Base de dados : MEDLINE
Pesquisa : C04.588.531 [Categoria DeCS]
Referências encontradas : 3490 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 349 ir para página                         

  1 / 3490 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29360854
[Au] Autor:Dolka I; Czopowicz M; Gruk-Jurka A; Wojtkowska A; Sapierzynski R; Jurka P
[Ad] Endereço:Department of Pathology and Veterinary Diagnostics, Faculty of Veterinary Medicine, Warsaw University of Life Sciences (SGGW), Warsaw, Poland.
[Ti] Título:Diagnostic efficacy of smear cytology and Robinson's cytological grading of canine mammary tumors with respect to histopathology, cytomorphometry, metastases and overall survival.
[So] Source:PLoS One;13(1):e0191595, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytology is a simple, rapid, and inexpensive method used for pre-operative diagnosis of canine mammary tumors (CMTs) in veterinary practice. Studies related to human breast cancer showed the Robinson's grading system-established for invasive ductal carcinoma, not otherwise specified (IDC, NOS) and used on cytological material-to not only closely correspond to the histopathological grading but also be helpful in assessing prognosis and selecting most suitable treatments before surgery. The objectives of this study were: to evaluate the accuracy of cytological diagnosis and cytological Robinson's grading system compared to the histopathological examination of CMTs; to compare of cytological features and cytomorphometric parameters with tumor behavior, as well as cytological and histological grading; and to determine an association of the Robinson's grading system and cytological background details with metastases, and patients' survival. We report substantial diagnostic accuracy in detecting simple types and high grade tumors. Cytological diagnosis of tumor behavior showed relatively low sensitivity and specificity compared to human studies, and this might be caused by the heterogeneous morphology of CMTs. The presence of mucosecretory material and extracellular matrix was not significantly associated with tumor behavior. We report a positive correlation between both grading systems and cytological features (included in Robinson's grading), the presence of necrotic debris, inflammation, and red blood cells. A negative correlation was determined only for the presence of extracellular matrix. The univariate and multivariate analyses confirmed a significantly higher risk of developing metastasis and shorter overall survival for dogs with tumors of grade 2 or 3 on cytology. In addition, these tumors were the most common cause of CMT-related deaths in dogs. Taken together, our findings suggest that the Robinson's method of cytological grading applied for malignant CMTs evaluated in cytological smears regardless of tumor type can be adapted to veterinary cytology. Additionally, some background features seem to aid malignancy assessment.
[Mh] Termos MeSH primário: Doenças do Cão/diagnóstico
Neoplasias Mamárias Animais/diagnóstico
Metástase Neoplásica
[Mh] Termos MeSH secundário: Animais
Biópsia
Doenças do Cão/patologia
Cães
Feminino
Neoplasias Mamárias Animais/patologia
Sensibilidade e Especificidade
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191595


  2 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29317486
[Au] Autor:Foster CT; Gualdrini F; Treisman R
[Ad] Endereço:Signalling and Transcription Group, Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:Mutual dependence of the MRTF-SRF and YAP-TEAD pathways in cancer-associated fibroblasts is indirect and mediated by cytoskeletal dynamics.
[So] Source:Genes Dev;31(23-24):2361-2375, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Both the MRTF-SRF and the YAP-TEAD transcriptional regulatory networks respond to extracellular signals and mechanical stimuli. We show that the MRTF-SRF pathway is activated in cancer-associated fibroblasts (CAFs). The MRTFs are required in addition to the YAP pathway for CAF contractile and proinvasive properties. We compared MRTF-SRF and YAP-TEAD target gene sets and identified genes directly regulated by one pathway, the other, or both. Nevertheless, the two pathways exhibit mutual dependence. In CAFs, expression of direct MRTF-SRF genomic targets is also dependent on YAP-TEAD activity, and, conversely, YAP-TEAD target gene expression is also dependent on MRTF-SRF signaling. In normal fibroblasts, expression of activated MRTF derivatives activates YAP, while activated YAP derivatives activate MRTF. Cross-talk between the pathways requires recruitment of MRTF and YAP to DNA via their respective DNA-binding partners (SRF and TEAD) and is therefore indirect, arising as a consequence of activation of their target genes. In both CAFs and normal fibroblasts, we found that YAP-TEAD activity is sensitive to MRTF-SRF-induced contractility, while MRTF-SRF signaling responds to YAP-TEAD-dependent TGFß signaling. Thus, the MRF-SRF and YAP-TEAD pathways interact indirectly through their ability to control cytoskeletal dynamics.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Fibroblastos Associados a Câncer/fisiologia
Citoesqueleto/metabolismo
Proteínas de Ligação a DNA/metabolismo
Neoplasias Mamárias Animais/fisiopatologia
Fosfoproteínas/metabolismo
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Linhagem Celular Tumoral
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Camundongos
Fosfoproteínas/genética
Transdução de Sinais
Transativadores/genética
Ativação Transcricional/genética
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (DNA-Binding Proteins); 0 (MKL1 protein, human); 0 (MKL1 protein, mouse); 0 (Phosphoproteins); 0 (Tead1 protein, mouse); 0 (Trans-Activators); 0 (Transcription Factors); 0 (Transforming Growth Factor beta1); 0 (Yap protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1101/gad.304501.117


