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[PMID]:28454682
[Au] Autor:Priglinger E; Wurzer C; Steffenhagen C; Maier J; Hofer V; Peterbauer A; Nuernberger S; Redl H; Wolbank S; Sandhofer M
[Ad] Endereço:AUVA Research Center, Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Linz, Austria; Austrian Cluster for Tissue Regeneration, Vienna, Austria. Electronic address: Eleni.Priglinger@trauma.lbg.ac.at.
[Ti] Título:The adipose tissue-derived stromal vascular fraction cells from lipedema patients: Are they different?
[So] Source:Cytotherapy;19(7):849-860, 2017 07.
[Is] ISSN:1477-2566
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AIMS: Lipedema is a hormone-related disease of women characterized by enlargement of the extremities caused by subcutaneous deposition of adipose tissue. In healthy patients application of autologous adipose tissue-derived cells has shown great potential in several clinical studies for engrafting of soft tissue reconstruction in recent decades. The majority of these studies have used the stromal vascular fraction (SVF), a heterogeneous cell population containing adipose-derived stromal/stem cells (ASC), among others. Because cell identity and regenerative properties might be affected by the health condition of patients, we characterized the SVF cells of 30 lipedema patients in comparison to 22 healthy patients. METHODS: SVF cells were analyzed regarding cell yield, viability, adenosine triphosphate content, colony forming units and proliferative capacity, as well as surface marker profile and differentiation potential in vitro. RESULTS: Our results demonstrated a significantly enhanced SVF cell yield isolated from lipedema compared with healthy patients. In contrast, the adipogenic differentiation potential of SVF cells isolated from lipedema patients was significantly reduced compared with healthy patients. Interestingly, expression of the mesenchymal marker CD90 and the endothelial/pericytic marker CD146 was significantly enhanced when isolated from lipedema patients. DISCUSSION: The enhanced number of CD90 and CD146 cells could explain the increased cell yield because the other tested surface marker were not reduced in lipedema patients. Because the cellular mechanism and composition in lipedema is largely unknown, our findings might contribute to a better understanding of its etiology.
[Mh] Termos MeSH primário: Tecido Adiposo/patologia
Lipedema/patologia
Células Estromais/citologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Adipogenia/fisiologia
Tecido Adiposo/citologia
Adulto
Antígeno CD146/metabolismo
Estudos de Casos e Controles
Diferenciação Celular
Células Cultivadas
Feminino
Seres Humanos
Meia-Idade
Células-Tronco/citologia
Células-Tronco/patologia
Células Estromais/metabolismo
Células Estromais/patologia
Antígenos Thy-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (MCAM protein, human); 0 (Thy-1 Antigens); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29186180
[Au] Autor:Persichini T; Funari A; Colasanti M; Sacchetti B
[Ad] Endereço:Department of Science, University ROMA TRE, Rome, Italy.
[Ti] Título:Clonogenic, myogenic progenitors expressing MCAM/CD146 are incorporated as adventitial reticular cells in the microvascular compartment of human post-natal skeletal muscle.
[So] Source:PLoS One;12(11):e0188844, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent observation identifies subendothelial (mural) cells expressing MCAM, a specific system of clonogenic, self-renewing, osteoprogenitors (a.k.a, "mesenchymal stem cells") in the microvascular compartment of post-natal human bone marrow (BM). In this study, we used MCAM/CD146, as a marker to localize, isolate and assay subendothelial clonogenic cells from the microvasculature of postnatal human skeletal muscle. We show here that these cells share with their BM counterpart, anatomic position (subendothelial/adventitial) and ex vivo clonogenicity (CFU-Fs). When assayed under the stringent conditions, these cells display a high spontaneous myogenic potential (independent of co-culture with myoblasts or of in vivo fusion with local myoblasts), which is otherwise only attained in cultures of satellite cells. These muscle-derived mural cells activated a myogenic program in culture. Cultured CD146+ cells expressed the myogenic factors (Pax7, Pax3 and Myf5), NCAM/CD56, desmin as well as proteins characteristic of more advanced myogenic differentiation, such as myosin heavy chain. In vivo, these cells spontaneously generate myotubes and myofibrils. These data identify the anatomy and phenotype of a novel class of committed myogenic progenitor in human post-natal skeletal muscle of subendothelial cells associated with the abluminal surface of microvascular compartment distinct from satellite cells.
