ライフサイエンスコーパス: mammary epithelium

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

2 d dissemination in both normal and malignant mammary epithelium.

3 essive transformation of HER2-overexpressing mammary epithelium.

4 and luminal epithelial cell lineages of the mammary epithelium.

5 of cyclin D1 in suppressing autophagy in the mammary epithelium.

6 en Brca1 loss and Kit over-expression in the mammary epithelium.

7 patterning or structural organization of the mammary epithelium.

8 ated form of MDM2 (MDM2DDS166D/S186D) in the mammary epithelium.

9 ncoproteins, such as SRC3 that can transform mammary epithelium.

10 ER(+)/PR(+) cell type in the wild-type (WT) mammary epithelium.

11 proper architecture and functionality of the mammary epithelium.

12 RANKL-dependent proliferative changes in the mammary epithelium.

13 ive proliferation and increased apoptosis of mammary epithelium.

14 terone and prolactin signaling in the murine mammary epithelium.

15 of its own signaling receptor (RANK) in the mammary epithelium.

16 ted expression of c-myc and cyclin D1 in the mammary epithelium.

17 nd proper hormone receptor expression in the mammary epithelium.

18 through generation of a targeted deletion in mammary epithelium.

19 nd Cxcr4 signaling axis, specifically within mammary epithelium.

20 mary epithelial cell line (MCF10A) and mouse mammary epithelium.

21 al for maintenance of homeostasis within the mammary epithelium.

22 significance of this steroid receptor in the mammary epithelium.

23 or constitutively active Ron receptor in the mammary epithelium.

24 MMP-26 is not expressed in normal mammary epithelium.

25 xpressed in virgin, lactating, or involuting mammary epithelium.

26 ate radiation-responsiveness of p53 in mouse mammary epithelium.

27 t PEA-15 is phosphorylated in situ in normal mammary epithelium.

28 ranching and epithelial proliferation in the mammary epithelium.

29 ssary for maintenance of p53 activity in the mammary epithelium.

30 l the cellular subtypes recognized in murine mammary epithelium.

31 are essential to the normal functions of the mammary epithelium.

32 has some "tumor suppressor" function in the mammary epithelium.

33 of several proteases in transdifferentiated mammary epithelium.

34 , strongly enhance tumorigenesis in p53-null mammary epithelium.

35 e in the differentiation and function of the mammary epithelium.

36 Pak1-ER pathway in promoting hyperplasia in mammary epithelium.

37 IRES-Cre transgene (NIC) specifically in the mammary epithelium.

38 d prolactin receptor mRNAs colocalize in the mammary epithelium.

39 tivating LEF-1, which is expressed in normal mammary epithelium.

40 gulates branching morphogenesis in the mouse mammary epithelium.

41 ce of the hyperplastic characteristic of the mammary epithelium.

42 ducing estrogen-induced proliferation in the mammary epithelium.

43 educes tumorigenesis in Brca1-knockout mouse mammary epithelium.

44 marked elevation in cyclin D1 expression in mammary epithelium.

45 veologenesis and milk secretion in PrlR(-/-) mammary epithelium.

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

47 ones expressing the erbB2 proto-oncogene in mammary epithelium.

48 lineage-specific transcriptional control in mammary epithelium.

49 activation of STAT1, STAT3, and STAT6 in the mammary epithelium.

50 gets is obligatory for the remodeling of the mammary epithelium.

51 e cell death machinery in the differentiated mammary epithelium.

52 s residing in the luminal compartment of the mammary epithelium.

53 Prlr) and ErbB4 expression in Xbp1-deficient mammary epithelium.

54 r EZH2 controls the differentiation clock of mammary epithelium.

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

56 a tumor-suppressive function for Par3 in the mammary epithelium.

57 Wnt/beta-catenin-dependent signaling in the mammary epithelium.

58 ching and altered the differentiation of the mammary epithelium.

59 ut not the Wnt/Myc) oncogenic pathway in the mammary epithelium.

60 dissemination of cells out of primary murine mammary epithelium.

61 identified as modulators of COX-2 in normal mammary epithelium.

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

63 forming growth factor beta (TGF-beta) in the mammary epithelium.

64 complexes on genes specifically expressed in mammary epithelium.

