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2 of cancer-induced BTP using female rats with mammary adenocarcinoma cells sealed within the tibia.
3 nsforming growth factor beta1 (TGF-beta1) in mammary adipose tissue in obese mice activates SMAD3 sig
4 reasing microRNA 140 (miR-140) expression in mammary adipose tissue through a novel negative-feedback
5 transcription factor, a master regulator of mammary alveologenesis and luminal cell differentiation,
6 question in the casein locus containing five mammary and two non-mammary genes under the control of a
7 d that patients receiving bilateral internal mammary artery (BIMA) conduits during coronary artery by
8 vival than those receiving a single internal mammary artery (SIMA), data on risk of repeat revascular
9 duit selection, including bilateral internal mammary artery and radial artery use; intraoperative gra
10 nary artery bypass grafting with an internal mammary artery and with 1 to 4 vein grafts were recruite
14 miR-31 is highly expressed in MaSC-enriched mammary basal cell population and in mammary tumors, and
15 . (2017) establish a model for post-pubertal mammary branching morphogenesis in which position-depend
16 ede mammary gland induction, but compromises mammary bud growth, as well as TEB formation, ductal out
18 elays formation of Eda-induced supernumerary mammary buds and normalizes the embryonic and postnatal
21 ix, MSC cultured with conditioned media from mammary cancer cells expressed increased levels of alpha
23 DF11 in vitro and suppresses triple-negative mammary cancer metastasis to the lung of syngeneic hosts
25 ession could be induced in murine chest wall mammary cancers with a topical toll-like receptor (TLR)-
26 yrosine kinase ERB2 (HER2), that define most mammary cancers, there are no targeted therapies for pat
27 polymorphisms as quantitative trait loci in mammary carcinogenesis, and they implicate distinct inte
28 olescence is a highly susceptible period for mammary carcinogenesis, but few prospective studies have
31 ouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cel
32 -control studies carried out in Germany: the Mammary Carcinoma Risk Factor Investigation (MARIE), a b
33 take of 2-(18)F-FEtOH in 4T1 and 67NR murine mammary carcinoma tumors grown in mice was measured usin
36 bal gene expression profiling of Ccn6(fl/fl) mammary carcinomas and comparison of orthologous genes w
37 ;MMTV-Cre mice developed invasive high grade mammary carcinomas with bona fide EMT, histologically si
38 Upon aging, the development of Wnt activated mammary carcinomas with squamous differentiation was acc
39 n validated against in-vivo data from murine mammary carcinomas, with particular focus placed on iden
42 pport a function for BRD4 in promoting basal mammary cell epithelial differentiation, at least in par
43 tional BRCA2 loss in a non-transformed human mammary cell line and see increased replication stress d
44 r by scavenging ROS or by halting the cyclic mammary cell population expansion, attenuated tumor recu
49 mmary microenvironment (niche) to direct non-mammary cells including testicular and embryonic stem ce
51 raction of transplanted normal MECs with non-mammary cells within the mammary fat-pads of recipient m
58 To study the in vivo effects of AZD4547 on mammary development, mammary epithelial cell (MEC) popul
62 or (Fgf) receptors have a recognized role in mammary ductal development and stem cell maintenance, bu
63 ast-specific PTEN deletion greatly restricts mammary ductal elongation and induces aberrant alveolar
65 Accordingly, stroma adjacent to invading mammary ducts of Sharpin(cpdm) mice displayed reduced co
66 f the border CTCF site separating the Csn1s1 mammary enhancer from neighboring genes resulted in the
67 is the predominant SENP transcript in human mammary epithelia but is significantly reduced in precan
69 total cell lysate obtained from normal human mammary epithelial (HME-1) cells treated with variable d
71 CaCo-2 colon, as well as normal human MCF10A mammary epithelial and human peripheral blood mononuclea
73 o effects of AZD4547 on mammary development, mammary epithelial cell (MEC) populations, and oncogenic
74 equired for ErbB4 ICD-mediated inhibition of mammary epithelial cell differentiation in a three-dimen
