ライフサイエンスコーパス: breast cancer

1 , or breastfeeding; and no family history of breast cancer.

2 clinical outcomes in treatment of resistant breast cancer.

3 ree, metastasis-free, or overall survival in breast cancer.

4 tastases in women with HER2-negative primary breast cancer.

5 s is crucial for metastatic dissemination in breast cancer.

6 rently required for the treatment of HER2(+) breast cancer.

7 with prognostic and therapeutic relevance in breast cancer.

8 tional drug that is now widely used to treat breast cancer.

9 anism underlying endocrine resistance in ER+ breast cancer.

10 represent a prognostic marker in ERalpha(+) breast cancer.

11 to determine the association with subsequent breast cancer.

12 nd spontaneous metastasis of triple-negative breast cancer.

13 cross-disease communication that accelerates breast cancer.

14 metastatic recurrence, particularly in basal breast cancer.

15 F1 or KMT2D, which are frequently mutated in breast cancer.

16 tastases in women with HER2-negative primary breast cancer.

17 linical and clinical imaging of ER and PR in breast cancer.

18 oach for the safe and effective treatment of breast cancer.

19 entified patients with stage I-III ER+/HER2- breast cancer.

20 lation treatment strategies in HER2-positive breast cancer.

21 d increased risk of relapse in patients with breast cancer.

22 tion genes should be offered to all men with breast cancer.

23 d were subsequently followed up for incident breast cancer.

24 herapy after primary surgery for early-stage breast cancer.

25 cancer, and 1% (95% CI, 0.2% to 5%) for male breast cancer.

26 tion therapy immunogenicity in patients with breast cancer.

27 acle that hinders their utility beyond ER(+) breast cancer.

28 ubiquitinases (DUB) in regulating ERalpha in breast cancer.

29 ion, prognosis, and companion diagnostics in breast cancer.

30 quency in advanced endocrine-resistant ER(+) breast cancer.

31 ifically open and unmethylated in basal-like breast cancer.

32 demonstrated in an orthotopic mouse model of breast cancer.

33 ial biomarkers for the clinical diagnosis of breast cancer.

34 nostic biomarkers and therapeutic targets in breast cancer.

35 ple for FEN1 blockade in tamoxifen-resistant breast cancer.

36 cing and patient-derived-xenograft models of breast cancer.

37 histopathology images from 23 patients with breast cancer.

38 transcriptional regulator in the majority of breast cancers.

39 ranscription factor expressed in over 50% of breast cancers.

40 ly diagnosis and postoperative monitoring of breast cancers.

41 (ER) modulator in patients with ER-positive breast cancers.

42 g is a cornerstone of adjuvant treatment for breast cancer, 25% of patients experience recurrent dise

43 ars were 53% (95% CI, 44% to 63%) for female breast cancer, 5% (95% CI, 2% to 10%) for ovarian cancer

44 Of the remaining 2228 women with breast cancer, 58 women with previous treatment or recur

45 ocrine Jag1-Notch1-Zeb1-VEGFA loop decreases breast cancer aggressiveness and thus enhances the effic

46 c surgery is associated with reduced risk of breast cancer among pre- and postmenopausal women.

47 tologically confirmed advanced HER2-negative breast cancer, an Eastern Cooperative Oncology Group per

48 e for refugees and nationals and prioritises breast cancer and childhood cancers.

49 physical activity levels and lower risks of breast cancer and colorectal cancer.

50 pressive microenvironment of triple negative breast cancer and facilitate the checkpoint blockade imm

51 Mice bearing MDA-MB-231 breast cancer and FaDu head neck cancer xenografts show

52 associations for estrogen positive (ER(+ve)) breast cancer and for colon cancer.

53 opausal women with HR-positive/HER2-negative breast cancer and high recurrence risk, as defined by cl

54 on distinguish EMT and papillary subtypes of breast cancer and identify said pathways as a means to e

55 eceptor for lactate, which is upregulated in breast cancer and plays an autocrine role to promote tum

56 r proliferation and underlying metastasis in breast cancer and provide an initial framework for explo

57 for >35% of patients diagnosed with invasive breast cancer and refined OS estimates.

