ライフサイエンスコーパス: TNBC

1 TNBC cells (MDA-MB-157, MDA-MB-231, and Hs578T) were tre

2 TNBC does not express estrogen receptor-alpha, progester

3 TNBC tumors that fail to respond to chemotherapy are cha

4 ype (p < 0.01) and drug resistant (p < 0.05) TNBC cells.

5 This study of 193 TNBC samples with patient survival information found an

6 and inhibited the tumor growth of MDA-MB-231 TNBC cell xenografts in the mammary fat pads of female n

7 ons revealed that the survival of MDA-MB-231 TNBC cells relied heavily on the BCL-2/BCL-XL signaling

8 gene silencing efficiency in GFP-MDA-MB-468 TNBC cells without any significant cytotoxicity.

9 These compounds were discovered from a TNBC phenotypic screen and possess a unique dual inhibit

10 In a TNBC xenograft mouse model, JNK-IN-8 significantly suppr

11 Design and optimization, driven with a TNBC tumor cell assay, identified potent and selective c

12 kdown more severely impaired migration in AA TNBC cells than White TNBC cells.

13 o the necessity of KIFC1 for migration in AA TNBC cells.

14 ndependent biomarker of poor prognosis in AA TNBC patients, potentially due to the necessity of KIFC1

15 pectively) in multivariable Cox models in AA TNBCs but not White TNBCs.

16 antly with Ki67 in White TNBCs but not in AA TNBCs, suggesting that nKIFC1 is not merely a surrogate

17 t merely a surrogate for proliferation in AA TNBCs.

18 CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell meta

19 sting oncogenic pathways in cystine-addicted TNBC with prominent mesenchymal features.

20 3-d]pyrimidines with potent activity against TNBC tumor cell lines.

21 could be used as targeted treatment against TNBC has been put forth based on estimates that 30-60% o

22 into IND-enabling studies as a single agent TNBC therapy.

23 ronment, tissue inflammation, and aggressive TNBC biology.

24 y to treat drug-resistant, highly aggressive TNBC tumors.

25 fferentially wired between normal breast and TNBC in tandem with isomiR or tRF dysregulation.

26 r better survival of patients with ER(-) and TNBC disease.

27 gated the potential link between obesity and TNBC in African American women.

28 the metabolic signature of HBOC syndrome and TNBC patients and to evaluate the potential contribution

29 ation among obesity, metabolic syndrome, and TNBC in African American women and mechanistic studies t

30 reatments for triple-negative breast cancer (TNBC) are urgently needed.

31 verexpressing triple negative breast cancer (TNBC) cell line.

32 hion in human triple-negative breast cancer (TNBC) cell lines.

33 show that, in triple-negative-breast cancer (TNBC) cells enriched with TICs, CCN5 significantly block

34 migration of triple-negative breast cancer (TNBC) cells is dependent on nuclear export of the orphan

35 enchymal-like triple-negative breast cancer (TNBC) cells that differ from one another in their relati

36 enhancers of triple negative breast cancer (TNBC) cells, (2) acts as a key regulator of the prolifer

37 nases against triple negative breast cancer (TNBC) cells.

38 Triple-negative breast cancer (TNBC) classified by transcriptional profiling as the mes

39 Triple-negative breast cancer (TNBC) comprises approximately 20% of all breast cancers

40 Triple-negative breast cancer (TNBC) has high rates of local recurrence and distant met

41 Triple-negative breast cancer (TNBC) is a breast cancer subtype characterized by marked

42 Triple-negative breast cancer (TNBC) is a highly aggressive, heterogeneous disease with

43 Triple-negative breast cancer (TNBC) is a molecularly heterogeneous cancer that is diff

44 Triple-negative breast cancer (TNBC) is a subtype of breast cancer in which the estroge

45 Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous carcinoma in wh

46 Triple-negative breast cancer (TNBC) is an aggressive disease lacking targeted therapy.

47 Triple-negative breast cancer (TNBC) is notoriously aggressive with high metastatic pot

48 he process of triple-negative breast cancer (TNBC) metastasis has not been addressed.

49 e tracing and triple negative breast cancer (TNBC) patient derived xenografts we demonstrate that the

50 Triple-negative breast cancer (TNBC) patients commonly exhibit poor prognosis and high

51 ally distinct triple-negative breast cancer (TNBC) patients is unknown.

