ライフサイエンスコーパス: breast tumor

1 rgizes with RT in control of syngeneic mouse breast tumor.

2 loid infiltration into the mammary gland and breast tumor.

3 REKA-Lipo-Dox) for the therapy of metastatic breast tumor.

4 motherapy and radiotherapy for their primary breast tumor.

5 ociated protein down-regulated in aggressive breast tumors.

6 erlying CHD4-mediated HIF transactivation in breast tumors.

7 and OR2W3 were abundant similar to invasive breast tumors.

8 ell lines, and with SNAI2 in patient-derived breast tumors.

9 s) are used clinically to treat BRCA-mutated breast tumors.

10 y derived from the epithelial compartment of breast tumors.

11 0.002) and G (l) (P = 0.0006) in orthotopic breast tumors.

12 role in suppressing metastatic competence of breast tumors.

13 ncer-derived lung tumors, but not in primary breast tumors.

14 e lung and co-expressed in a large number of breast tumors.

15 reported in brain metastatic but not primary breast tumors.

16 cation of genomic segments, in HER2-positive breast tumors.

17 arian, 10% of BRCA1 breast, and 46% of BRCA2 breast tumors.

18 impairment of the growth of 1q21.3-amplified breast tumors.

19 r cell lines and tissue specimens of primary breast tumors.

20 ion of T cell responses against AT-3-induced breast tumors.

21 h PIK3R1 expression significantly reduced in breast tumors.

22 hallmark of cancer, observable in >/=75% of breast tumors.

23 egatively correlated with Foxa1 in the human breast tumors.

24 help predict metastatic potential of luminal breast tumors.

25 sion observed in a large percentage of human breast tumors.

26 and centrosomal gene signature expression in breast tumors.

27 amples coming from brain, ovarian, lung, and breast tumors.

28 o suppress metastasis of HER2-overexpressing breast tumors.

29 tissue in patients with benign and malignant breast tumors.

30 n for the treatment of HER2+, PTEN-deficient breast tumors.

31 aterial-enhanced MR imaging in patients with breast tumors.

32 it is not known how PTHrP is upregulated in breast tumors.

33 as well as ex vivo-cultured ERalpha-positive breast tumors.

34 nrichment with APOBEC-signature mutations in breast tumors.

35 rs, including colorectal, neuroblastoma, and breast tumors.

36 ents with benign and patients with malignant breast tumors.

37 nt tissues of clinically characterized human breast tumors.

38 ting may treat neurofibromin-deficient ER(+) breast tumors.

39 3 zinc finger 2 mutants in ER-alpha positive breast tumors.

40 in clinical/experimental obesity-associated breast tumors.

41 l management strategy for poorly immunogenic breast tumors.

42 a MCF-7 cell line and in mice bearing MCF-7 breast tumors.

43 ient to segregate normal breast tissues from breast tumors.

44 upregulated heparanase in hormone-responsive breast tumors.

45 In primary TAMs from human and murine breast tumors, 5-LO expression was absent or low when co

46 triggered a potent inflammatory response in breast tumors able to induce long-lasting CD8(+) T cell-

47 In breast tumors, activation of the nuclear factor kappaB (

48 t and prevent local recurred triple negative breast tumors after surgical resection.

49 ncreased skipping of TRA2beta-PE detected in breast tumors, altering breast cancer cell viability, pr

50 Deregulated Notch signaling within the breast tumor and its tumor microenvironment (TME) is lin

51 ort of patients with invasive breast cancer, breast tumor and matched normal tissue sample data (as o

52 wed that miR-221 was abundantly expressed in breast tumor and metastatic MDA-MB-231 cells and its lev

53 Here we show that, in cultured breast tumor and non-tumorigenic mammary epithelial cell

54 lyses were performed on DNA from unprocessed breast tumor and tumor cells propagated from the same tu

55 Using transcriptomic samples for 1047 breast tumors and 110 healthy breast tissues from TCGA,

56 s this, we performed single-cell genomics of breast tumors and adjacent normal cells propagated for a

57 r cell migration, amplified in human primary breast tumors and associated with metastasis-free surviv

58 n tumors and normal tissues, with a focus on breast tumors and cell lines.

