ライフサイエンスコーパス: breast tumour

1 of mutations that are absent in the primary breast tumour.

2 ication in about 50% of mice with orthotopic breast tumours.

3 lence of TP53 somatic mutations in ER+ Asian breast tumours.

4 r cell lines and in a variable percentage of breast tumours.

5 implicated Apc mutations in the aetiology of breast tumours.

6 s prepared from a series of ERalpha-positive breast tumours.

7 tumours and (c) RASSF1 mutation analysis in breast tumours.

8 tor with the DBD of RFX4 occur in some human breast tumours.

9 overexpressed in approximately two thirds of breast tumours.

10 RNA levels are low in a large proportion of breast tumours.

11 o occur in the majority of invasive sporadic breast tumours.

12 s increased in ageing cerebral cortex and in breast tumours.

13 nd BRCA2 and in a control series of sporadic breast tumours.

14 alignant cell growth, were reported in human breast tumours.

15 n 14/27 carcinoma cell lines and 3/6 primary breast tumours.

16 f cell lines, including several derived from breast tumours.

17 ouse colon carcinomas and poorly immunogenic breast tumours.

18 ines and 952 whole-genome sequenced lung and breast tumours.

19 g therapeutic intervention for TBX2-addicted breast tumours.

20 y for PI3Kbetai/AKTi sensitive and resistant breast tumours.

21 inguish their transcriptomes in 1780 primary breast tumours.

22 ting complete regression of CPI-unresponsive breast tumours.

23 lates with cell cannibalism in primary human breast tumours.

24 ate target genes and somatic driver genes in breast tumours.

25 ceptor and directly correlated with FOXM1 in breast tumours.

26 fic haematopoietic activity present in human breast tumours.

27 lified in approximately 10.5% of ER-positive breast tumours.

28 ognostic power of HOTAIR in aggressive HER2+ breast tumours.

29 ntributing to the aggressive phenotype of TN breast tumours.

30 nged the survival of mice bearing metastatic breast tumours.

31 maging in female mice bearing metastatic 4T1 breast tumours.

32 c is transcriptionally regulated by GATA3 in breast tumours.

33 umour cell lines (65%, 13/20) and in primary breast tumours (38%, 15/40).

34 was important to clinical outcome in primary breast tumours a tissue microarray (TMA) containing biop

35 echnique and its indications with regards to breast tumours according to the existing literature.

36 n 7/7 normal breast tissues but only in 9/12 breast tumours analysed.

37 In total, 47 paired breast tumour and metastatic axillary lymph node samples

38 l, and copy number profiles of 560 Malaysian breast tumours and a comparative analysis of breast canc

39 le in vivo scenarios, including treatment of breast tumours and acute injury in the liver and modelli

40 gene expression analysis of matched primary breast tumours and bone metastasis-derived patient-deriv

41 hose mRNA was found to be expressed in human breast tumours and breast cancer cell lines.

42 messenger RNA is upregulated in most primary breast tumours and breast cancer cell lines.

43 The results show that breast tumours and cell lines comprise a large milieu of

44 X was found to be upregulated in a subset of breast tumours and cell lines.

45 sed in metastatic cells and metastatic human breast tumours and destabilizes transcripts containing T

46 We screened TOX3 for mutations in 133 breast tumours and identified four mutations (three miss

47 17q23 amplification occurs in 20% of primary breast tumours and is associated with poor outcome.

48 ffective treatments for reducing the size of breast tumours and levels of ER phosphorylation when giv

49 es with interleukin-11 expression in primary breast tumours and low interleukin-11 correlates with re

50 HOTAIR is increased in expression in primary breast tumours and metastases, and HOTAIR expression lev

51 ssed in human breast cancer cells, malignant breast tumours and metastases.

52 Our analysis revealed alterations in 2/70 breast tumours and none of the ovarian carcinomas.

53 -L1 expression were observed between primary breast tumours and paired axillary lymph nodes.