52 Triple negative breast cancer (TNBC) remains a serious unmet medical need with discoura

53 Triple-negative breast cancer (TNBC) remains an aggressive disease without effective ta

54 raft model of triple negative breast cancer (TNBC) resulted in tumor growth inhibition.

55 osed with the triple-negative breast cancer (TNBC) subtype have the worst prog-nosis.

56 cacy in mouse triple-negative breast cancer (TNBC) syngeneic models with a TGI (tumor growth inhibiti

57 ving force in triple-negative breast cancer (TNBC), contributing to the maintenance of a chemoresista

58 landmarks in triple-negative breast cancer (TNBC), functional validation of candidate cancer genes (

59 e (ER(-)) and triple-negative breast cancer (TNBC), nitric oxide synthase-2 (NOS2) and cyclooxygenase

60 Triple-negative breast cancer (TNBC), the deadliest form of this disease, lacks a targe

61 rogression of triple negative breast cancer (TNBC), the most aggressive form of breast cancer, partly

62 pregulated in triple-negative breast cancer (TNBC), where they contribute to its aggressive pathogene

63 resistance of triple negative breast cancer (TNBC).

64 in basal-like triple-negative breast cancer (TNBC).

65 rexpressed in triple-negative breast cancer (TNBC).

66 in basal-like triple-negative breast cancer (TNBC).

67 es, including triple negative breast cancer (TNBC).

68 patients with triple-negative breast cancer (TNBC).

69 patients with triple-negative breast cancer (TNBC).

70 iagnosed with triple-negative breast cancer (TNBC).

71 rrelated with triple-negative breast cancer (TNBC).

72 r, and ERBB2 (triple-negative breast cancer [TNBC]).

73 Triple negative breast cancers (TNBC) are aggressive tumors, with high rates of metastat

74 Triple-negative breast cancers (TNBC) are highly aggressive, lack FDA-approved targeted

75 of PARPi in triple-negative breast cancers (TNBC) can be expanded by targeting MYC-induced oncogenic

76 up to 50% of triple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially

77 Triple-negative breast cancers (TNBC) remain clinically challenging with a lack of optio

78 herapies for triple negative breast cancers (TNBC) that lack expression of estrogen and progesterone

79 s, including triple-negative breast cancers (TNBC), to utilize glutamine for survival and growth.

80 Basal-like/triple-negative breast cancers (TNBCs) are among the most aggressive forms of breast can

81 Triple-negative breast cancers (TNBCs) are more common among African-ancestry population

82 Why some triple-negative breast cancers (TNBCs) have high and others have low immune cell infiltr

83 ssed in most triple-negative breast cancers (TNBCs), may be a potential target for antibody-drug conj

84 ach produces a simple ontology that captures TNBC heterogeneity and informs how tumor-associated prop

85 Surprisingly, clinical TNBCs retain the GDF11 locus and expression of the prote

86 Culturing TNBC cells in suspension increased the CSC-like populati

87 gene expression profiling of patient-derived TNBC tumors demonstrates that an IFN-beta metagene signa

88 invasive breast cancer, 16 (24.2%) developed TNBC compared with 7 (7.4%) of the 94 WA patients who de

89 10-year probability estimate for developing TNBC was 0.56% (95% CI, 0.32%-1.0%) for AA patients and

90 rformed miRNA-profiling studies in different TNBC subtypes to identify miRNAs that significantly cont

91 Pi yielded synthetic lethality in MYC-driven TNBC cells.

92 ce endothelial-mesenchymal transition (EMT), TNBC cells could produce plasminogen activator inhibitor

93 durable regressions (>1 year) of established TNBC tumors in vivo Overall, our results illustrate conv

94 cancer cells in cultures of EGFR-expressing TNBC-derived cells.

95 explanation as to why EGFR inhibitors failed TNBC patients and support how combining a select antioxi

96 Finally, TNBC lung metastases have lower LD abundance than their

97 -C as a novel immunotherapeutic approach for TNBC treatment.Significance: These findings show how upr

98 may provide a novel therapeutic approach for TNBC.

99 t be considered as BRCA1-like biomarkers for TNBC and HBOC syndrome.

100 ing NF-kappaB and MMP7 that is essential for TNBC cell invasiveness, thereby providing implications t

101 y persisted as a significant risk factor for TNBC.

