ライフサイエンスコーパス: breast cancer

1 ), A549 (lung adenocarcinoma) and MDA-MB-231(breast cancer).

2 advanced adenomas), endometrial cancers, and breast cancer.

3 decision making in patients with unilateral breast cancer.

4 several known histopathological subtypes of breast cancer.

5 ith brain metastases at time of diagnosis of breast cancer.

6 crine therapy resistance in OXPHOS-dependent breast cancer.

7 e whose heterozygous mutations predispose to breast cancer.

8 (2), respectively, and 82% had stage I or II breast cancer.

9 ohistochemically in patients with metastatic breast cancer.

10 tic hormone receptor-positive, HER2-negative breast cancer.

11 s that are commonly used in the treatment of breast cancer.

12 ma but generally fail in brain metastases of breast cancer.

13 n age >/= 65 years who reported a history of breast cancer.

14 se orthotopic model of human triple-negative breast cancer.

15 th breast cancer compared with women without breast cancer.

16 suppressor BRCA2 predominantly predispose to breast cancer.

17 its potential risks on venous thrombosis and breast cancer.

18 lated to the pathogenesis of triple-negative breast cancer.

19 geted therapy in patients with HER2-positive breast cancer.

20 ctory, estrogen receptor-positive metastatic breast cancer.

21 one therapeutic efficacy in ERalpha-negative breast cancer.

22 tumour growth in a transgenic mouse model of breast cancer.

23 patients who underwent recent treatment for breast cancer.

24 tly correlates with poor survival outcome in breast cancer.

25 ne are linked causally to increased risks of breast cancer.

26 en-dependent diseases like endometriosis and breast cancer.

27 b with ET in early HER2-positive/HR-positive breast cancer.

28 onal transgenic mouse models of PyMT-induced breast cancer.

29 as associated with a modestly higher risk of breast cancer.

30 a potential therapeutic approach to control breast cancer.

31 rowth factor receptor 2-positive early-stage breast cancer.

32 atients with different molecular subtypes of breast cancer.

33 cyclines in patients with early TOP2A-normal breast cancer.

34 tumor progression in an aggressive model of breast cancer.

35 potential therapeutic target for metastatic breast cancer.

36 milar to that seen in patients with invasive breast cancer.

37 use they experience the highest incidence of breast cancer.

38 patients with locally relapsed or metastatic breast cancer.

39 ome microRNAs (miRNAs) are known to suppress breast cancer.

40 hanism for the involvement of this region in breast cancer.

41 scular preventive therapy after diagnosis of breast cancer.

42 sts of passengers in cell lines and in human breast cancers.

43 ER2 has been reported in around 25% of human breast cancers.

44 coamplification of MED1 and HER2 in certain breast cancers.

45 es for understanding the etiology of certain breast cancers.

46 rom 520 patients with metastatic prostate or breast cancers.

47 clinical outcome in estrogen receptor+ (ER+) breast cancers.

48 e interaction between MALAT1 and depleted in breast cancer 1 (DBC1) was validated using RNA pull-down

49 ast cancer analysis, 426 were diagnosed with breast cancer, 109 with ovarian cancer, and 245 with con

50 Although all had a biologic sister with breast cancer, 16.5% had average or lower risk of breast

51 In 13 breast cancers, 8 had a low binding (mean density, 844 +

52 s, were significantly increased for invasive breast cancer (9 more cases [95% CI, 1 to 19]), probable

53 The primary tumors were breast cancer (92 patients, 426 scans), non-Hodgkin lymp

54 and the linkages between iron metabolism and breast cancer, a predictive mathematical model of an exp

55 tients with ERBB2 (HER2)-positive metastatic breast cancer; a clinically effective biosimilar may hel

56 t cancer, 16.5% had average or lower risk of breast cancer according to the Breast Cancer Risk Assess

57 h 18,908 BRCA1 mutation carriers (9,414 with breast cancer), all of European origin.