54 ene expression changes are found in clinical breast tumours and patient-derived xenograft samples tha

55 Relevant data on contralateral breast tumours and side-effects were included from an ov

56 ker which may prove of use in the staging of breast tumours and the stratification of breast cancer p

57 the growth of spontaneously formed malignant breast tumours and their associated metastases in mice.

58 lucidate how the molecular interplay between breast tumours and their microenvironment drives aggress

59 egions of persyn mRNA and the persyn gene in breast tumours and tumour cell lines.

60 MMP-3), a stromal enzyme upregulated in many breast tumours, and found that MMP-3 can cause epithelia

61 roduced in both basal-like and luminal human breast tumours, and its expression levels are tightly co

62 he mammalian extracellular matrix, including breast tumours, and osteoarthritic cartilage.

63 The anti-breast tumour antibody SM3 has a high selectivity in rea

64 ular composition of the immune infiltrate in breast tumours appear to exist, and these differences ar

65 s comprise 40% of all metastatic tumours and breast tumours are among the tumours that most commonly

66 Most BRCA1-associated breast tumours are basal-like yet originate from luminal

67 vidence that cancer stem cells (CSCs) within breast tumours are capable of metastasis, but the mechan

68 Human breast tumours are diverse in their natural history and

69 Breast tumours are embedded in a collagen I-rich extrace

70 phenotype expressed by the vast majority of breast tumours are luminal.

71 High SOX11 levels in breast tumours are significantly associated with distant

72 The status of p53 was investigated in breast tumours arising in germ-line carriers of mutant a

73 mplification in approximately 12% of primary breast tumours, as well as in breast, ovarian, colon, pr

74 pes within the basal subgroup of ER negative breast tumours, associated with apoptotic and immune res

75 eceptor negative luminal progenitor cells in breast tumour biopsies of hormone receptor negative canc

76 L/CD154) is expressed in CD40-positive human breast tumour biopsies, suggesting that the constitutive

77 ed to normal breast tissues (BN) and primary breast tumours (BP).

78 e Met-DNA tested is detectable in some human breast tumours but not in normal tissue.

79 show that lncRNA-based profiling categorizes breast tumours by their known molecular subtypes in brea

80 RASSF2 suppressed breast tumour cell growth in vitro and in vivo, while th

81 metastatic breast cancer cells and represses breast tumour cell intravasation and bone metastasis in

82 promoter region of DUTT1 gene in the HTB-19 breast tumour cell line (not expressing DUTT1) showed co

83 ate brk transcript is expressed in the human breast tumour cell line T-47D.

84 ion of the range of transcripts encoded in a breast tumour cell line, compared to normal breast, sugg

85 RASSF2 was frequently methylated in breast tumour cell lines (65%, 13/20) and in primary bre

86 sion could be switched back on in methylated breast tumour cell lines after treatment with 5'-aza-2'd

87 mplification has been previously detected in breast tumour cell lines and in colon tumours; here, we

88 r 60% of breast carcinoma tissue samples and breast tumour cell lines, but not normal mammary tissue

89 osphorylation events in two triple- negative breast tumour cell lines, MFM223 and SUM52, that exhibit

90 overlapping homozygous deletions in lung and breast tumour-cell lines have defined a minimal critical

91 major histocompatibility complex class I on breast tumour cells and that treatment with BML-210 subs

92 human epidermal growth factor receptor 2 on breast tumour cells can be halted by disengaging the T c

93 induced by hypoxia in tumours in vivo and in breast tumour cells in vitro, and that C/EBPdelta-defici

94 vascular mimicry drives the ability of some breast tumour cells to contribute to distant metastases

95 s are functionally active in patient-derived breast tumour cells, cell lines, and cancer-associated f

96 hysiological bone matrices seeded with human breast tumour cells, the presence of bone mineral reduce

97 ey factor secreted exclusively by aggressive breast tumour cells, which induces CAF conversion.

98 e metastasis in mice bearing RKIP-expressing breast tumour cells.