102 esents an effective therapeutic strategy for TNBC treatment.

103 associated with inherent susceptibility for TNBC pathogenetic pathways.

104 e kinase as a clinically relevant target for TNBC.

105 entify EphA2 as a novel molecular target for TNBC.

106 naling is a potential therapeutic target for TNBC.

107 s toward developing an effective therapy for TNBC.

108 splatin and WEE1 inhibition is promising for TNBCs treatment, and for overcoming their cisplatin resi

109 reveals a cell-biological vulnerability for TNBCs lacking therapeutically actionable mutations.

110 ome of tumor-associated stroma isolated from TNBC (n = 57).

111 How TNBC's high invasiveness is driven by FOXC1 and its down

112 late expression of these genes in four human TNBC cell lines.

113 nd generated immunogenic cell death in human TNBC cell lines.

114 NF-kappaB transcriptional activity in human TNBC cells and suppressed downstream NF-kappaB target ge

115 In human TNBC cells, BETd-246 induced degradation of BET proteins

116 ing growth inhibition and apoptosis of human TNBC cells.

117 In mouse xenograft models of human TNBC, administration of C1572 suppressed tumor growth an

118 Conclusion:(89)Zr-transferrin targets human TNBC primary tumors significantly better than (18)F-FDG,

119 ing the EGFR and PYK2/FAK kinases to improve TNBC therapy.

120 hanism-based therapeutic strategy to improve TNBC treatment.

121 found that JNK regulated c-Jun activation in TNBC cells and that JNK activation correlated with c-Jun

122 tivation correlated with c-Jun activation in TNBC tumors.

123 High glutaminase (GLS) activity in TNBC tumors resulted in low cellular glutamine pool size

124 However, the function of AR in TNBC and the mechanisms by which AR-targeted therapy red

125 of this newly discovered regulatory axis in TNBC.

126 d extraterminal protein inhibitors (BETi) in TNBC revealed these drugs cause multinucleation, indicat

127 epithelial cells and tumorigenic capacity in TNBC is independent of expression of EMT-associated gene

128 ition (EMT) and induction of beta-catenin in TNBC cells, and these TGF-beta-induced responses and nuc

129 e subtypes of mesenchymal carcinoma cells in TNBC.

130 tter response to neoadjuvant chemotherapy in TNBC (P < 0.0001) but not in non-TNBC patients.

131 the response to neoadjuvant chemotherapy in TNBC, implying a potential role for 3q genes in the mech

132 ents or in 768 pairwise drug combinations in TNBC cell lines to identify synergistic combinations tra

133 ciated with the observed race disparities in TNBC.

134 This cohesiveness was widely disrupted in TNBC.

135 chanism of lipid metabolism dysregulation in TNBC through the prometastatic protein, CUB-domain conta

136 BETd-246 was more potent and effective in TNBC cells than its parental BET inhibitor compound BETi

137 how how MUC1 contributes to immune escape in TNBC, and they offer a rationale to target MUC1-C as a n

138 s sufficient to suppress PD-L1 expression in TNBC cells.

139 einase-7 (MMP7) were upregulated by FOXC1 in TNBC cells.

140 ion of several new tumor suppressor genes in TNBC demonstrate the utility of two-step forward genetic

141 expression and lower clonal heterogeneity in TNBC and HER2(+) cancers suggest an immune pruning effec

142 icroenvironmental (stromal) heterogeneity in TNBC has not been well characterized.

143 n level of c-Jun was significantly higher in TNBC tumors than in non-TNBC tumors, and high c-Jun mRNA

144 errogate MYC via TfR-targeted PET imaging in TNBC.

145 an unusual mechanism of its inactivation in TNBC.

146 AR levels increased in TNBC cells grown in forced suspension culture compared w

147 erall mutation, neoantigen, and CNV loads in TNBC and HER2(+) cancers.

148 and chemotherapy response and were lowest in TNBC patients with residual disease.

149 promotes CSC self-renewal and maintenance in TNBC.

150 driver gene FXR1 with distant metastasis in TNBC (P = 0.01) was further validated by immunohistochem

151 ed the effects of BET proteins on mitosis in TNBC.