58 iated relative risk for male than for female breast cancer, although absolute excess risks for males

59 but we did see a 19% excess risk of invasive breast cancer among those with AF (adjusted hazard ratio

60 40-55 years) eligible for the contralateral breast cancer analysis, 426 were diagnosed with breast c

61 e range [IQR], 30-46 years) eligible for the breast cancer analysis, 5066 women (median age, 38 years

62 Here we adopt this powerful approach to breast cancer and analyse 515 cells from 11 patients.

63 I trial, 2,012 women with early TOP2A-normal breast cancer and at least one high-risk factor were ran

64 In specimens from breast cancer and melanoma patients, CD39(+)CD8(+) T cel

65 gnificant difference between triple-negative breast cancer and non-triple-negative breast cancer (P =

66 rans-repression, with clear implications for breast cancer and other diseases.

67 44 years who were diagnosed with early-stage breast cancer and received a CPM increased in many state

68 vant systemic therapy (NST) in patients with breast cancer and to outline a model of pathologic respo

69 Using ExonArray analysis of 176 breast cancers and 9 normal breast tissues we demonstrat

70 RF1 expression is increased in HER2-positive breast cancers and correlates with HER2-positive status

71 er (TNBC) comprises approximately 20% of all breast cancers and is the most aggressive mammary cancer

72 -infiltrating lymphocytes in triple-negative breast cancers and while MEK inhibition can promote recr

73 etween 0 (thyroid, ascites) and 8.48 months (breast cancers)-and were sometimes based on modeled data

74 In fact, most triple-negative breast cancers are poor-prognosis tumors with a complex

75 In a population in which most breast cancers are self-detected, previous clinical brea

76 arcinoma in situ (DCIS) lesions and invasive breast cancers as well as with increased mortality in pa

77 Tumor recurrence remains the main reason for breast cancer-associated mortality, and there are unmet

78 treatment solutions to benefit patients with breast cancer at high risk of recurrence.

79 improve early diagnosis directly by finding breast cancers at earlier stages or indirectly by height

80 Examination of molecular signatures of breast cancer (based on complex gene expression patterns

81 Breast cancer (BC) has a higher incidence in young Leban

82 Adjuvant radiotherapy (RT) in breast cancer (BC) is often used to eradicate remaining

83 Triple-negative (TN) breast cancer (BC) shares histological characteristics w

84 types with lower SSTR expression, including breast cancer (BC).

85 he high mortality rates associated with most breast cancers (BC).

86 men diagnosed with unilateral stage I to III breast cancer between 1998 and 2012 within the Surveilla

87 h signaling pathways that predict aggressive breast cancer biology.

88 me, sensitive electrochemical detection of a breast cancer biomarker microRNA (miRNA), mir-21 was ach

89 st1 expression is associated with basal-like breast cancer (BLBC) with poor prognosis owing to its ro

90 m), we demonstrated specific localization to breast cancer bone metastases in mice.

91 Patients with breast cancer (BrCa) brain metastases (BrM) have limited

92 e advances in the diagnosis and treatment of breast cancer, breast cancers still cause significant mo

93 ual identification of presence and extent of breast cancer by a pathologist is critical for patient m

94 regulated autophagy suppresses metastasis in breast cancer by preventing tumor fibrosis.

95 ondary cancers in women with newly diagnosed breast cancer by using histologic or imaging follow-up a

96 ng or targeted therapy, we screened invasive breast cancers by immunohistochemistry for the presence

97 associated with ESR1-positive and -negative breast cancer can physically interact.

98 ollow-up (2004 to 2011), 2,407 first primary breast cancer cases were identified.

99 t strategies to prevent cancer metastasis in breast cancer cases.

100 nation for exercise-dependent suppression of breast cancer cell growth.

101 ific demethylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylati

102 yrosine 537, in the estrogen-responsive MCF7 breast cancer cell line.

103 us to discriminate between normal and human breast cancer cell lines (fibrocystic and metastatic sta

104 fold more potent at inhibiting the growth of breast cancer cell lines (MCF7, MCF7/VP16, BT474, T47D,

105 rbon monoxide (CO) reduced GSH/GSSG in three breast cancer cell lines by inhibiting CBS.