59 interrogate transcriptome data from primary breast tumors and find that among genes in 17q23, PRR11

60 odeling based on analysis of fifteen primary breast tumors and find that apparent clonal change betwe

61 publicly available ERalpha ChIP-seq data in breast tumors and found a striking resemblance in the ER

62 ld efficiently inhibit the in situ growth of breast tumors and further restrict their lung metastasis

63 igh degree in basal-like versus luminal-like breast tumors and healthy mammary tissue.

64 our data suggest that patients with hypoxic breast tumors and hypomethylated EGFR status may benefit

65 single-cell RNA sequencing of primary human breast tumors and identified new subsets of stromal mese

66 ent with prior reports, we observed in human breast tumors and in a mouse model of breast cancer that

67 ts, an independent cohort of triple-negative breast tumors and normal breast tissue was analyzed for

68 Gene expression data of breast tumors and normal tissues in the TCGA database we

69 otent synthetic lethality in triple-negative breast tumors and other aggressive tumors characterized

70 antly expressed in hormone-receptor-positive breast tumors and play a role in modulating pathway choi

71 romising for visualizing ErbB2 expression in breast tumors and serve as an adjunct during surgery to

72 ignaling contribute to D-2HG accumulation in breast tumors and show that D-2HG is an oncogenic metabo

73 D-2HG is the predominant enantiomer in human breast tumors and show that the D-2HG-producing mitochon

74 become capable of first homing to orthotopic breast tumors and then capturing angiogenin to prevent t

75 d magnetic resonance imaging data taken from breast tumors and time-course microarray gene expression

76 in expression, compared with matched primary breast tumors, and in patients with brain metastases, hy

77 driving dedifferentiation and malignancy of breast tumors, and loss of this binding activates variou

78 lified in 11% and/or overexpressed in 15% of breast tumors, and overexpression of MYST3 correlated wi

79 n levels are high in breast cancer cells and breast tumors, and the gene is often amplified in basal

80 wo E2F1-driven highly aggressive bladder and breast tumors, and use network analysis methods to ident

81 However, many breast tumors are a heterogeneous mixture of cell types

82 Breast tumors are characterized into subtypes based on t

83 Breast tumors are stiffer and more hypoxic than nonmalig

84 multi-regional sampling in a triple-negative breast tumor, arising in a LS patient over 10 years.

85 While it is common to stratify and treat breast tumors as a single entity, insights from studies

86 t cancer cells and its expression in primary breast tumors associated with a higher likelihood of met

87 lesion avidity were obtained for the primary breast tumor, axillary lymph nodes, and extraaxillary ly

88 lesion avidity were obtained for the primary breast tumor, axillary lymph nodes, and extraaxillary ly

89 ty of a clinical HMI system to differentiate breast tumors based on their relative HMI displacements,

90 ated that doxorubicin (DOX) treatment of 4T1 breast tumor-bearing mice led to the induction of IL-13R

91 sed on measurements of tumor volume, 4T1-luc breast tumor bioluminescence, and survival.

92 or the first time that histological types of breast tumors can be classified using subtle morphologic

93 an oncoprotein that is often overproduced in breast tumors, can block breast cancer cell anoikis via

94 of the whole-genome sequencing data for 215 breast tumors catalogued 99 recurrent gene fusions, 57%

95 a defining characteristic in BRCA-deficient breast tumors caused by genetic or epigenetic alteration

96 blished results revealed roles for SEMA7A in breast tumor cell growth, motility, invasion, and tumor-

97 n in vivo as a potential mechanism for early breast tumor cell invasion.

98 ancer-associated lncRNAs were studied in two breast tumor cell lines, MCF-7 and MDA-MB-231.

99 mposition of the tumor spheroids (MDA-MB-231 breast tumor cells + mesenchymal stem cells (MSCs)/human

100 icantly higher in the presence of metastatic breast tumor cells as compared to non-metastatic ones.

101 DeltaNp63 is able to drive the migration of breast tumor cells by inducing the expression of MTSS1.

102 ingle-cell traction force measurements using breast tumor cells embedded within 3D collagen matrices.

103 ory effect on the metastatic colonization of breast tumor cells in the lung.

104 ificantly reduced metastatic colonization by breast tumor cells in vivo.

