One advantage of this class of agents in this patient population is the toxicity of t T Aided by Is very acceptable. RTI has a chronic dose administered alone or in combination with other pharmacological KU-55933 compounds of the underlying disease to maintain a controlled clinical condition EEA EEA. On another front, RTI seems that the optimal treatment for patients with AML after remission Aged people and other poor risk features. While there are only limited data suggest synergistic or additive combination with chemotherapy IFT provides another avenue of exploration. Vorl based on the promising tolerance characterizing data t, the biological activity of t and clinical response in some patients with AML Tipifarnib required with other studies. The challenge is to defi ne the use of these new agents, if in the course of the disease, it should be administered, and.
In what combinations with other therapies in this context the new agents do not have to duplicate the mechanisms of action are combined and represent a DAPT step in the direction of the potential increase in positive AML. Another challenge is the identification of a sensitive type of leukemia Chemistry chemistry is based on a specific genetic advantages. A common set of genes that are regulated by tipifarnib found. The expression of these candidate genes as markers Nnte be k T Wirkstoffaktivit. In par, recent studies have genes which confer resistance or pr decorates Diktiv response to Tipifarnib sq.m identified possible. Although these markers are not yet validated their identifi cation Sentieren likely an important step in the F Ability of patients F stories, their reaction.
The cure rate for adult myeloid leukemia mie Acute with the economy still insufficient. Risk characteristics such as age poor AML Re confinement Lich myelodysplasia and before the treatment-related AML cytogenetic events and leukocytosis secondary Re disease in the absence of re identify extramedull cytogenetic patients who are not only less likely to remission obtained with cytotoxic chemotherapy anf llig survive But shorter disease-free. despite intensive induction and post-remission treatment In particular, the response rate and survival of adults with AML and RESTRICTION more about.Limited. Part of this poor response refers to the F Ability of Elderly patients Unf chemotherapy is not very tolerable Possible is. Equally important, however, is the genetic complexity Tt and strength of the pension Inh MLA herk cytotoxic effects of anticancer drugs Mmlichen.
AML occurring in the age group often a blood disease tt main chlich MDS, which has developed from a background of exposure to toxins. These MDS AML have a complex genetic profile, probably due to the cumulative genomic Sch L ‘. Farnesyl transferase inhibitors, small molecule inhibitors of signal transduction, cell growth and survival pathways inhibited critical. These agents are potent and selective inhibitors of intracellular Ren enzyme farnesyltransferase competition Res farnesyl transfer with a high carbon content to a cysteine in the N terminus of a polypeptide of the C-catalyzed substrate. Re numerous intracellular Re polypeptides confinement, Lich small GTP-binding polypeptides Ras, Rho and lamin B Rheb F promotion Families and the proteins that interact with microtubules centromere completion o F mitosis, are substrates for prenylation via FTase.