99 ns are critical for the survival of ERBB2+ve breast tumour cells.

100 normalized growth of transplanted MMTV-PyMT breast tumours cells.

101 This study compared breast tumour characteristics between YPM women (under 3

102 w this HIV differential varies by patient or breast tumour characteristics.

103 Sequencing studies of breast tumour cohorts have identified many prevalent mut

104 n addition, Brn-3b expression is elevated in breast tumours compared to levels in normal mammary cell

105 ly, subsets of CSCs in some human and murine breast tumours contain lower ROS levels than correspondi

106 These results suggest that development of breast tumours correlates with overexpression of the wil

107 r-associated CpG island of the CLCA2 gene in breast tumours demonstrated that the absence of expressi

108 of the ErbB-ligand, Heregulinbeta1 (HRG), to breast tumour-derived T47D cells promotes D-cyclin expre

109 nly prognostic miRNA signatures derived from breast tumours devoid of somatic copy-number aberrations

110 table photothermal effect to kill 4T1 murine breast tumours established on BALB/c mice.

111 cell line xenografts and primary ERalpha(+) breast tumour explants, and had increased anti-prolifera

112 Most breast tumours express the oestrogen receptor and are tr

113 benign lesions, approximately two-thirds of breast tumours expressed appreciable levels, and 27% of

114 mitogenesis, and raises the possibility that breast tumours expressing BRK may acquire a resistance t

115 We demonstrate that breast tumours fall along a continuum constrained by thr

116 nables an evaluation of the residual size of breast tumours following neoadjuvant systemic therapy (N

117 lational gene network response that enhances breast tumour formation and growth.

118 ptomic profiles of pre-treatment biopsies of breast tumours from 168 patients treated with chemothera

119 s in a set of 65 surgical specimens of human breast tumours from 42 different individuals, using comp

120 We also find that breast tumours from carriers of heterozygous mutations i

121 d miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss o

122 d approach combining statistical analysis of breast tumour gene expression data and experimental vali

123 genomic characterization of 64 HER2-positive breast tumour genomes that exhibit four subgroups, based

124 al and stromal compartments are required for breast tumour growth and progression.

125 kdown of lncRNA-JADE significantly inhibited breast tumour growth in vivo.

126 o models, we found that neuronal SP promoted breast tumour growth, invasion and metastasis.

127 protein (AP)-2gamma transcription factor in breast tumours has been identified as an independent pre

128 ly disrupting mutations of BRCA1 in sporadic breast tumours has suggested that other mechanisms, incl

129 Here we develop a polyclonal mouse model of breast tumour heterogeneity, and show that distinct clon

130 sequences generated using DNA derived from a breast tumour (histological grade; poorly differentiated

131 We took core biopsy samples from primary breast tumours in 24 patients before treatment and then

132 Compared to breast tumours in Caucasian women, we show an increased

133 levels of lncRNA-JADE were observed in human breast tumours in comparison with normal breast tissues.

134 rate the importance of the genetic makeup of breast tumours in dictating pro-metastatic systemic infl

135 ly labelled polyacrylamide beads injected in breast tumours in mice as well as mathematical modelling

136 the detection and image-guided resection of breast tumours in vivo using a smartphone with modified

137 f Sox9 reduces growth of tamoxifen-resistant breast tumours in vivo.

138 and transcriptomic study of 2,000 individual breast tumours, in the context of the human genome-scale

139 Accordingly, increased hypoxia in mouse breast tumours increases hypermethylation, while restora

140 of heterozygosity (LOH) analyses of sporadic breast tumours indicate that there are many other putati

141 ular composition of the immune infiltrate in breast tumours influence survival and treatment response

142 ssion of miR-10b in otherwise non-metastatic breast tumours initiates robust invasion and metastasis.