65 itor cells has been shown to exist among the mammary epithelium.

66 miRNAs 365-1 and 6365, as a STAT5 target in mammary epithelium.

67 intaining normal stem cell subpopulations in mammary epithelium.

68 nical signals that regulate branching in the mammary epithelium.

69 ich deletion of c-Src can be targeted to the mammary epithelium.

70 atment from the antiproliferative effects on mammary epithelium.

71 negative (ER(+)/PR(-)) cell type in the PRKO mammary epithelium, a cell type that is equivalent to th

72 shown recently to induce hyperplasia in the mammary epithelium, a phenotype also manifested by overe

73 his study provides new insights into how the mammary epithelium adapts to control amino acid uptake t

74 ermines the correct dorsoventral position of mammary epithelium along the flank.

75 udy tested the hypotheses that Brca1 loss in mammary epithelium alters the estrogenic growth response

76 deletion of the type II TGF-beta receptor in mammary epithelium, an increased level of TGF-beta prote

77 xhibited an 80% reduction of Stat5 levels in mammary epithelium and a concomitant reduction of STAT5-

78 Lkb1 loss-induced structural alterations in mammary epithelium and BM fragmentation.

79 tem cells residing in the basal layer of the mammary epithelium and breast TICs originating in the lu

80 MTA1 dysregulation in mammary epithelium and cancer cells triggered downregula

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

82 in increased vascularization of hyperplastic mammary epithelium and dramatic acceleration of tumor ap

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

84 ilar PTEN(lo)/pERK(hi)/pAKT(hi) phenotype as mammary epithelium and exhibited high activation of estr

85 we examine the expression of 4.1B in murine mammary epithelium and find that 4.1B is dramatically up

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

87 Bmi1 expression was induced in the AEBP1(TG) mammary epithelium and HC11 mammary epithelial cells co-

88 TET proteins and a powerful oncogene in the mammary epithelium and hematopoietic system.

89 or Hus1 in the survival and proliferation of mammary epithelium and identify a role for p53 in mammar

90 a key role in growth and development of the mammary epithelium and in breast cancer.

91 lactation, and serotonin was detected in the mammary epithelium and in milk.

92 fines distinct progenitor populations in the mammary epithelium and is critical for mammary progenito

93 to be associated with WNT signalling in the mammary epithelium and is specifically upregulated in mo

94 During pregnancy the mammary epithelium and its supporting vasculature rapidl

95 sembly of multiprotein complexes to regulate mammary epithelium and keratinocyte differentiation and

96 Transplantation experiments of mammary epithelium and of whole mammary glands implicate

97 changes in Wnt/beta-catenin signaling in the mammary epithelium and offers insights into the developm

98 ween the known oncogenic activity of PDK1 in mammary epithelium and PPARdelta activation.

99 tivated H-Ras induces ARC in both the normal mammary epithelium and resulting tumors of intact mice.

100 ucted from benign biopsies containing normal mammary epithelium and scored by computational image ana

101 g pathways regulating the cross-talk between mammary epithelium and stroma that could predispose the

102 Thus, Ptch1 functions in the mammary epithelium and stroma to regulate ductal morphog

103 to be shown to have a functional role in the mammary epithelium and the first marker to be shown to b

104 ndent on interactions between the developing mammary epithelium and the surrounding stromal tissues.

105 cteristics of these programs in normal human mammary epithelium and their similarity to those in stem

106 ike growth factor I pathway in AIB1(-/-)-ras mammary epithelium and tumor cells was responsible in pa

107 e polyoma middle T oncoprotein (PyMT) in the mammary epithelium, and its comparison to human breast t

108 JAM-A is robustly expressed in normal human mammary epithelium, and its expression is down-regulated

109 contributes to lipogenic differentiation in mammary epithelium, and perk deletion inhibits the susta

110 totic response is TGF-beta1 dependent in the mammary epithelium, and that both apoptosis and inhibiti

111 aSCs) reside in the basal compartment of the mammary epithelium, and their neoplastic counterparts, m

112 to inactivate p53 and/or Rb strictly in the mammary epithelium, and to determine recurrent genomic c

113 within normal, pre-malignant and neoplastic mammary epithelium, and using complementary gain-of-func

114 miR-200a regulates the Keap1/Nrf2 pathway in mammary epithelium, and we find that epigenetic therapy

115 Therefore, ER-expressing cells of the mammary epithelium are distinct from the mammary stem ce

116 ctional implications of this receptor in the mammary epithelium are not known.