106 To investigate this question, we developed breast cancer cell lines expressing an inducible, consti

107 defects by direct and indirect assays in 12 breast cancer cell lines to estimate the spontaneous occ

108 h GSK1016790A reduced viability of two basal breast cancer cell lines with pronounced endogenous over

109 1 in total RNA extracted from human lung and breast cancer cell lines, discriminating between the can

110 tic cancer tissues as well as pancreatic and breast cancer cell lines.

111 ells, also inhibit endothelial phenotypes of breast cancer cells adopted in response to a nutrient-de

112 Here, we first demonstrated that breast cancer cells and pancreatic adenocarcinoma cells

113 the human genome, are overexpressed in some breast cancer cells and tissues but without regard to ca

114 g than seen with EGF, provoking responses in breast cancer cells associated with differentiation rath

115 ine and reveal that enhancers transcribed in breast cancer cells direct critical gene regulatory netw

116 with DAC to reduce the viability of luminal breast cancer cells in in vitro assays.

117 ration and activated apoptosis in MDA-MB-231 breast cancer cells in vitro and in vivo.

118 ngeneic studies with orthotopically injected breast cancer cells in wild-type and RAGE-knockout C57BL

119 Accordingly, E+P treatment of breast cancer cells increased ER binding to the NEMO pro

120 Breast cancer cells often develop resistance to endocrin

121 estigate the unique transhesive profiles for breast cancer cells that are adapted to colonize differe

122 A repair while elevated levels can sensitize breast cancer cells to doxorubicin leading to apoptotic

123 imental tumor construct, MCF7 and MDA-MB-231 breast cancer cells were coinjected into the mammary fat

124 we demonstrate that treatment of human MCF-7 breast cancer cells with pro-inflammatory cytokines resu

125 diation in both a nematode in vivo model and breast cancer cells, and could potentially be utilized a

126 Here, we characterize, in breast cancer cells, the molecular effects of a recently

127 Indeed, when CXCR7 was silenced in breast cancer cells, their metastatic ability was inhibi

128 S nanoparticles that target HER2 and CD44 in breast cancer cells, we demonstrate labeling of fixed ce

129 ate level of PAK4 protein in triple negative breast cancer cells.

130 intrasinusoidal infiltration of the liver by breast cancer cells.

131 epletion impairs the metastatic potential of breast cancer cells.

132 unction, contributes to PARPi sensitivity in breast cancer cells.

133 /HER2 in normal mammary epithelial cells and breast cancer cells.

134 promote invadopodial maturation in invasive breast cancer cells.

135 ted regulation of invasion and metastasis in breast cancer cells.

136 vitro and cell-based model of MMP-dependent breast cancer cellular invasiveness, this N-TIMP2 mutant

137 Purpose Aromatase inhibitors are established breast cancer chemoprevention interventions.

138 g disease regression in treatment-refractory breast cancer chest wall metastases but responses are sh

139 than 50% of estrogen receptor (ER)-positive breast cancers coexpress the progesterone receptor (PR),

140 epidermal growth factor receptor 2-negative breast cancer compared with the TC6 regimen.

141 ence and disability pension among women with breast cancer compared with women without breast cancer.

142 Triple-negative breast cancer, compared with non-TNBC, likely arises fro

143 ent and Therapy Response Prediction in Early Breast Cancer) compares pathologic complete response (pC

144 results from The Cancer Genome Atlas (TCGA) breast cancer data set (n = 1215) to calculate previousl

145 Here, we analyzed human breast cancer data to identify transcriptional programs

146 ion about the use of hormonal contraception, breast-cancer diagnoses, and potential confounders.

147 nvasive breast cancer, median age at initial breast cancer diagnosis was 60.6 years (age range, 24.9-

148 Women were followed until February 2015 or breast cancer diagnosis.

149 h shorter patient delay and earlier stage at breast cancer diagnosis.

150 ists, and behavioral scientists to eliminate breast cancer disparities related to racial/ethnic ident

151 hly effective in inhibiting ERalpha-negative breast cancer due at least in part to epigenetic reactiv

152 h ovarian cancer, and 245 with contralateral breast cancer during follow-up.