143 Here we show that TGFbeta increases breast tumour-initiating cell (BTIC) numbers but only in

144 Mutating KLF4 methylation sites suppresses breast tumour initiation and progression, and immunohist

145 breast carcinogenesis and the progression of breast tumours into lethal, treatment-refractory systemi

146 Overexpression of miR-182 promotes breast tumour invasion and TGFbeta-induced osteoclastoge

147 id composition in adipose tissue adjacent to breast tumour is observed in ex vivo and animal models.

148 of aggressiveness and metastatic features in breast tumours is accompanied by the elevated PML expres

149 Immune infiltration of breast tumours is associated with clinical outcome.

150 ptor 2 (HER2; also known as ERBB2) status of breast tumours is emphasised in various national guideli

151 er evolution during the expansion of primary breast tumours is limited(1,2).

152 pression was not detectable in one out of 18 breast tumour lines analysed by RT-PCR.

153 that only a fraction of the ERBB2-amplified breast tumour lines are truly addicted to the ERBB2 onco

154 overlapping homozygous deletions in lung and breast tumour lines.

155 mense potential of this device for automated breast tumour margin assessment to minimise repeat invas

156 af kinase inhibitory protein (RKIP) inhibits breast tumour metastasis in part via let-7.

157 demonstrate that inhibition of CDK4/6 blocks breast tumour metastasis in the triple-negative breast c

158 escribed pathway in which a component of the breast tumour microenvironment alters cellular structure

159 y microfluidic device for co-culture of a 3D breast tumour model and a 2D endothelium model for cross

160 c antitumour immunity in ovarian, colon, and breast tumour models in multiple anatomic locations.

161 Current breast tumour models, such as those from oncogenically t

162 High expression of LOX in primary breast tumours or systemic delivery of LOX leads to oste

163 nal interaction of mouse- or patient-derived breast tumour organoids and tumour-specific cytotoxic T

164 Here we report that microRNA-30c, a human breast tumour prognostic marker, has a pivotal role in c

165 n deficiency, is known to be associated with breast tumour progression, resistance to conventional th

166 ing an involvement of the encoded protein in breast tumour progression.

167 nd that their upregulation may contribute to breast tumour progression.

168 ated quality of life (HRQOL) and ipsilateral breast tumour recurrence (IBTR) outcomes in this populat

169 cancer at below average risk of ipsilateral breast tumour recurrence (IBTR).

170 fferences in the hazard rate for ipsilateral breast tumour recurrence in the first decade after treat

171 the univariate hazard ratio for ipsilateral breast tumour recurrence in women assigned to no radioth

172 However, the 5-year rate of ipsilateral breast tumour recurrence is probably low enough for omis

173 s as first salvage treatment for ipsilateral breast tumour recurrence occurred in 279 (79%) of 354 pa

174 outcome was the biopsy-confirmed ipsilateral breast tumour recurrence rate determined using the Kapla

175 for longer-term outcomes such as ipsilateral breast tumour recurrence rates and contralateral breast

176 w-up of 5 years (IQR 3.84-6.05), ipsilateral breast tumour recurrence was 1.3% (95% CI 0.2-2.3; n=5)

177 20-year cumulative incidence of ipsilatelal breast tumour recurrence was 16.4% (99% CI 14.1-18.8) in

178 Ipsilateral breast tumour recurrence was significantly lower in the

179 Ipsilateral breast tumour recurrence was the first treatment failure

180 , p<0.0001), subsequent risks of ipsilateral breast tumour recurrence were similar in both groups (0.

181 endpoint of the original trial, ipsilateral breast tumour recurrence, and the co-primary endpoint, o

182 The primary endpoint was ipsilateral breast tumour recurrence.

183 ly-stage breast cancer decreases ipsilateral breast-tumour recurrence (IBTR), yielding comparable res

184 26.4 months (IQR 15.2-39.6), no ipsilateral breast tumour recurrences occurred in these 31 patients.

