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  1 / 2747 MEDLINE  
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PMID:28464874
Autor:Han Y; Li J; Han S; Jia S; Zhang Y; Zhang W
Dirección:Mammary Surgery Department, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China. hany1@sj-hospital.org.
Título:Diagnostic value of endoscopic appearance during ductoscopy in patients with pathological nipple discharge.
Fuente:BMC Cancer; 17(1):300, 2017 May 02.
ISSN:1471-2407
País de publicación:England
Idioma:eng
Resumen:BACKGROUND: To explore the features of ductoscopic appearance that may be diagnostic in patients with pathologic nipple discharge (PND) and to discuss the diagnostic criteria for intraductal tumors. METHODS: We reviewed 247 patients with PND but without a palpable mass who were evaluated using either surgical biopsy or excision. Data concerning patient age, duration of discharge, discharge color, and the details of endoscopic appearance were analyzed according to the pathological results. RESULTS: The postoperative diagnosis in 61 patients (24.70%) was a nonmass lesion, and 186 patients (76.52%) had an intraductal tumor. Among those with intraductal lesions, 10 patients (4.05%) had a malignant tumor, including 4 (1.62%) with ductal carcinoma in situ and 6 (2.43%) with invasive ductal carcinoma. On univariate analysis, patients of older age with spontaneous and bloody discharge were more likely to suffer from intraductal lesions. On logistic regression analysis, bloody nipple discharge, morphology, and a broad lesion base revealed by ductoscopy showed a statistically significant correlation with malignancy (p = 0.001, p < 0.001, p = 0.022, respectively). CONCLUSIONS: Both clinical features and endoscopic appearance are significant for the precise diagnosis of an intraductal lesion seen on ductoscopy. The endoscopic features of bloody discharge, morphology, and a broad lesion base are independent risk factors for malignancy and represent new criteria for the diagnosis of patients with PND.
Tipo de publicación:JOURNAL ARTICLE


  2 / 2747 MEDLINE  
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PMID:29022488
Autor:Joshi PS; Modur V; Cheng J; Robinson K; Rao K
Dirección:1 Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Título:Characterization of immortalized human mammary epithelial cell line HMEC 2.6.
Fuente:Tumour Biol; 39(10):1010428317724283, 2017 Oct.
ISSN:1423-0380
País de publicación:United States
Idioma:eng
Resumen:Primary human mammary epithelial cells have a limited life span which makes it difficult to study them in vitro for most purposes. To overcome this problem, we have developed a cell line that was immortalized using defined genetic elements, and we have characterized this immortalized non-tumorigenic human mammary epithelial cell line to establish it as a potential model system. human mammary epithelial cells were obtained from a healthy individual undergoing reduction mammoplasty at SIU School of Medicine. The cells were transduced with CDK4R24C followed by transduction with human telomerase reverse transcriptase. Post all manipulation, the cells displayed a normal cell cycle phase distribution and were near diploid in nature, which was confirmed by flow cytometry and karyotyping. In vitro studies showed that the cells were anchorage dependent and were non-invasive in nature. The cell line expressed basal epithelial markers such as cytokeratin 7, CD10, and p63 and was negative for the expression of estrogen receptor and progesterone receptor. Upon G-band karyotyping, the cell line displayed the presence of a few cytogenic abnormalities, including trisomy 20 and trisomy 7, which are also commonly present in other immortalized mammary cell lines. Furthermore, the benign nature of these cells was confirmed by multiple in vitro and in vivo experiments. Therefore, we think that this cell line could serve as a good model to understand the molecular mechanisms involved in the development and progression of breast cancer and to also assess the effect of novel therapeutics on human mammary epithelial cells.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)


  3 / 2747 MEDLINE  
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PMID:28938116
Autor:Hannezo E; Scheele CLGJ; Moad M; Drogo N; Heer R; Sampogna RV; van Rheenen J; Simons BD
Dirección:Cavendish Laboratory, Department of Physics, University of Cambridge, Cambridge CB3 0HE, UK; The Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; The Wellcome Trust/Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge CB2
Título:A Unifying Theory of Branching Morphogenesis.
Fuente:Cell; 171(1):242-255.e27, 2017 Sep 21.
ISSN:1097-4172
País de publicación:United States
Idioma:eng
Resumen:The morphogenesis of branched organs remains a subject of abiding interest. Although much is known about the underlying signaling pathways, it remains unclear how macroscopic features of branched organs, including their size, network topology, and spatial patterning, are encoded. Here, we show that, in mouse mammary gland, kidney, and human prostate, these features can be explained quantitatively within a single unifying framework of branching and annihilating random walks. Based on quantitative analyses of large-scale organ reconstructions and proliferation kinetics measurements, we propose that morphogenesis follows from the proliferative activity of equipotent tips that stochastically branch and randomly explore their environment but compete neutrally for space, becoming proliferatively inactive when in proximity with neighboring ducts. These results show that complex branched epithelial structures develop as a self-organized process, reliant upon a strikingly simple but generic rule, without recourse to a rigid and deterministic sequence of genetically programmed events.
Tipo de publicación:JOURNAL ARTICLE