105 We orthotopically implanted PyMT breast tumor cells into the mammary fat pads of syngenei

106 lso discovered that TSLP is expressed by the breast tumor cells themselves and acts to block breast c

107 In vivo, breast tumor cells utilize a specialized mode of migrati

108 tion of GLI-mediated signaling in epithelial breast tumor cells via EMT cell-induced production and s

109 ve an enhanced selectivity for HER2-positive breast tumor cells with high purity, reproducibility, an

110 alter migration and morphology of metastatic breast tumor cells, and this effect depends on the cells

111 c regulator of the innate immune response in breast tumor cells, and ZMYND8 may be a possible target

112 increases interleukin (IL)-33 released from breast tumor cells, which is crucial for the induction o

113 targeted monomeric CDK4 and CDK6 (CDK4/6) in breast tumor cells.

114 CM) with their ability to degrade the ECM in breast tumor cells.

115 drug delivery or for enumerating circulating breast tumor cells.

116 CXCL8/IL-8 chemokine expression in lung and breast tumor cells.

117 properties in GnRH-R-expressing prostate and breast tumor cells.

118 nd necessary for the viability and growth of breast tumor cells.

119 to suppress chemokine receptor expression in breast tumor cells.

120 inting to ATIP3 as a predictive biomarker of breast tumor chemosensitivity.

121 ed elevated levels of FN and MMP9 in patient breast tumors compared with healthy mammary glands.

122 tochemical analysis of a collection of human breast tumors confirmed that low expression of RASA1 is

123 cohort of 43 ER+ HER2- and ER- HER2- primary breast tumors, confirming many of the exon events identi

124 ted at both the mRNA and DNA levels in human breast tumors, consistent with its role in promoting cel

125 o found that increased miR-663 expression in breast tumors consistently correlates with increased pat

126 LGR4 expression in breast tumors correlated with poor prognosis.

127 Infiltration of T cells in breast tumors correlates with improved survival of patie

128 Elevated SIRT5 expression in human breast tumors correlates with poor patient prognosis.

129 geneity of hematopoietic cell populations in breast tumors corresponded to the amount of diversity pr

130 Notably, in three human breast tumors data sets the MTSS1/p63 co-expression is a

131 Analysis of mRNA expression profiles in breast tumors demonstrates that those with lower Trex1 a

132 ell line expressing or lacking single TF, 2) Breast tumors divided along PAM50 designations 3) Whole

133 ce in these relationships when stratified by breast tumor estrogen receptor (ER) status.

134 he data were integrated into a model showing breast tumors exhibit features on the proteomic, lipidom

135 Patients bearing primary ER(+) breast tumors, exhibiting a transcriptomic signature of

136 in both murine xenograft and patient-derived breast tumor explant models.

137 Whether plasma 25(OH)D interacts with breast tumor expression of vitamin D receptor (VDR) and

138 In human breast tumors, expression of genes associated with the w

139 In triple-negative breast tumors, factors associated with lower disease-fre

140 DGFRbeta and PDGFB has been noted in patient breast tumors for decades, how PDGFB-to-PDGFRbeta tumor-

141 e in vivo mouse models containing orthotopic breast tumors for in vivo SPECT/MRI and biodistribution

142 uterine serous tumors for ETV6 and 45 basal breast tumors for MITF and confirm that the correspondin

143 ing an excellent capacity for distinguishing breast tumors from black vs white patients (cross-valida

144 -positive and progesterone receptor-positive breast tumors from five patient cases using DW-MRI and [

145 djacent to tumor (normal pairs, n = 11), and breast tumors from NHB and NHW women (n = 64), with fewe

146 amed BGP successfully distinct 4T1 and MC4L2 breast tumors from normal lesions.

147 xplored a tissue microarray of 1,432 primary breast tumors from patients who underwent surgery betwee

148 Breast tumor FTV measured by MR imaging is a strong pred

149 ly from lung cancer in a collection of 4,801 breast tumor gene expression data.

150 Analysis of breast tumor gene expression datasets revealed an invers

151 s distinguish functional protein modules for breast tumor groups, with co-expression of EGFR and MET

152 functions and in the development of primary breast tumor growth and metastasis.Significance: Tumor-d

153 ogeneity confers some selective advantage on breast tumor growth and progression.

154 HC3-mediated protein palmitoylation supports breast tumor growth by modulating cellular oxidative str

155 iets of GTPs and BSp significantly inhibited breast tumor growth in ERalpha-negative mouse xenografts

156 h inducible MYST3 shRNAs potently attenuated breast tumor growth in mice.