117 xpression during the malignant conversion of mammary epithelium as a contributing factor of breast ca

118 ch the Cx26 gene was specifically ablated in mammary epithelium at different stages of development us

119 bition is acting directly on hormone-induced mammary epithelium at early stages in tumorigenesis, and

120 STAT5 activation in Erbb4(Flox/Flox)Wap-Cre mammary epithelium at parturition.

121 human breast parenchyma, specifically in the mammary epithelium; (b) human breast parenchyma can supp

122 functional ablation of the Jak2 gene in the mammary epithelium before and after neoplastic transform

123 In contrast, loss of Cx26 in mammary epithelium before puberty resulted in abrogated

124 ete loss of exon 11 of Brca1 specifically in mammary epithelium (Brca1-MG-Deltaex11) were studied in

125 R-cad is expressed in nontransformed mammary epithelium but absent from tumorigenic cell line

126 ation and cellular homeostasis in the normal mammary epithelium but also the contribution of differen

127 o implicated in neoplastic transformation of mammary epithelium, but responsible mechanisms are uncle

128 se, promotes the malignant progression of a mammary epithelium by activating and stabilizing vinculi

129 odel in which activation of PPARdelta in the mammary epithelium by endogenous or synthetic ligands re

130 PRB regulates branching morphogenesis in the mammary epithelium by modulating the response of the FGF

131 dence that albumin is transported across the mammary epithelium by the same pathway as immunoglobulin

132 ogeneous transgene expression throughout the mammary epithelium can be achieved.

133 Mammary epithelium can functionally regenerate upon tran

134 (88) phosphorylation-inactive DLC1 mutant in mammary epithelium cells and in a transgenic animal mode

135 st cancer (IBC) cells and RhoC-overexpressed mammary epithelium cells.

136 the core 2-based glycans observed in normal mammary epithelium cells.

137 t analyses showed that in XOR+/- females the mammary epithelium collapses, resulting in premature inv

138 During pregnancy, Elf5-null mammary epithelium completely failed to initiate alveolo

139 The adult mouse mammary epithelium contains self-sustained cell lineages

140 educing AIB1/SRC-3 levels or activity in the mammary epithelium could potentiate therapies aimed at i

141 ucible suppression of NF-kappaB in the adult mammary epithelium delayed the onset and number of new t

142 Brca2 sustain a wide range of carcinoma and mammary epithelium deleted for Brca1 or Brca2 is highly

143 ing both human HER2 and mutant PIK3CA in the mammary epithelium developed tumors with shorter latenci

144 umor cells were incorporated into the normal mammary epithelium, developed ductal intraepithelial neo

145 polyomavirus middle T antigen (PyVmT) in the mammary epithelium displayed increased pulmonary metasta

146 ssion of the mdm2 transgene (BLGmdm2) to the mammary epithelium disrupts the cell cycle, causing mult

147 e mouse homolog of TFAP2C, Tcfap2c, in mouse mammary epithelium driven by MMTV-Cre promoted aberrant

148 mary cell normally expresses RANKL in the WT mammary epithelium during pregnancy.

149 for the proliferation and differentiation of mammary epithelium during pregnancy.

150 hypomorphic mutation leads to HDR defects in mammary epithelium during puberty and pregnancy, includi

151 r cells (MaSCs) maintain self-renewal of the mammary epithelium during puberty and pregnancy.

152 PTEN is overexpressed in ductal and alveolar mammary epithelium during puberty, pregnancy, lactation,

153 ally homogeneous transgene expression in the mammary epithelium during puberty, pregnancy, lactation,

154 dance in stem/progenitor cells of lactogenic mammary epithelium during successive pregnancy/lactation

155 Loss of Cx26 in mammary epithelium during the later part of pregnancy di

156 t NF-kappaB activity specifically within the mammary epithelium during tumor development in the polyo

157 The p53-null normal mammary epithelium exhibits the same dependence as p53 w

158 Induction of this microRNA cluster impacts mammary epithelium fate by regulating apoptosis and insu

159 ect of the conditional knockout of Fn in the mammary epithelium [Fn(MEp-/-)] on postnatal mammary gla

160 for the short-term delivery of genes to the mammary epithelium for both research and therapeutic pur

161 Mammary epithelium from p53 null mice was transplanted s

162 Proliferative mammary epithelium from R-ketorolac-treated mice display

163 dress this question we have now investigated mammary epithelium from transgenic mice that express act

164 we show that heightened PKA activity in the mammary epithelium generates tumors.