58 miological bidirectional association between breast cancer and schizophrenia may partly be explained

59 Given this population's high incidence of breast cancer and younger age of onset compared to the g

60 electively downregulated in ERalpha-positive breast cancers and breast cancers driven by ERBB2.

61 are detected at the invasive front of human breast cancers and independently predict metastatic rath

62 for coronary artery disease, 13% to 76% for breast cancer, and 11% to 80% for colon cancer.

63 )F-ISO-1) to image solid tumors in lymphoma, breast cancer, and head and neck cancer has been previou

64 pes, including lymphoma, lung, glioblastoma, breast cancer, and several forms of leukemia, with prima

65 an elevated risk of developing contralateral breast cancer, and that the PRS can considerably improve

66 the management approaches used for men with breast cancer are like those used for women.

67 nisms through which they are associated with breast cancer are not well known.

68 lly adopted strategy to treat colorectal and breast cancers as well as age-related macular degenerati

69 cer from 1990 onward with follow-up from the Breast Cancer Association Consortium.

70 0-90(th) percentile) have a lifetime risk of breast cancer at 55% (95% CI 49-61%), which increases to

71 a prospective cohort of women diagnosed with breast cancer at age <= 40 years and enrolled patients b

72 Screening mammography aims to identify breast cancer at earlier stages of the disease, when tre

73 Breast cancer (BC) is one of the most prevalent cancers

74 We hypothesized that in breast cancer (BC), where mutation is less common, tumor

75 ERBB2 levels spiked in metastatic breast cancer between 10.0 and 4.0 months pre-diagnosis.

76 urora B expression is elevated in basal-like breast cancer (BLBC) compared with other breast cancer s

77 en therapeutic advances; however, basal-like breast cancer (BLBC) remains clinically intractable.

78 ncluded menopausal status, family history of breast cancer, body mass index, hormone replacement ther

79 ial responses in patients with HER2-positive breast cancer brain metastases.

80 develops in estrogen receptor positive (ER+) breast cancer, but the underlying molecular mechanisms a

81 can reduce tumor growth and invasiveness of breast cancer by noncanonical mechanisms unrelated to th

82 tMap by investigating the molecular basis of breast cancers capable of metastasizing to the brain-a p

83 us was defined using age as a proxy, whereby breast cancer cases or deaths at age 50 years or older w

84 ded 301 premenopausal and 399 postmenopausal breast cancer cases.

85 Analysis of PREX1 mRNA expression in breast cancer cDNA arrays and a METABRIC cohort revealed

86 Complementary studies using human breast cancer cell culture models revealed that siRNA-me

87 In human breast cancer cell lines and 4T1 mouse mammary tumor cel

88 nase-targeted therapy in a subset of HER2(+) breast cancer cell lines and allow cancer cells to proli

89 binding with its promoter region in luminal breast cancer cell lines and indirectly through a distal

90 Compound 1 was cytotoxic for both breast cancer cell lines and the majority of cells died

91 erum or 0.024 wt % of the total protein from breast cancer cell lysates.

92 argeting miRNAs and examine their effects on breast cancer cell migration through exosome-mediated de

93 Here, using human breast cancer cell models, we identified a pathway in wh

94 indicated that 8a decreases triple-negative breast cancer cell viability, and immunoblotting reveale

95 NA templates and validated with DNA from two breast cancer cell-lines and two patient tumour tissue s

96 Breast cancer cells 'educate' lymphatic endothelial cell

97 ll-characterized cellular reference samples (breast cancer cells and B cells), captured either separa

98 latelets promote the metastasis of colon and breast cancer cells and suggests that GPVI represents a

99 the mesenchymal phenotype of triple-negative breast cancer cells and that CBFbeta-depleted cells unde

100 pe cells adopt MAPK-dependent circuitries in breast cancer cells and that the kinase TTK is important

101 oratories, we characterised a range of human breast cancer cells and their protein-level responses to

102 opy the PYCR1 knockdown in MCF10A H-RAS(V12) breast cancer cells by inhibiting de novo proline biosyn

103 e compared across an isogenic panel of human breast cancer cells derived from MDA-MB-231 cells.