  4 / 2747 MEDLINE  
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PMID:28859163
Autor:Che W; Bao Y; Tang F
Dirección:Huashan Hospital of Fudan University, Shanghai, China.
Título:Down-regulation of C35 decreased the cell viability and migration of breast ductal carcinoma cells.
Fuente:PLoS One; 12(8):e0183941, 2017.
ISSN:1932-6203
País de publicación:United States
Idioma:eng
Resumen:BACKGROUND: Resistance to human epidermal growth factor receptor-2 (HER2)-targeted therapies is common, and results in treatment failure and new tumor progression. C35 is over-expressed in many invasive breast cancer endogenously, and functions as an oncogene in breast cancer cell lines. METHODS: The current study aims to investigate effects of C35 on cell viability and migration of HER2-positive breast tumor cells and explore possible mechanisms. The protein expression of C35 in BT-474 breast ductal carcinoma cells was interfered by siRNAs. MTT assay was utilized to detect the viability of BT474 breast ductal carcinoma cells after transfection. The migration of BT474 breast ductal carcinoma cells was examined by cell wound scratch assay. RESULTS: In addition, the protein expression of C35, HER2, AKT and p-AKT in breast ductal carcinoma cells were detected by Western Blot. The protein expression of C35 was weaker in siRNA1 and siRNA2 groups compared with the control group. The relative expression ratio of C35 to ß-actin decreased significantly in siRNA2 and siRNA1 groups. When C35 expression was interfered by siRNA1 and siRNA2 for 48 h, the viability of BT474 breast ductal carcinoma cells decreased compared with the control group. In addition, the migration of breast ductal carcinoma cells decreased when C35 expression was interfered by siRNA1 for 24 h, and interfered by siRNA1 and siRNA2 for 48 h.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Intracellular Signaling Peptides and Proteins); 0 (MIEN1 protein, human); 0 (Neoplasm Proteins); 0 (RNA, Small Interfering); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)


  5 / 2747 MEDLINE  
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PMID:28831952
Autor:Sosa-Castillo E; Rodríguez-Cruz M; Moltó-Puigmartí C
Dirección:Laboratorio de Nutrición Molecular,Unidad de Investigación Médica en Nutrición,Hospital de Pediatría,Centro Médico Nacional Siglo XXI,Instituto Mexicano del Seguro Social,06725 Ciudad de México,Mexico.
Título:Genomics of lactation: role of nutrigenomics and nutrigenetics in the fatty acid composition of human milk.
Fuente:Br J Nutr; 118(3):161-168, 2017 Aug.
ISSN:1475-2662
País de publicación:England
Idioma:eng
Resumen:Human milk covers the infant's nutrient requirements during the first 6 months of life. The composition of human milk progressively changes during lactation and it is influenced by maternal nutritional factors. Nowadays, it is well known that nutrients have the ability to interact with genes and modulate molecular mechanisms impacting physiological functions. This has led to a growing interest among researchers in exploring nutrition at a molecular level and to the development of two fields of study: nutrigenomics, which evaluates the influence of nutrients on gene expression, and nutrigenetics, which evaluates the heterogeneous individual response to nutrients due to genetic variation. Fatty acids are one of the nutrients most studied in relation to lactation given their biologically important roles during early postnatal life. Fatty acids modulate transcription factors involved in the regulation of lipid metabolism, which in turn causes a variation in the proportion of lipids in milk. This review focuses on understanding, on the one hand, the gene transcription mechanisms activated by maternal dietary fatty acids and, on the other hand, the interaction between dietary fatty acids and genetic variation in genes involved in lipid metabolism. Both of these mechanisms affect the fatty acid composition of human milk.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Dietary Fats); 0 (Fatty Acids)


