ライフサイエンスコーパス: mammary

1 hile depletion of DeltaNp63 inhibits primary mammary adenocarcinoma development, oscillatory expressi

2 dy, which revealed a significant increase of mammary adenocarcinoma incidence in the stop-dose animal

3 pecies analysis between the TAp63 metastatic mammary adenocarcinoma mouse model and models of human b

4 MP9-DOX-NPs by 3.7-fold in an orthotopic 4T1 mammary adenocarcinoma mouse model.

5 Primary mammary adipose stromal cells derived from women with ob

6 ies implicate MMe macrophage accumulation in mammary adipose tissue as a mechanism for promoting TNBC

7 Here, we show that obesity reprograms mammary adipose tissue macrophages to a pro-inflammatory

8 astic nephroma, secretory breast cancer, and mammary analog secretory carcinoma of the salivary gland

9 e reveal in mouse interfollicular epidermal, mammary and hair follicle epithelia that genotoxicity do

10 kines, which were collectively important for mammary and metastatic lung engraftment.

11 Glandular epithelia, including the mammary and prostate glands, are composed of basal cells

12 Whereas the use of the left internal mammary artery as a conduit is associated with the highe

13 The left internal mammary artery graft is done by sternal-sparing approach

14 val attributable to use of the left internal mammary artery graft.

15 and survival advantages of the left internal mammary artery.

16 d as a composite graft based on the internal mammary artery.

17 loop, vertically transmitted via the entero-mammary axis.

18 ian quality and breeding success, as well as mammary branching impairment.

19 ication of the mammary placode or descending mammary bud, it is essential for both the prenatal hormo

20 of hypoxia-induced molecular alterations in mammary CAFs.

21 We confirmed that other mammary cancer cells embedded in tissue-mimetic hydrogel

22 s present in domesticated mammals with a low mammary cancer incidence.

23 of mammals with a naturally low incidence of mammary cancer mediate the elimination of cancer cells.

24 Here, we utilize mammary cancer models to temporally delete essential aut

25 Using a triple-negative mammary cancer mouse model and chronic neural interface

26 Using a mouse model of HR(+) mammary cancer, we demonstrate that a preestablished dis

27 ts of this polymorphism on susceptibility to mammary cancer, we used a humanized p53 mouse model, hom

28 s development in a mouse model of aggressive mammary cancer-induced peritoneal carcinomatosis.

29 dimethylbenz[a]anthracene (DMBA) to initiate mammary cancer.

30 ng tumor cells (CTCs) in two mouse models of mammary cancer: genetically modified MMTV-PyMT mice and

31 Our model of mammary carcinogenesis allowed for the exploration of ti

32 isease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional

33 fferences between OW and FF; (2) evidence of mammary carcinogenicity, estrogenicity, or genotoxicity;

34 vo HSPC-transduced mice with implanted mouse mammary carcinoma (MMC) tumors, after initial tumor grow

35 Using syngeneic cancer cells (EO771 mammary carcinoma and B16-F10 melanoma cells) injected i

36 However, the effects of acidity on mammary carcinoma cell morphology and phenotype have not

37 Acidification also increased mammary carcinoma cell motility when cultured with fibro

38 Acidification decreased overall mammary carcinoma cell viability, while increasing their

39 al effects of environmental acidification on mammary carcinoma cells in standard two-dimensional cult

40 ance and extracellular vesicle production by mammary carcinoma cells that promote tumor expansion.

41 agy genes increased the sensitivity of mouse mammary carcinoma cells to radiation therapy in vitro an

42 ncreased extracellular vesicle production by mammary carcinoma cells.

43 d hyperthermia in a neu deletion (NDL) mouse mammary carcinoma model (Her2(+), ER/PR negative).

44 ered peritumorally in vivo in the EMT6 mouse mammary carcinoma model, OxLys-SNAs significantly increa

45 Like other cancers, mammary carcinoma progression involves acidification of

46 usly showed that mitochondrial SNPs regulate mammary carcinoma tumorigenicity and metastatic potentia

47 ell (MCF-7, tamoxifen-resistant MCF-7, mouse mammary carcinoma, MDA-MB-231, and BT-549) viability, mi

48 LRRK2-mutated mammary carcinomas are enriched with stop-gain, truncati

49 MMTV-PyMT mice, which spontaneously develop mammary carcinomas, with MC-deficient C57BL/6-Kit(W-sh/W

50 nd adipocytes repopulation, estrogen-induced mammary cell death was via lysosome-mediated programmed

51 ng quantitative, multidimensional imaging of mammary cell ensembles from GCaMP6 transgenic mice, we r

52 in the organoid models of premalignant human mammary cell lines.