153 Health Study (WCHS) in the African American Breast Cancer Epidemiology and Risk Consortium.

154 receptor tyrosine kinase 2 (ErbB2)-positive breast cancer (ErbB2(KI)), which exhibits aberrant beta-

155 s between medications of interest and second breast cancer events was observed when surveillance was

156 The majority of breast cancers expresses the estrogen receptor (ER(+)) a

157 Traditional treatments for breast cancer fail to address therapy-resistant cancer s

158 olling mammary stem cell (MaSC) activity and breast cancer formation remain poorly understood.

159 by age and menopausal status in over 11,000 breast-cancer-free women aged 35-85 years, from 40 ethni

160 In six of the 52 patients, breast cancer had been diagnosed at an outside instituti

161 carcinogenic effects, but protection against breast cancer has not been established.

162 Evidence on everolimus in breast cancer has placed hyperglycemia among the most co

163 neoadjuvant chemotherapy (NAC) for operable breast cancer has raised questions about optimal local t

164 xC(-) activity in vivo and its potential for breast cancer imaging.

165 relation of T2D to incidence of ER- and ER+ breast cancer in data from the Black Women's Health Stud

166 Family history was pertinent for breast cancer in her mother, sister, and maternal aunt.

167 Alcohol consumption was not associated with breast cancer in other categories of family history and

168 ctive cohort study, we evaluated the risk of breast cancer in relation to indoor heating and cooking

169 data set, was highly enriched in basal-like breast cancers in young individuals of African descent.

170 ctive to counteract the invasive behavior of breast cancer, indicating that blocking PI3K-AKT pathway

171 Substantial evidence suggests that breast cancer initiation, recurrence and drug resistance

172 for 1 year, unless disease recurrence or new breast cancer, intolerable adverse events, or consent wi

173 optimized lead compound (38u) that represses breast cancer invasion and migration.

174 erior therapeutic efficacy.MEK inhibition in breast cancer is associated with increased tumour infilt

175 Breast cancer is the most common cancer among women and

176 Foxa1 expression is linked with luminal breast cancer (LBC) with good prognosis, whereas Twist1

177 to systemic therapy alone for patients with breast cancer liver metastasis.

178 d by nasopharyngeal carcinoma CNE2 cells and breast cancer MDA-MB-231 cells, where these tumor cells

179 Among 7541 women with invasive breast cancer, median age at initial breast cancer diagn

180 ors and heterogeneous receptor expression in breast cancer metastases.

181 regulation of kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential

182 ional evidence that LOXL2 is a key driver of breast cancer metastasis in two conditional transgenic m

183 ysiologic role and new function for LOXL2 in breast cancer metastasis.

184 ecent work in a TP53(-/-)BRCA1-mutant murine breast cancer model indicates that double blockade with

185 The majority of breast cancer models for drug discovery are based on ort

186 significantly contribute to the diversity of breast cancer molecular subtypes and explain much of the

187 associations of vitamin D with lower risk of breast cancer morbidity and mortality.

188 terms of reduction of disease recurrence and breast cancer mortality.

189 During the same period, deaths after breast cancer (n = 134) were significantly reduced (40 d

190 eatment with chemotherapy and a diagnosis of breast cancer, non-Hodgkin lymphoma, or gynecologic canc

191 tential vanilloid 4 (TRPV4) in a subgroup of breast cancers of the basal molecular subtype.

192 In cell models of human breast cancer or in a cyclin D1-deficient model, we obse

193 Breast cancer originates from this epithelium, but the m

194 gative breast cancer and non-triple-negative breast cancer (P = .009, .003, and .001, respectively).

195 Consistently, breast cancer patient samples portrayed a strong and sig

196 n analyzed gene expression profiles of human breast cancer patients and patient-derived xenograft (PD

197 gical procedure performed, demonstrates that breast cancer patients receiving neoadjuvant chemotherap

198 In node-positive breast cancer patients treated with neoadjuvant chemothe

199 , representing novel therapeutic targets for breast cancer patients who smoke.

200 Importantly, breast cancer patients whose tumors express both low str

201 reliable prognostic biomarker in ER positive breast cancer patients, and predictive of preclinical se

202 ay significantly increase response rates for breast cancer patients, especially those with HER2 and E

203 d in cancers and signifies poor prognosis of breast cancer patients.