165 acids, exhibit markedly opposing effects on mammary epithelium growth and differentiation.

166 Deletion of Stat5 during pregnancy, after mammary epithelium had entered Stat5-mediated differenti

167 cell fate in individual cells in the intact mammary epithelium has not been possible to date.

168 nactivation and activation of genes in mouse mammary epithelium have been widely used to study geneti

169 In vitro models of normal mammary epithelium have correlated increased extracellul

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

171 sue revealed robust elafin expression in the mammary epithelium; however, elafin expression was drama

172 ositive cells isolated from the virgin mouse mammary epithelium identified 861, 326 and 488 genes as

173 operties of the p53 null preneoplastic mouse mammary epithelium in a p53 wild-type environment.

174 nce of the functional differentiation of the mammary epithelium in an in vivo system.

175 e transcription factor BCL-6 is expressed in mammary epithelium in nonpregnant animals as well as dur

176 investigating trafficking events within the mammary epithelium in real time.

177 Differentiation of mammary epithelium in vivo requires signaling through pr

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

179 ut mouse model with targeted ablation in the mammary epithelium, in combination with ex vivo three-di

180 f human breast cancer is the BALB/c p53-null mammary epithelium, in which deletion of the tumor suppr

181 Cre-recombinase-mediated Ptch1 ablation in mammary epithelium increased proliferation and branching

182 Conditional ablation of Igf1r in the mouse mammary epithelium increased the latency of Kras*-induce

183 logic and ex vivo analyses of MMTV-Neu mouse mammary epithelium indicated that EphA2 enhanced tumor p

184 he activation of Wnt signaling components in mammary epithelium induces not only glandular tumors but

185 publication that WAP-TGF-beta1 expression in mammary epithelium induces premature stem cell senescenc

186 ly active form of the Notch1 receptor in the mammary epithelium induces the rapid development of preg

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

188 The mechanisms by which the mammary epithelium integrates cues from the ECM with int

189 EPO might maintain mammary epithelium integrity, thereby reducing viral loa

190 Loss of EphA2 decreased penetration of mammary epithelium into fat pad, reduced epithelial prol

191 Transplants of mammary epithelium into p53+/m recipient mice demonstrat

192 alpha-overexpressing and cyclin D1-deficient mammary epithelium into the cleared fat pad of wild-type

193 The mouse mammary epithelium is composed of three main cell types

194 Mammary epithelium is comprised of an inner layer of lum

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

196 tions suggest that ERalpha expression in the mammary epithelium is essential for normal ductal morpho

197 The mammary epithelium is highly responsive to local and sys

198 The mammary epithelium is indispensable for the continued su

199 The mammary epithelium is organized as a bilayer of luminal

200 e that the developmental defect of PrlR(-/-) mammary epithelium is rescued by an exogenously expresse

201 The mammary epithelium is thought to be stabilized by cell-c

202 stem cells (CSCs) in constantly replenishing mammary epithelium is unclear.

203 fferentiation-specific genes was observed in mammary epithelium lacking both EZH2 and STAT5, suggesti

204 ontrolled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the lumina

205 Differentiation of mammary epithelium lacking the miR-193b locus was accele

206 verexpression of the proto-oncogene Wnt-1 in mammary epithelium leads to mammary hyperplasia and subs

207 e Ron receptor tyrosine kinase in the murine mammary epithelium leads to mammary tumor formation.