53 t, luminal breast cancer and non-transformed mammary cells maintain viability upon POLE suppression b

54 m, via the secretion of bioactive factors by mammary cells, that is present in domesticated mammals w

55 at differed between normal luminal and basal mammary cells.

56 late infection; adenopathies in the internal mammary chain; granulomas in the capsule of the implant,

57 Prolonged mammary CPX exposure was highly correlated to improved e

58 through SMAD members has distinct effects on mammary development and homeostasis.

59 rs and ligands are also important for normal mammary development, suggesting the potential for conser

60 s provide a valuable platform for studies of mammary differentiation, transformation, and breast canc

61 demonstrate that slowing drug release in the mammary duct after intraductal administration overcomes

62 icrofluidic platform that juxtaposes a human mammary duct in proximity to a perfused endothelial vess

63 rom alveolar units and its passage along the mammary ductal network.

64 ic evaluation of quantifiable aspects of the mammary ductal tree, and c) compare those methods.

65 ies demonstrated reduced decorin surrounding mammary ducts and enhanced TGFbeta1 activity within mamm

66 een established, localized transport via the mammary ducts may be improved with tailored drug deliver

67 e most significant inflammatory mediators of mammary engraftment and lung metastatic growth in triple

68 Coexpression of EZH2(T416D) in mammary epithelia of HER2/Neu transgenic mice reprograms

69 ped a new methodology based on primary mouse mammary epithelial acini, where oncogenes can be switche

70 ausal variants and target genes in six human mammary epithelial and breast cancer cell lines.

71 eome, we used mouse models of pre-neoplastic mammary epithelial and cancer stem cells to reveal the c

72 Finally, mammary epithelial cell exposure to SAM milk pellets sho

73 and redirect cancer cells to adopt a normal mammary epithelial cell fate in vivo.

74 in cultured cells was studied using a human mammary epithelial cell line that expresses SULT1A3 at l

75 and the cis-regulatory networks of two human mammary epithelial cell lines (184A1 and MCF10A) are inv

76 Furthermore, mammary epithelial cell lines were exposed to milk pelle

77 in apicobasal polarity defects and increased mammary epithelial cell proliferation associated with hy

78 density-induced increase in Akt activity and mammary epithelial cell proliferation.

79 letion of macrophages in obese mice enhanced mammary epithelial cell stem/progenitor activity, elevat

80 etabolic programs in cancer cells, influence mammary epithelial cell tumorigenicity and aggressivenes

81 er resolution representation of the multiple mammary epithelial cell types in the organoids, and demo

82 optotic roles of P. zopfii GT-II in cultured mammary epithelial cells (from cattle and mice) and muri

83 D) colony organization of premalignant human mammary epithelial cells (HMECs) is one of the indices o

84 -II (but not GT-I) invaded bovine and murine mammary epithelial cells (MECs) and induced apoptosis, a

85 series of cellular and molecular changes in mammary epithelial cells (MECs) of female adults.

86 feasible with conventional static hydrogels, mammary epithelial cells (MECs) were cultured on methacr

87 miR-489, we sorted different populations of mammary epithelial cells and determined that miR-489 was

88 pha (ER-alpha) forms a regulatory network in mammary epithelial cells and in breast cancer with the t

89 x perturbation experiment with primary human mammary epithelial cells and multiplex cryopreserved tum

90 tumors initiated from different precancerous mammary epithelial cells are distinct.

91 logy observed in mammary epithelium in vivo, mammary epithelial cells cultured on soft microenvironme

92 Breast and mammary epithelial cells experience different local envi

93 utilizes a premalignant phenotype of normal mammary epithelial cells lacking PTEN.

94 R-loops and DNA damage were also detected in mammary epithelial cells of mice treated with BP-3 and P

95 and survival of E-cadherin-deficient murine mammary epithelial cells on stiff matrices like fibrilla

96 This dramatic impact was also observed in mammary epithelial cells with constitutively high levels

97 In primary mammary epithelial cells, fermentative glycolysis, and i

98 ation and localization was altered in STM KO mammary epithelial cells, leading to decreased protein s

99 In normal luminal mammary epithelial cells, miR-223 acted cell autonomousl

100 he density-dependent proliferation of murine mammary epithelial cells, we developed a fluorescence-ac

101 ducts and enhanced TGFbeta1 activity within mammary epithelial cells.