75 trength between metastatic and nonmetastatic mammary epithelial cell lines, which occur over concentr
79 ANCE Here, we use an in vitro model of human mammary epithelial cell transformation to assess how mal
81 ing Lgr5-EGFP-IRES-CreERT2, to demonstrate a mammary epithelial cell-autonomous requirement of CBL an
86 ctin promotes lactational differentiation of mammary epithelial cells (MECs) via its cognate receptor
87 nd receptors are recruited to the surface of mammary epithelial cells (MECs), and the vesicle transpo
90 m cell-like populations from non-tumorigenic mammary epithelial cells and non-aggressive breast cance
92 proteins that maintain the growth of starved mammary epithelial cells contingent upon epithelial cell
93 r-, progesterone receptor-, or ki67-positive mammary epithelial cells in the transgenic mice at the l
95 stimulation by FGF2, and Ptprb knockdown in mammary epithelial cells resulted in a higher level of f
98 gnalling is decreased, matrix-attached human mammary epithelial cells upregulate and internalize beta
99 nges over time, here, we study the motion of mammary epithelial cells within engineered monolayers, i
102 of MCF-7 breast cancer cells versus MCF-10A mammary epithelial cells, when subjected to individual a
103 and DOCK5 extends to non-transformed MCF10A mammary epithelial cells, with DOCK5 'dialing-up' and GI
111 in breast cancer and provide a link between mammary epithelial involution, tumorigenesis, and the ph
112 reast cancer metastasis, we have generated a mammary epithelial progression series of increasingly ag
113 R-ketorolac treatment significantly reduced mammary epithelial proliferation, based on Ki67 staining
114 ce concomitantly exhibit an expansion of the mammary epithelial stem cell (MaSC) enriched basal/myoep
115 11b acts as a central intrinsic regulator of mammary epithelial stem cell quiescence and exhaustion a
118 sembly of multiprotein complexes to regulate mammary epithelium and keratinocyte differentiation and
119 PRB regulates branching morphogenesis in the mammary epithelium by modulating the response of the FGF
122 Cre-recombinase-mediated Ptch1 ablation in mammary epithelium increased proliferation and branching
123 nd genetic changes within the pre-neoplastic mammary epithelium of mice with and without stromal PTEN
124 nal deletion of both mPot1a and p53 in mouse mammary epithelium resulted in development of highly inv
125 sgenics to delete Apc and/or Apc2 from mouse mammary epithelium to elucidate the significance of thes
126 aSCs) reside in the basal compartment of the mammary epithelium, and their neoplastic counterparts, m
132 nse drug extravasation than in contralateral mammary fat pad tissue, which is consistent with enhance
133 vivo shRNA knockdown of Ptprb in the cleared mammary fat pad transplant assay resulted in smaller epi
135 ormal MECs with non-mammary cells within the mammary fat-pads of recipient mice that had their endoge
136 of phosphatase and tensin homolog (PTEN) in mammary fibroblasts induces an oncogenic secretome that
137 mensional coculture assay for the effects of mammary fibroblasts on associated breast cancer cells.
138 in locus containing five mammary and two non-mammary genes under the control of at least seven putati
140 levated serotonin concentrations in both the mammary gland and circulation compared to controls.
141 benzo-a-pyrene (BaP) metabolism in the mouse mammary gland and develop a circadian in vitro model for
142 gly, this signature is present in the normal mammary gland and is progressively lost in patients with
143 vide new insights into the role of SEMA3B in mammary gland and provides a new branch of GATA3 signali
144 rowth-hormone concentrations that may affect mammary gland and pubertal development.We evaluated the
145 t, WAP-Cre x Tph1 (FL/FL) dams had decreased mammary gland and serum serotonin concentrations compare
146 (V) chains are an abundant product of normal mammary gland basal cells, and that alpha3(V) ablation i
147 y that SHARPIN regulates the normal invasive mammary gland branching morphogenesis in an epithelial c
148 properties of stem cells that participate in mammary gland branching morphogenesis remain contested.
