ライフサイエンスコーパス: breast tumor

1 motherapy and radiotherapy for their primary breast tumor.

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

3 o suppress metastasis of HER2-overexpressing breast tumors.

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

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

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

7 nrichment with APOBEC-signature mutations in breast tumors.

8 ) were inversely associated with risk of ER- breast tumors.

9 ng lung metastasis and 12-HETE production in breast tumors.

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

11 nanoparticles inhibits in vivo growth of 4T1 breast tumors.

12 ly co-occurs with PI3K pathway activation in breast tumors.

13 , which was further substantiated in primary breast tumors.

14 hese molecules in multiple subtypes of human breast tumors.

15 pinges on a pro-tumorigenic role of MTSS1 in breast tumors.

16 differentiation between malignant and benign breast tumors.

17 and a modulator of tumor microenvironment in breast tumors.

18 with poor prognosis in triple-negative human breast tumors.

19 most highly upregulated protein in RESTless breast tumors.

20 gene) are associated with aggressiveness of breast tumors.

21 molecular subtype within the triple negative breast tumors.

22 ed the search for the cellular precursors of breast tumors.

23 ded insight into the origin and evolution of breast tumors.

24 integral component of HER2 biology in HER2+ breast tumors.

25 reported in brain metastatic but not primary breast tumors.

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

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

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

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

30 h PIK3R1 expression significantly reduced in breast tumors.

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

32 egatively correlated with Foxa1 in the human breast tumors.

33 help predict metastatic potential of luminal breast tumors.

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

35 and centrosomal gene signature expression in breast tumors.

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

37 Women with breast tumors 3 cm or larger scheduled for NACT underwen

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

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

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

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

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

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

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

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

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

47 lated RNA from samples obtained from primary breast tumors and also from brain metastatic lesions fol

48 essed in luminal, estrogen-receptor positive breast tumors and cell lines.

49 TNBC, we evaluated phosphatase expression in breast tumors and characterized their contributions to i

50 and ERalpha in recurrent tamoxifen-resistant breast tumors and conducted a genome-wide target gene pr

51 ng the most aggressive and therapy-resistant breast tumors and currently possess almost no molecular

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

53 Using RNA-sequencing data from breast tumors and germline genotypes from The Cancer Gen

54 UCL1 expression is highest in HER2-amplified breast tumors and inhibiting HER2 activity in tumor cell

55 y offer a strategy to treat taxane-resistant breast tumors and metastases.

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

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

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

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

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

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

62 indings into the examination of 1100 primary breast tumors and six breast cancer cell lines.

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

64 SD3 was highly expressed in ERalpha-positive breast tumors and treatment with estradiol increased SUS

65 ACSS2 exhibits copy-number gain in human breast tumors, and ACSS2 expression correlates with dise

66 icroenvironmental heterogeneity for advanced breast tumors, and highlight that ecological statistics

67 plicing factor SRSF1 is upregulated in human breast tumors, and its overexpression promotes transform

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

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

70 ions were identified in 23% of HER2-positive breast tumors, and these mutations were associated with

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

72 Breast tumors are characterized by an extensive desmopla

73 Breast tumors are characterized into subtypes based on t

74 Breast tumors are stiffer and more hypoxic than nonmalig

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

76 y correlated with PI3K pathway activation in breast tumors as assessed by gene expression and phospho

77 fic APA profiling identified triple-negative breast tumors as having the highest levels of APA.

78 esonance (MR) imaging protocol developed for breast tumor assessment and to compare it with 7-T diffu

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

80 h SRC expression defines basal-like and HER2 breast tumors associated with poor clinical outcome.

81 tions where 60 subjects with newly diagnosed breast tumors (at least 2 cm in the longest dimension) w

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

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

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

85 In human breast tumors, beclin 1 expression is inversely correlat

86 In breast tumor biopsies from women diagnosed with BrCA we

87 tibody, not only eradicating the primary 4T1 breast tumor but also significantly preventing metastasi

88 nt expression of MAGI3(pPA) in primary human breast tumors but not in tumor-adjacent normal tissues.

89 a poor clinical outcome in patients with ER+ breast tumors by enhancing stem-like properties in these

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

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

92 ere found to be important for BCAR3-mediated breast tumor cell chemotaxis toward serum and invasion i

93 3 (BCAR3) promotes adhesion disassembly and breast tumor cell invasion.

94 Analysis of breast tumor cell lines showed that REST directly repres

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

96 at exerted potent antitumor activity against breast tumor cell lines.