204 nd correlate with metastatic status in human breast cancer patients.

205 tween Src kinases, paxillin, and survival of breast cancer patients.

206 sidual cancer cells from neoadjuvant-treated breast cancer patients.

207 prognostic marker and therapeutic target in breast cancer patients.

208 monstrate the feasibility of our approach in breast cancer patients.

209 even independent data sets with totally 1079 breast cancer patients.

210 static niche formation and poor prognosis in breast cancer patients.

211 lateral cancer are a small proportion of the breast cancer population.

212 utation carriers leading to an international breast cancer prevention trial, and insights into the in

213 m phase 2 clinical trial of 15 patients with breast cancer previously treated in an academic medical

214 h centrally confirmed HER2-positive advanced breast cancer previously treated with both trastuzumab a

215 HD levels were independently associated with breast cancer prognostic characteristics and patient pro

216 ess response miRNA whose activity may define breast cancer progression and survival.

217 al relationships between Twist1 and Foxa1 in breast cancer progression are unknown.

218 es in patients with HER2-positive metastatic breast cancer randomized to an antibody-based (trastuzum

219 tential benefits of vitamin D for preventing breast cancer recurrence and mortality, yet data from pr

220 potential to serve as imaging biomarkers of breast cancer recurrence risk.

221 Tumor recurrence is the leading cause of breast cancer-related death.

222 Conclusion Older patients with breast cancer remain largely underrepresented in coopera

223 Metastatic breast cancer remains challenging to treat, and most pat

224 brain metastases at the time of diagnosis of breast cancer, representing 0.41% of the entire cohort a

225 -response elements and significantly induced breast cancer resistance protein (BCRP) gene transcripti

226 sporters, multidrug resistance protein 2 and breast cancer resistance protein.

227 differences shown for lung, colorectal, and breast cancers, respectively.

228 lower risk of breast cancer according to the Breast Cancer Risk Assessment Tool (Gail score).

229 graphic density (MD) is one of the strongest breast cancer risk factors.

230 ntal samples and extensive data on potential breast cancer risk factors.

231 according to genetic risk based on lifetime breast cancer risk from birth, as estimated by BOADICEA

232 Purpose Genetic testing for breast cancer risk is evolving rapidly, with growing use

233 ic load) increase the complexity of studying breast cancer risk related to racial/ethnic identity.

234 We analyze in depth two regulatory variants-breast cancer risk SNP rs11055880 and leukemia risk-asso

235 en from 25 to 76 years of age with increased breast cancer risk who underwent CE spectral mammography

236 ndpoint was participation (ie, attendance at breast cancer screening) within 90 days of the date of t

237 Breast cancer-specific survival assessed by Kaplan-Meier

238 h probably contributes to poorer overall and breast cancer-specific survival.

239 currence and drug resistance is supported by breast cancer stem cells (BCSCs).

240 Breast cancer stem cells represent the tumor subpopulati

241 potently inhibited tumorigenic potentials of breast cancer stem-like cells and rendered them sensitiv

242 he diagnosis and treatment of breast cancer, breast cancers still cause significant mortality.

243 A healthy control subjects from the Carolina Breast Cancer Study (CBCS) and the Women's Circle of Hea

244 e internet-based system of the International Breast Cancer Study Group, was stratified by type of pre

245 than 70% of recurrent tumors, regardless of breast cancer subtype.

246 the tumor-suppressive function of PTPN23 in breast cancer supports the identification of FYN as a th

247 Purpose Persistent pain after breast cancer surgery is a well-recognized problem, with

248 n strategies for those who undergo bilateral breast cancer surgery.

249 ee patients were recruited from the Shanghai Breast Cancer Survival Study, a longitudinal study of pa

250 eight loss intervention for African American breast cancer survivors (AABCS) on weight, body composit

251 been identified and contribute to hereditary breast cancer syndromes.