[Mh] Termos MeSH primário: Microvasos/metabolismo
Músculo Esquelético/citologia
[Mh] Termos MeSH secundário: Antígeno CD146/metabolismo
Técnicas de Cocultura
Seres Humanos
Músculo Esquelético/irrigação sanguínea
Músculo Esquelético/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (MCAM protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188844


  3 / 626 MEDLINE  
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[PMID]:28646020
[Au] Autor:Tripathi SC; Fahrmann JF; Celiktas M; Aguilar M; Marini KD; Jolly MK; Katayama H; Wang H; Murage EN; Dennison JB; Watkins DN; Levine H; Ostrin EJ; Taguchi A; Hanash SM
[Ad] Endereço:Department of Clinical Cancer Prevention, University of Texas MD Anderson Cancer Center, Houston, Texas.
[Ti] Título:MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway.
[So] Source:Cancer Res;77(16):4414-4425, 2017 Aug 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite favorable responses to initial therapy, small-cell lung cancer (SCLC) relapse occurs within a year and exhibits resistance to multiple drugs. Because of limited accessibility of patient tissues for research purposes, SCLC patient-derived xenografts (PDX) have provided the best opportunity to address this limitation. Here, we sought to identify novel mechanisms involved in SCLC chemoresistance. Through in-depth proteomic profiling, we identified MCAM as a markedly upregulated surface receptor in chemoresistant SCLC cell lines and in chemoresistant PDX compared with matched treatment-naïve tumors. MCAM depletion in chemoresistant cells reduced cell proliferation and reduced the IC inhibitory concentration of chemotherapeutic drugs This MCAM-mediated sensitization to chemotherapy occurred via SOX2-dependent upregulation of mitochondrial 37S ribosomal protein 1/ATP-binding cassette subfamily C member 1 (MRP1/ABCC1) and the PI3/AKT pathway. Metabolomic profiling revealed that MCAM modulated lactate production in chemoresistant cells that exhibit a distinct metabolic phenotype characterized by low oxidative phosphorylation. Our results suggest that MCAM may serve as a novel therapeutic target to overcome chemoresistance in SCLC. .
[Mh] Termos MeSH primário: Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Carcinoma de Pequenas Células do Pulmão/tratamento farmacológico
Carcinoma de Pequenas Células do Pulmão/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD146/genética
Antígeno CD146/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/fisiologia
Resistência a Medicamentos Antineoplásicos
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fatores de Transcrição SOXB1/genética
Transdução de Sinais
Carcinoma de Pequenas Células do Pulmão/genética
Carcinoma de Pequenas Células do Pulmão/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (MCAM protein, human); 0 (SOXB1 Transcription Factors); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-2874


  4 / 626 MEDLINE  
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[PMID]:28592632
[Au] Autor:Connacher MK; Tay JW; Ahn NG
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO 80309.
[Ti] Título:Rear-polarized Wnt5a-receptor-actin-myosin-polarity (WRAMP) structures promote the speed and persistence of directional cell migration.
[So] Source:Mol Biol Cell;28(14):1924-1936, 2017 Jul 07.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In contrast to events at the cell leading edge, rear-polarized mechanisms that control directional cell migration are poorly defined. Previous work described a new intracellular complex, the Wnt5a-receptor-actomyosin polarity (WRAMP) structure, which coordinates the polarized localization of MCAM, actin, and myosin IIB in a Wnt5a-induced manner. However, the polarity and function for the WRAMP structure during cell movement were not determined. Here we characterize WRAMP structures during extended cell migration using live-cell imaging. The results demonstrate that cells undergoing prolonged migration show WRAMP structures stably polarized at the rear, where they are strongly associated with enhanced speed and persistence of directional movement. Strikingly, WRAMP structures form transiently, with cells displaying directional persistence during periods when they are present and cells changing directions randomly when they are absent. Cells appear to pause locomotion when WRAMP structures disassemble and then migrate in new directions after reassembly at a different location, which forms the new rear. We conclude that WRAMP structures represent a rear-directed cellular mechanism to control directional migration and that their ability to form dynamically within cells may control changes in direction during extended migration.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Miosina não Muscular Tipo IIB/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina
Actinas/metabolismo
Actinas/fisiologia
Actomiosina/fisiologia
Antígeno CD146/metabolismo
Antígeno CD146/fisiologia
Polaridade Celular/fisiologia
Miosinas
Miosina não Muscular Tipo IIB/fisiologia
Proteínas Wnt
Proteína Wnt-5a
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CD146 Antigen); 0 (MCAM protein, human); 0 (WNT5A protein, human); 0 (Wnt Proteins); 0 (Wnt-5a Protein); 9013-26-7 (Actomyosin); EC 3.6.1.- (Nonmuscle Myosin Type IIB); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E16-12-0875


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[PMID]:28420427
[Au] Autor:Esteves CL; Sheldrake TA; Mesquita SP; Pesántez JJ; Menghini T; Dawson L; Péault B; Donadeu FX
[Ad] Endereço:The Roslin Institute, University of Edinburgh, Edinburgh, UK. cristina.esteves@roslin.ed.ac.uk.