97 gulin was enriched in ERalpha-positive human breast tumor cells and required for estrogen-dependent g

98 of BCAR3 is in complex with Cas in invasive breast tumor cells and that these proteins colocalize in

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

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

101 t tumor suppressor that induces apoptosis of breast tumor cells by selectively enhancing mRNA decay o

102 Loss of REST renders MCF7 and MDA-MB-231 breast tumor cells dependent on IRS1 activity for colony

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

104 udy, we show that GM-CSF produced by primary breast tumor cells induced the activation of plasmacytoi

105 Silencing ARF6 or JIP3/JIP4 in breast tumor cells results in MT1-MMP endosome mispositi

106 an epigenetically distinct subpopulation of breast tumor cells that have an enhanced capacity to col

107 enhanced signaling, growth, and migration in breast tumor cells that occur upon REST loss.

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

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

110 ound that MCPIP1 expression was repressed in breast tumor cells, and overexpression of MCPIP1 induced

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

112 ensitivity to radiation in p53 mutant Hs578t breast tumor cells, HN6 head and neck tumor cells, and H

113 lthough CRD-BP mRNA expression is induced in breast tumor cells, levels remain approximately 1000-fol

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

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

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

117 drug delivery or for enumerating circulating breast tumor cells.

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

119 PKA regulatory subunit, induced spontaneous breast tumors characterized by enhanced type-II PKA acti

120 e we report that miR-873 is downregulated in breast tumor compared with normal tissue.

121 on was highest in estrogen receptor-positive breast tumors compared with many other cancer subtypes,

122 ressed the GM-CSF receptor were increased in breast tumors compared with noninvolved adjacent breast

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

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

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

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

127 confirmed that only a fraction of vessels in breast tumors contain SMA(+) TECs, suggesting that not a

128 LGR4 expression in breast tumors correlated with poor prognosis.

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

130 package with an application to multi-source breast tumor data from The Cancer Genome Atlas.

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

132 breast MR imaging, enables quantification of breast tumor deformation and displacement secondary to c

133 magnetic resonance (MR) imaging to quantify breast tumor deformation and displacement secondary to t

134 riendly 2-min dynamic acquisition to monitor breast tumor DeltaBF to neoadjuvant chemotherapy using (

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

136 nvestigated the effect of LIMK inhibition on breast tumor development and on paclitaxel-resistant tum

137 ng to nuclear SREBP-1a was also critical for breast tumor development in vivo.

138 tumors, we generated genetic mouse models of breast tumors driven by concurrent Her2 activation and P

139 ive breast cancer recurrence and new primary breast tumors during a mean of 7.3 years of study follow

140 hosts, limiting the outgrowth of KRas-driven breast tumors, even though trametinib largely failed to

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

142 propose a method to identify CDR3 reads in a breast tumor exome and validate it using deep TCRB seque

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

144 Breast tumors exposed to high circulating levels of TSLP

145 We have previously shown that in human breast tumors expressing both CSF1 and CSF1R, invasion i

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

147 istration to mice bearing uPA-overexpressing breast tumors, FAM-labeled uCendR peptide and uCendR-coa

148 t healthy volunteers and 17 patients with 20 breast tumors (five benign, 15 malignant).

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

150 n, ribavirin, safely and potently suppresses breast tumor formation.

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

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

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

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

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

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

157 e has demonstrated that CAIX is required for breast tumor growth and metastasis; however, the mechani

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

159 al relevance, demonstrating that TP53 mutant breast tumor growth can be suppressed by pharmacologic T

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

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

162 strated stable SOX2 repression and long-term breast tumor growth inhibition, which lasted for >100 da

163 rlying mechanism by which Sema 3A suppresses breast tumor growth is still unexplored.

164 matrix (ECM), is thought to be critical for breast tumor growth, invasion and metastasis.

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

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

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

168 Macrophage infiltration and recruitment in breast tumors has been correlated with poor prognosis in

169 ignaling and cell survival and HER2-enriched breast tumors have a poor outcome when Akt is upregulate

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

171 ure studies using (18)F-fluciclovine PET for breast tumor imaging as well as for detection of locoreg

172 administration blocked the growth of primary breast tumors in several murine models and reduced the d

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

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

175 Here, we comprehensively profiled 817 breast tumors, including 127 ILC, 490 ductal (IDC), and

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

177 AM preconditioned by breast tumors inhibited Th1 and favored generation of Th

178 e combination in inducing differentiation of breast tumor-initiating cells in vivo Furthermore, gene

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

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

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

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

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

184 The microenvironment of breast tumors is often hypoxic, and because apoptosis is

185 We find that gene expression in metastatic breast tumors is pervasively correlated with gene expres

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

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

188 However, the degree to which metastatic breast tumors locally reprogram stromal cells as they di

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

190 We recreate the breast tumor mechanical environment by controlling the m

191 tween FLT1 and inflammatory responses within breast tumor metastases.

192 capacity is a major biological correlate of breast tumor metastatic potential.

