCC1806 triple-negative breast cancer cells with or without ASCT

81 Treatment of triple-negative breast cancer cells with topoisomerase i

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

83 When applied to human triple-negative breast cancer cells, we observe proporti

84 ed a miR-21-associated invasive phenotype in triple-negative breast cancer cells.

85 nce reovirus infectivity and cytotoxicity of triple-negative breast cancer cells.

86 marrow, all derived from parental MDA-MB-231 triple-negative breast cancer cells.

87 hanced infective and cytotoxic properties in triple-negative breast cancer cells.

88 iruses that more efficiently infect and kill triple-negative breast cancer cells.

89 ating regulation of the estrogen receptor in triple-negative breast cancer cells.

90 hat the level of alpha-parvin is elevated in triple-negative breast cancer cells.

91 inhibitors more efficiently infect and kill triple-negative breast cancer cells.IMPORTANCE Patients

92 type III IFNs can activate STAT1 and STAT2, triple-negative breast cancer cellular proliferation is

93 hich showed that MLK4 is highly expressed in triple-negative breast cancer compared to other molecula

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

95 Triple-negative breast cancer constitutes a subset of br

96 mittee on Cancer (AJCC) Stage I-III invasive triple-negative breast cancer diagnosed from 2004 to 201

97 Fifteen patients had triple-negative breast cancer (estrogen receptor/progest

98 The 108 patients with triple-negative breast cancer had received a median of 3

99 ancer cells.IMPORTANCE Patients afflicted by triple-negative breast cancer have decreased survival an

100 and carboplatin in patients with metastatic triple-negative breast cancer; however, the regimen was

101 , 2004, and Dec, 31, 2014, 16 062 women with triple-negative breast cancer in the database met the in

102 cacy of antigen-specific CD8 T cells against triple-negative breast cancer in vivo.

103 We also define a subgroup of triple-negative breast cancers in which cancer rarely re

104 Median overall survival for metastatic triple-negative breast cancer is approximately 1 year vs

105 Triple-negative breast cancer is more likely to recur th

106 Triple-negative breast cancer is viewed clinically as an

107 cancer, including breast cancer (especially triple-negative breast cancer), leukemias, brain tumors,

108 ity in vitro in 2D monolayers of MDA-MB-231 (triple negative breast cancer), MCF7 (breast cancer) and

109 cancer 4T1, murine glioblastoma GL261, human triple negative breast cancer MDA-MB-231, human pancreat

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

111 The orthotopic 4T1 murine triple negative breast cancer model was studied.

112 ent tumor inhibition in a poorly immunogenic triple negative breast cancer model.

113 mAbs in a syngeneic orthotopic E0771 murine triple-negative breast cancer model, whereby tumor-beari

114 Here, using a syngeneic triple negative breast cancer murine model we investigat

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

116 We apply clonealign to triple-negative breast cancer patient-derived xenografts

117 currence free survival among ER-positive and triple negative breast cancer patients and was independe

118 vely correlated with that of TWIST1 in human triple-negative breast cancer patients.

119 tin therapy in a co-clinical trial involving triple-negative breast cancer PDXs.

120 ccessfully applied this system in a model of triple-negative breast cancer, providing the proof of co

121 Metastatic triple-negative breast cancers showed an increase in the

122 of ovarian (ST070), endometrial (ST040) and triple negative breast cancers (ST502, ST738), EC2629 sh

123 obtained tumour sample for determination of triple-negative breast cancer status and PD-L1 status by

124 Using a murine model of metastatic triple-negative breast cancer, systemic delivery of thes

125 s that PDLIM2 expression defines a subset of triple-negative breast cancer that may benefit from targ

126 or early stage bone and lung metastasis from triple-negative breast cancer that should be given prior

127 serves attention as a potential new drug for triple-negative breast cancer therapy.