  3 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29061783
[Au] Autor:Vetvicka V; Vetvickova J
[Ad] Endereço:University of Louisville, Department of Pathology, Louisville, KY, U.S.A. vaclav.vetvicka@louisville.edu.
[Ti] Título:Fucoidans Stimulate Immune Reaction and Suppress Cancer Growth.
[So] Source:Anticancer Res;37(11):6041-6046, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Fucoidans are gaining popularity as natural immunomodulators. The aim of this study was to compare the immunological activities or both purified samples and commercially available mixtures containing fucoidan. MATERIALS AND METHODS: We evaluated the effects of various samples on phagocytosis, mitogenic response, natural killer (NK) activity, antibody formation and inhibition of breast cancer growth. RESULTS: We found significant immunostimulating activity, but the strength of these effects was different among individual samples. CONCLUSION: Fucoidans have strong immunostimulating potential, including inhibition of cancer, with isolated samples offering better activity than commercial mixtures.
[Mh] Termos MeSH primário: Inflamação/prevenção & controle
Células Matadoras Naturais/imunologia
Macrófagos/imunologia
Neoplasias Mamárias Animais/prevenção & controle
Polissacarídeos/farmacologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/farmacologia
Animais
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Fatores Imunológicos
Inflamação/imunologia
Inflamação/patologia
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/patologia
Macrófagos/efeitos dos fármacos
Macrófagos/patologia
Neoplasias Mamárias Animais/imunologia
Neoplasias Mamárias Animais/patologia
Camundongos
Camundongos Endogâmicos BALB C
Fagocitose/efeitos dos fármacos
Linfócitos T/efeitos dos fármacos
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antineoplastic Agents); 0 (Immunologic Factors); 0 (Polysaccharides); 9072-19-9 (fucoidan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


  4 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29033361
[Au] Autor:Wang Z; Zhang F; He J; Wu P; Tay LWR; Cai M; Nian W; Weng Y; Qin L; Chang JT; McIntire LB; Di Paolo G; Xu J; Peng J; Du G
[Ad] Endereço:Department of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, 6431 Fannin St., Houston, TX 77030, USA.
[Ti] Título:Binding of PLD2-Generated Phosphatidic Acid to KIF5B Promotes MT1-MMP Surface Trafficking and Lung Metastasis of Mouse Breast Cancer Cells.
[So] Source:Dev Cell;43(2):186-197.e7, 2017 Oct 23.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Little is known about the cellular events promoting metastasis. We show that knockout of phospholipase D (PLD2), which generates the signaling lipid phosphatidic acid (PA), inhibits lung metastases in the mammary tumor virus (MMTV)-Neu transgenic mouse breast cancer model. PLD2 promotes local invasion through the regulation of the plasma membrane targeting of MT1-MMP and its associated invadopodia. A liposome pull-down screen identifies KIF5B, the heavy chain of the motor protein kinesin-1, as a new PA-binding protein. In vitro assays reveal that PA specifically and directly binds to the C terminus of KIF5B. The binding between PLD2-generated PA and KIF5B is required for the vesicular association of KIF5B, surface localization of MT1-MMP, invadopodia, and invasion in cancer cells. Taken together, these results identify a role of PLD2-generated PA in the regulation of kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential therapeutic target for metastatic breast cancer.
[Mh] Termos MeSH primário: Cinesina/metabolismo
Neoplasias Pulmonares/secundário
Neoplasias Mamárias Animais/patologia
Metaloproteinase 14 da Matriz/metabolismo
Ácidos Fosfatídicos/metabolismo
Fosfolipase D/fisiologia
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Movimento Celular/fisiologia
Feminino
Seres Humanos
Cinesina/genética
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Células MCF-7
Neoplasias Mamárias Animais/genética
Neoplasias Mamárias Animais/metabolismo
Metaloproteinase 14 da Matriz/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ligação Proteica
Transporte Proteico
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphatidic Acids); EC 3.1.4.- (phospholipase D2); EC 3.1.4.4 (Phospholipase D); EC 3.4.24.80 (Matrix Metalloproteinase 14); EC 3.6.1.- (Kif5b protein, mouse); EC 3.6.4.4 (Kinesin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