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

194 The breast tumor microenvironment (TMEN) is a unique niche w

195 roteoglycan chains are key components of the breast tumor microenvironment that critically influence

196 atase and, hence, estrogen production in the breast tumor microenvironment.

197 he ethnic disparity in the aggressiveness of breast tumors might be transmitted through social influe

198 sis and anti-tumor effects in the VEGFR2-luc breast tumor model proven by BLI, WB and immunohistochem

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

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

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

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

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

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

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

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

207 terodimerization with ErbB2 overexpressed in breast tumors or other cancers.

208 nd dramatically reduced growth of MDA-MB-231 breast tumors or U87 gliomas in murine xenografts.

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

210 the importance of EGF receptor signaling in breast tumor pathogenesis and therapeutic response.

211 Studying the role of IL17 in invasive breast tumor pathogenesis, we found that metastatic prim

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

213 Breast tumor perfusion was calculated from this short dy

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

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

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

217 otein and RNA expression in ERalpha-positive breast tumors predicted favorable outcome in patients tr

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

219 e differences and the phenotypic reversal of breast tumor pro-angiogenic TEM to a weak pro-angiogenic

220 nical models to study mechanisms involved in breast tumor progression as well as antitumor drug effec

221 a candidate tumor suppressor that attenuates breast tumor progression by binding with its co-receptor

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

223 Breast tumor progression is accompanied by changes in th

224 Understanding what drives breast tumor progression is of utmost importance for blo

225 might be functionally important to regulate breast tumor progression.

226 maphorin 7a may be novel target for blocking breast tumor progression.

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

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

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

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

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

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

233 stage breast cancer significantly reduces in-breast tumor recurrence and improves overall survival.

234 Ipsilateral breast tumor recurrence.

235 -PXXP interaction screen, we identified Brk (breast tumor-related kinase) as a high-affinity p27 kina

236 lear whether cellular heterogeneity within a breast tumor results from transformation of bipotent bas

237 files with gene expression profiles of human breast tumors revealed significant linkage between right

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

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

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

241 increased tissue factor expression in human breast tumor samples.

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

243 imate HER2 (ERBB2) activation status for 662 breast-tumor samples and found that the Rsubread data re

244 locus analysis in normal breast tissues and breast tumors showed that the g (risk) allele of rs10941

245 Analysis of a large set of breast tumors shows a significant correlation between cy

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

247 gulated in a significant proportion of human breast tumor specimens.

248 ate had a reduced capability to migrate into breast tumor spheroids, the majority of cells remaining

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

250 Breast tumor subtype-specific APA profiling identified t

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

252 gene signature associated with proliferative breast tumor subtypes, cell-cycle progression, and DNA r

253 rotenoid exposure as well as associations by breast tumor subtypes.

254 and limited analyses have been conducted by breast tumor subtypes.

255 , as well as the ability of HER2 to generate breast tumors, suggesting that interactions between PMCA

256 treatment are functional characteristics of breast tumors that do not respond to AIs.

257 ibe a set of mutations associated with human breast tumors that occur in a common structural motif of

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

259 ly, within some of these genes in BRCA1 null breast tumors, there are specific insertion/deletion mut

260 In breast tumors, this effect is partially mediated by the

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

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

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

264 und that CDK11(p110) was highly expressed in breast tumor tissues and cell lines.

265 determining the expression of CDK11(p110) in breast tumor tissues and examining the phenotypic change

266 25 were significantly overexpressed in human breast tumor tissues and were associated with reduced ov

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

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

269 In breast tumor tissues, GLI1 expression enhanced tissue id

270 ation of TGFbeta/SMAD3 signaling by HOXB7 in breast tumor tissues.

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

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

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

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

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

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

277 .38-fold higher mRNA levels in AI-responsive breast tumors vs non-responders (P<0.001).

278 differentiation between malignant and benign breast tumors was analyzed by dividing the sample into e

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

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

281 stant subcutaneous in situ R3230 and MATBIII breast tumors was evaluated.

282 lication by Yates and colleagues, the ITH of breast tumors was examined and shown to have important i

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

284 ts diagnosed with either malignant or benign breast tumors were prospectively recruited.

285 ttractive strategy to target triple negative breast tumors, which currently lacks molecularly targete

286 and CDKN1B expression are relatively high in breast tumors while EGFR expression is relatively high i

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

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

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

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

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

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

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

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

295 ithin a tumor ECM preparation (Matrigel) and breast tumor xenograft slices ex vivo.

296 In this paper, breast tumor xenografts grown from MDA-MB-231-HRE-tdToma

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

298 models of orthotopic primary triple-negative breast tumor xenografts, including a patient-derived xen

299 MSI volume data from MDA-MB-231-HRE-tdTomato breast tumor xenografts.

300 l vascular endothelial cells and human MCF-7 breast tumor xenografts.