The second Phase III trial in previously untreated metastatic performed Acceptable melanoma patients and a control unit treatment arm, best Strengthens the benefits observed with ipilimumab treatment.13 This study randomized patients with previously untreated metastatic melanoma MLN8237 with ipilimumab placebo plus dacarbazine or dacarbazine. OS was significantly longer than this in the group receiving ipilimumab plus dacarbazine than in the group receiving dacarbazine alone: 11.2 months versus 9.1 months. Interestingly ipilimumab obtained in sub-groups of patients over the types of human leukocyte antigens, tumor mutations or prognostic factors such as serum lactate observed basis. This best CONFIRMS the clinical benefit of ipilimumab and the growing number of immunotherapy for patients with advanced melanoma. These tests showed the ipilimumab clinical benefit of immune modulation in metastatic melanoma.
The most important areas for future research focus on improving the provision of risks of immunotherapy for metastatic disease and the evaluation of the agent of the disease with a high risk from the start. Reduction of H abundance and severity and improved management of side effects, the identification of markers of BIBF1120 sensitivity of the tumor and the patient’s risk of adverse events: In the first case, the effort has been ben following areas CONFIRMS concentrated heavy side and evaluation combination strategies are there either the tumor-specific immune response and / or the target tumor cell proliferation and survival pathways. In the latter case, attempts are underway to resect the benefit of ipilimumab in melanoma patients evaluated.
Agents, and the results of the tests of therapies on the immune system are summarized in Table 1. Tumor-targeting drugs are in n Discussed in the next section. Molecular pathways ver Changed genetic in melanoma cells Crucial Ver Modifications that have increased to the oncogenic potential in melanoma Identified hen. Key mutations that result in constitutive activation of tumor growth and survival pathways occur in CKIT receptor tyrosine kinase and the RAS / RAF / MEK / ERK and phosphoinositide-3-OH kinase / protein kinase B / phosphatase tensin homolog gel deleted And signal transduction systems on chromosome 10th Although simple possibility M Conceive them as independent-Dependent significant interactions occur and the simultaneous activation of the signaling pathways play a r In the pathogenesis of malignant melanoma.
Demonstration that improves the mutant BRAF inhibitor vemurafenib survival in patients with metastatic melanoma shows that targeting aberrant protein k pathways with kinase inhibitors can Conduct clinical benefit.15 Below, we describe some of the main roads and agents for these target elements ways designed. Signal RAS / RAF / MEK / ERK pathway, the RAS / RAF / MEK / ERK plays an r Organogenesis in the normal, however, when aberrantly activated, it can b Sartigen cell proliferation, cause inhibition of apoptosis, and mitogen-activated protein kinase invasion.16 These relays extracellular Binary signals from the plasma membrane of the cell to one over the nucleus ordered series of different phosphorylation events.