208 PTEN overexpression in mammary epithelium leads to reduced cell number and impa

209 lized beta-catenin (DeltaE3 beta-catenin) in mammary epithelium leads to the transdifferentiation int

210 These results suggest that p27(+/-) mammary epithelium may be more susceptible to oncogene-i

211 duced transformed properties in normal human mammary epithelium (MCF10A); in contrast, Int6 silencing

212 lone or combined with p53 heterozygosity, in mammary epithelium mimic several aspects of the most agg

213 rexpressing ErbB2 (also known as Neu) in the mammary epithelium (MMTV-Neu mice), but not in mice over

214 ressing the polyomavirus middle T antigen in mammary epithelium (MMTV-PyV-mT mice).

215 both promoters target Cre gene expression to mammary epithelium, MMTV-Cre is also expressed in spleen

216 o protection was seen in our BALB/c p53-null mammary epithelium model, indicating a p53 dependency fo

217 ism of GSK3beta activity is oncogenic in the mammary epithelium; mutation or pharmacologic down-regul

218 HIF-1alpha was conditionally deleted in the mammary epithelium of a transgenic mouse model for metas

219 onversely, targeted deletion of FIP1C in the mammary epithelium of an ErbB2 model coexpressing Cre re

220 ncer, we deleted PPARgamma expression in the mammary epithelium of an in vivo model of basal breast c

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

222 e report here that ErbB3 loss in the luminal mammary epithelium of mice impaired Akt and MAPK signali

223 nd genetic changes within the pre-neoplastic mammary epithelium of mice with and without stromal PTEN

224 adipose tissue surrounding the cancer-prone mammary epithelium of MMTV-Neu mice influences tumor dev

225 virus to deliver the ErbB2 oncogene into the mammary epithelium of our previously reported MMTV-tva t

226 expression were substantially reduced in the mammary epithelium of PIKE-/- mice.

227 highly enriched transcription factor in the mammary epithelium of pubertal mice.

228 is, we targeted N-cadherin expression in the mammary epithelium of the MMTV-Neu mouse.

229 eu gene under its endogenous promoter in the mammary epithelium of the mouse results in accelerated l

230 cycline-inducible expression of RANKL in the mammary epithelium of the progesterone receptor knockout

231 system to express conditionally FGF-3 in the mammary epithelium of transgenic mice.

232 xhibits the same dependence as p53 wild-type mammary epithelium on ovarian hormones for growth.

233 action but has no direct effect on the mouse mammary epithelium or Met-1 and MCNeuA cells.

234 rom these mice as well as cells derived from mammary epithelium, ovary, and neonatal brain were obser

235 a) is expressed in many cell types including mammary epithelium, ovary, macrophages, and B- and T-cel

236 in which local synthesis of serotonin by the mammary epithelium plays an important role in the negati

237 Conditional ablation of Myc in the mammary epithelium prevented the induction of regressing

238 ast growth factor receptor-1 (iFGFR1) in the mammary epithelium rapidly increased the expression of s

239 1), a protein abundantly expressed in normal mammary epithelium, regulates Wnt signaling, maintaining

240 n of ROCK kinase activity in EphA2-deficient mammary epithelium rescued branching defects in primary

241 Deletion of gp130 specifically from mammary epithelium resulted in a complete loss of Stat3

242 Conditional loss of ErbB3 in mammary epithelium resulted in a delay of PIK3CA(H1047R)

243 Expression of SNCG in mammary epithelium resulted in a significant stimulation

244 Targeted deletion of Brca1 in mammary epithelium resulted in carcinomas and adenocarci

245 surprisingly, deletion of HIF-1alpha in the mammary epithelium resulted in decreased pulmonary metas

246 Conditional deletion of HIF-1alpha in the mammary epithelium resulted in delayed tumor onset and r

247 nal deletion of both mPot1a and p53 in mouse mammary epithelium resulted in development of highly inv

248 Hus1 inactivation in the mammary epithelium resulted in genome damage that induce

249 nscription factor STAT3 in involuting murine mammary epithelium, resulting in delayed involution and

250 Loss of Tgfbr2 in the mammary epithelium results in lobular-alveolar hyperplas

251 llation of the RANKL signaling axis into the mammary epithelium results in precocious ductal side-bra

252 tro differentiated adipocyte cell line, with mammary epithelium showed that when activated, adipocyte

253 , on laser capture microdissected c-jun(-/-) mammary epithelium, showed that endogenous c-jun regulat

254 show that targeted deletion of FAK in mouse mammary epithelium significantly suppresses mammary tumo

255 tive regulator of the cell cycle, is a human mammary epithelium-specific marker that is downregulated

256 Thus, NSCs and their progeny enter mammary epithelium-specific niches and adopt the functio

257 th these findings, R-cad knockdown in normal mammary epithelium stimulated invasiveness and disrupted

258 of mammalian tissues including the lactating mammary epithelium, suggesting additional roles for XOR

259 In normal human mammary epithelium, TGFbeta induces progenitor activity

260 or, Tgfbr2, was conditionally deleted in the mammary epithelium (Tgfbr2MGKO).

