ライフサイエンスコーパス: breast tumour

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

2 implicated Apc mutations in the aetiology of breast tumours.

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

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

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

6 overexpressed in approximately two thirds of breast tumours.

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

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

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

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

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

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

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

14 ceptor and directly correlated with FOXM1 in breast tumours.

15 fic haematopoietic activity present in human breast tumours.

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

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

18 ntributing to the aggressive phenotype of TN breast tumours.

19 nged the survival of mice bearing metastatic breast tumours.

20 lates with cell cannibalism in primary human breast tumours.

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

22 c is transcriptionally regulated by GATA3 in breast tumours.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 Human breast tumours are diverse in their natural history and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 overlapping homozygous deletions in lung and breast tumour lines.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 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)

125 20-year cumulative incidence of ipsilatelal breast tumour recurrence was 16.4% (99% CI 14.1-18.8) in

126 Ipsilateral breast tumour recurrence was the first treatment failure

127 The primary endpoint was ipsilateral breast tumour recurrence.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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