185 The primary endpoint was ipsilateral breast tumour relapse (IBTR) analysed by intention to tr

186 5-year incidence of ipsilateral breast tumour relapse after 40 Gy was 2.1% (1.4 to 3.1);

187 The primary endpoint was ipsilateral breast tumour relapse; assuming a 2% 5-year incidence fo

188 In a cohort of 71 breast tumour resection samples, automated scoring showe

189 ry and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical fo

190 expression profiles of a set of 33 familial breast tumours revealed that FOXA1 promoter methylation

191 Expression studies in human breast tumour samples demonstrate correlation between No

192 First ex vivo imaging of breast tumour samples revealed excellent contrast betwee

193 fresh frozen (FF) sequential patient-matched breast tumour samples.

194 sequencing for the detection of mutations in breast-tumour samples from 16 patients, and to monitor t

195 ncies, we established a meta-cohort of 1,828 breast tumours spanning pre-invasive, primary invasive a

196 those observed in normal breast tissue or in breast tumour specimens revealed features of the express

197 id composition spectra were acquired from 17 breast tumour specimens, 15 healthy female volunteers an

198 re compared using PUFA spectra from 17 human breast tumour specimens, 15 healthy female volunteers, a

199 molecules was found in cancer cell lines and breast tumour specimens.

200 was methylated in 16 out of 20 p53-negative breast tumour specimens.

201 However, A3B-null breast tumours still have this mutational bias.

202 on 17q23 and is often over-expressed in this breast tumour subset.

203 ypically occurs years after the removal of a breast tumour, suggesting that disseminated cancer cells

204 oestrogen receptor alpha positive (ERalpha) breast tumours, suggesting a potential interaction betwe

205 also observe elevated immune scores in Asian breast tumours, suggesting potential clinical response t

206 their multiple occurrence in BRCA-associated breast tumours suggests that these novel p53 mutants are

207 Strikingly, breast tumour suppression on Skp2 deficiency can be resc

208 r our data refute a role for CAVEOLIN-1 as a breast tumour suppressor gene in vivo.

209 el TBX2-repressed target genes including the breast tumour suppressor NDRG1 (N-myc downregulated gene

210 o co-repress EGR1-target genes including the breast tumour suppressor NDRG1.

211 Cre-mediated excision of exon 11 of the breast-tumour suppressor gene Brca1 in mouse mammary epi

212 of the vasculature in an experimental human breast tumour that overexpresses HER2 in mice, and that

213 tudy, we sequence 173 genes in 2,433 primary breast tumours that have copy number aberration (CNA), g

214 Importantly, we find that patients with breast tumours that overexpress Jumonji demethylases hav

215 In human breast tumours, the EMT-transcription factors strongly c

216 scence in-situ hybridisation of two cores of breast tumour tissue in a microarray, done in a central

217 with the therapeutic elimination of primary breast tumours to prevent recurrent metastatic disease.

218 ganization and the transcription profiles of breast tumours to promote growth and metastasis; this is

219 pare the expression of PD-1/PD-L1 in primary breast tumours to that in metastatic axillary lymph node

220 atment with BML-210 substantially sensitized breast tumours to the inhibitor of the checkpoint progra

221 overlapping homozygous deletions in lung and breast tumours/tumour lines and defined a small region o

222 bility for the lymphocytic infiltrate in 998 breast tumours using a novel virtual biopsy method.

223 BP and in BBM and their originating primary breast tumours using Combined Bisulphite and Restriction

224 was observed in both primary and metastatic breast tumours, varying in degree from extreme selective

225 lantation and the second case is a malignant breast tumour which is hyperechogenic on sonography.

226 verexpression of the ERBB2 proto-oncogene in breast tumours, which occurs in 25-30% of patients, corr

227 that SOX11 may be a potential biomarker for breast tumours with elevated risk of developing metastas

228 eport the miRNA expression profiles of 1,302 breast tumours with matching detailed clinical annotatio

229 MTA1s expression is increased in human breast tumours with no or low nuclear ER.

230 f capturing and studying tumour biology, and breast tumour xenografts are generally assumed to be rea

231 In human breast tumour xenografts, inhibition of the PAR-complex-