149 isplay convergent co-option by placental and mammary gland cell types to optimize offspring success.
150 ow-dose effects include persistent delays in mammary gland development (perfluorooctanoic acid; PFOA)
151 The p53 family member, p63, is critical for mammary gland development and contains transactivation d
152 have revealed its specific roles in pubertal mammary gland development and potential contributions to
154 e studies showed that it is not required for mammary gland development during puberty, it is not clea
156 se environmental chemical exposure on normal mammary gland development in rats to motivate and evalua
157 Here, we examined the role of SHARPIN in mammary gland development, a process strongly regulated
158 be used to study the hormonal regulation of mammary gland development, and to test newly synthesized
164 t has minimal or less effect on normal human mammary gland epithelial cells (HMECs) and estrogen rece
165 mapping of accessible chromatin in the mouse mammary gland epithelial EpH4 cell line and its Ras-tran
168 into wild-type stroma, fully repopulate the mammary gland fat pad, undergo unperturbed ductal outgro
169 essing EMT-associated genes in normal murine mammary gland homeostasis and human breast cancer still
172 cterized by dynamic tissue remodeling in the mammary gland involving ductal elongation, resolution in
174 her analysis of the function of TAp63 in the mammary gland is critical for improved diagnosis and pat
176 In mouse models, PELP1 overexpression in the mammary gland leads to premalignant lesions and eventual
177 trolled variables across tumor and non-tumor mammary gland microvasculature with and without applicat
178 m and progenitor cell subpopulations driving mammary gland morphogenesis and homoeostasis are poorly
180 helial, stromal and systemic roles in murine mammary gland organogenesis, yet specific functions rema
183 n of neoplastic cells within the duct of the mammary gland that have not invaded into the surrounding
184 RCA-/-, p53-/- breast tumor tissue or normal mammary gland tissue with methyl-tert-butyl ether (MTBE)
185 revealed a shift from high triglycerides in mammary gland to high phospholipid levels in tumors.
186 te the interactions between CSCs and CAFs in mammary gland tumors driven by combined activation of Wn
187 e developed an ex vivo culture method of the mammary gland where the direct action of estrogens can b
188 EMT in vivo, in developing mouse embryos and mammary gland, and in vitro, in cultured 3D cell aggrega
189 ases basal levels of autophagy in the normal mammary gland, highlighting the potential of vitamin D a
199 exposure influences BaP metabolism in mouse mammary glands and describe an in vitro model that can b
207 in (PTHrP) in their developing epidermis and mammary glands] with those from wild type, we show that
208 cidate the significance of these proteins in mammary homeostasis and delineate their influences on Wn
210 but not in serum, suggesting that an entero-mammary link may exist for food-specific antibody-secret
211 tion factor that regulates genes involved in mammary luminal cell differentiation and tumor suppressi
212 e we report that induced p53 loss in Krt8(+) mammary luminal cells leads to their clonal expansion wi
213 addition to GATA3, FoxM1b also represses the mammary luminal differentiation marker FoxA1 by promoter
214 was to evaluate (64)Cu-DOTA-alendronate as a mammary microcalcification-targeting PET imaging agent,
215 y, we demonstrated the ability of the normal mammary microenvironment (niche) to direct non-mammary c
217 Brca2(-/-);p53(-/-) and Brca1(-/-);p53(-/-) mammary mouse tumours, suggesting that mitotic progressi
220 reERT; mT/mG), we show that Cbl/Cbl-b DKO in mammary organoids leads to hyperactivation of AKT-mTOR s
223 d early treatment discontinuation within the Mammary Prevention.3 (MAP.3) breast cancer prevention tr
227 s to characterize dams with a lactation- and mammary-specific disruption of Lrp5 (WAP-Cre x Lrp5 (FL/
229 ss these questions in the Wap locus with its mammary-specific super-enhancer separated by CTCF sites
230 nctions of specific microRNAs in controlling mammary stem cell (MaSC) activity and breast cancer form
232 background, as well as a tamoxifen-inducible mammary stem cell (MaSC)-specific Cbl and Cbl-b double k
233 hway components, the oncogene c-Myc, and the mammary stem cell regulator Id4 This signature drove clu
235 sition of mammary epithelial cells (MECs) to mammary stem cells (MaSCs) and to tumor-initiating cells
236 show that Ptprb is highly expressed in adult mammary stem cells and also, although at lower levels, i
237 transcriptional effector, acts within mouse mammary stromal cells to direct a hormone-responsive nic
239 ithelium, and their neoplastic counterparts, mammary TICs (MaTICs), are thought to serve as the TICs
240 se data indicate a crucial role for TAp63 in mammary TICs and provide a mechanism for its role as a t
241 rograms promote stemness and thereby support mammary tissue outgrowth and tumors of basal origin.