152 TGF-beta-induced nuclear export of NR4A1 in TNBC cells plays an essential role in cell migration, SM

153 NF-kappaB signaling inhibition by NO2-OA in TNBC cells were multifaceted, as NO2-OA (a) inhibited th

154 ngly associated with lung metastasis only in TNBC (P < 0.0001, Hazard ratio (HR) 1.44, 95% confidence

155 Similar patterns were seen in OS.In TNBC (n = 174), 5-year BCSS was higher in patients with

156 en shown to be specifically overexpressed in TNBC and associated with poor clinical outcome.

157 d (3) is associated with a poor prognosis in TNBC breast cancer patients.

158 s a candidate biomarker of poor prognosis in TNBC, and they offer a preclinical proof of concept for

159 protein levels showing a marked reduction in TNBC.

160 asal-type breast cancer cells mostly seen in TNBC tumors.

161 n effects of C1572 and induced senescence in TNBC cells.

162 clear factor kappaB (NF-kappaB) signaling in TNBC.

163 ed CSC phenotype through Notch1 signaling in TNBC.

164 t, the T/B values increased significantly in TNBC, but did not change in MCF-7 tumors.

165 gnificantly increased glutamine pool size in TNBC tumors.

166 a driver and candidate therapeutic target in TNBC.

167 atopoietic system, its downstream targets in TNBC are still unclear.

168 ct with more alkylation-sensitive targets in TNBC cells to inhibit growth and viability.

169 To identify new intervention targets in TNBC, we used large-scale, loss-of-function screening to

170 ke cell (CSC) phenotype and tumorigenesis in TNBC are not well defined.

171 was discovered recently to be upregulated in TNBC.

172 enhance the efficacy of chemotherapy even in TNBCs with low AR expression by targeting a CSC-like cel

173 MUC1 expression in TNBCs also correlated inversely with CD8, CD69, and GZMB

174 ics and the extent of immune infiltration in TNBCs.

175 ngs indicate that repressed IFN signaling in TNBCs with CSC-like properties is due to high levels of

176 pressed tumor cell growth in vivo, including TNBC patient-derived xenografts.

177 Cs-when mixed with TNBC cells-could increase TNBC cell metastatic potency.

178 results suggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 and CCL5 signaling and il

179 bility in vitro, attenuated TNFalpha-induced TNBC cell migration and invasion, and inhibited the tumo

180 ealed that NO2-OA more selectively inhibited TNBC function.

181 PCSK5 reconstitution mobilizes the latent TNBC reservoir of GDF11 in vitro and suppresses triple-n

182 EGFR is highly expressed in basal-like TNBC and is considered as a potential therapeutic target

183 n of LPIN1 increases apoptosis in basal-like TNBC cell lines, whereas it has minimal or less effect o

184 lly inhibits the proliferation of basal-like TNBC cells in vitro and attenuates tumor growth in a mou

185 induction in basal and mesenchymal stem-like TNBC.

186 asal-like) and MDA-MB-231 (mesenchymal-like) TNBC cell lines in which NO induced COX2 and PGE2 induce

187 aplastic TNBC as a surrogate for mesenchymal TNBC, DAT and DAE had notable activity in mesenchymal TN

188 evaluate potential regimens for mesenchymal TNBC.

189 henotypes of tumors derived from mesenchymal TNBC cells.

190 While assays to identify mesenchymal TNBC are under development, metaplastic breast cancer se

191 PTK6 downregulation in mesenchymal TNBC cells suppressed migration and three-dimensional cu

192 and DAE had notable activity in mesenchymal TNBC.

193 TNBC, as well as nonmetaplastic, mesenchymal TNBC, especially when PI3K pathway aberrations are ident

194 Up to 30% of mesenchymal TNBC can be classified histologically as metaplastic bre

195 ATHER TNBC cohort (n = 109) and the METABRIC TNBC cohort (n = 203).

196 of TNBC patients (n = 383) and the METABRIC TNBC dataset (n = 217), we found CDK7 mRNA levels to be

197 izumab in patients with advanced metaplastic TNBC.

198 Center of patients with advanced metaplastic TNBC.

199 erformed to test DAT and DAE for metaplastic TNBC, as well as nonmetaplastic, mesenchymal TNBC, espec

200 Using metaplastic TNBC as a surrogate for mesenchymal TNBC, DAT and DAE ha

201 Fifty-two women with metaplastic TNBC (median age, 58 years; range, 37-79 years) were tre

202 xenograft tumors, as well as lung metastatic TNBC cell line-derived xenograft tumors, by both killing

203 patients with relapsed/refractory metastatic TNBC who received a 10 mg/kg starting dose on days 1 and

204 heavily pretreated patients with metastatic TNBC.