102 g-term proliferation of normal and malignant mammary epithelial cells.

103 ation at the cortical cytoskeleton in normal mammary epithelial cells.

104 coplasma infection was investigated in mouse mammary epithelial cells.

105 effectors of this process, we developed a 3D mammary epithelial culture model, in which dissemination

106 SOX11 is an embryonic mammary epithelial marker that is normally silenced prio

107 t inducible LINC complex disruption in human mammary epithelial MCF-10A cells and canine kidney epith

108 ubstantially lower effect on non-tumorigenic mammary epithelial MCF10A cells (67% viability).

109 we identified CD177 as a novel regulator of mammary epithelial proliferation and breast cancer patho

110 molog Zfp217, and increased Akt activity and mammary epithelial proliferation.

111 or beta-1 (TGFbeta1) is a major regulator of mammary epithelial stem/progenitor cells, and its activi

112 d the generation of bioelectric gradients in mammary epithelial tissues.

113 promote dedifferentiation of wild-type Pygo2 mammary epithelial tumor cells.

114 Loss of CD177 leads to hyperproliferative mammary epithelium and contributes to breast cancer path

115 ehaviors and bidirectional signaling between mammary epithelium and endothelium during homeostasis an

116 pubertal hormone-dependent branching of the mammary epithelium and for proper alveologenesis during

117 and miR-34a in particular, is implicated in mammary epithelium homoeostasis.

118 apitulates the acinar morphology observed in mammary epithelium in vivo, mammary epithelial cells cul

119 Selective targeting of CCR2 in the PyVmT mammary epithelium inhibited tumor growth and invasion,

120 relevant drivers of breast cancers in intact mammary epithelium is critical for understanding tumorig

121 The mammary epithelium is indispensable for the continued su

122 egnancy reprograms enhancer chromatin in the mammary epithelium of mice and influences the transcript

123 Immunostaining of mouse mammary epithelium was performed to quantify R-loops and

124 ics and induce oncogenic changes in a normal mammary epithelium.

125 xpressed in a subset of luminal cells in the mammary epithelium.

126 of Twist1 and is not expressed in the normal mammary epithelium.

127 d high-throughput cancer driver discovery in mammary epithelium.

128 essing tumor initiation suggesting prolonged mammary exposure may improve efficacy.

129 overall survival of mice when injected into mammary fat pad of syngeneic mice, and demonstrated syne

130 ell line (AT-3, Gpr81-negative) implanted in mammary fat pad of wild-type mice and Gpr81-null mice.

131 se model, tumor cells were inoculated to the mammary fat pad or the proximal tibia.

132 tumor cells, as well as tumor weight in the mammary fat pad.

133 ly high probe activation compared to healthy mammary fat pads and surrounding tissue.

134 y implanted PyMT breast tumor cells into the mammary fat pads of syngeneic LysMcre, HIF-1alpha (fl/fl

135 s during the dry period will adversely alter mammary function, health and milk production for the sub

136 Indeed, postnatal mammary gland (MG) development is controlled locally by

137 , an improper glucose supply often threatens mammary gland (MG) health.

138 e phenotype of the ventral prostate (VP) and mammary gland (MG) in ERbeta(crispr-/-) mice was similar

139 ion model, P. zopfii GT-II replicated in the mammary gland and caused severe inflammation with infilt

140 r tissue-specific promoters of the pancreas, mammary gland and other secretory tissues, as well as an

141 V-PyMT mice redirects SmgGDS splicing in the mammary gland and slows tumorigenesis in this aggressive

142 ntly transduce progenitor cells of the adult mammary gland and use that as a platform to functionally

143 Tissue-resident macrophages in the mammary gland are found in close association with epithe

144 eration, but not normal proliferation of the mammary gland associated with pregnancy or other normal

145 in regulating bone marrow, skin, muscle, and mammary gland biology is emerging, but the role of adipo

146 uctal epithelial branching in the developing mammary gland by regulating macrophage dynamics.