[Ti] Título:Isolation and characterization of equine native MSC populations.
[So] Source:Stem Cell Res Ther;8(1):80, 2017 Apr 18.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In contrast to humans in which mesenchymal stem/stromal cell (MSC) therapies are still largely in the clinical trial phase, MSCs have been used therapeutically in horses for over 15 years, thus constituting a valuable preclinical model for humans. In human tissues, MSCs have been shown to originate from perivascular cells, namely pericytes and adventitial cells, which are identified by the presence of the cell surface markers CD146 and CD34, respectively. In contrast, the origin of MSCs in equine tissues has not been established, preventing the isolation and culture of defined cell populations in that species. Moreover, a comparison between perivascular CD146 and CD34 cell populations has not been performed in any species. METHODS: Immunohistochemistry was used to identify adventitial cells (CD34 ) and pericytes (CD146 ) and to determine their localization in relation to MSCs in equine tissues. Isolation of CD34 (CD34 /CD146 /CD144 /CD45 ) and CD146 (CD146 /CD34 /CD144 /CD45 ) cell fractions from equine adipose tissue was achieved by fluorescence-activated cell sorting. The isolated cell fractions were cultured and analyzed for the expression of MSC markers, using qPCR and flow cytometry, and for the ability to undergo trilineage differentiation. Angiogenic properties were analyzed in vivo using a chorioallantoic membrane (CAM) assay. RESULTS: Both CD34 and CD146 cells displayed typical MSC features, namely growth in uncoated tissue culture dishes, clonal growth when seeded at low density, expression of typical MSC markers, and multipotency shown by the capacity for trilineage differentiation. Of note, CD146 cells were distinctly angiogenic compared with CD34 and non-sorted cells (conventional MSCs), demonstrated by the induction of blood vessels in a CAM assay, expression of elevated levels of VEGFA and ANGPT1, and association with vascular networks in cocultures with endothelial cells, indicating that CD146 cells maintain a pericyte phenotype in culture. CONCLUSION: This study reports for the first time the successful isolation and culture of CD146 and CD34 cell populations from equine tissues. Characterization of these cells evidenced their distinct properties and MSC-like phenotype, and identified CD146 cells as distinctly angiogenic, which may provide a novel source for enhanced regenerative therapies.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/citologia
Cultura Primária de Células/veterinária
[Mh] Termos MeSH secundário: Tecido Adiposo/citologia
Angiopoietina-1/genética
Angiopoietina-1/metabolismo
Animais
Antígenos CD34/genética
Antígenos CD34/metabolismo
Antígeno CD146/genética
Antígeno CD146/metabolismo
Células Cultivadas
Cavalos
Células Mesenquimais Estromais/metabolismo
Pericitos/citologia
Pericitos/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiopoietin-1); 0 (Antigens, CD34); 0 (CD146 Antigen); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1186/s13287-017-0525-2


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[PMID]:28419140
[Au] Autor:Khatun M; Sorjamaa A; Kangasniemi M; Sutinen M; Salo T; Liakka A; Lehenkari P; Tapanainen JS; Vuolteenaho O; Chen JC; Lehtonen S; Piltonen TT
[Ad] Endereço:Department of Obstetrics and Gynecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.
[Ti] Título:Niche matters: The comparison between bone marrow stem cells and endometrial stem cells and stromal fibroblasts reveal distinct migration and cytokine profiles in response to inflammatory stimulus.