104 Here, we found that melanoma and lung and breast cancer cells experiencing stress from oncogene in

105 Methods: ER+, PR+ T47D breast cancer cells expressing wild-type (WT) ER or an a

106 AZP-531 also suppresses the growth of breast cancer cells in vitro and in xenografts, and may

107 When cocultured with breast cancer cells in vitro, MCs hindered activation of

108 Here, we show that breast cancer cells maintained in hypoxia release small

109 Pulsed magnetic field exposure of human breast cancer cells that express a sialic-acid rich glyc

110 panel of cell lines derived from MDA-MB-231 breast cancer cells that vary in their metastatic potent

111 unctional DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3B-mediated mutations and double

112 e have employed varying EMT models of murine breast cancer cells to identify the key players establis

113 P followed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the proteasome inhibito

114 In breast cancer cells under normoxia, CHD4 enrichment at H

115 Investigating the behavior of breast cancer cells via reaction kinetics may help unrav

116 educed drug responsiveness was observed when breast cancer cells were maintained in 3D under fluid fl

117 nvironments reminiscent of metastatic sites, breast cancer cells were more resistant to the estrogen

118 akdown and concomitant drug release, when in breast cancer cells with increased levels of reducing ag

119 pressed MYC-mediated apoptosis in p53-mutant breast cancer cells with UBR5/MYC coamplification.

120 ast array of long noncoding RNAs (lncRNA) in breast cancer cells, but their biological functions rema

121 haracterize effects of unacylated ghrelin on breast cancer cells, define its mechanism of action, and

122 rs distinct features to ER-negative DCIS.com breast cancer cells, leading to populations enriched wit

123 icinal plant Arabidopsis thaliana with human breast cancer cells, selectively suppresses cancer cell

124 hibitors of ciliogenesis in normal and basal breast cancer cells.

125 ved from parental MDA-MB-231 triple-negative breast cancer cells.

126 ls of cell cycle regulators were examined in breast cancer cells.

127 tabolism has been unsuccessful so far in the breast cancer clinical setting, with major unresolved ch

128 We also determined that breast cancer co-culture stimulated lymphangiogenic sign

129 Disparities in Outcomes Study, a prospective breast cancer cohort study, we implemented active mobile

130 t Cancer International Consortium (METABRIC) breast cancer cohort, FGFR4-induced and FGFR4-repressed

131 By analysing two published breast cancer cohort, we signifies that MOVICS can serve

132 , including ovarian cancer, medulloblastoma, breast cancer, colorectal cancer, and lung cancer.

133 Application to breast cancer data revealed a linear, branching evolutio

134 the estimated difference in 8-year risk for breast cancer death between continuing and stopping scre

135 We discovered that breast-cancer-derived lung metastases, but not the corre

136 digital breast tomosynthesis (DBT) improves breast cancer detection and recall rates compared with t

137 clinical trials have shown a reduced rate of breast cancer development in high-risk women in the init

138 rms in the regulation of gene expression and breast cancer development.

139 LIBRA measures on mammograms obtained before breast cancer diagnosis and compare their performance to

140 Similarly, we show that after the breast cancer diagnosis, individuals with elevated PRS h

141 In the African Breast Cancer-Disparities in Outcomes Study, a prospecti

142 Pregnancy after breast cancer does not increase the risk of recurrence;

143 lated in ERalpha-positive breast cancers and breast cancers driven by ERBB2.

144 We identified 771 incident cases of breast cancer during follow-up (median time: 5.2 years).

145 In human breast cancer E2F2, status was also correlated with a pa

146 HDI) faced a greater burden of premenopausal breast cancer for both new cases and deaths compared wit

147 erapy was the standard treatment of advanced breast cancer for three decades until the discovery of t

148 opean ancestry diagnosed with first invasive breast cancer from 1990 onward with follow-up from the B

149 t gene-environmental studies have focused on breast cancers generally, the preponderance of which occ

150 ofiles, enumeration of copy numbers of eight breast cancer genes by multicolor fluorescence in situ h

151 affect genomic regions containing well-known breast-cancer genes.