128 he basis for improved therapy for basal-like triple-negative breast cancer through rational combinati

129 et consisting of 1315 hormone sensitive, 634 triple negative breast cancer (TNBC) and 1365 breast can

130 Analysis of Triple Negative Breast cancer (TNBC) and Triple Positive

131 However, treatment options for metastatic triple negative breast cancer (TNBC) are quite limited d

132 his workflow was applied to the study of two Triple Negative Breast Cancer (TNBC) cell lines and reve

133 contributes to the aggressive properties of triple negative breast cancer (TNBC) cell lines via upre

134 Like triple negative breast cancer (TNBC) cells, the lack of

135 Triple negative breast cancer (TNBC) does not respond to

136 Triple negative breast cancer (TNBC) encompasses molecul

137 This is particularly important for triple negative breast cancer (TNBC) for which chemother

138 Triple negative breast cancer (TNBC) has poor survival,

139 A third of patients with triple negative breast cancer (TNBC) have relapsed disea

140 Triple negative breast cancer (TNBC) is an aggressive br

141 Triple negative breast cancer (TNBC) is an aggressive di

142 iomarkers for the diagnosis and treatment of triple negative breast cancer (TNBC) is complicated by t

143 esponse to neoadjuvant chemotherapy (NAC) in triple negative breast cancer (TNBC) is highly prognosti

144 Due to the lack of the three main receptors, triple negative breast cancer (TNBC) is refractive to st

145 lved in the mechanism by which recurrence of Triple Negative Breast Cancer (TNBC) occurs.

146 enic molecule aflibercept, and the other for triple negative breast cancer (TNBC) patients treated wi

147 tin therapy in a co-clinical trial involving triple negative breast cancer (TNBC) PDX.

148 CT2 depletion in a syngeneic murine model of triple negative breast cancer (TNBC) prevented tumor gro

149 Triple negative breast cancer (TNBC) remains the most ag

150 Triple negative breast cancer (TNBC) represents 15-20% o

151 Triple negative breast cancer (TNBC) represents the most

152 Triple negative breast cancer (TNBC), an aggressive brea

153 Chemoresistance is a major obstacle in triple negative breast cancer (TNBC), the most aggressiv

154 antibody-drug conjugate (ADC) development in triple negative breast cancer (TNBC), which has limited

155 effective therapy is yet available to treat triple negative breast cancer (TNBC), which has poor pro

156 for the specific targeting and treatment of triple negative breast cancer (TNBC).

157 e most frequently mutated or deleted gene in triple negative breast cancer (TNBC).

158 filtrating lymphocytes (TILs) in early-stage triple negative breast cancer (TNBC).

159 tumor recurrence in human cancers including triple negative breast cancer (TNBC).

160 (ADSL) as an EglN2 hydroxylase substrate in triple negative breast cancer (TNBC).

161 as a promising strategy for the treatment of triple negative breast cancer (TNBC).

162 y was tested using the very aggressive human triple negative breast cancer (TNBC, MDA-MB-231 cells) g

163 s involved in tumor behavior and outcomes of triple negative breast cancers (TNBC).

164 Triple-negative breast cancer (TNBC) accounts for 10 to

165 Triple-negative breast cancer (TNBC) accounts for 15-20%

166 High recurrence and metastasis of triple-negative breast cancer (TNBC) after operation is

167 receptor (ER)+ and ER- breast cancer, and of triple-negative breast cancer (TNBC) among black women.

168 lymphoma 11A (BCL11A) is highly expressed in triple-negative breast cancer (TNBC) and drives metastat

169 Triple-negative breast cancer (TNBC) and HER2-positive b

170 ablish this tumor-intrinsic role of PD-L1 in triple-negative breast cancer (TNBC) and non-small cell

171 (BBDIs) are candidate therapeutic agents for triple-negative breast cancer (TNBC) and other cancer ty

172 f a variety of cancer cells, including human triple-negative breast cancer (TNBC) and patient-derived

173 majority of clinical deaths in patients with triple-negative breast cancer (TNBC) are due to chemores

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

175 receptor 3 (HER3) have been investigated as triple-negative breast cancer (TNBC) biomarkers.

176 a drug-treated, phenotypically heterogeneous triple-negative breast cancer (TNBC) cell line to elucid

177 We find a greater dependency on OGT among triple-negative breast cancer (TNBC) cell lines, which r

178 oncogenic MUC1-C protein is overexpressed in triple-negative breast cancer (TNBC) cells and contribut

179 mily is poorly expressed in mesenchymal-like triple-negative breast cancer (TNBC) cells and ectopic m

180 P-Responsive Gene) is greatly induced within triple-negative breast cancer (TNBC) cells subjected to

181 We report here that treating triple-negative breast cancer (TNBC) cells with the fatt

182 inhibitor of CDK12 and CDK13, which disables triple-negative breast cancer (TNBC) cells.

183 in ERCC1-defective NSCLC and BRCA1-defective triple-negative breast cancer (TNBC) cells.