147 This work uses a novel mouse mammary gland cancer model to show that tumors initiated

148 We show that in MCF-7 mammary gland cells, AGO1 associates with transcriptiona

149 conserved signaling pathways between normal mammary gland development and breast cancer.

150 h receptors and ligands contribute to normal mammary gland development and breast tumor progression.

151 HER2 signaling pathway; however, its role in mammary gland development and HER2-induced tumor initiat

152 Myoepithelial cells play key roles in normal mammary gland development and in limiting pre-invasive t

153 ta reveals that TET2 plays a pivotal role in mammary gland development and luminal lineage commitment

154 in the adipose stroma, and are important for mammary gland development and tissue homeostasis.

155 riments was tested in two studies related to mammary gland development and tumorigenesis.

156 e factors are enriched for genes integral to mammary gland development as well as epithelial cell bio

157 ly unknown mechanism controlling the rate of mammary gland development during puberty and highlights

158 his Review, we outline the various stages of mammary gland development in the mouse, with a particula

159 ental processes, including those involved in mammary gland development.

160 se that the unique biology of the postpartum mammary gland drives tumor progression.

161 expressing a hyperactive STAT5 mutant in the mammary gland during postlactational remodeling.

162 P-Cre transgene, commonly used to target the mammary gland during pregnancy, induces metastatic pineo

163 ssociation with stemness, contributes to the mammary gland homeostasis, evolution of early neoplastic

164 The objective was to test whether goat's mammary gland immune response to E. coli lipopolysacchar

165 iomarkers and possible treatments for bovine mammary gland inflammation.

166 The mammary gland is a highly vascularized tissue capable of

167 The mammary gland is a unique tissue and the defining featur

168 th stable barcodes, we found that each mouse mammary gland is generated from a defined number of ~120

169 s role in epithelial tissue organization and mammary gland morphogenesis in vivo has not been investi

170 In a three-dimensional (3D) model of mammary gland morphogenesis, sEV treatment induced hallm

171 peculate that secreted sphingomyelins in the mammary gland of mammals with a naturally low incidence

172 d in tissues that are softer than the normal mammary gland or the primary breast tumor, such as bone

173 intaining homeostasis within the nulliparous mammary gland stroma.

174 e subpopulation within the mouse nulliparous mammary gland that is characterized by the expression of

175 tions of this theory on datasets of pubertal mammary gland tips and embryonic kidney tips, as well as

176 ling during the transformation of the normal mammary gland to breast cancer hinders the development o

177 transferases (PRMT) are directly involved in mammary gland transformation and tumor progression.

178 In mammary gland tumor models, Angpt2(443) differentially a

179 the possible roles of PRMT overexpression in mammary gland tumorigenesis, we generated Cre-activated

180 her BPA showed effects on the developing rat mammary gland using new quantitative and established sem

181 n linked to ductal development in the virgin mammary gland, but less is known regarding the effects o

182 tem cells (MSCs) injected into contralateral mammary gland, evidenced by the lack of tumor growth at

183 regulation of branching morphogenesis in the mammary gland, whereby stromal ACKR2 modulates levels of

184 t as well as epigenetic reprogramming in the mammary gland, which can affect cell fate decisions in p

185 s on effects on progenitor cell pools in the mammary gland.

186 ose stroma and fibrous capsule of the virgin mammary gland.

187 rement of VANGL family members in the murine mammary gland.

188 lar mechanisms of PRMT overexpression in the mammary gland.

189 x10 has multiple functions in the developing mammary gland.

190 s to match the requirements of the lactating mammary gland.

191 l division and apicobasal polarity in normal mammary glands and to establish a protumorigenic program

192 Analyses showed that susceptible mammary glands from E-R72 (R72 x MMTV-Erbb2/Neu) mice de

193 evaluated after the administration of LPS in mammary glands of dairy goats under thermal-neutral (TN;

194 Branching organs, including the salivary and mammary glands, lung, and kidney, arise as epithelial bu

195 tis, they do not address the regeneration of mammary glandular tissue and have been associated to the

196 ogical and immunological changes critical to mammary health.

197 mics indicated that heat stress affected the mammary immune response to simulated infection, which co

198 milk production, they are effector cells of mammary immunity.

199 In a murine mammary infection model, P. zopfii GT-II replicated in t

200 ever, how estrogen and neutrophils influence mammary involution are unknown.

