We believe that interferon Cuscutin alpha may also prevent cytokine signaling by bone marrow stromal cells that support proliferation and survival of malignant cells in the MPN. Recently Manshouri et al. showed that humoral factors to protect from bone marrow stromal cells with malignant secreted JAK2V617F therapeutic effect of JAK2 inhibitors. Thus, the combination of interferon alpha JAK2 inhibitors and a more effective therapeutic treatment for the treatment of patients with MPN only be JAK2 inhibitors. Other immunomodulatory drugs are also tested in patients NPP, especially in patients with myelofibrosis.
Thalidomide and lenalidomide with or without prednisone showed how the increased effectiveness Hte production of cytokines in these patients inhibit by the Gr Inhibit S spleen, myelofibrosis and angiogenesis. Pomalidomide, another analog, is currently with or without prednisone in large Agomelatine en evaluated clinical trials in patients with myelofibrosis treatment. These immunomodulatory drugs are candidates with JAK2 inhibitors as therapeutic targeting patients are assigned to MPN. Herk Mmliche therapies such as hydroxyurea are also effective in the treatment of patients with MPN, not only for treatment but also cytoreduction as a treatment to reduce the burden JAK2V617F. Recently Bessi et al. showed that hydroxyurea, the mutant JAK2 more than 50% in untreated patients with PV and ET to reduce.
This effect has a synergy with the therapeutic effect of JAK2 inhibitors. Hydroxycarbamide a drug candidate for combination with inhibitors of JAK2 JAK2 inhibitors are effective to alleviate the symptoms of my clinical patients with BCR-ABL negative MPN. Combination with other therapies, to show the synergies and other biological properties, the JAK2 inhibitors promises to be the most effective treatment for these diseases. Third Lockable Remarks JAK2 tyrosine kinase is a gene which plays an r Important role in the development of hematopoietic h ESE normal in the signal path with cytokines STAT3 and STAT5 proteins. Hyperactivation of JAK2 in MPN done by different genetic mechanisms. JAK2 inhibitors have been developed to further suppress cytokine cascade is initiated by the activation of JAK2, independently Ngig mechanism of the underlying genetic.
In Phase II / III clinical trials of JAK2 inhibitors are effective embroidered l the symptoms Clinics and improving my Lebensqualit t. Recently it was shown that even in the core of JAK2 are cells, where it plays an r In the transcriptional regulation of genes regulated by JAK2 inhibitors HP1a.Whether can r The suppression of the r JAK2 nuclear or not, it is still unknown, but it him opens new perspectives for the combined use of epigenetic therapy with JAK2 inhibitors for the treatment of NPP. Has recently also been shown that JAK2 inhibitors are not able to aim h Hematopoietic Preferences Shore cells uncommitted Ethical responsibility for the initiation of myeloproliferative disease.