  5 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28945747
[Au] Autor:Gentile LB; Nagamine MK; Biondi LR; Sanches DS; Toyota F; Giovani TM; de Jesus IP; da Fonseca IIM; Queiroz-Hazarbassanov N; Diaz BL; Salles Gomes COM; Dagli MLZ
[Ad] Endereço:Laboratory of Experimental and Comparative Oncology, Department of Pathology, School of Veterinary Medicine and Animal Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
[Ti] Título:Establishment of primary mixed cell cultures from spontaneous canine mammary tumors: Characterization of classic and new cancer-associated molecules.
[So] Source:PLoS One;12(9):e0184228, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There are many factors which make canine cancer like cancer in humans. The occurrence of spontaneous mammary tumors in pet dogs, tumor genetics, molecular targets and exposure to the same environmental risk factors are among these factors. Therefore, the study of canine cancer can provide useful information to the oncology field. This study aimed to establish and characterize a panel of primary mixed cell cultures obtained from spontaneous canine mammary tumors. Eight established cell cultures obtained from one normal mammary gland, one complex adenoma, one mixed adenoma, two complex carcinomas and two mixed carcinomas were analyzed. The gene expression levels of classic molecular cancer players such as fibroblast growth factor receptor (FGFR) 2, breast cancer (BRCA) 1, BRCA2 and estrogen receptor (ESR) 1 were evaluated. For the first time, three orphan nuclear receptors, estrogen-related receptors (ERRs) α, ß and γ were studied in canine mammary cancer. The highest expression level of ERRα was observed in complex carcinoma-derived cell culture, while the highest levels of ERRß and γ were observed in cells derived from a mixed carcinoma. Meanwhile, complex carcinomas presented the highest levels of expression of ESR1, BRCA1 and FGFR2 among all samples. BRCA2 was found exclusively in complex adenoma. The transcription factor GATA3 had its highest levels in mixed carcinoma samples and its lowest levels in complex adenoma. Proliferation assays were also performed to evaluate the mixed cell cultures response to ER ligands, genistein and DES, both in normoxia and hypoxic conditions. Our results demonstrate that morphological and functional studies of primary mixed cell cultures derived from spontaneous canine mammary tumors are possible and provide valuable tool for the study of various stages of mammary cancer development.
[Mh] Termos MeSH primário: Doenças do Cão/metabolismo
Neoplasias Mamárias Animais/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína BRCA1/metabolismo
Proteína BRCA2/metabolismo
Ciclo Celular
Linhagem Celular Tumoral
Proliferação Celular
Células Cultivadas
Cães
Receptor alfa de Estrogênio/metabolismo
Feminino
Citometria de Fluxo
Ploidias
Cultura Primária de Células
Reação em Cadeia da Polimerase em Tempo Real
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA1 Protein); 0 (BRCA2 Protein); 0 (Estrogen Receptor alpha); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184228