[So] Source:PLoS One;12(4):e0175986, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Intrinsic inflammatory characteristics play a pivotal role in stem cell recruitment and homing through migration where the subsequent change in niche has been shown to alter these characteristics. The bone marrow mesenchymal stem cells (bmMSCs) have been demonstrated to migrate to the endometrium contributing to the stem cell reservoir and regeneration of endometrial tissue. Thus, the aim of the present study was to compare the inflammation-driven migration and cytokine secretion profile of human bmMSCs to endometrial mesenchymal stem cells (eMSCs) and endometrial fibroblasts (eSFs). MATERIALS AND METHODS: The bmMSCs were isolated from bone marrow aspirates through culturing, whereas eMSCs and eSFs were FACS-isolated. All cell types were tested for their surface marker, proliferation profiles and migration properties towards serum and inflammatory attractants. The cytokine/chemokine secretion profile of 35 targets was analysed in each cell type at basal level along with lipopolysaccharide (LPS)-induced state. RESULTS: Both stem cell types, bmMSCs and eMSCs, presented with similar stem cell surface marker profiles as well as possessed high proliferation and migration potential compared to eSFs. In multiplex assays, the secretion of 16 cytokine targets was detected and LPS stimulation expanded the cytokine secretion pattern by triggering the secretion of several targets. The bmMSCs exhibited higher cytokine secretion of vascular endothelial growth factor (VEGF)-A, stromal cell-derived factor-1 alpha (SDF)-1α, interleukin-1 receptor antagonist (IL-1RA), IL-6, interferon-gamma inducible protein (IP)-10, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)1α and RANTES compared to eMSCs and/or eSFs after stimulation with LPS. The basal IL-8 secretion was higher in both endometrial cell types compared to bmMSCs. CONCLUSION: Our results highlight that similar to bmMSCs, the eMSCs possess high migration activity while the differentiation process towards stromal fibroblasts seemed to result in loss of stem cell surface markers, minimal migration activity and a subtler cytokine profile likely contributing to normal endometrial function.
[Mh] Termos MeSH primário: Células da Medula Óssea/citologia
Movimento Celular
Citocinas/imunologia
Endométrio/citologia
Fibroblastos/citologia
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Células da Medula Óssea/imunologia
Antígeno CD146/análise
Antígeno CD146/imunologia
Proliferação Celular
Células Cultivadas
Citocinas/análise
Endométrio/imunologia
Feminino
Fibroblastos/imunologia
Seres Humanos
Inflamação/imunologia
Lipopolissacarídeos/imunologia
Meia-Idade
Receptor beta de Fator de Crescimento Derivado de Plaquetas/análise
Receptor beta de Fator de Crescimento Derivado de Plaquetas/imunologia
Células-Tronco/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (Cytokines); 0 (Lipopolysaccharides); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175986


  7 / 626 MEDLINE  
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[PMID]:28364041
[Au] Autor:Colomb F; Wang W; Simpson D; Zafar M; Beynon R; Rhodes JM; Yu LG
[Ad] Endereço:From the Gastroenterology Research Unit, Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE and.
[Ti] Título:Galectin-3 interacts with the cell-surface glycoprotein CD146 (MCAM, MUC18) and induces secretion of metastasis-promoting cytokines from vascular endothelial cells.
[So] Source:J Biol Chem;292(20):8381-8389, 2017 May 19.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The galactoside-binding protein galectin-3 is increasingly recognized as an important player in cancer development, progression, and metastasis via its interactions with various galactoside-terminated glycans. We have shown previously that circulating galectin-3, which is increased up to 30-fold in cancer patients, promotes blood-borne metastasis in an animal cancer model. This effect is partly attributable to the interaction of galectin-3 with unknown receptor(s) on vascular endothelial cells and causes endothelial secretion of several metastasis-promoting cytokines. Here we sought to identify the galectin-3-binding molecule(s) on the endothelial cell surface responsible for the galectin-3-mediated cytokine secretion. Using two different galectin-3 affinity purification processes, we extracted four cell membrane glycoproteins, CD146/melanoma cell adhesion molecule (MCAM)/MUC18, CD31/platelet endothelial cell adhesion molecule-1 (PECAM-1), CD144/VE-cadherin, and CD106/Endoglin, from vascular endothelial cells. CD146 was the major galectin-3-binding ligand and strongly co-localized with galectin-3 on endothelial cell surfaces treated with exogenous galectin-3. Moreover, galectin-3 bound to -linked glycans on CD146 and induced CD146 dimerization and subsequent activation of AKT signaling. siRNA-mediated suppression of CD146 expression completely abolished the galectin-3-induced secretion of IL-6 and G-CSF cytokines from the endothelial cells. Thus, CD146/MCAM is the functional galectin-3-binding ligand on endothelial cell surfaces responsible for galectin-3-induced secretion of metastasis-promoting cytokines. We conclude that CD146/MCAM interactions with circulating galectin-3 may have an important influence on cancer progression and metastasis.