201 Estrogen exposure during mammary involution drives tumor growth through neutrophi

202 ammatory microenvironment during post-partum mammary involution promotes parity-associated breast can

203 diated by ERalpha and unique to the phase of mammary involution.

204 nd p120-1, including bronchial epithelia and mammary luminal epithelial cells.

205 s that are known to coordinately orchestrate mammary luminal lineage specification and endocrine resp

206 The normal mammary microenvironment can suppress tumorigenesis and

207 bution to luminal and basal epithelia during mammary morphogenesis.

208 Functionally, by using pancreatic and mammary organoid cultures, we found that YAP/TAZ-regulat

209 t tumors and compare tumors localized to the mammary pad and tumor cells injected into the iliac arte

210 were injected into BALB/c mice either in the mammary pad or into the iliac artery, urine was collecte

211 The mammary persistence of CPX from CPX NS, CPX-Zn NS, and C

212 irement of Sox10 in the specification of the mammary placode or descending mammary bud, it is essenti

213 Therefore, both stem and non-stem cells in mammary precancerous lesions can contribute to the event

214 tor of NODAL/SMAD2 signaling, is produced by mammary progenitor cells and, concomitantly, suppresses

215 tial of the basal compartment, which harbors mammary repopulating cells.

216 ng to genetic instability in mice carrying a mammary specific disruption of breast cancer associated

217 Here, using our recently established mammary specific Tet2 deletion mouse model, the data rev

218 Mammary-specific activation of PKA in mouse models leads

219 P2 (t-ASPP2) as a driver of ILC in mice with mammary-specific loss of E-cadherin.

220 is conversion as, in both cases, a subset of mammary spheroids remained insensitive to local matrix s

221 e likely causally related to its function in mammary stem and precursor cells, this is not the case f

222 o implicated Sox10 as an important factor in mammary stem and precursor cells.

223 bpopulations of cells that contribute to the mammary stem and progenitor cell hierarchy and we sugges

224 tro; however, whether and how TET2 regulates mammary stem cell fate and mammary tumorigenesis in vivo

225 ermined that miR-489 was highly expressed in mammary stem cells.

226 nd enhanced TGFbeta1 within the ECM of obese mammary tissue may enhance breast cancer risk.

227 ivery systems to control release and prolong mammary tissue persistence of a lipophilic metal complex

228 In the second arm, mammary tissue persistence of CPX followed the rank orde

229 the rapid ductal clearance of CPX, prolongs mammary tissue persistence, improves efficacy against DC

230 markably, 88% of estrogen-regulated genes in mammary tissue were mediated through neutrophils, which

231 ersus luminal-like breast tumors and healthy mammary tissue.

232 Mammary-tissue-restricted cytochrome P450 4Z1 (CYP4Z1) h

233 es via long-term propagation of normal human mammary tissues.

234 trix and induces precancerous lesions in the mammary tissues.

235 P exposure at a human-equivalent dose on the mammary transcriptome in rats and to subsequently examin

236 Mammary treatment with LPS resulted in febrile response

237 n BC studies (n = 294) or from within canine mammary tumor associated regions (n = 471).

238 Here we report on Mammary Tumor Associated RNA 25 (MaTAR25), a nuclear enr

239 AK is required for their activity to promote mammary tumor cell migration.

240 matin associated lncRNA that plays a role in mammary tumor cell proliferation, migration, and invasio

241 ry tumor progression in mice and showed that mammary tumor cells become highly susceptible to replica

242 eta(D849V) also promoted brain metastases of mammary tumor cells expressing high PDGFB when injected

243 extracellular vesicles released from hypoxic mammary tumor cells facilitate intercellular communicati

244 Mice were injected with Cl66 murine mammary tumor cells, Cl66 cells resistant to doxorubicin

245 human breast cancer cell lines and 4T1 mouse mammary tumor cells, PD-L1 expression was regulated by t

246 opic tumor growth and intracranial growth of mammary tumor cells, while mesenchymal-specific expressi

247 exerted proproliferative signals on adjacent mammary tumor cells.

248 significantly reduced intracranial growth of mammary tumor cells.

249 stem cells and validation in KB2P1.21 mouse mammary tumor cells.

250 breast cancer mouse model exhibits enhanced mammary tumor development with deficient ERalpha express

251 E-cadherin alone does not predispose mice to mammary tumor development, indicating that additional pe

252 cell proliferation and migration, as well as mammary tumor formation and metastasis.