157 Loss of HIF1/2alpha abolished CHD4-mediated breast tumor growth in mice.

158 ing and one lead compound potently inhibited breast tumor growth in murine xenograft models.

159 tumor, which directly restrained basal-like breast tumor growth in vivo.

160 umor-promoting signaling and acceleration of breast tumor growth under obese conditions.

161 endothelial cell tube formation in vitro and breast tumor growth, angiogenesis and metastasis in vivo

162 between BITC, p53/LKB1 and p73/LKB1 axes in breast tumor growth-inhibition.

163 n proliferation and cell death is pivotal to breast tumor growth.

164 of metastatic disease, and its expression in breast tumors has been associated with poor clinical out

165 Forty percent of ErbB2-positive breast tumors have an activating mutation in p110alpha,

166 ue microarray comprised of 363 primary human breast tumors, high PDGFB protein expression was prognos

167 de on its side wall and multiple copies of a breast-tumor-homing peptide at its tip.

168 modulated the microenvironment of orthotopic breast tumors in mice, and significantly reduced tumor g

169 Bioinformatic analysis of human breast tumors in The Cancer Genome Atlas database showed

170 s tumor-specific contrast in human xenograft breast tumors in vivo.

171 r findings were substantiated in a cohort of breast tumors in which IGF-1R expression was positively

172 measurements acquired routinely on a single breast tumor, including histopathology, MRI, and molecul

173 We combine this stochastic breast tumor induction model with inverted light-sheet i

174 types obtained from paired nonneoplastic and breast tumor-infiltrated tissues, all of which showed ex

175 unosuppressive tumor microenvironment during breast tumor initiation and progression, and prompt furt

176 These data establish a novel mechanism of breast tumor initiation involving IMP3 and they provide

177 The PAM50 classifier is widely used for breast tumor intrinsic subtyping based on gene expressio

178 ological inhibition of this pathway prevents breast tumor invasion and metastasis in vivo.

179 The chemotherapy of aggressive breast tumor is usually accompanied by a poor prognosis

180 findings, elevated MBNL1 expression in human breast tumors is associated with reduced metastatic rela

181 cular pathways underlying the development of breast tumors is critical for improving diagnosis, treat

182 Metabolic reprogramming in breast tumors is linked to increases in putative oncogen

183 se-associated phenotypes are mediated by the breast tumor kinase, Brk (PTK6), via the hypoxia-inducib

184 Neoadjuvant lapatinib therapy in HER2(+) breast tumors lead to a significant increase of phospho-

185 Prior to migration, breast tumor leader cells (K14(+)) were present througho

186 red in this environment the responses of two breast tumor lineages characterized by different molecul

187 actors altered neutrophil lipid profiles and breast tumor lung metastasis in mice.

188 DOX-MDSC promote breast tumor lung metastasis through MDSC miR-126a(+) ex

189 Measurements on about 313 human breast tumor margins showed more than 90% accuracy and n

190 ntralateral breast with radiomic features of breast tumors may improve the accuracy of digital mammog

191 Here, we show that in the human breast tumor microenvironment (TME), the presence of inc

192 Our results indicate that in the breast tumor microenvironment, IL-6 secreted from myoepi

193 10%) and PTX-PM (10%) in a syngeneic 4T1-luc breast tumor model based on measurements of tumor volume

194 ration of an immuno-nanoparticle in a murine breast tumor model drives a robust tumor site-specific A

195 In a xenograft breast tumor model, the SED alone or the ultrasound alon

196 onder phenomenon in an aggressive MCF10-CA1a breast tumor model.

197 nd drug-induced alterations in an orthotopic breast tumor model.

198 important to develop three-dimensional (3D) breast tumor models that recapitulate size-induced micro

199 In highly hypoxic murine or human xenograft breast tumor models, we found that administering either

200 associations were analyzed within individual breast tumor molecular subtypes, across multiple tumor t

201 depletion in mice decreases the invasion of breast tumors; moreover, epithelial tumor cells coxenogr

202 Fibroblasts from primary breast tumors, normal breast tissue, and lung tissue hav

203 primary breast epithelial cells and primary breast tumors obtained immediately following surgical ex

204 ls and its level was significantly higher in breast tumor or MDA-MB-231 cells than in distal non-tumo

205 ggest that only two thirds of postmenopausal breast tumors overexpress aromatase.

