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Wyszukujesz frazę "tumour invasion" wg kryterium: Temat


Wyświetlanie 1-2 z 2
Tytuł:
Numerical experiments with model equations of cancer invasion of tissue
Autorzy:
Kolev, M.
Zubik-Kowal, B.
Powiązania:
https://bibliotekanauki.pl/articles/206179.pdf
Data publikacji:
2011
Wydawca:
Polska Akademia Nauk. Instytut Badań Systemowych PAN
Tematy:
in vivo tumorigenicity
cancer cells
proliferation
chemotaxis
haptotaxis
extracellular matrix
tumour invasion
mathematical model
animal models
approximations
Opis:
In this paper we investigate a mathematical model of cancer invasion of tissue, which incorporates haptotaxis, chemotaxis, proliferation and degradation rates for cancer cells and the extracellular matrix, kinetics of urokinase receptor, and urokinase plasminogen activator cycle. We solve the model using spectrally accurate approximations and compare its numerical solutions with laboratory data. The spectral accuracy allows to use low-dimensional matrices and vectors, which speeds up the computations of the numerical solutions and thus to estimate the parameter values for the model equations. Our numerical results demonstrate correlations between numerical data computed from the mathematical model and in vivo tumour growth rates from prostate cell lines.
Źródło:
Control and Cybernetics; 2011, 40, 3; 779-791
0324-8569
Pojawia się w:
Control and Cybernetics
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
TGF beta signalling and its role in tumour pathogenesis.
Autorzy:
Kaminska, Bozena
Wesolowska, Aleksandra
Danilkiewicz, Malgorzata
Powiązania:
https://bibliotekanauki.pl/articles/1041410.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Smad propteins
RNA interference.
TGF beta signal transduction
tumour invasion
cancer therapy
MAP kinases
Opis:
Transforming growth factor beta (TGF-β) is a multifunctional cytokine involved in the regulation of cell proliferation, differentiation and survival/or apoptosis of many cells. Knock-out experiments in mice for the three isoforms of TGF-β have demonstrated their importance in regulating inflammation and tissue repair. TGF-β is implicated in the pathogenesis of human diseases, including tissue fibrosis and carcinogenesis. TGF-β receptors act through multiple intracellular pathways. Upon binding of TGF-β with its receptor, receptor-regulated Smad2/3 proteins become phosphorylated and associate with Smad4. Such complex translocates to the nucleus, binds to DNA and regulates transcription of specific genes. Negative regulation of TGF-β/Smad signalling may occur through the inhibitory Smad6/7. Furthermore, TGF-β-activated kinase-1 (TAK1) is a component of TGF-β signalling and activates stress-activated kinases: p38 through MKK6 or MKK3 and c-Jun N-terminal kinases (JNKs) via MKK4. In the brain TGF-β, normally expressed at the very low level, increases dramatically after injury. Increased mRNA levels of the three TGF-β isoforms correlate with the degree of malignancy of human gliomas. TGF-βs are secreted as latent precursors requiring activation into the mature form. TGF-β may contribute to tumour pathogenesis by direct support of tumour growth and influence on local microenvironment, resulting in immunosuppression, induction of angiogenesis, and modification of the extracellular matrix. TGF-β1,2 may stimulate production of vascular endothelial growth factor (VEGF) as well as plasminogen activator inhibitor (PAI-I), that are involved in vascular remodelling occurring during angiogenesis. Blocking of TGF-β action inhibits tumour viability, migration, metastases in mammary cancer, melanoma and prostate cancer model. Reduction of TGF-β production and activity may be a promising target of therapeutic strategies to control tumour growth.
Źródło:
Acta Biochimica Polonica; 2005, 52, 2; 329-337
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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