242 e results in elevated expression of Ramp3 in mammary tissue through augmented promoter-enhancer inter
244 in situ cancers growing within primary human mammary tissues and is also required for metastasis in v
249 1), A77636, inhibited proliferation of 4T1.2 mammary tumor cells as well as MDA-MB-231 breast cancer
255 ssess the contribution of endogenous Muc4 to mammary tumor growth properties, we first created a gene
256 enhanced, whereas overexpression, suppressed mammary tumor growth, consistent with a significant asso
259 2 transgenic mice dramatically shortened the mammary tumor latency and accelerated tumor growth due t
265 or mammary-specific deletion inhibited mouse mammary tumor virus (MMTV)- PyMT- and MMTV- Wnt1-driven
266 c acid (PA), inhibits lung metastases in the mammary tumor virus (MMTV)-Neu transgenic mouse breast c
267 ance between mesenchymal Wingless-type Mouse Mammary Tumor Virus integration site family, member 10B
269 tered breast cancer development in the mouse mammary tumor virus-polyoma middle T-antigen model.
270 ce were generated and crossed with the Mouse Mammary Tumor Virus-Polyoma Middle T-Antigen mouse.
273 In this study, we generated a mouse model of mammary tumorigenesis harboring the MMTV-HER2 oncogene a
274 we found that ERalpha and ERbeta expression, mammary tumorigenesis, and survival are energy balance d
278 ed with muscle was observed in both the SSM3 mammary tumors (2.4 +/- 0.17 vs. 1.6 +/- 0.14 percentage
279 on on two separate transposon screens of 123 mammary tumors and 20 B-cell acute lymphoblastic leukemi
280 howed that HER2(+)/PIK3CA(H1047R) transgenic mammary tumors are resistant to the HER2 antibodies tras
281 for the sensitive and specific detection of mammary tumors as well as the differentiation of maligna
282 cyclin D1 expression are suppressed, primary mammary tumors from Muc4(ko)/NDL female mice exhibit sim
284 These mice developed multiple independent mammary tumors of which the majority resembled human ILC
287 ng C-Met signaling were confirmed in vivo in mammary tumors using the in vivo invasion assay and intr
288 nriched mammary basal cell population and in mammary tumors, and is regulated by NF-kappaB signaling.
289 of Cdh1 does not predispose mice to develop mammary tumors, implying that mutations in additional ge
290 v mice bearing estrogen-dependent SSM3 mouse mammary tumors, male athymic nude mice bearing androgen-
296 ells, and that alpha3(V) ablation in a mouse mammary tumour model inhibits mammary tumour progression
297 asis, an MMTV-PyMT transgenic mouse model of mammary tumour progression and clinical breast cancer sa
298 ion in a mouse mammary tumour model inhibits mammary tumour progression by reducing the proliferative
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