206 Importantly, when breast tumors overexpressed GRPR, high GRPR expression w

207 ty considering case-control, segregation and breast tumor pathology information was 3.23 x 10(-8) Our

208 Breast tumor perfusion was calculated from this short dy

209 In the clinic, breast tumors poorly infiltrated with immune cells are m

210 ntial diagnosis and therapy of heterogeneous breast tumors poses a major clinical challenge.

211 Finally, in primary breast tumors, PR-A expression was correlated negatively

212 n CD11b(hi) CD206(+) TAMs infiltrating mouse breast tumors prevents pulmonary metastasis and tumor ly

213 9 downregulation functionally contributes to breast tumor progression by recruiting macrophages to th

214 ion and cooperates with PTEN loss to promote breast tumor progression in mice.

215 To investigate the role of Hic-5 in breast tumor progression in vivo, Hic-5(-/-) mice were g

216 Breast tumor progression is accompanied by changes in th

217 ent and in limiting pre-invasive to invasive breast tumor progression, yet their differentiation and

218 e stromal ECM to promote non-cell autonomous breast tumor progression.

219 might be functionally important to regulate breast tumor progression.

220 bute to normal mammary gland development and breast tumor progression.

221 Presented herein, an unbiased analysis of breast tumor proteomes, inclusive of 9995 proteins quant

222 uced the cumulative incidence of ipsilateral breast tumor recurrence (IBTR) as a first event within 1

223 Time to ipsilateral breast tumor recurrence (IBTR) as first event.

224 termine the 5-year difference in ipsilateral breast tumor recurrence (IBTR) between 30 Gy in 5 once-d

225 eta-analysis of margin width and ipsilateral breast tumor recurrence (IBTR) from a systematic review

226 he effect of postoperative RT on ipsilateral breast tumor recurrence (IBTR) in a large randomized tri

227 To compare ipsilateral breast tumor recurrence (IBTR) in women with DCIS treate

228 Prognostic factors of ipsilateral breast tumor recurrence (IBTR) may change over time foll

229 Ipsilateral breast tumor recurrence.

230 In breast tumors, relationships between FOXA1 methylation a

231 he The Cancer Genome Atlas database of human breast tumors revealed a set of genes that are associate

232 e luminal mammary epithelial cells and ER(+) breast tumors revealed significant difference in the res

233 designed a two-stage study, including 1,000 breast tumor RNA-seq data from The Cancer Genome Atlas (

234 ts expression, variability, and structure in breast tumor RNA-sequencing data, a different dataset fr

235 We also analyze 416 nuclei from a frozen breast tumor sample and 380 nuclei from normal breast ti

236 = 0.0105) was found using a panel of primary breast tumor samples (n = 35), supporting a synergetic r

237 combination reduced the viability of patient breast tumor samples in an explant system.

238 g human-in-mouse xenograft luminal and basal breast tumor samples that are known to have significant

239 ively correlates with SNAI2 protein level in breast tumor samples, and higher USP20 expression is ass

240 versely correlates with NOTCH in human ER(+) breast tumor samples.

241 nd associated with metastatic progression in breast tumor samples.

242 ships between matched primary and metastasis breast tumor samples.

243 HER2 positive breast cancer cells and human breast tumor samples.

244 dopamine can be detected in human and mouse breast tumor samples.

245 odistribution studies in mice engrafted with breast tumors showed a distinct accumulation of cy-2-glu

246 Using patient breast tumor specimens, breast cancer cell lines, and a

247 cially observed in 60% of bladder and 53% of breast tumor specimens, whereas the expression of nectin

248 Using fSTREAM we assessed human breast tumors stained in vivo with fluorescent bevacizum

249 ns could predict clinical phenotypes such as breast tumor status and estrogen receptor status (AUC =

250 In the breast tumor-stroma interplay, paracrine factors such as

251 Patients with other breast tumor subtypes or older breast cancer patients di

252 than the normal mammary gland or the primary breast tumor, such as bone marrow, brain, and lung.