252 Now, almost 90 years after its first use in breast cancer, technology developments in diagnostic ima

253 eptor-positive, HER2-negative, node-positive breast cancer, the MammaPrint assay may be used in patie

254 -based adjuvant chemotherapy for early-stage breast cancer, the use of scalp cooling vs no scalp cool

255 (FERMT2) promotes metastatic progression of breast cancer through the recruitment and subversion of

256 generating PIP2, is positively expressed in breast cancer tissues, which correlates intimately with

257 related with beta-catenin and PKM2 levels in breast cancer tissues.

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

259 Triple-negative breast cancer (TNBC) patients commonly exhibit poor prog

260 eceptor-negative (ER(-)) and triple-negative breast cancer (TNBC), nitric oxide synthase-2 (NOS2) and

261 ese and to be diagnosed with triple-negative breast cancer (TNBC).

262 ghly activated in basal-like triple-negative breast cancer (TNBC).

263 Triple-negative breast cancers (TNBC) are highly aggressive, lack FDA-ap

264 ggressive cancers, including triple-negative breast cancers (TNBC), to utilize glutamine for survival

265 Triple-negative breast cancers (TNBCs) are more common among African-anc

266 se Trop-2, expressed in most triple-negative breast cancers (TNBCs), may be a potential target for an

267 orubicin (Cyclo/Dox), a common treatment for breast cancer, to female BALB/c mice near the beginning

268 TILs in patients with advanced HER2-positive breast cancer treated with either pertuzumab or placebo

269 r who are at risk for receiving nonguideline breast cancer treatment, which probably contributes to p

270 l of targeting YAP-BCAR4-glycolysis axis for breast cancer treatment.

271 In clinical specimens of breast cancer, TRIB1 levels correlated with expression o

272 oller of Wnt/beta-catenin signaling-mediated breast cancer tumorigenesis, metastasis, and cancer stem

273 We characterized T cells infiltrating both breast cancer tumors and the surrounding normal breast t

274 were used to identify females with invasive breast cancer undergoing planned mastectomy.

275 regnancy 6 months or more after diagnosis of breast cancer, vs 87.5% (95% CI, 86.5%-88.4%) for women

276 ears of follow-up, the incidence of invasive breast cancer was 5.7%, and the incidence of colorectal

277 alculated pore size of a brain metastasis of breast cancer was approximately 10-fold smaller than gli

278 41611 consecutively tested white women with breast cancer was estimated at 10.2%.

279 Results Breast cancer was screening-detected in 16 women (age ra

280 ation of hormonal contraception, the risk of breast cancer was still higher among the women who had u

281 d States from 2009 to 2013, the incidence of breast cancer was the highest of any cancer and the deat

282 risk of receiving nonguideline treatment of breast cancer were assessed in multivariable logistic re

283 The pharmacokinetic parameters of breast cancer were calculated by using the Tofts model w

284 States or Puerto Rico who had a sister with breast cancer were eligible.

285 013, 235 women undergoing PM for Stage 0-III breast cancer were randomized to undergo either standard

286 led trial, patients with HER2-positive early breast cancer were randomly assigned to receive treatmen

287 omy and breast reconstruction for unilateral breast cancer were recruited for this prospective observ

288 follow-up (mean = 6.4 years), 1,843 invasive breast cancers were diagnosed.

289 s highly dysregulated in aggressive forms of breast cancers, which overexpress CPEB2B.

290 constitute a large subgroup of patients with breast cancer who are at risk for receiving nonguideline

291 Women with stages I to III breast cancer who received all or part of their treatmen

292 ents with hormone receptor-positive advanced breast cancer who were not given dexamethasone mouthwash

293 Conclusion Patients with breast cancer who were treated in community oncology cli

294 ER2-negative, locally advanced or metastatic breast cancer, who had relapsed on or after endocrine th

295 odels to investigate whether associations of breast cancer with body mass index (BMI; weight (kg)/hei

296 uce the expression of pro-apoptotic genes in breast cancer with mutant p53.

297 e available on the survival of patients with breast cancer with preexisting mental illness, and elder

298 es to immune escape in an aggressive form of breast cancer, with potential implications for a novel i

299 major advances in the treatment of advanced breast cancer, with several targeted therapies that enha

300 antibody targets p5365-73 peptide-expressing breast cancer xenografts, significantly inhibiting tumor