205 iferative and apoptotic activity in multiple TNBC backgrounds.

206 ng single agent in vivo efficacy in multiple TNBC xenograft models without significant body weight lo

207 I: 73.2-85.9) and lowest in triple-negative (TNBC) (74.8%; 95% CI: 66.6-81.2; P < 0.0001).

208 ER(+), 207 HER2(+), and 191 triple-negative (TNBC) cancers from The Cancer Genome Atlas.

209 ign breast disease (BBD) predicts future non-TNBC.

210 otherapy in TNBC (P < 0.0001) but not in non-TNBC patients.

211 nificantly higher in TNBC tumors than in non-TNBC tumors, and high c-Jun mRNA level was associated wi

212 acterize the extent to which TNBC versus non-TNBC stem cells may differ.

213 le-negative breast cancer, compared with non-TNBC, likely arises from different pathogenetic pathways

214 put forth based on estimates that 30-60% of TNBC express high levels of EGFR.

215 ) decreased the tumor-initiating capacity of TNBC cells and reduced tumor volume and viability when a

216 his study is the largest analysis to date of TNBC in the context of racial/ethnic identity and BBD as

217 mportant implications for the development of TNBC therapeutics to specifically block CDCP1-driven FAO

218 ontributors to the race-based disparities of TNBC.Significance: This big data-driven study comparing

219 ccompanied by markedly reduced expression of TNBC signature genes.

220 Herein, we review the genomic findings of TNBC and discuss current efforts in precision medicine a

221 tio) was linked to an increased incidence of TNBC in premenopausal and postmenopausal African America

222 essential for FOXC1-induced invasiveness of TNBC cells in vitro.

223 In an immunocompetent model of TNBC in which Eo771/MUC1-C cells were engrafted into MUC

224 fts and a patient-derived xenograft model of TNBC.

225 n and genetically engineered mouse models of TNBC reduced tumor growth in culture and in vivo.

226 vestigated in multiple preclinical models of TNBC.

227 aging were compared in preclinical models of TNBC.

228 reased ACSL activity in two animal models of TNBC.

229 1) doxorubicin uptake dynamics in a panel of TNBC cell lines, and (2) cell population response to dox

230 Gene expression profiling of TNBC has identified molecular subtypes and representativ

231 Nos significantly inhibited proliferation of TNBC wild type (p < 0.01) and drug resistant (p < 0.05)

232 brain but not bone metastasis regardless of TNBC status.

233 e transcriptomic data from a collated set of TNBC patients (n = 383) and the METABRIC TNBC dataset (n

234 sion and somatic mutation profile subsets of TNBC that reflect biological behavior more accurately an

235 e luminal androgen receptor (LAR) subtype of TNBC.

236 on assays revealed that ex vivo treatment of TNBC cells with C1572 reduced CSC levels by 28-fold.

237 oncept for several combination treatments of TNBC, which offer near-term prospects for clinical trans

238 ulator of the proliferation and viability of TNBC cells, but not Luminal A cells, and (3) is associat

239 mplified or overexpressed in the majority of TNBCs.

240 ese cancers may also represent the subset of TNBCs that could derive benefit from immune checkpoint i

241 s, which then acts in a paracrine fashion on TNBC cells to enhance their migration, invasion, and met

242 ptor negativity, presence of a basal-like or TNBC phenotype and reduced distant metastasis free survi

243 ation and metastasis of FOXC1-overexpressing TNBC cells were attenuated by knocking out WNT5A, but co

244 sential for the growth of MYC-overexpressing TNBC cells and may identify new therapeutic targets for

245 dard of (18)F-FDG PET for MYC-overexpressing TNBC.

246 cohorts with good prognosis and immune-poor TNBC cohorts with poor prognosis.

247 d neoantigen counts than did lymphocyte-poor TNBCs with poor prognosis.

248 r endothelial cells as well as TEM8-positive TNBC cells.

249 aling underlies the driving force to prevent TNBC growth and progression.