253 Obese women have higher risk of bearing breast tumors that are highly aggressive and resistant t

254 We identified a subset of luminal A primary breast tumors that give rise to HER2-enriched (HER2E) su

255 We show in mouse breast tumors that the action of the collagen receptor D

256 ning mammography, the proportion of detected breast tumors that were small (invasive tumors measuring

257 nd to be highly fibrotic, and unlike primary breast tumors, they exclude cytotoxic T lymphocytes (CTL

258 Intravital microscopy of NP spread in breast tumor tissue confirmed a significant difference i

259 cal variables and miRNA expression levels in breast tumor tissue is moderately predictive of risk of

260 Extraction of 10 mg BRCA-/-, p53-/- breast tumor tissue or normal mammary gland tissue with

261 study we compared the expression of DXME in breast tumor tissue samples from patients representing t

262 regions of interest within the phantoms and breast tumor tissue.

263 Expression studies in breast tumor tissues found SNP rs2787486 to be associate

264 ly, immunohistochemical analysis of clinical breast tumor tissues showed that high p62 expression lev

265 In breast tumor tissues, CD154 expression inversely correla

266 In breast tumor tissues, GLI1 expression enhanced tissue id

267 Furthermore, in human triple-negative breast tumor tissues, mitofusin and myoglobin levels wer

268 splay screens in mice bearing 4T1 metastatic breast tumors to identify peptides that target peritonea

269 f ERCC6 (1.8%) and ERCC8 (0.3%) mutations in breast tumors to known breast cancer susceptibility gene

270 nt has been implicated in the progression of breast tumors to metastasis.

271 Clinical and experimental data show that breast tumors treated with a p110alpha-specific inhibito

272 ical specimen and apply this measure to five breast tumors treated with neoadjuvant HER2-targeted the

273 e transcriptional profiles of murine Her2(+) breast tumor TUBO cells and their derived CSC-enriched t

274 ptional-regulatory events affected by APA in breast tumors, tumor datasets were analyzed for recurren

275 The basal-like 4T1 breast tumor underwent apoptosis and necrosis with the i

276 ted with HIF target gene expression in human breast tumors; upregulation of CHD4 and other known HIF

277 etastases, but not the corresponding primary breast tumors, use the serine biosynthesis pathway to su

278 ity and efficacy of DMDD to treat metastatic breast tumors using an in vivo mouse model of the 4T1 ma

279 SF imaging in porcine heart tissue and mouse breast tumor via local injections were studied and demon

280 oncometabolite, 2-hydroxyglutarate (2HG), in breast tumors was associated with MYC signaling, but not

281 Precontrast T1 relaxation in fat and breast tumors was computed with and without B1 correctio

282 Induction of PAQR4 in breast tumors was found to be subtype-independent and co

283 D4 and other known HIF coactivators in human breast tumors was mutually exclusive.

284 his was mediated even when growth of primary breast tumors was not affected by these treatments.

285 olecular signatures of SEPT9 upregulation in breast tumors, we overexpressed several of its isoforms

286 zation, measurements of benign and malignant breast tumors were conducted (n = 63) to compare perform

287 with subcutaneous triple negative xenograft breast tumors) were found to specifically target, elimin

288 dopamine has been directly detected in human breast tumors, which could inform future investigation i

289 Metabolic imaging of the primary breast tumor with (18)F-fluorodeoxyglucose ([(18)F]FDG)

290 howing the significant expression changes in breast tumors with a false discovery rate (FDR) < 1% in

291 of immune competent mice bearing orthotopic breast tumors with anti-mouse CD47 antibodies resulted i

292 ification of FYN as a therapeutic target for breast tumors with heterozygous or homozygous loss of PT

293 cer mouse model, MMTV-PyMT (PyMT), developed breast tumors with lung metastasis; however, mice delete

294 In the present study, we compared DNAm in breast tumors with normal-adjacent breast samples from T

295 e differentiation of malignant versus benign breast tumors with PET.

296 sion of PTPN23 in Comma 1Dbeta cells induced breast tumors within 56 wk.

297 e metabolite can be imaged by MALDI-MSI in a breast tumor xenograft model.

298 imaging data acquired from eight orthotopic breast tumor xenografts (i.e. a tumor 'ensemble').

299 ve and estrogen receptor (ER)-positive human breast tumor xenografts with or without VEGF overexpress

300 In human breast tumors, ZMYND8 was negatively correlated with ISG