  6 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28825599
[Au] Autor:Taylor NA; Vick SC; Iglesia MD; Brickey WJ; Midkiff BR; McKinnon KP; Reisdorf S; Anders CK; Carey LA; Parker JS; Perou CM; Vincent BG; Serody JS
[Ad] Endereço:Lineberger Comprehensive Cancer Center.
[Ti] Título:Treg depletion potentiates checkpoint inhibition in claudin-low breast cancer.
[So] Source:J Clin Invest;127(9):3472-3483, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Claudin-low breast cancer is an aggressive subtype that confers poor prognosis and is found largely within the clinical triple-negative group of breast cancer patients. Here, we have shown that intrinsic and immune cell gene signatures distinguish the claudin-low subtype clinically as well as in mouse models of other breast cancer subtypes. Despite adaptive immune cell infiltration in claudin-low tumors, treatment with immune checkpoint inhibitory antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programmed death receptor 1 (PD-1) were ineffective in controlling tumor growth. CD4+FoxP3+ Tregs represented a large proportion of the tumor-infiltrating lymphocytes (TILs) in claudin-low tumors, and Tregs isolated from tumor-bearing mice were able to suppress effector T cell responses. Tregs in the tumor microenvironment highly expressed PD-1 and were recruited partly through tumor generation of the chemokine CXCL12. Antitumor efficacy required stringent Treg depletion combined with checkpoint inhibition; delays in tumor growth were not observed using therapies that modestly diminished the number of Tregs in the tumor microenvironment. This study provides evidence that the recruitment of Tregs to the tumor microenvironment inhibits an effective antitumor immune response and highlights early Treg recruitment as a possible mechanism for the lack of response to immune checkpoint blockade antibodies in specific subtypes of cancer that are heavily infiltrated with adaptive immune cells.
[Mh] Termos MeSH primário: Pontos de Checagem do Ciclo Celular
Claudinas/metabolismo
Linfócitos do Interstício Tumoral/imunologia
Linfócitos T Reguladores/imunologia
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Biomarcadores Tumorais/metabolismo
Linfócitos T CD4-Positivos/imunologia
Antígeno CTLA-4/metabolismo
Quimiocina CXCL12/metabolismo
Análise por Conglomerados
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Linfócitos do Interstício Tumoral/citologia
Neoplasias Mamárias Animais/tratamento farmacológico
Neoplasias Mamárias Animais/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Análise de Sequência com Séries de Oligonucleotídeos
Receptor de Morte Celular Programada 1/metabolismo
Neoplasias de Mama Triplo Negativas/imunologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (CXCL12 protein, human); 0 (Chemokine CXCL12); 0 (Claudins); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE


  7 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28783168
[Au] Autor:Simond AM; Rao T; Zuo D; Zhao JJ; Muller WJ
[Ad] Endereço:Department of Biochemistry, Rosalind and Morris Goodman Cancer Research Centre, McGill University, Montreal, Quebec, Canada.
[Ti] Título:ErbB2-positive mammary tumors can escape PI3K-p110α loss through downregulation of the Pten tumor suppressor.
[So] Source:Oncogene;36(43):6059-6066, 2017 Oct 26.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Breast cancer is the most common cancer among women and 30% of patients will be diagnosed with an ErbB2-positive tumor. Forty percent of ErbB2-positive breast tumors have an activating mutation in p110α, a catalytic subunit of phosphoinositide 3-kinase. Clinical and experimental data show that breast tumors treated with a p110α-specific inhibitor often circumvent inhibition and resume growth. To understand this mechanism of resistance, we crossed a p110α conditional (p110α ) mouse model with mice that overexpress the ErbB2/Neu-IRES-Cre transgene (NIC) specifically in the mammary epithelium. Although mammary-specific deletion of p110α dramatically delays tumor onset, tumors eventually arise and are dependent on p110ß. Through biochemical analyses we find that a proportion of p110α-deficient tumors (23%) display downregulation of the Pten tumor suppressor. We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110α to p110ß in vivo. These results provide insight into the molecular mechanism by which ErbB2-positive breast cancer escapes p110α inhibition.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Classe I de Fosfatidilinositol 3-Quinases/genética
Neoplasias Mamárias Animais/genética
PTEN Fosfo-Hidrolase/genética
Receptor ErbB-2/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Modelos Animais de Doenças
Epitélio/metabolismo
Epitélio/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Glândulas Mamárias Animais/metabolismo
Glândulas Mamárias Animais/patologia
Neoplasias Mamárias Animais/metabolismo
Neoplasias Mamárias Animais/patologia
Camundongos Transgênicos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.137 (1-phosphatidylinositol 3-kinase p110 subunit, mouse); EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Erbb2 protein, mouse); EC 2.7.10.1 (Receptor, ErbB-2); EC 3.1.3.67 (PTEN Phosphohydrolase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.264