152 tudies provide insight into the landscape of breast cancer genomics with the genomic characterization

153 systems against malignant lung metastasis of breast cancer have been extensively studied, while metas

154 lanoma and other cancers, clinical trials in breast cancer have reported low responses to these thera

155 studies are often performed in patients with breast cancer; however, incidental radiotracer uptake in

156 nsisting of tumor/TIL maps for 1090 invasive breast cancer images from The Cancer Genome Atlas.

157 ed incidence rates (ASIRs) for premenopausal breast cancer in 20 of 44 populations and significantly

158 ficantly increasing ASIRs for postmenopausal breast cancer in 24 of 44 populations.

159 while 19% of them had a positive history of breast cancer in first- or second-degree relatives.

160 omy, was significantly associated with lower breast cancer incidence and lower breast cancer mortalit

161 Obesity is known to increase breast cancer incidence and mortality, but the underlyin

162 , was significantly associated with a higher breast cancer incidence but no significant difference in

163 In breast cancer, increased ECM stiffness promotes epitheli

164 ogene and cooperate with HER2/neu to enhance breast cancer initiation and metastasis, despite having

165 In the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast

166 romatase inhibitors (MAP.3 and International Breast Cancer Intervention Study II [IBIS-II]).

167 d negative prognostic value in patients with breast cancer, inversely correlating with mitochondrial

168 Invasive breast cancer is believed to evolve from non-invasive du

169 Prognosis in young patients with breast cancer is generally poor, yet considerable differ

170 The burden of disease and economic impact of breast cancer is intensifying in LMICs.

171 Breast cancer is the most common cancer, and the second

172 Breast cancer is the second leading cause of cancer-rela

173 BC), representing ~15% of globally diagnosed breast cancer, is typically an incurable malignancy due

174 a Mammography Project for Risk Prediction of Breast Cancer (KARMA), 2011-2017.

175 ly expanding the population of patients with breast cancer likely to benefit from PARPi beyond gBRCA1

176 In breast cancer, malignant cells recruit and educate macro

177 Furthermore, a synergistic effect on breast cancer (MCF-7) and melanoma (SK-MEL-5) was proven

178 oduli and mass of adherent colon (HT-29) and breast cancer (MCF-7) cells from the interphase through

179 h of these miRNAs was transfected into human breast cancer MDA-MB-231 cells.

180 nes, colon cancer (HT29) and AQP1-expressing breast cancer (MDA), and low-AQP1-expressing SW480.

181 d fibroblasts in mouse models of spontaneous breast cancer metastasis and in patients with breast can

182 uced small extracellular vesicles accelerate breast cancer metastasis, and targeted inhibition of tum

183 Lungs are one of the main sites of breast cancer metastasis.

184 icing regulatory factor that impedes EMT and breast cancer metastasis.

185 ibutions of pre- and post-EMT tumor cells in breast cancer metastasis.See related commentary by Bunz,

186 We further apply this to a breast cancer model to evaluate differential methylation

187 nthesis using a histologically heterogeneous breast cancer model, highlighting metabolic vulnerabilit

188 Here, we use mouse and human breast cancer models to identify a collective signal gen

189 In melanoma and breast cancer models, it is shown that gCM-MNs significa

190 t result in substantial reductions in 8-year breast cancer mortality compared with stopping screening

191 with lower breast cancer incidence and lower breast cancer mortality, whereas prior randomized use of

192 r incidence but no significant difference in breast cancer mortality.

193 Furthermore, Tet2 deletion-PyMT breast cancer mouse model exhibits enhanced mammary tumo

194 Staging for breast cancer now includes anatomic and biologic factors

195 of the two most frequently mutated genes in breast cancers, occurring in 30-40% of cases.

196 miR-223 expression was decreased in breast cancer of luminal and HER2 subtypes and inversely

197 one previous line of treatment for advanced breast cancer or relapsed within 12 months of neoadjuvan

198 rgeted therapy agents that are used to treat breast cancer, pancreatic cancer, colorectal cancer, or

199 ator of mammary epithelial proliferation and breast cancer pathogenesis likely via the modulation of

200 In a breast cancer patient cohort coupled with in silico anal

201 proof-of-principle, we apply MutSpace to 560 breast cancer patient samples and demonstrate that our m

202 d the alternative splicing of CLSTN1 predict breast cancer patient survival.