184 EMI1 as a modulator of PARPi sensitivity in triple-negative breast cancer (TNBC) cells.

185 prediction by in vitro studies of aggressive triple-negative breast cancer (TNBC) cells.

186 o be inhibition of HS cleavage in MDA-MB-231 triple-negative breast cancer (TNBC) cells.

187 Triple-negative breast cancer (TNBC) commonly develops r

188 Triple-negative breast cancer (TNBC) comprises approxima

189 Triple-negative breast cancer (TNBC) constitutes 10 to 1

190 Here we show that triple-negative breast cancer (TNBC) exhibits a hyper-ac

191 cation of key molecular networks involved in triple-negative breast cancer (TNBC) growth and metastas

192 Triple-negative breast cancer (TNBC) has few therapeutic

193 unohistochemical surrogate subtypes of which triple-negative breast cancer (TNBC) has the highest ris

194 Of these subtypes, triple-negative breast cancer (TNBC) has the worst progn

195 Platinum compounds have activity in triple-negative breast cancer (TNBC) in germline BRCA mu

196 Triple-negative breast cancer (TNBC) in which the three

197 eferred neoadjuvant regimens for early-stage triple-negative breast cancer (TNBC) include anthracycli

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

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

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

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

202 Triple-negative breast cancer (TNBC) is among the most a

203 Triple-negative breast cancer (TNBC) is an aggressive br

204 Triple-negative breast cancer (TNBC) is an aggressive ca

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

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

207 Compared with other breast cancer subtypes, triple-negative breast cancer (TNBC) is associated with

208 Triple-negative breast cancer (TNBC) is characterized by

209 Triple-negative breast cancer (TNBC) is characterized by

210 Treatment of patients with triple-negative breast cancer (TNBC) is limited by a lac

211 eath protein 1 (PD-1) blockade in metastatic triple-negative breast cancer (TNBC) is low(1-5), highli

212 Triple-negative breast cancer (TNBC) is more aggressive

213 Triple-negative breast cancer (TNBC) is the deadliest fo

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

215 Lacking targetable molecular drivers, triple-negative breast cancer (TNBC) is the most clinica

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

217 In several triple-negative breast cancer (TNBC) models, Six2 enhanc

218 mechanisms driving metastatic progression in triple-negative breast cancer (TNBC) patients are poorly

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

220 Triple-negative breast cancer (TNBC) patients have the w

221 2 (PAR2) contributes significantly to human triple-negative breast cancer (TNBC) progression by rele

222 Tumor-associated macrophages (TAM) promote triple-negative breast cancer (TNBC) progression.

223 proximately 40% of patients with stage I-III triple-negative breast cancer (TNBC) recur after standar

224 the circadian transcription factor BMAL1 in triple-negative breast cancer (TNBC) specifically under

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

226 Triple-negative breast cancer (TNBC) subtype is among th

227 oint blockade in breast cancer with focus on triple-negative breast cancer (TNBC) subtype.

228 ssion of ZEB1 in basal-like tumor cells, two triple-negative breast cancer (TNBC) subtypes, to demons

229 In lymph node-positive, triple-negative breast cancer (TNBC) tissues, low miR-14

230 Using models of triple-negative breast cancer (TNBC) with different intr

231 cers with limited treatment options, such as triple-negative breast cancer (TNBC)(1,3).

232 progression, occurs in 65% of patients with triple-negative breast cancer (TNBC), a disease commonly

233 vitro and murine models of cancer, including triple-negative breast cancer (TNBC), a highly aggressiv

234 cinoma in situ lesions but were uncoupled in triple-negative breast cancer (TNBC), a subtype in which

235 on-small cell lung cancer (NSCLC) but not in triple-negative breast cancer (TNBC), although these can

236 in was present in 60% of tumors diagnosed as triple-negative breast cancer (TNBC), and only 20% of ot

237 proliferation of multiple cancers, including triple-negative breast cancer (TNBC), and these growth d

238 ally unmet need for effective treatments for triple-negative breast cancer (TNBC), as it remains the

239 ZNF165, a CT antigen frequently expressed in triple-negative breast cancer (TNBC), associates with SM

240 sing therapeutic agents for the treatment of triple-negative breast cancer (TNBC), but the rapid emer

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

242 macrophages that define 'immune subtypes' of triple-negative breast cancer (TNBC), including neutroph

243 ressive nature of several cancers, including triple-negative breast cancer (TNBC), independently of i