[Mh] Termos MeSH primário: Galectina 3/metabolismo
Fator Estimulador de Colônias de Granulócitos/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Interleucina-6/metabolismo
Multimerização Proteica
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/metabolismo
Antígeno CD146/genética
Antígeno CD146/metabolismo
Caderinas/genética
Caderinas/metabolismo
Galectina 3/genética
Fator Estimulador de Colônias de Granulócitos/genética
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Interleucina-6/genética
Metástase Neoplásica
Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/patologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD146 Antigen); 0 (Cadherins); 0 (Galectin 3); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (MCAM protein, human); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (cadherin 5); 0 (galectin-3, human); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170402
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.783431


  8 / 626 MEDLINE  
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[PMID]:28347241
[Au] Autor:Tampaki EC; Tampakis A; Nonni A; Kontzoglou K; Patsouris E; Kouraklis G
[Ad] Endereço:1 2nd Department of Propedeutic Surgery, Athens University Medical School, Laiko General Hospital, Athens, Greece.
[Ti] Título:Nestin and cluster of differentiation 146 expression in breast cancer: Predicting early recurrence by targeting metastasis?
[So] Source:Tumour Biol;39(3):1010428317691181, 2017 Mar.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to investigate the relationship between the expression of stem-cell markers nestin and cluster of differentiation 146 with clinicopathological characteristics in breast cancer and to determine whether a prognostic impact of nestin and CD146 expression exists regarding occurrence of disease relapse in breast cancer. A total of 141 patients who were histologically diagnosed with breast cancer and underwent radical operations from November 2006 to October 2013 in Laiko General Hospital, National and Kapodistrian University of Athens, were enrolled in the study. CD146 and nestin protein expression were evaluated using immunohistochemistry. Nestin expression was observed in 18.4% (26/141) of the cases, while CD146 expression was observed in 35.5% (50/141) of the cases. Nestin expression is significantly higher in younger patients with breast cancer. Nestin and CD146 expression were not correlated with the tumor size and the presence of lymph node metastasis. On the contrary, a significantly higher expression of nestin and CD146 was observed with triple-negative cancers (p < 0.0001 for both markers), low differentiated tumors (p = 0.021 for nestin and p = 0.008 for CD146), and increased Ki-67 expression (p = 0.007 for nestin and p < 0.0001 for CD146). The nestin-positive group of patients and the CD146-positive group of patients presented significantly higher rates of disease recurrence (log-rank test, p = 0.022 for nestin and p = 0.003 for CD146) with a distant metastasis, 30 months after the primary treatment. CD146 but not nestin, however, predicted independently (p = 0.047) disease recurrence. Nestin and CD146 are expressed in breast cancer cells with highly aggressive potency. They might contribute to disease relapse in breast cancer by activating the epithelial-mesenchymal transition pathway and assist tumor neovascularization.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Nestina/biossíntese
[Mh] Termos MeSH secundário: Neoplasias da Mama/cirurgia
Antígeno CD146/biossíntese
Estudos de Casos e Controles
Diferenciação Celular/fisiologia
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Metástase Neoplásica
Recidiva Local de Neoplasia/metabolismo
Recidiva Local de Neoplasia/patologia
Estadiamento de Neoplasias
Valor Preditivo dos Testes
Neoplasias de Mama Triplo Negativas/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
Neoplasias de Mama Triplo Negativas/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (MCAM protein, human); 0 (NES protein, human); 0 (Nestin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317691181


  9 / 626 MEDLINE  
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[PMID]:28333070
[Au] Autor:Luz MC; Perez MM; Azzalis LA; Sousa LV; Adami F; Fonseca FL; Alves BD
[Ad] Endereço:Clinical Laboratory, Faculdade de Medicina do ABC (FMABC), Av. Príncipe de Gales, 821, CEP 09060-650 Santo André, SP, Brazil. mb.luz@uol.com.br.
[Ti] Título:Evaluation of MCT1, MCT4 and CD147 Genes in Peripheral Blood Cells of Breast Cancer Patients and Their Potential Use as Diagnostic and Prognostic Markers.
