Danusertib Fic for HCC The goal is to continue to improveFic for HCC

The goal is to continue to improve, if possible m, Get the results with sorafenib and erh Hen the number of patients who benefit from treatment can k. Our Gain Ndnis of pr Ziser and fine complex mechanisms HCC development, local growth mechanisms of angiogenesis and distant spread, ie the M Possibility offer, new therapies that will develop more effective. Molecular pathogenesis of HCC when handling the molecular mechanisms for the development and Danusertib progression of HCC, we have to. Nature of these heterogeneous tumor HCC in a healthy liver to develop a diseased liver, but not cirrhosis or, h Open more often, in cirrhosis. Can lead to cancer of various causes, Sch Caused by the toxic substances viruses, as in the case of chronic infections of hepatitis loan Be st. Quite generally, liver carcinogenesis represented as shown in Figure 1. K at the molecular level Can the mechanisms that are summarized in the pathogenesis of HCC in two main groups.
First, the activation of said paths ugetieren specified triggering Sen multiplication and then Border development of cancer, such as those of the mitogen-receptor of the epidermal growth factor-activated protein kinase, Wnt, Cryptotanshinone insulin Hnlichen growth factor, or the target of rapamycin in S and the second group includes the activation of more generic way of mechanisms common to most types of cancer, which are for the activation of angiogenesis, resistance to apoptosis, inactivation of specific control points the cell cycle or the limitless replicative potential preserve. All these changes Ver Can k, At least potentially, either with drugs that are already addressed in the market, although most of the time prescribed for other indications or with molecules in various stages of pr Clinical and clinical development or. EGFR targeting agents mentioned above Hnt, tr Path of EGFR gt essential for proliferation, apoptosis resistance and invasive behavior of HCC cells.
Three small molecules specifically tested the receptor tyrosine kinase EGFR and EGFR-neutralizing monoclonal Bodies were for clinical use in HCC. Erlotinib Erlotinib has shown anti-tumor activity of t Against HCC in pr Have clinical models and clinical studies. In the first study, 38 patients with HCC who had been treated intermediate to advanced clinical classification to Barcelona liver cancer, 39 with extrahepatic metastases EGFR inhibitor, administered orally at a dose of 150 mg. The objective response rate was low, which is not surprising given the cytostatic pleased t that the cytotoxic drug. However, the progression-free survival at 6 months was 32, and the median survival time was 13 months. Both figures are remarkable, even if it is at least partially explained by the fact Rt that a Gro Part of Enro