203 cal outcome in tamoxifen treated ER-positive breast cancer patients by repressing estrogen signaling

204 A significant proportion of breast cancer patients develop bone metastases, but the

205 RNA sequencing of freshly isolated CTCs from breast cancer patients revealed a subset with strong rib

206 del to predict tumor response for two HER2 + breast cancer patients treated with the same therapeutic

207 Annual mortality rates among breast cancer patients were significantly greater in LMI

208 MLK3 inhibitor in pan T cells, isolated from breast cancer patients, also increases cytotoxic CD8(+)

209 In breast cancer patients, PREX1 levels are significantly i

210 ssociated with better overall survival among breast cancer patients, while high fruit juice consumpti

211 ratio is associated with reduced survival of breast cancer patients.

212 utic strategies to improve the prognosis for breast cancer patients.

213 natures are predictive of survival for human breast cancer patients.

214 ed variation to genes that may contribute to breast cancer predisposition.

215 igned patients with HER2-positive metastatic breast cancer previously treated with trastuzumab, pertu

216 x, keeping it in the active state to enhance breast cancer progression, but also rendering the cells

217 Thus, although involved in breast cancer progression, HOXB13 is not a material brea

218 ized for its role in promoting metastasis of breast cancer, prostate cancer, and melanoma.

219 vel alternative splicing biomarkers from the breast cancer proteome.

220 doxorubicin-cyclophosphamide for stage I-III breast cancer received paclitaxel 175 mg/m(2) every 2 we

221 434 (10%) of 4480 women had a breast cancer recurrence (280 [9%] POAI; 154 [10%] contr

222 -1.12); p=0.40 with the proportion free from breast cancer recurrence at 5 years of 91.0% (95% CI 89.

223 Breast cancer remains the leading cancer-related cause o

224 ods: Five patients with a prior diagnosis of breast cancer, renal cell cancer, or leukemia underwent

225 factor receptor 2 (HER2)-negative metastatic breast cancer represents a major milestone in cancer the

226 iation and endocrine response that underlies breast cancer resistance to anti-estrogen treatments.

227 3)C MRI enabled successful identification of breast cancer response after one cycle of neoadjuvant ch

228 ensity change, which are all associated with breast cancer risk and can indicate women at short-term

229 identified MD loci also are associated with breast cancer risk in an independent meta-analysis (P <

230 ch gene expression could potentially explain breast cancer risk phenotypes.

231 s Statement, we discuss the current state of breast cancer risk prediction, risk-stratified preventio

232 e obese breast microenvironment may increase breast cancer risk.

233 Continuing annual breast cancer screening past age 75 years did not result

234 in the United States instead of DM alone for breast cancer screening.

235 y et al. showed the high potential of AI for breast cancer screening.

236 ls to improve the accuracy and efficiency of breast cancer screening.

237 reatment of mice with disseminated ER+ human breast cancer showed that D9 plus MK-2206 blocked format

238 otein expression in pre-treatment samples on breast cancer-specific and distant metastasis-free survi

239 uggests the frequent coexistence of multiple breast cancer states within a PDTX model, the majority o

240 onses in the treatment of BC/TNBC along with breast cancer stem cells have been discussed in details.

241 e citrullinating enzyme PADI4 in suppressing breast cancer stem cells through epigenetic repression o

242 Synergy was also observed against breast cancer stem cells.

243 ated a possible role for PADI4 in regulating breast cancer stem cells.

244 The Young Women's Breast Cancer Study is a prospective cohort of women dia

245 The phenotypes of each breast cancer subtype are defined by their transcriptome

246 gative breast cancer (TNBC) is an aggressive breast cancer subtype.

247 ve breast cancer (TNBC), the most aggressive breast cancer subtype.

248 Knowledge of fundamental differences between breast cancer subtypes has driven therapeutic advances;

249 ike breast cancer (BLBC) compared with other breast cancer subtypes.

250 ts to define extended signatures of distinct breast cancer subtypes.

251 s in these pathways as promising targets for breast cancer subtypes.

252 soforms did not significantly differ between breast cancer subtypes.

253 ritance of monoallelic germline mutations in breast cancer susceptibility gene type 1 or 2 (BRCA1/2)

254 cancer progression, HOXB13 is not a material breast cancer susceptibility gene.