  8 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28750038
[Au] Autor:Wang W; Gordon JL; Philbrick KA; Yang X; Branscum AJ; Löhr CV; Haschek WM; Turner RT; Iwaniec UT; Helferich WG
[Ad] Endereço:Food Science and Human Nutrition, University of Illinois, Urbana, Illinois, United States of America.
[Ti] Título:Low calcium diet increases 4T1 mammary tumor carcinoma cell burden and bone pathology in mice.
[So] Source:PLoS One;12(7):e0180886, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Breast cancer metastasizes to bone in the majority of patients with advanced disease. We investigated the effects of inadequate dietary calcium (Ca) on bone turnover, tumor growth, and bone response to tumor in tibia inoculated with 4T1 mammary carcinoma cells. Nine-month-old female Balb/c mice were placed on an adequate Ca (5 g/kg diet, n = 30) or low Ca (80 mg/kg diet, n = 31) diet for 14 days, then injected intratibially with 1,000 4T1 cells (transfected with luciferase for bioluminescence imaging), and sacrificed at 5, 10, or 21 days post-inoculation (n = 7-10 mice/group). Control mice (n = 6/group) were injected with carrier and sacrificed at 10 days post-inoculation. Tibiae with muscle intact were excised and evaluated by microcomputed tomography and histology. In vivo bioluminescent imaging revealed that 4T1 cells metastasized to lung. Therefore, lungs were removed for quantification of tumor. Mice fed low Ca exhibited higher bone turnover and higher tibial lesion scores than mice fed adequate Ca. Lesion severity, manifested as cortical osteolysis and periosteal woven bone formation, and tumor cell infiltration to muscle, increased with time, irrespective of diet. However, for most skeletal endpoints the rates of increase were greater in mice consuming low Ca compared to mice consuming adequate Ca. Infiltration of tumor cells into adjacent muscle, but not metastasis to lung, was also greater in mice consuming low Ca diet. The findings suggest that high bone turnover due to Ca insufficiency results in greater local mammary tumor cell growth, cortical osteolysis, woven bone formation, and invasion to muscle in mice.
[Mh] Termos MeSH primário: Cálcio na Dieta/farmacologia
Neoplasias Mamárias Animais/patologia
Tíbia/patologia
Carga Tumoral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Remodelação Óssea/efeitos dos fármacos
Osso Esponjoso/diagnóstico por imagem
Osso Esponjoso/efeitos dos fármacos
Osso Esponjoso/patologia
Linhagem Celular Tumoral
Progressão da Doença
Feminino
Camundongos Endogâmicos BALB C
Metástase Neoplásica
Tíbia/diagnóstico por imagem
Tíbia/efeitos dos fármacos
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium, Dietary)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180886


