Ensayos clínicos

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Cells with increased oncogene activity adopt a secretory phenotype. For example, increased levels of c-Src not only inhibit differentiation but also induce the expression of extracellular matrix (ECM) proteins such as fibronectin (1), a protein critically involved in cell migration. The abnormal secretion of ECM proteins stems from the inability of c-Src overexpressing cells to sense their environment and to act in-sync with local tissue demand, likely because of a constitutive activation of ECM biosensors such as focal adhesion kinase (FAK). We hypothesize that the secretion of ECM proteins is an early event in malignant transformation induced by increased oncogene activity, resulting from constitutive activation of signaling cascades that are otherwise responsive to changes of the extracellular environment. To test our hypothesis, and to exploit its consequences or diagnostic applications, we propose the following specific aims:

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