244 In triple-negative breast cancer (TNBC), miR-127 downregula

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

246 Highly heterogenous cancers, such as triple-negative breast cancer (TNBC), remain challenging

247 Triple-negative breast cancer (TNBC), representing ~15%

248 Triple-negative breast cancer (TNBC), the most aggressiv

249 ause HEXIM1 is often down-regulated in human triple-negative breast cancer (TNBC), these cells are pa

250 To define transcriptional dependencies of triple-negative breast cancer (TNBC), we identified tran

251 Triple-negative breast cancer (TNBC), which has the high

252 Triple-negative breast cancer (TNBC), which lacks estrog

253 Taxanes are the mainstay of treatment in triple-negative breast cancer (TNBC), with de novo and a

254 Studies of triple-negative breast cancer (TNBC)-a highly aggressive

255 eting nanoparticle (CDN) and test it against triple-negative breast cancer (TNBC).

256 functions in breast cancer, with a focus on triple-negative breast cancer (TNBC).

257 formation and metastasis of human basal-like triple-negative breast cancer (TNBC).

258 is a promising strategy for the treatment of triple-negative breast cancer (TNBC).

259 originate from epithelial tissues, including triple-negative breast cancer (TNBC).

260 anscriptomic data of a cohort of 465 primary triple-negative breast cancer (TNBC).

261 tin ligase, ITCH, modulates DDR machinery in triple-negative breast cancer (TNBC).

262 and BMI1 in the epigenetic reprogramming of triple-negative breast cancer (TNBC).

263 gnosis in various types of cancer, including triple-negative breast cancer (TNBC).

264 ey for optimal cancer therapy, especially in triple-negative breast cancer (TNBC).

265 oxygen tension and deacetylase inhibition in triple-negative breast cancer (TNBC).

266 tumors, which phenotypically resemble human triple-negative breast cancer (TNBC).

267 makes it a potential drug candidate against triple-negative breast cancer (TNBC).

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

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

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

271 Targeted therapeutics are needed for triple-negative breast cancer (TNBC).

272 , which is associated with poor prognosis in triple-negative breast cancer (TNBC).

273 ry engraftment and lung metastatic growth in triple-negative breast cancer (TNBC).

274 ciation between pCR and survival outcomes in triple-negative breast cancer (TNBC).

275 ted with increased incidence and severity of triple-negative breast cancer (TNBC); however, mechanism

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

277 Over 80% of triple-negative breast cancers (TNBC) express mutant p53

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

279 ), progesterone receptor, and HER2 (known as triple-negative breast cancer; TNBC).

280 rt a genomic and transcriptional analysis of triple negative breast cancers (TNBCs) from an East Asia

281 Poorly immunogenic tumors, including triple negative breast cancers (TNBCs), remain resistant

282 lent in many malignancies such as aggressive triple-negative breast cancers (TNBCs) and it is associa

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

284 cy of BRCA1 promoter hypermethylation in 237 triple-negative breast cancers (TNBCs) from a population

285 Operable triple-negative breast cancers (TNBCs) have a higher ris

286 Triple-negative breast cancers (TNBCs) lack progesterone

287 Stromal heterogeneity in human triple-negative breast cancers (TNBCs) remains poorly un

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

289 Here we utilize xenograft mouse models of triple-negative breast cancer to explore the importance

290 alized NCEH1 activity at the leading edge of triple-negative breast cancer tumors, suggesting roles f

291 d locally recurrent inoperable or metastatic triple-negative breast cancer using a block method (bloc

292 agnostic samples of tumour tissue confirming triple-negative breast cancer was a prerequisite for enr

293 en receptor-positive breast cancer and basal triple-negative breast cancer, which is associated with

294 y-confirmed, locally recurrent or metastatic triple-negative breast cancer who had no more than two p

295 -chemotherapy among patients with metastatic triple-negative breast cancer with CPS of 10 or more.

296 iptional activity in the GR positive HCC1806 triple negative breast cancer xenograft model.

297 cell lung, as well as MDA-MB-436 and SUM149 triple negative breast cancer xenograft models.

298 biting OTULIN or Wnt/beta-catenin sensitizes triple-negative breast cancer xenograft tumors to chemot

299 so inhibited the growth of hematological and triple negative breast cancer xenografts at well-tolerat

300 ion is specific to tumor-initiating cells in triple-negative breast cancer xenografts that rely on LE