  6 / 2747 MEDLINE  
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PMID:28800960
Autor:Chean J; Chen CJ; Shively JE
Dirección:Department of Molecular Immunology, Beckman Research Institute of City of Hope, 1450 E. Duarte Road, Duarte, CA 91010, USA.
Título:ETS transcription factor ELF5 induces lumen formation in a 3D model of mammary morphogenesis and its expression is inhibited by Jak2 inhibitor TG101348.
Fuente:Exp Cell Res; 359(1):62-75, 2017 Oct 01.
ISSN:1090-2422
País de publicación:United States
Idioma:eng
Resumen:The loss of expression of a single gene can revert normal tissue to a malignant phenotype. For example, while normal breast has high lumenal expression of CEACAM1, the majority of breast cancers exhibit the early loss of this gene with the concurrent loss of their lumenal phenotype. MCF7 cells that lack CEACAM1 expression and fail to form lumena in 3D culture, regain the normal phenotype when transfected with CEACAM1. In order to probe the mechanism of this gain of function, we treated these cells with the clinically relevant Jak2 inhibitor TG101348 (TG), expecting that disruption of the prolactin receptor signaling pathway would interfere with the positive effects of transfection of MCF7 cells with CEACAM1. Indeed, lumen formation was inhibited, resulting in the down regulation of a set of genes, likely involved in the complex process of lumen formation. As expected, inhibition of the expression of many of these genes also inhibited lumen formation, confirming their involvement in a single pathway. Among the genes identified by the inhibition assay, ETS transcription factor ELF5 stood out, since it has been identified as a master regulator of mammary morphogenesis, and is associated with prolactin receptor signaling. When ELF5 was transfected into the parental MCF7 cells that lack CEACAM1, lumen formation was restored, indicating that ELF5 can replace CEACAM1 in this model system of lumenogenesis. We conclude that the event(s) that led to the loss of expression of CEACAM1 is epistatic in that multiple genes associated with a critical pathway were affected, but that restoration of the normal phenotype can be achieved with reactivation of certain genes at various nodal points in tissue morphogenesis.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (ELF5 protein, human); 0 (Neoplasm Proteins); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-ets); 0 (Pyrrolidines); 0 (RNA, Antisense); 0 (RNA, Messenger); 0 (SOCS2 protein, human); 0 (STAT5 Transcription Factor); 0 (STAT5A protein, human); 0 (Sulfonamides); 0 (Suppressor of Cytokine Signaling Proteins); 0 (TG101348); 0 (Tumor Suppressor Proteins); EC 2.7.10.2 (Janus Kinase 2)


  7 / 2747 MEDLINE  
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PMID:28604702
Autor:Mayorca-Guiliani AE; Madsen CD; Cox TR; Horton ER; Venning FA; Erler JT
Dirección:Biotech Research and Innovation Centre (BRIC), University of Copenhagen (UCPH), Copenhagen, Denmark.
Título:ISDoT: in situ decellularization of tissues for high-resolution imaging and proteomic analysis of native extracellular matrix.
Fuente:Nat Med; 23(7):890-898, 2017 Jul.
ISSN:1546-170X
País de publicación:United States
Idioma:eng
Resumen:The extracellular matrix (ECM) is a master regulator of cellular phenotype and behavior. It has a crucial role in both normal tissue homeostasis and disease pathology. Here we present a fast and efficient approach to enhance the study of ECM composition and structure. Termed in situ decellularization of tissues (ISDoT), it allows whole organs to be decellularized, leaving native ECM architecture intact. These three-dimensional decellularized tissues can be studied using high-resolution fluorescence and second harmonic imaging, and can be used for quantitative proteomic interrogation of the ECM. Our method is superior to other methods tested in its ability to preserve the structural integrity of the ECM, facilitate high-resolution imaging and quantitatively detect ECM proteins. In particular, we performed high-resolution sub-micron imaging of matrix topography in normal tissue and over the course of primary tumor development and progression to metastasis in mice, providing the first detailed imaging of the metastatic niche. These data show that cancer-driven ECM remodeling is organ specific, and that it is accompanied by comprehensive changes in ECM composition and topological structure. We also describe differing patterns of basement-membrane organization surrounding different types of blood vessels in healthy and diseased tissues. The ISDoT procedure allows for the study of native ECM structure under normal and pathological conditions in unprecedented detail.
Tipo de publicación:JOURNAL ARTICLE