255 s of EpCAM positive cancer cell lines (MCF-7 breast cancer, SW480 colon cancer, and PC3 prostate canc

256 higher double-positive signal in basal-like breast cancer than in luminal A or luminal B subtypes.

257 one and lung metastasis from triple-negative breast cancer that should be given prior to conventional

258 On the syngeneic mouse model of breast cancer, the iron-crosslinked Rososomes exhibit be

259 found that the d-spacing of the EMT positive breast cancer tissue (FFPE (dewaxed)) is within the rang

260 ty, and enabled the cellular architecture of breast cancer tissue to be characterized on the basis of

261 urrence in estrogen receptor- positive (ER+) breast cancer tissue.

262 Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA database

263 ancer cells, including human triple-negative breast cancer (TNBC) and patient-derived TNBC cells in v

264 of HS cleavage in MDA-MB-231 triple-negative breast cancer (TNBC) cells.

265 Triple negative breast cancer (TNBC) is an aggressive breast cancer subt

266 Treatment of patients with triple-negative breast cancer (TNBC) is limited by a lack of effective m

267 In triple-negative breast cancer (TNBC), miR-127 downregulation correlates

268 Triple-negative breast cancer (TNBC), representing ~15% of globally diag

269 tance is a major obstacle in triple negative breast cancer (TNBC), the most aggressive breast cancer

270 py is yet available to treat triple negative breast cancer (TNBC), which has poor prognosis due to fr

271 nd lung metastatic growth in triple-negative breast cancer (TNBC).

272 ng the very aggressive human triple negative breast cancer (TNBC, MDA-MB-231 cells) growing in the br

273 ically engineered orthotopic mouse models of breast cancer to show that while depletion of DeltaNp63

274 uantified the global macroeconomic burden of breast cancer to underscore the critical importance of i

275 e 10-year cumulative IBTR incidence in early breast cancer treated with external APBI using IMRT tech

276 Adverse effects of breast cancer treatment can negatively affect survivors'

277 When examining breast cancer trends, we noted significantly increasing

278 in distinct patterns in different classes of breast cancer tumor samples.

279 In mice engrafted with HER2-positive breast cancer tumors, coinjection of MCs increased tumor

280 C signature 3 observed in BRCA1/BRCA2-mutant breast cancer tumors.

281 luding humans and proteomic data to classify breast cancer tumours.

282 In patients with breast cancer, TWIST1 and PRKD1 expression correlated wi

283 lk of additional ten women not known to have breast cancer, two of them contained cells that were enr

284 he identification of groups at high risk for breast cancer, type 2 diabetes, inflammatory bowel disea

285 ed therapies, patients with advanced HER2(+) breast cancer ultimately develop drug resistance.

286 with pre-BMT chest radiation or a history of breast cancer were excluded.

287 pausal women at increased risk of developing breast cancer were recruited and were randomly assigned

288 endocrine therapies to reduce risk of future breast cancer, while testing DCIS for PgR is considered

289 Men with hormone receptor-positive breast cancer who are candidates for adjuvant endocrine

290 Furthermore, patients with early-stage breast cancer who experienced cardiovascular events afte

291 factor receptor 2 (HER2)-positive metastatic breast cancer who have disease progression after therapy

292 ies patients with early-stage, HER2-positive breast cancer who might be candidates for escalated or d

293 In patients with HER2-positive breast cancer with BMs, the addition of tucatinib to tra

294 GWAS datasets suggested an increased risk of breast cancer with ERCC6 (main effect: 1.29 <= OR <= 2.9

295 -year-old woman with a previous diagnosis of breast cancer with liver metastasis presented with a com

296 reast cancer metastasis and in patients with breast cancer with lung metastasis.

297 factor receptor 2 (HER2)-negative metastatic breast cancer with prior clinical benefit from endocrine

298 s during bevacizumab therapy in two types of breast cancer xenografts (KPL-4 and MDA-MB-468).

299 to tumor-initiating cells in triple-negative breast cancer xenografts that rely on LEFTY1 for growth.

300 Young-onset breast cancers (YOBC) tend to be aggressive and may be e