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  • ACTIVATION  (2)
  • CANCER CELLS  (2)
  • 1
    Keywords: HUMAN-BREAST ; MEDIA ; MMP-9 ; tumor microenvironment ; E ; THERAPIES ; SERUM ; PROGRESSION ; prevention ; BREAST-CANCER ; breast cancer ; culture ; BREAST ; microenvironment ; CANCER-CELLS ; SERA ; THERAPY ; human ; tumor ; CELL ; CANCER ; CANCER CELLS ; CELLS
    Type of Publication: Book chapter
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  • 2
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; SURVIVAL ; carcinoma ; PATHWAY ; PATHWAYS ; GENE ; ACTIVATION ; MECHANISM ; prognosis ; tumour ; FREQUENCY ; polymorphism ; DELETION ; AMPLIFICATION ; immunohistochemistry ; PROMOTER ; MUTATION ; CDKN2A ; inactivation ; p53 ; PATHOGENESIS ; SPORADIC PRIMARY MELANOMAS ; REGION ; microsatellite instability ; MUTATIONS ; CARCINOMAS ; HISTOLOGIC TYPE ; K-RAS ; METHYLATION ; ENDOMETRIAL CANCER ; BRAF ; K-ras mutation ; Ras ; SUBSET ; KRAS MUTATIONS ; interaction ; ESTROGEN ; SUPPRESSOR ; BRAF MUTATIONS ; K-RAS MUTATIONS ; KRAS ; MISMATCH-REPAIR ; PROMOTER REGION ; CDKN2A (p16) ; P16(INK4) ; POPULATION-BASED SERIES ; PROMOTER METHYLATION
    Abstract: Several pathways have been implicated in the pathogenesis of endometrial carcinoma. Based on recent reports, BRAF mutations provide an alternative route for activation of the RAS signalling pathway. The CDKN2A (p16) tumour suppressor gene is also altered in several tumour types. We therefore wanted to assess the pattern and prognostic impact of BRAF mutations and p16 alterations in endometrial carcinomas. Only 1 of 48 tumours (2%) was found to have a BRAF mutation in exon 15, whereas 8 of 45 tumours (18%) had a K-ras mutation. Homozygous deletion, amplification, promoter region methylation or mutation of the p16 gene was seen in 6 cases (13%), and 18 cases (38%) carried polymorphisms in the p16 gene. All tumours with presence of p16 methylation, non-sense mutation, deletion or amplification exhibited loss of p16 expression as evaluated by immunohistochemistry. Presence of a p16 hit was significantly correlated with high FIGO stage (p = 0.04), high histologic grade (p = 0.02), estrogen receptor negativity (p = 0.05), pathologic expression of p53 (p = 0.02), pathologic expression of p16 (p = 0.05) and poor survival (p 0.02). There was also a significant correlation between loss of p16 expression and K-ras mutations, pathologic p53 expression and serous papillary/clear cell histologic types (p = 0.05/p = 0.001/p = 0.002). In. conclusion, BRAF mutation is an infrequent finding in endometrial carcinomas. Loss of p16 expression is seen in all cases with alterations of the p16 gene. The presence of a p16 hit might be important in a subset of endometrial carcinomas with aggressive clinical behaviour. However, the mechanism of p16 inactivation remains unclear for the majority of cases exhibiting loss of expression, but the interactions with K-ras and p53 should be further studied. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15723290
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  • 3
    Keywords: RECEPTOR ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; proliferation ; SURVIVAL ; tumor ; CELL ; human ; KINASE ; PATHWAY ; PATHWAYS ; SUPPORT ; EXPOSURE ; SITE ; DIFFERENTIATION ; MONOCLONAL-ANTIBODY ; NF-KAPPA-B ; ACTIVATION ; FAMILY ; BINDING ; PHOSPHORYLATION ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; MEMBRANE ; METASTASIS ; REGION ; CANCER-CELLS ; EXTRACELLULAR-MATRIX ; BETA ; ADHESION ; MIGRATION ; FACTOR-KAPPA-B ; INTEGRIN ; NF-kappa B ; RECEPTORS ; MMP ; FIBRONECTIN ; TUMOR-METASTASIS ; SERUM ; FAMILIES ; basement membrane ; cell adhesion ; GELATINASE-A ; MMP-2 ; INTEGRINS ; RGD ; NUCLEAR ; EVENTS ; ERK ; MMP-9 ; pharmacology ; MT1-MMP ; TISSUE INHIBITOR ; ENGLAND ; matrix metalloproteinase ; MATRIX-METALLOPROTEINASE ; MEDICINE ; MEDIA ; interactions ; MT1-MMP MMP-14 ; PI-3K
    Abstract: Interactions between tumour cells and the extracellular matrix (ECM) strongly influence tumour development, affecting cell survival, proliferation and migration. Many of these interactions are mediated through a family of cell surface receptors named integrins. Fibronectin and its integrin receptors play important roles in tumour development. The alpha 5 beta 1 integrin interacts with the central cell adhesive region of fibronectin and requires both the RGD and synergy sites for maximal binding. Matrix metalloproteinases (MMPs) are a family of zinc dependent endopeptidases. They are capable of digesting the different components of the ECM and basement membrane. The ECM gives structural support to cells and plays a central role in cell adhesion, differentiation, proliferation and migration. Binding of ECM to integrins modulates expression and activity of the different MMPs. Our experimental findings demonstrate that cultivation of human breast cancer cells, MCF-7, in serum free medium in the presence of fibronectin upregulates the activity of MMP-2 and MMP-9. Blocking of alpha 5 beta 1 integrin with anti-alpha 5 monoclonal antibody inhibits the fibronectin-induced MMP activation response appreciably. This strongly indicates alpha 5 beta 1 mediated signalling events in activation of MMP-2 and MMP-9. Phosphorylation of FAK and PI-3 kinase and the nuclear translocation of ERK and NF-kappa B upon fibronectin binding demonstrate possible participation of the FAK/PI-3K/ERK signalling pathways in the regulation of MMP-2 activity. (c) 2007 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18243246
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