ライフサイエンスコーパス: TNBC

1 TNBC has a high frequency of tumor protein p53 (Tp53/p53

2 TNBC is an aggressive cancer phenotype, with low 5-year

3 TNBC lacks effective treatments.

4 TNBC lacks expression of the targetable receptors found

5 TNBC reliance on IRE1alpha is an important vulnerability

6 TNBCs with high HER3-EGFR scores exhibited significantly

7 cg06588802 in LINC00299 was measured in 154 TNBC cases and 159 breast cancer-free matched controls u

8 Using MDA-MB-468 and SUM-159PT TNBC cells, along with LC-MS/MS and HPLC metabolomics pr

9 we analyzed tumor and serial bloods from 26 TNBC patients collected prior, during, and after NAC.

10 In a multi-institutional cohort of 510 TNBC patients, we analyzed the impact of HER3, EGFR, or

11 A subset of 60 TNBC samples were RNA-sequenced using massive parallel s

12 es (MLNPs), designed to address the aberrant TNBC biology through the placement of redox responsive c

13 MLNPs exhibited higher cytotoxicity against TNBC and breast cancer cells which present high intracel

14 nd tested their therapeutic efficacy against TNBC metastasis.

15 polymerase (PARP) inhibitor olaparib against TNBC cells.

16 TRIM37 drives aggressive TNBC biology by promoting resistance to chemotherapy and

17 ription and splicing and promotes aggressive TNBC phenotypes.

18 ies, no such targeted therapy exists for all TNBC patients.

19 Amid TNBC subtypes, BCL2L14-ETV6 is most frequently detected

20 us therapeutic advantages in treating BC and TNBC.

21 astatic estrogen receptor-positive (ER+) and TNBC clinical tissue specimens compared to healthy breas

22 associated with lower risk of ER+, ER-, and TNBC (e.g., highest compared with lowest quartile: TNBC

23 ssociated with reduced risk of ER+, ER-, and TNBC among black women.

24 tone acetylation, HIF-1alpha expression, and TNBC tumor growth were all reduced in vivo.

25 r association between methylation levels and TNBC overall (P = 0.062).

26 Comparing MBC and TNBC protein profiles we show MBC-specific increases rel

27 wal of cancer stem cells (CSCs) in vitro and TNBC tumor formation in vivo.

28 , and remodels the cellular TME, attenuating TNBC growth in mice.

29 h excellent responses in the treatment of BC/TNBC along with breast cancer stem cells have been discu

30 noparticle, exosomes for the treatment of BC/TNBC and other molecular targets available such as poly

31 Shannon index was significantly lower in BNH TNBC tumor tissue as compared to matched NAT zone.

32 are key inducers of the neural genes in both TNBC and NTNBC, but the inducer-responder relationships

33 -A expression, and tumor vasculature of both TNBC and HER2-positive trastuzumab-refractory breast can

34 Pi) have efficacy in triple negative breast (TNBC) and ovarian cancers (OCs) harboring BRCA mutations

35 Triple-negative breast cancer (TNBC) accounts for 10 to 20% of breast cancer, with chem

36 Triple-negative breast cancer (TNBC) accounts for 15-20% of breast cancer cases in the

37 metastasis of triple-negative breast cancer (TNBC) after operation is a leading cause of breast cance

38 ancer, and of triple-negative breast cancer (TNBC) among black women.

39 ensitive, 634 triple negative breast cancer (TNBC) and 1365 breast cancer patients with information o

40 expressed in triple-negative breast cancer (TNBC) and drives metastatic disease.

41 Triple-negative breast cancer (TNBC) and HER2-positive breast cancer are particularly a

42 ic agents for triple-negative breast cancer (TNBC) and other cancer types, but inherent and acquired

43 cluding human triple-negative breast cancer (TNBC) and patient-derived TNBC cells in vitro, and atten

44 Analysis of Triple Negative Breast cancer (TNBC) and Triple Positive Breast Cancer (TPBC) tissues f

45 patients with triple-negative breast cancer (TNBC) are due to chemoresistance and aggressive metastas

46 vestigated as triple-negative breast cancer (TNBC) biomarkers.

47 in MDA-MB-231 triple-negative breast cancer (TNBC) cells.

48 Triple-negative breast cancer (TNBC) constitutes 10 to 15% of all breast cancer and is

49 Triple negative breast cancer (TNBC) does not respond to checkpoint blockade immunother

50 Triple negative breast cancer (TNBC) encompasses molecularly different subgroups, with

51 e activity in triple-negative breast cancer (TNBC) in germline BRCA mutation carriers (BRCA carriers)

52 Triple-negative breast cancer (TNBC) in which the three major receptors i.e. estrogen r

53 Triple-negative breast cancer (TNBC) is a subtype of breast cancer unresponsive to trad

54 Triple-negative breast cancer (TNBC) is among the most aggressive forms of breast cance

55 Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype associated

56 Triple negative breast cancer (TNBC) is an aggressive breast cancer subtype.

57 Triple-negative breast cancer (TNBC) is an aggressive cancer subtype for which effectiv

58 Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer characteriz

59 cer subtypes, triple-negative breast cancer (TNBC) is associated with relatively poor outcomes due to

60 Triple-negative breast cancer (TNBC) is characterized by its aggressive biology, early

61 rapy (NAC) in triple negative breast cancer (TNBC) is highly prognostic and determines whether adjuva

62 patients with triple-negative breast cancer (TNBC) is limited by a lack of effective molecular therap

63 rine model of triple negative breast cancer (TNBC) prevented tumor growth.

64 (TAM) promote triple-negative breast cancer (TNBC) progression.

65 Triple negative breast cancer (TNBC) represents 15-20% of the over one million new brea

66 ctor BMAL1 in triple-negative breast cancer (TNBC) specifically under conditions of hyperinsulinemia.

67 or cells, two triple-negative breast cancer (TNBC) subtypes, to demonstrate that ZEB1 represses POLQ

68 ode-positive, triple-negative breast cancer (TNBC) tissues, low miR-149 expression correlated with ma

69 ing models of triple-negative breast cancer (TNBC) with different intratumoral immune contexture, we

70 uncoupled in triple-negative breast cancer (TNBC), a subtype in which p53 is usually mutated.

71 Triple negative breast cancer (TNBC), an aggressive breast cancer subtype lacking estro

72 reatments for triple-negative breast cancer (TNBC), as it remains the most aggressive subtype of brea

73 expressed in triple-negative breast cancer (TNBC), associates with SMAD3 to modulate transcription o

74 treatment of triple-negative breast cancer (TNBC), but the rapid emergence of resistance necessitate

75 In triple-negative breast cancer (TNBC), miR-127 downregulation correlates with decreased

76 cers, such as triple-negative breast cancer (TNBC), remain challenging immunotherapeutic targets.

77 Triple-negative breast cancer (TNBC), representing ~15% of globally diagnosed breast ca

78 r obstacle in triple negative breast cancer (TNBC), the most aggressive breast cancer subtype.

79 able to treat triple negative breast cancer (TNBC), which has poor prognosis due to frequent metastas

80 Studies of triple-negative breast cancer (TNBC)-a highly aggressive malignancy with a dismal postt

81 re needed for triple-negative breast cancer (TNBC).

82 prognosis in triple-negative breast cancer (TNBC).

83 l outcomes in triple-negative breast cancer (TNBC).

84 tic growth in triple-negative breast cancer (TNBC).

85 st it against triple-negative breast cancer (TNBC).

86 treatment of triple negative breast cancer (TNBC).

87 th a focus on triple-negative breast cancer (TNBC).

88 ressive human triple negative breast cancer (TNBC, MDA-MB-231 cells) growing in the brains of athymic

89 Over 80% of triple-negative breast cancers (TNBC) express mutant p53 (mtp53) and some contain oncoge

90 outcomes of triple negative breast cancers (TNBC).

91 ation in 237 triple-negative breast cancers (TNBCs) from a population-based study using reported whol

92 Operable triple-negative breast cancers (TNBCs) have a higher risk of relapse than non-TNBCs with

93 ity in human triple-negative breast cancers (TNBCs) remains poorly understood, limiting the developme

94 s, including triple negative breast cancers (TNBCs), remain resistant to current immunotherapies, due

95 ast cancer progression in secretome-cultured TNBC cells.

96 TAT5B), and STAT6 in p53- and PTEN-deficient TNBC cells.

97 ell proliferation of p53- and PTEN-deficient TNBC in vitro and inhibited tumor growth in vivo, but ha

98 ive breast cancer (TNBC) and patient-derived TNBC cells in vitro, and attenuates chemotherapy-induced

99 rsus stromal compartments of patient-derived TNBCs (N = 10) using a panel of 39 markers.

100 inhibition in a panel of genetically diverse TNBC cells.

101 eated stage II-III histologically documented TNBC were randomly assigned (1:1) to receive chemotherap

102 has prognostic and predictive value in early TNBC patients.

103 standard chemotherapy in patients with early TNBC.

104 bispecific antibodies for TNBC and emerging TNBC targets for future bispecific antibody development.

105 levant, inflammatory amplifier that enhances TNBC engraftment and dissemination in association with n

106 hibited the proliferation of LIPG-expressing TNBC cells but not LIPG-negative luminal breast cancer c

107 56 formalin-fixed, paraffin-embedded (FFPE) TNBCs.

108 Single-cell RNA sequencing of five TNBCs revealed two cancer-associated fibroblast (CAF) an

109 ew discusses novel bispecific antibodies for TNBC and emerging TNBC targets for future bispecific ant

110 ion may serve as a circulating biomarker for TNBC.

111 romising targeted therapeutic candidates for TNBC through in vitro screening of 1,363 drugs in patien

112 as part of the current standard of care for TNBC.

113 echanism to T cell-mediated cytotoxicity for TNBC cells.

114 To address the unmet need for TNBC treatment, we recently determined that tissue facto

115 efore provides therapeutic opportunities for TNBC and other highly aggressive human cancers of epithe

116 argeted therapeutics to improve outcomes for TNBC patients.

117 targeting the SFK/CDCP1/PKCdelta pathway for TNBC treatment.

118 geted radionuclide therapy has potential for TNBC and merits further exploration in a clinical settin

119 transcriptional activity and is required for TNBC tumor growth in vivo using an orthotopic xenograft

120 liposomal spherical nucleic acids (SNAs) for TNBC therapy.

121 d effective novel therapeutic strategies for TNBC.

122 es, with effects that appeared strongest for TNBC (OR: 0.58; 95% CI: 0.35, 0.94); no association was

123 lish ADAR1 as a novel therapeutic target for TNBC tumors.

124 potential to open a new area of therapy for TNBC.

125 t cancer; logistic regressions were used for TNBC.

126 addition, in SFK_pY416(-) samples, FOXA1(+) TNBC tended to be SFK_pY527(+) (classic inactive SFK), a

127 Y527(+) (classic inactive SFK), and FOXA1(-) TNBC tended to be SFK_pY527(-) (SFK poised for activatio

128 uently in forkhead box protein A1 (FOXA1)(-) TNBCs.

129 juvants and encapsulate lysates derived from TNBC cell lines as antigens.

130 9 (LINC00299) gene in blood-derived DNA from TNBC patients compared with healthy controls implying th

131 hile both subtypes involve neural functions, TNBC has substantially more up-regulated neural genes th

132 -or node negative with tumor 1 cm or greater-TNBC, with prior anthracycline- and/or taxane-containing

133 Seventy percent had TNBC.

134 protein levels were higher in HER3-EGFR-high TNBCs based on immunohistochemistry (p = 0.036).

135 In vivo, tumour growth of implanted human TNBC cells and the number of circulating 4T1 mouse tumou

136 thereby promote growth and survival of human TNBC cells.

137 26 did not have an autocrine effect on human TNBC cells, but rather its effect on engraftment and gro

138 This paradigm will be tested in a phase I/II TNBC clinical trial.

139 ment of improved viral oncolytics.IMPORTANCE TNBC is unresponsive to hormone therapies, leaving patie

140 In TNBC cells, knockdown of ADAR1 attenuates proliferation

141 rocessed to mature, functional miR-127-3p in TNBC tumor cells.

142 way is often found to be highly activated in TNBC, however the precise functions of the ERK isoforms

143 h a highly abnormal loss of redox control in TNBC cells.

144 ms by which r2Reovirus induces cell death in TNBC cells.

145 mechanism of reovirus-induced cell death in TNBC.

146 ed that combined p53- and PTEN-deficiency in TNBC activates expression of the transcription factor me

147 se, BCL2L14-ETV6 was exclusively detected in TNBC, and interrogation of four independent patient coho

148 ng approach to prevent metastatic disease in TNBC exploits lipid anabolism as a metabolic vulnerabili

149 ns by showing that miR-149 downregulation in TNBC enhances reciprocal growth factor signaling between

150 response to enhance therapeutic efficacy in TNBC.

151 our suppressive transcription factor Elf5 in TNBC cells activates intrinsic interferon-gamma (IFN-gam

152 s unknown whether IRE1alpha adapts the ER in TNBC cells and modulates their TME, and whether IRE1alph

153 nsitivity to the EGFR inhibitor erlotinib in TNBC cells by promoting the synthesis of the antiapoptot

154 rectly targeting CSF1, miR-149 expression in TNBC cell lines (MDA-MB-231 and BT-549) inhibited the re

155 o elucidate the role of MEGF11 expression in TNBC cells, both in vitro and in vivo, and in human tiss

156 found that YM155 reduces EGFR expression in TNBC cells, shedding light on its potential mechanism of

157 ibited starvation-induced autophagic flux in TNBC cells that were dependent on autophagy for survival

158 LQ by ZEB1 fostered micronuclei formation in TNBC tumor cell lines.

159 tential target to suppress PD-L1 function in TNBC.

160 re predicted to enhance adaptive immunity in TNBC while glia development, along with a few other neur

161 ion of combined BET and CDK4/6 inhibition in TNBC and suggest novel mechanisms of action for these dr

162 tudy and potentially future investigation in TNBC patients.

163 se models, silencing or inactivating IRIS in TNBC cells lowered the levels of circulating GM-CSF, sup

164 tor, synergize with the BET inhibitor JQ1 in TNBC lines.

165 IRE1alpha knockout in TNBC cells markedly reversed substantial ultrastructural

166 receptor 1 (IFNGR1) at the protein level in TNBC.

167 raw revealed increased methylation levels in TNBC cases compared with controls in the young age group

168 stem cell (CSC) phenotype and metastasis in TNBC.

169 We found that MEOX1 is expressed only in TNBC cells with frequent deficiencies in p53 and PTEN, a

170 promotes metastasis and the CSC phenotype in TNBC.

171 ee in all samples but only phosphorylated in TNBC tumor cells that expressed SFK_pY416.

172 h to glycolysis and reduce ATP production in TNBC cells.

173 a pro-tumorigenic gene expression program in TNBC.

174 hanced infective and cytotoxic properties in TNBC cells.

175 hanced oncolytic properties of r2Reovirus in TNBC to interactions between a type 3 M2 gene segment an

176 ds promise for potential clinical success in TNBC.

177 ions as a tumor and metastasis suppressor in TNBC and that delivery of miR-127 may hold promise as a

178 stasis and a potential therapeutic target in TNBC as well as other diseases reliant upon IL26-mediate

179 me axis is a potential therapeutic target in TNBC.

180 he clinical investigation of this therapy in TNBC.

181 correlated the extent of this uncoupling in TNBC cell lines with the importance of NRF2 in the 3D gr

182 y be a targetable metabolic vulnerability in TNBC.

183 highly expressed in breast cancer including TNBC.

184 ivation in multiple solid cancers, including TNBC.

185 and differentiated-PVL cells in independent TNBC patient cohorts revealed strong associations with c

186 assortant reovirus, r2Reovirus, that infects TNBC cells more efficiently and induces cell death with

187 treated mice with intracardially inoculated TNBC cells and found the combination to inhibit lung and

188 gression of pre-invasive TN-DCIS to invasive TNBC are needed.

189 IRISOE TNBC cells expressed low levels of calreticulin (the "ea

190 Accordingly, IRISOE TNBC tumors had significantly few CD8(+)/PD-1(+) cytotox

191 TGFbeta1 receptors on their surface, IRISOE TNBC cells channeled TGFbeta1/TbetaRI/II signaling towar

192 Coinjecting macrophages with IRISOE TNBC cells induced earlier metastasis in athymic mice ac

193 we report BRCA1-IRIS-overexpressing (IRISOE) TNBC cells secrete high levels of GM-CSF in a hypoxia-in

194 totoxic across multiple models of basal-like TNBC and reduces PDX mammary tumor growth in vivo.

195 Infection of different MSL lineage TNBC cells with r2Reovirus results in caspase 3-dependen

196 gated spheroid-forming cells in a metastatic TNBC model.

197 ic 4T07 (nonmetastatic) and 4T1 (metastatic) TNBC tumor grafts (n = 3-5).

198 s to identify PRK2 binding partners in mouse TNBC cells revealed proteins that are important for both

199 survival benefit in highly metastatic murine TNBC models poorly responsive to PD-1 blockade.

200 hanced ADR or cisplatin inhibition of murine TNBC tumors in vivo and reduced systemic levels of pro-i

201 lysis of transcriptomic data of TNBC and non-TNBC (NTNBC) tissue samples from the TCGA database, focu

202 NBCs) have a higher risk of relapse than non-TNBCs with standard therapy.

203 ressed higher levels of STING, and PTEN-null TNBC cell lines were hyperresponsive to STING agonists.

204 PTEN-null TNBC cells expressing a phosphomimetic version of Rab7-S

205 Consistent with this data, PTEN-null TNBC tumors expressed higher levels of STING, and PTEN-n

206 end point, decreased Ki67, occured in 12% of TNBC.

207 rts detected BCL2L14-ETV6 in 4.4 to 12.2% of TNBC tumors.

208 yses, HR deficiency was identified in 69% of TNBC with the mutational-signature-based HRDetect assay.

209 und that intratumoral regions and ALNs(-) of TNBC contained higher concentrations of markers related

210 TAK1 is implicated in aggressive behavior of TNBC, while means are not fully understood.

211 her investigation of the distinct biology of TNBC vs. NTNBC.

212 After central confirmation of TNBC status by immunohistochemistry, patients were rando

213 utational analysis of transcriptomic data of TNBC and non-TNBC (NTNBC) tissue samples from the TCGA d

214 Here, we uncovered a molecular dependence of TNBC tumors on the TRIM37 network, which enables tumor c

215 presented opportunity for the development of TNBC-targeting immunotherapies.

216 cs profiling, we found here that exposure of TNBC cells to the cytotoxic chemotherapy drugs cisplatin

217 synergistically inhibited in vitro growth of TNBC and HER2-positive trastuzumab-resistant BT474-TtzmR

218 a preclinical assessment of immunotherapy of TNBC using TF-CAR-NK cell as single agent therapy and in

219 nd enhance cell motility and invasiveness of TNBC and benign breast epithelial cells.

220 In three mouse models of TNBC, CDN administration inhibits tumor growth and subst

221 axane response in multiple in vivo models of TNBC, including a patient-derived xenograft, without ind

222 Py8119 orthotopic syngeneic mouse models of TNBC.

223 identified IL26 as a novel key modulator of TNBC metastasis and a potential therapeutic target in TN

224 (PD) decreased the viability and motility of TNBC cells, sensitized TNBC cells to chemotherapy, and r

225 equencing studies have revealed a paucity of TNBC-specific mutations.

226 fective strategy to improve the prognosis of TNBC.

227 More recently, in 2017, the proliferation of TNBC and other cancer cell lines was reported to be unaf

228 stantially reduced the in vivo propensity of TNBC cells.

229 The models span a range of TNBC subtypes and exhibit a diverse set of putative driv

230 pharmacologic resource that is reflective of TNBC.

231 intake was associated with decreased risk of TNBC, and increased sun exposure was associated with red

232 d protein levels in primary tumor samples of TNBC and NSCLC patients.

233 explanation for the increased sensitivity of TNBC to Hsp90 inhibition.

234 s DFMO-induced preferential sensitization of TNBC cells to chemotherapy, reported here suggest that O

235 the highest efficacy against 3D spheroids of TNBC, in addition the MLNPs also induced higher levels o

236 rs are shown to overexpressed on surfaces of TNBC.

237 150 isoform, is required for the survival of TNBC cell lines.

238 -NK immunotherapy for effective treatment of TNBC and may warrant further preclinical study and poten

239 for the localized and targeted treatment of TNBC did not caused any noticeable toxicity and thus sig

240 body-based therapeutics for the treatment of TNBC have gained recent attention in the scientific comm

241 were effective in vivo for the treatment of TNBC in cell line- and patient's tumor-derived xenograft

242 of cell/tissue viability in the treatment of TNBC.

243 s an important strategy for the treatment of TNBC.

244 y have clinical utility for the treatment of TNBC.

245 (called L-ICON) for preclinical treatment of TNBC.

246 for the specific targeting and treatment of TNBC.

247 vitro and in cells, reduced the viability of TNBC cells and had oral bioavailability in mice.

248 downstream of TBK1/IKKepsilon in a subset of TNBCs and reveals previously unrecognized cross-talk wit

249 We confirmed that a subset of TNBCs have elevated expression of HLA-DR in tumor epithe

250 umor-infiltrating lymphocytes in a subset of TNBCs with high tumor-infiltrating lymphocyte content.

251 ting LIPG phospholipase activity, impacts on TNBC tumor formation and malignant features.

252 LNs(-) were associated with the luminal A or TNBC subtype.

253 Furthermore, oxidizing TNBC cells prior to lysis and incorporation into SNAs (O

254 HIF functions, we found using a preclinical TNBC xenograft mouse model, and an existing selective Sp

255 potential therapeutic target for preventing TNBC recurrence.

256 However, how r2Reovirus promotes TNBC cell death is not known.

257 e.g., highest compared with lowest quartile: TNBC OR: 0.53; 95% CI: 0.31, 0.91; P-trend = 0.02).

258 onstrated that LIPG differentially regulates TNBC malignancy through its enzymatic and non-enzymatic

259 ility and motility of TNBC cells, sensitized TNBC cells to chemotherapy, and restricted the TNBC stem

260 or difluoromethylornithine (DFMO) sensitized TNBC cells to chemotherapy, but this was not observed in

261 as BRCA1 pathogenic variants in early-stage TNBC and that hypermethylated and mutated cases have sim

262 In patients with early-stage TNBC, neoadjuvant treatment with atezolizumab in combina

263 results by pCR in patients with early-stage TNBC.

264 ide as neoadjuvant treatment for early-stage TNBC.

265 romising DNA-based biomarker for early-stage TNBC.

266 o circulating tumor cells (CTCs) to suppress TNBC lung metastasis.

267 These results suggest that BCL11A sustains TNBC cell invasion and metastatic growth by repressing M

268 trochemotherapy (ECT), to effectively target TNBC cells.

269 GLI1/tGLI1 inhibitors synergistically target TNBC and HER2 breast cancer since these two pathways are

270 nd prolonged overall survival in both tested TNBC models.

271 iological Chemistry, Geck et al. report that TNBC cells are highly sensitive to inhibition of the de

272 Cytotoxicity data showed that TNBC cell lines are more sensitive to TAK1 inhibitor com

273 ted neural genes than NTNBC, suggesting that TNBC is more complex than NTNBC; (2) non-neural function

274 TCGA data showed that TNBCs express high levels of RBG regulators, and elevate

275 hibition of metastasis by TriplatinNC in the TNBC 4T1 syngeneic tumour model.

276 osphorylation (OXPHOS), which redirected the TNBC metabolism to mitochondria.

277 BC cells to chemotherapy, and restricted the TNBC stem cell population.

278 With a lack or targeted therapies, TNBC is challenging to treat and carries a poor prognosi

279 Thus, TNBC cells critically rely on IRE1alpha to adapt their E

280 hibition of this pathway sensitizes cells to TNBC-relevant chemotherapy, uncovering new opportunities

281 on, and transcriptional phenotype similar to TNBC tumors with BRCA1-inactivating variants, and it can

282 identify which adjuvant chemotherapy-treated TNBC patients have a higher risk of treatment resistance

283 ith shorter survival in chemotherapy-treated TNBC patients.

284 ARP inhibitors in 43 patients with untreated TNBC.

285 inverse pattern for the Shannon index, when TNBC tumor tissue was compared to the matched NAT.

286 her LINC00299 methylation is associated with TNBC in a prospective nested breast cancer case-control

287 in the ALNs(-) were factors associated with TNBC, whereas CD83 dendritic cells in the ALNs(-) were a

288 sociation of LINC00299 hypermethylation with TNBC in young women.

289 ul surface target in 50-85% of patients with TNBC and developed a second-generation TF-targeting anti

290 1 expression in the tumours of patients with TNBC strongly suggest that this signalling axis could be

291 Patients with TNBC tumors expressing high levels of ERK2 have a poorer

292 y-five studies with over 4,000 patients with TNBC were identified.

293 ciated with improved EFS/OS in patients with TNBC who received neoadjuvant therapy, regardless of pCR

294 mportant prognostic factors in patients with TNBC, although the relative importance of lymphocyte sub

295 rrent treatment modalities for patients with TNBC, the immunogenic nature of this aggressive disease

296 improve clinical outcomes for patients with TNBC, who currently lack effective targeted therapeutic

297 xplains the worse prognosis of patients with TNBC.

298 tment strategies for Elf5(low) patients with TNBC.

299 and reduces metastasis risk in patients with TNBC.

300 sly found to be ineffective in patients with TNBC.