250 es TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback l

251 When compared with a previously published TNBC subtyping scheme, the STROMA4 method better capture

252 ciated with poor prognosis within the RATHER TNBC cohort (n = 109) and the METABRIC TNBC cohort (n =

253 JQ1 reduced TNBC growth in vitro and in vivo and inhibited xenograft

254 NO2-OA reduced TNBC cell growth and viability in vitro, attenuated TNFa

255 knockdown increases LD abundance and reduces TNBC 2D migration in vitro, which can be partially rescu

256 summarizes the existing literature regarding TNBCs and stem cells as they pertain to the burden of br

257 her, our data demonstrate that JNK regulates TNBC tumorigenesis by promoting CSC phenotype through No

258 c agent to eradicate CSCs for drug-resistant TNBC treatment.

259 ant role for the treatment of drug-resistant TNBC.

260 number alteration levels between immune-rich TNBC cohorts with good prognosis and immune-poor TNBC co

261 This study suggests that immune-rich TNBCs may be under an immune surveillance that continuou

262 Lymphocyte-rich TNBCs with good prognosis had significantly lower mutati

263 WEE1 inhibition sensitizes TNBCs and cisplatin resistant cancer cells to cisplatin-

264 In BRCA-mutant/sporadic TNBC patients, amplification of the MYC gene is correlat

265 factor activity in highly mesenchymal SUM159 TNBC cells can repress expression of the epithelial tran

266 loid-derived suppressor cells in a syngeneic TNBC mouse model.

267 rison showed that (89)Zr-transferrin targets TNBC tumors significantly better (P < 0.05-0.001) than (

268 ed xenograft tumors, by both killing TEM8(+) TNBC tumor cells and targeting the tumor endothelium to

269 vestigated whether BETi JQ1 could impair the TNBC response induced by hypoxia and exert anti-tumour e

270 The same phenotype was also observed in the TNBC cell line MDA-MB-157.

271 NuRD, and SIN3A from the cell lysate of the TNBC cell line SUM149.

272 e receptor, or the HER2 oncogene; therefore, TNBC lacks targets for molecularly-guided therapies.

273 idative phosphorylation, which contribute to TNBC migration and metastasis.

274 e JNK/c-Jun signaling pathway contributes to TNBC tumorigenesis.

275 orts in precision medicine as they relate to TNBC.

276 ltration and assign prognostic categories to TNBCs.

277 tic targeting of TEM8 as a strategy to treat TNBC.Significance: These findings offer a preclinical pr

278 lly effective against multiple RB1-wild-type TNBC models.

279 ch seeks to characterize the extent to which TNBC versus non-TNBC stem cells may differ.

280 y in 163 African American (AA) and 144 White TNBC tissue microarrays (TMAs) pooled from four hospital

281 paired migration in AA TNBC cells than White TNBC cells.

282 correlated significantly with Ki67 in White TNBCs but not in AA TNBCs, suggesting that nKIFC1 is not

283 ariable Cox models in AA TNBCs but not White TNBCs.

284 whether AA identity remains associated with TNBC for women with a prior diagnosis of BBD.

285 ZNF326 expression associated with TNBC patient survival, with ZNF326 protein levels showin

286 th inherently low GLS activity compared with TNBC, displayed a larger baseline glutamine pool size th

287 ere, we demonstrate that ECs-when mixed with TNBC cells-could increase TNBC cell metastatic potency.

288 ve than T+CEF in the subset of patients with TNBC (HR, 0.53; 95% CI, 0.31-0.92; P = .02; and HR, 0.55

289 this pathway are manifested in patients with TNBC and in The Cancer Genome Atlas database.

290 d cancer family history of 315 patients with TNBC enrolled between August 1, 2011, and December 31, 2

291 Patients with TNBC had favorable survival outcomes when treated with t

292 Patients with TNBC suffer a poor prognosis due in part to a lack of mo

293 Among patients with TNBC who received chemotherapy, elevated ITGB4 expressio

294 Of the 291 patients with TNBC, all were women; the mean (SD) age was 48 (11) year

295 us affects therapy response in patients with TNBC.

296 orter disease-free survival of patients with TNBC.

297 ve the prognosis for high-risk patients with TNBC.

298 are no targeted therapies for patients with TNBC.

299 and CCL5-targeting therapy for patients with TNBC.

300 Within TNBC, the wiring of the affected pathways with isomiRs a