  8 / 2747 MEDLINE  
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PMID:28586101
Autor:Huang X; Schurman N; Handa K; Hakomori S
Dirección:Division of Biomembrane Research, Pacific Northwest Research Institute, Seattle, WA, USA.
Título:Functional role of glycosphingolipids in contact inhibition of growth in a human mammary epithelial cell line.
Fuente:FEBS Lett; 591(13):1918-1928, 2017 Jul.
ISSN:1873-3468
País de publicación:England
Idioma:eng
Resumen:We have demonstrated previously the involvement of certain glycosphingolipids (GSLs) in 'contact inhibition' (dependent on cell-to-cell contact) of cell growth. Here, we examined the roles of specific GSLs in contact inhibition of the human epithelial cell line MCF10A. Contact-inhibited cells show increased expression of the ganglioside GD3 and the globo-series GSL Gb3, and of the mRNAs for the corresponding sialyltransferases ST8SIA1 (GD3 synthase) and galactosyltransferase A4GALT (Gb3 synthase). siRNA knockdown (KD) of ST8SIA1 and/or A4GALT significantly suppresses contact inhibition. Exogenous addition of GD3 or Gb3 inhibits proliferation of low-density cells. Our findings suggest that GSLs play functional roles in contact inhibition of these cells and that Merlin/NF2, a tumor suppressor protein, is involved in the GSL function.
Tipo de publicación:LETTER
Nombre de substancia:0 (Glycosphingolipids); 0 (RNA, Messenger); 0 (RNA, Small Interfering); EC 2.4.1.- (Galactosyltransferases); EC 2.4.1.- (UDP-galactose-lactosylceramide alpha 1-4-galactosyltransferase); EC 2.4.99.- (Sialyltransferases); EC 2.4.99.8 (alpha-N-acetylneuraminate alpha-2,8-sialyltransferase)


  9 / 2747 MEDLINE  
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PMID:28533107
Autor:Murphy MP; Niedziela DA; Keane OM
Dirección:Animal & Bioscience Department, Teagasc, Grange, Dunsany, Co. Meath, Ireland.
Título:EHS matrix incubated in media containing penicillin retains sufficient concentrations of antibiotic to inhibit growth of susceptible microorganisms.
Fuente:J Microbiol Methods; 139:103-106, 2017 Aug.
ISSN:1872-8359
País de publicación:Netherlands
Idioma:eng
Resumen:In studying the interaction between bacteria and host cells in vitro, the latter are frequently cultured on commercially available biotic matrices such as Matrigel® or Geltrex®. To avoid contamination, host cells are commonly grown in the presence of antibiotics. However, we present here the finding that cell culture on such a matrix in the presence of antibiotics interferes with the outcome of subsequent infection experiments by virtue of diminished bacterial survival. By comparing outcomes for penicillin-susceptible and resistant strains of Staphylococcus aureus, we show that residual penicillin remains in the matrix despite the antibiotics' withdrawal from culture. Hence, the use of antibiotics should be avoided in this context.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Anti-Bacterial Agents); 0 (Culture Media); 0 (Penicillins)


  10 / 2747 MEDLINE  
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PMID:28530657
Autor:Celià-Terrassa T; Liu DD; Choudhury A; Hang X; Wei Y; Zamalloa J; Alfaro-Aco R; Chakrabarti R; Jiang YZ; Koh BI; Smith HA; DeCoste C; Li JJ; Shao ZM; Kang Y
Dirección:Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.
Título:Normal and cancerous mammary stem cells evade interferon-induced constraint through the miR-199a-LCOR axis.
Fuente:Nat Cell Biol; 19(6):711-723, 2017 Jun.
ISSN:1476-4679
País de publicación:England
Idioma:eng
Resumen:Tumour-initiating cells, or cancer stem cells (CSCs), possess stem-cell-like properties observed in normal adult tissue stem cells. Normal and cancerous stem cells may therefore share regulatory mechanisms for maintaining self-renewing capacity and resisting differentiation elicited by cell-intrinsic or microenvironmental cues. Here, we show that miR-199a promotes stem cell properties in mammary stem cells and breast CSCs by directly repressing nuclear receptor corepressor LCOR, which primes interferon (IFN) responses. Elevated miR-199a expression in stem-cell-enriched populations protects normal and malignant stem-like cells from differentiation and senescence induced by IFNs that are produced by epithelial and immune cells in the mammary gland. Importantly, the miR-199a-LCOR-IFN axis is activated in poorly differentiated ER breast tumours, functionally promotes tumour initiation and metastasis, and is associated with poor clinical outcome. Our study therefore reveals a common mechanism shared by normal and malignant stem cells to protect them from suppressive immune cytokine signalling.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (LCOR protein, human); 0 (MicroRNAs); 0 (Mirn199 microRNA, mouse); 0 (Mlr2 protein, mouse); 0 (Repressor Proteins); 0 (Transcription Factors); 0 (mirn199 microRNA, human); 9008-11-1 (Interferons)



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