253 ected from oncogene-driven spontaneous mouse mammary tumor growth and associated lung metastasis.

254 to inhibit macrophage accumulation and slow mammary tumor growth in mouse models while also reducing

255 le models of basal-like TNBC and reduces PDX mammary tumor growth in vivo.

256 ion of autophagy strongly attenuates primary mammary tumor growth, impaired autophagy promotes sponta

257 brain tumor growth while minimally impacting mammary tumor growth.

258 led that R72 mice had a significantly higher mammary tumor incidence and reduced latency in both DMBA

259 vasion, and metastasis; however, its role in mammary tumor initiation remains unknown.

260 traceable MMTV-Wnt1-driven in vivo chimeric mammary tumor model comprising an admixture of low-Myc-

261 Using the MMTV-PyVmT/FVB mammary tumor model, we demonstrate a novel role for CCL

262 Here, using an MMTV-PyMT mouse mammary tumor model, we discovered that deletion of TGFb

263 s to the lungs in a 4T1 syngeneic orthotopic mammary tumor model.

264 n both DMBA-induced and MMTV-Erbb2/Neu mouse mammary tumor models compared to P72 mice.

265 VPA/hydralazine reduced mammary tumor multiplicity and lengthened tumor latency

266 block dissemination of both murine and human mammary tumor organoids.

267 ally realistic microvessel in coculture with mammary tumor organoids.

268 we established its functional importance in mammary tumor progression in mice and showed that mammar

269 Using a p53-null model of early stage mammary tumor progression, we found that Gas6 is highly

270 Therefore, we tested the extent to which mammary tumor resection attenuates tumor-induced neuroin

271 lasma membrane targeting of the B-type mouse mammary tumor virus (MMTV) and C-type HIV-1, which assem

272 ell protein 0 (ICP0) promoter, and the mouse mammary tumor virus long terminal repeat (MMTV-LTR).

273 tate, and pancreas) and a mouse model of the mammary tumor were employed to evaluate the effect of ur

274 t2 deletion does not inhibit and exacerbates mammary tumorigenesis and metastasis, but cell-autonomou

275 histone chaperone FACT is upregulated during mammary tumorigenesis and necessary for the viability an

276 ow TET2 regulates mammary stem cell fate and mammary tumorigenesis in vivo remains to be determined.

277 perates with oncogenic PI3K to promote rapid mammary tumorigenesis, the additional loss of PTEN prote

278 ole for SIRT5 in metabolic reprogramming and mammary tumorigenesis.

279 ss the effect of defined allelic variants on mammary tumorigenesis.

280 Here, we used RNA-profiling of canine mammary tumors (CMTs) coupled with a robust analysis fra

281 nhibition blocks transformation in cells and mammary tumors characterized by PIK3CA C-terminal mutati

282 We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M)

283 In vivo, irradiated autophagy-incompetent mammary tumors elicited robust immunity, leading to impr

284 f 173 and 225 unique ECM proteins from mouse mammary tumors have been identified using 1D and 2D RPLC

285 further reduced local invasion of orthotopic mammary tumors in vivo, and joint up-regulation of Cx43

286 herefore, here we tested the extent to which mammary tumors or tumor resection ("survivors") in mice

287 tissues of mice and rats bearing orthotopic mammary tumors without observation of acute toxic side e

288 as well as a delayed formation of detectable mammary tumors, thus suggesting a causal relationship be

289 ion of Mad1 accelerates growth of orthotopic mammary tumors, which show decreased levels of p53 and i

290 death response evident in early and advanced mammary tumors.

291 with hyperplasia and development of de novo mammary tumors.

292 pplied to the knee, on metastasized bone and mammary tumors.

293 oated control in mice bearing 4T1 orthotopic mammary tumors.

294 ably, it also reduced remotely the growth of mammary tumors.

295 performance of the probes in mouse models of mammary tumours and of metastatic lung cancer, as well a

296 rganotypic culture, intravital microscopy of mammary tumours in mice and in silico modelling, we iden

297 /10-expressing tumours to eradicate HER-2(+) mammary tumours in vivo.

298 In mammary tumours, high-energy radiation is associated wit

299 Here, we analyse the genetic architecture of mammary tumours, lymphomas and sarcomas induced by high

300 y repressed tumour formation in mice bearing mammary tumours.