261 s primarily originate from the subset of the mammary epithelium that is negative for PR and probably

262 In the mammary epithelium, the bulk of the tissue is composed o

263 y a phenotype consistent with progenitors of mammary epithelium: They exclude Hoechst dye 33342, and

264 les may reduce cellular proliferation in the mammary epithelium; this is one mechanism by which such

265 Here we report that the loss of Xbp1 in the mammary epithelium through targeted deletion leads to po

266 methyltransferases to the differentiation of mammary epithelium, thus opening the possibility of biol

267 ling can skew the homeostatic balance of the mammary epithelium to drive malignant progression; howev

268 sgenics to delete Apc and/or Apc2 from mouse mammary epithelium to elucidate the significance of thes

269 this question, we overexpressed GPNMB in the mammary epithelium to generate MMTV/GPNMB transgenic mic

270 or the major proliferative response of mouse mammary epithelium to progesterone during mammary lactat

271 uced proliferation of morphologically normal mammary epithelium, transgenic PRL restored it to rates

272 Finally, FVB strain transgenic mammary epithelium transplanted into nontransgenic recip

273 Serial mammary epithelium transplants demonstrate that p53+/m e

274 rming growth factor-beta receptor (DNIIR) in mammary epithelium under control of the MMTV promoter/en

275 reby CSF-1 was specifically expressed in the mammary epithelium under the regulation of the MMTV-prom

276 ansgenic mice expressing HGF specifically in mammary epithelium under the transcriptional control of

277 The mammary epithelium undergoes extensive growth and remode

278 ent and neoplasia, we disrupted this gene in mammary epithelium using a Cre-loxP approach.

279 nsfer of the activated neu oncogene into the mammary epithelium using a replication-defective retrovi

280 otype on the transcriptome of 'normal' mouse mammary epithelium using a unique in vivo model of prene

281 expressing the NF-kappaB p100/p52 subunit in mammary epithelium using the beta-lactoglobulin milk pro

282 cancer, Vhl was conditionally deleted in the mammary epithelium using the Cre/loxP system.

283 We deleted the PPARgamma gene in mammary epithelium using WAP-Cre transgenic mice and in

284 , but responses to ionizing radiation in the mammary epithelium vary among developmental stages.

285 However, hyperplastic mammary epithelium was a mixture of GFP/Akt1E17K-positiv

286 iated functional differentiation of Shh-null mammary epithelium was indistinguishable from wild type

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

288 expression of CXCL12 characteristic of human mammary epithelium was silenced by promoter hypermethyla

289 To investigate the role of Trsp in mouse mammary epithelium, we deleted this gene by using transg

290 eta driven model of transformation of normal mammary epithelium, we demonstrate that the class III hi

291 f the endogenous c-jun gene within the mouse mammary epithelium, we have identified its selective rol

292 chnology to specifically knockout FAK in the mammary epithelium, we showed that FAK is not required f

293 Transgenic mice expressing rtTA in the mammary epithelium were crossed with reporter lines bear

294 e that ectopically express PTEN and Wnt-1 in mammary epithelium were generated.

295 omas tested (n = 21) and, compared to normal mammary epithelium, were overexpressed in approximately

296 f RIP140 leads to a catastrophic loss of the mammary epithelium, whereas RIP140 overexpression augmen

297 st that R-cad is an adhesion molecule of the mammary epithelium, which acts as a critical regulator o

298 enerated chimeric mammary glands using mouse mammary epithelium with an inherited predisposition for

299 man primary breast tumors relative to normal mammary epithelium, with highest levels observed in brea

300 Breast cancer manifests itself in the mammary epithelium, yet there is a growing recognition t