mitochondria, IB kinase phosphorylation ? and thus the degradation of the NF B ? and mutual regulation of the tumor suppressor gene p53. Zus tzlich Akt regulates LY2886721 cell proliferation and growth of the target T t activity Glycogen synthase kinase and preventing the degradation of cyclin D1, as well as targeting mTOR. mTOR, also known as rapamycin associated protein is known, is a serine-threonine kinase, which is used as a molecular sensor growth and proliferation in response to N nutrients, growth factors, insulin, and regulated. abh ngig mTOR-dependent-dependent phosphorylation of several downstream molecules for cap-dependent-dependent translational function of proteins and cell cycle from G1 to S phase Recently there have been indications that exciting PI3K Akt pathway is an important target is at, treatment antimyeloma. Akt is constitutively activated in myeloma cells of the patient, but it is not of interest in non-malignant cells of the same patient.
Perhaps more importantly, enabled many of the most important factors for the growth of myeloma, such as IL-6, VEGF and NVP-BEP800 IGF-1-ligand for the receptor tyrosine kinase PI3K Pathway and the act of IL-6, the factor e-growing myeloma, it has been shown that phosphorylation of Akt and its downstream rtigen goals in a time and dose-dependent rtigen-dependent induction. Zus Tzlich IL-6 overcomes dexamethasone induces apoptosis by activation of Akt PI3K. Given the importance of the PI3K Akt in tumorigenesis, many drugs are being evaluated for a variety of malignancies. MM is currently evaluating three drugs. Perifosine Perifosine, an orally active, the connection to Rt alkyl phosphocholine a new class of anti-tumor signaling in Membranpermeabilit t, phospholipid metabolism, and mitogens. Importantly, perifosine was shown to the activation of Akt without affecting the activity of t of the PI3K-dependent-Dependent or T phosphoinositide-dependent-Dependent kinase inhibit Zun Highest it has been shown in vitro that p21WAF1 expression and cell cycle arrest in carcinomas of the head and epidermis Shuizhengguanli Sen and two Phase I studies in solid tumors have been performed.
MM, Hideshima and colleagues have not found that perifosine Akt activation inhibits the resistance of caspase-dependent-Dependent apoptosis JNK-dependent-Dependent herk Mmlichen therapy and sensitive MM cell lines overcomes the survival advantage of the interaction between MM cells and BMSCs and is cytotoxic peripheral mononuclear Ren Re blood cells. Zus tzlich anti-tumor effects in a mouse model has the MM M nozzles. After all, playing his pleotropic effects and calculated on the basis of clinical pr first perifosine an r useful in combination with other therapies and standards. In combination with standard therapies, such as dexamethasone, used melphalan and doxorubicin increased Hte perifosine MM cytotoxicity t t in vitro. Interestingly, the proteasome inhibitor, was found to activate Akt and that bortezomib combination of perifosine blocked this activation. This result is