[So] Source:Int J Mol Sci;18(4), 2017 Mar 23.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with breast cancer-the deadliest cancer among women-are at constant risk of developing metastasis. Oxidative stress and hypoxia are common feature of tumor cells that can proliferate even in a resultant metabolic acidosis. Despite the low extracellular pH, intracellular pH of tumor cells remains relatively normal, or even more alkaline due to the action of a membrane protein family known as monocarboxylate transporters (MCTs). The objective of this study was to verify the diagnostic and prognostic value of , and in tumor and peripheral blood samples of patients with breast cancer undergoing chemotherapic treatment. METHODS: Differential expression of , and obtained by qPCR was determined by 2 method between biological samples (tumor and serial samples of peripheral) of patients ( = 125) and healthy women ( = 25). RESULTS: tumor samples with higher histological grades have shown higher expression of these markers; this higher expression was also observed in blood samples obtained at diagnosis of patients when compared to healthy women and in patients with positive progression of the disease (metastasis development). CONCLUSION: markers studied here could be a promising strategy in routine laboratory evaluations as breast cancer diagnosis and prognosis.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Neoplasias da Mama/sangue
Antígeno CD146/sangue
Transportadores de Ácidos Monocarboxílicos/sangue
Proteínas Musculares/sangue
Simportadores/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD146 Antigen); 0 (Monocarboxylic Acid Transporters); 0 (Muscle Proteins); 0 (SLC16A4 protein, human); 0 (Symporters); 0 (monocarboxylate transport protein 1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE


  10 / 626 MEDLINE  
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[PMID]:28319067
[Au] Autor:Sechler M; Parrish JK; Birks DK; Jedlicka P
[Ad] Endereço:Cancer Biology Graduate Training Program.
[Ti] Título:The histone demethylase KDM3A, and its downstream target MCAM, promote Ewing Sarcoma cell migration and metastasis.
[So] Source:Oncogene;36(29):4150-4160, 2017 Jul 20.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ewing Sarcoma is the second most common solid pediatric malignant neoplasm of bone and soft tissue. Driven by EWS/Ets, or rarely variant, oncogenic fusions, Ewing Sarcoma is a biologically and clinically aggressive disease with a high propensity for metastasis. However, the mechanisms underpinning Ewing Sarcoma metastasis are currently not well understood. In the present study, we identify and characterize a novel metastasis-promotional pathway in Ewing Sarcoma, involving the histone demethylase KDM3A, previously identified by our laboratory as a new cancer-promoting gene in this disease. Using global gene expression profiling, we show that KDM3A positively regulates genes and pathways implicated in cell migration and metastasis, and demonstrate, using functional assays, that KDM3A promotes migration in vitro and experimental, post-intravasation, metastasis in vivo. We further identify the melanoma cell adhesion molecule (MCAM) as a novel KDM3A target gene in Ewing Sarcoma, and an important effector of KDM3A pro-metastatic action. Specifically, we demonstrate that MCAM depletion, like KDM3A depletion, inhibits cell migration in vitro and experimental metastasis in vivo, and that MCAM partially rescues impaired migration due to KDM3A knock-down. Mechanistically, we show that KDM3A regulates MCAM expression both through a direct mechanism, involving modulation of H3K9 methylation at the MCAM promoter, and an indirect mechanism, via the Ets1 transcription factor. Finally, we identify an association between high MCAM levels in patient tumors and poor survival, in two different Ewing Sarcoma clinical cohorts. Taken together, our studies uncover a new metastasis-promoting pathway in Ewing Sarcoma, with therapeutically targetable components.
[Mh] Termos MeSH primário: Epigenômica/métodos
Histona Desmetilases com o Domínio Jumonji/metabolismo
Sarcoma de Ewing/metabolismo
Sarcoma de Ewing/patologia
[Mh] Termos MeSH secundário: Adolescente
Animais
Antígeno CD146/genética
Antígeno CD146/metabolismo
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Criança
Regulação para Baixo
Perfilação da Expressão Gênica
Xenoenxertos
Seres Humanos
Histona Desmetilases com o Domínio Jumonji/genética
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Metástase Neoplásica
Regiões Promotoras Genéticas
Sarcoma de Ewing/enzimologia
Sarcoma de Ewing/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD146 Antigen); 0 (MCAM protein, human); EC 1.14.11.- (Jumonji Domain-Containing Histone Demethylases); EC 1.14.11.- (KDM3A protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170321
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.44



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