  9 / 3490 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28683102
[Au] Autor:Case A; Brisson BK; Durham AC; Rosen S; Monslow J; Buza E; Salah P; Gillem J; Ruthel G; Veluvolu S; Kristiansen V; Puré E; Brown DC; Sørenmo KU; Volk SW
[Ad] Endereço:Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
[Ti] Título:Identification of prognostic collagen signatures and potential therapeutic stromal targets in canine mammary gland carcinoma.
[So] Source:PLoS One;12(7):e0180448, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increasing evidence indicates that the tumor microenvironment plays a critical role in regulating the biologic behavior of breast cancer. In veterinary oncology, there is a need for improved prognostic markers to accurately identify dogs at risk for local and distant (metastatic) recurrence of mammary gland carcinoma and therefore would benefit from adjuvant therapy. Collagen density and fiber organization have been shown to regulate tumor progression in both mouse and human mammary tumors, with certain collagen signatures predicting poor outcomes in women with breast cancer. We hypothesized that collagen signatures in canine mammary tumor biopsies can serve as prognostic biomarkers and potential targets for treatment. We used second harmonic generation imaging to evaluate fibrillar collagen density, the presence of a tumor-stromal boundary, tumor associated collagen signatures (TACS) and individual collagen fiber characteristics (width, length and straightness) in grade I/II and grade III canine mammary tumors. Collagen density, as well as fiber width, length and straightness, were inversely correlated with patient overall survival time. Notably, grade III cases were less likely to have a tumor-stromal boundary and the lack of a boundary predicted poor outcome. Importantly, a lack of a defined tumor-stromal boundary and an increased collagen fiber width were associated with decreased survival even when tumor grade, patient stage, ovariohysterectomy status at the time of mammary tumor excision, and histologic evidence of lymphovascular invasion were considered in a multivariable model, indicating that these parameters could augment current methods to identify patients at high risk for local or metastatic progression/recurrence. Furthermore, these data, which identify for the first time, prognostic collagen biomarkers in naturally occurring mammary gland neoplasia in the dog, support the use of the dog as a translational model for tumor-stromal interactions in breast cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Colágeno/metabolismo
Glândulas Mamárias Animais/diagnóstico por imagem
Neoplasias Mamárias Animais/diagnóstico por imagem
Microambiente Tumoral
[Mh] Termos MeSH secundário: Animais
Biópsia
Colágeno/ultraestrutura
Progressão da Doença
Cães
Matriz Extracelular/metabolismo
Matriz Extracelular/ultraestrutura
Feminino
Metástase Linfática
Glândulas Mamárias Animais/patologia
Glândulas Mamárias Animais/cirurgia
Neoplasias Mamárias Animais/mortalidade
Neoplasias Mamárias Animais/patologia
Neoplasias Mamárias Animais/cirurgia
Microscopia de Fluorescência por Excitação Multifotônica
Gradação de Tumores
Estadiamento de Neoplasias
Prognóstico
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180448


  10 / 3490 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28650466
[Au] Autor:Roarty K; Pfefferle AD; Creighton CJ; Perou CM; Rosen JM
[Ad] Endereço:Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
[Ti] Título:Ror2-mediated alternative Wnt signaling regulates cell fate and adhesion during mammary tumor progression.
[So] Source:Oncogene;36(43):5958-5968, 2017 Oct 26.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cellular heterogeneity is a common feature in breast cancer, yet an understanding of the coexistence and regulation of various tumor cell subpopulations remains a significant challenge in cancer biology. In the current study, we approached tumor cell heterogeneity from the perspective of Wnt pathway biology to address how different modes of Wnt signaling shape the behaviors of diverse cell populations within a heterogeneous tumor landscape. Using a syngeneic TP53-null mouse model of breast cancer, we identified distinctions in the topology of canonical Wnt ß-catenin-dependent signaling activity and non-canonical ß-catenin-independent Ror2-mediated Wnt signaling across subtypes and within tumor cell subpopulations in vivo. We further discovered an antagonistic role for Ror2 in regulating canonical Wnt/ß-catenin activity in vivo, where lentiviral shRNA depletion of Ror2 expression augmented canonical Wnt/ß-catenin signaling activity across multiple basal-like models. Depletion of Ror2 expression yielded distinct phenotypic outcomes and divergent alterations in gene expression programs among different tumors, despite all sharing basal-like features. Notably, we uncovered cell state plasticity and adhesion dynamics regulated by Ror2, which influenced Ras Homology Family Member A (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1) activity downstream of Dishevelled-2 (Dvl2). Collectively, these studies illustrate the integration and collaboration of Wnt pathways in basal-like breast cancer, where Ror2 provides a spatiotemporal function to regulate the balance of Wnt signaling and cellular heterogeneity during tumor progression.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Proteínas Desgrenhadas/genética
Neoplasias Mamárias Animais/genética
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Proteínas rho de Ligação ao GTP/genética
Quinases Associadas a rho/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Adesão Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Mamárias Animais/patologia
Camundongos
Proteína Supressora de Tumor p53/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dishevelled Proteins); 0 (Dvl2 protein, mouse); 0 (Tumor Suppressor Protein p53); 0 (beta Catenin); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.10.1 (Ror2 protein, mouse); EC 2.7.11.1 (Rock1 protein, mouse); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.206



página 1 de 349 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde