Other h Dermatological malignancies are at the foot of the LMC trudge followed. BCR / ABL negative myeloproliferative neoplasia, especially Polyzyth Mie classic vera, essential Thrombozyth Chemistry and prim Re myelofibrosis, at present, the attention of many scientists in the fields H Dermatology, oncology, pathology, genetics and pharmacology, after identification of the Janus BMS-536924 BMS536924 kinase 2 mutation in a significant number of patients with these conditions in 2005.1 In this article, we aim to investigate the r JAK2 abnormalities in the pathogenesis, diagnosis, classification, severity and management of h dermatological malignancies. Classification of tumors myelo Abnormalit th That the JAK2 are Haupt Chlich identified in myeloproliferative neoplasms Of, we summarize the current classification system for these diseases. Leuk mie acute, chronic leukemia and myelodysplastic syndrome mie: They generally fall into three main groups. Chronic leukemia premiums In BCR / ABL , is the independent positive BCR / ABL CML c-Met Inhibitors Ngig be characterized by clinicopathological features, if they are present as acute leukemia Mie’s, W During BCR / ABL NPP is negative in herk Divided mmliche, non-conventional MPN with or without dysplasia and myelodysplastic syndrome. Diagnosis and classification of these changes St On figures from the peripheral blood, the percentage myelosis explosion type, the presence of dysplasia especially the extent biochemical fibrosis, based clinical features, and in particular genetics.2 4 JAK2 abnormalities are not only with myeloid neoplasms the most Classics are connected, but they are also associated with other tumors myelo seen the, au he BCR / ABL-positive CML and acute leukemia mie lympho than where it is rarely reported, as we sp’ll see th. One of the interesting things about the clinical characteristics of tumors myelo Has a tendency to transform into acute leukemia Mie, Sun MPN classic, heart tee their behavior before Leuk Chemistry, progress and regression for each 5 other.3 why carry an abnormal gene to various diseases Why classical progress and regression MPN What are the r JAK2 Abnormalit th In the pathogenesis of h Dermatological malignancy Th JAK Janus kinase family is a family of non-receptor tyrosine kinase is intracellular Ren that transduce signals mediated by cytokines. Currently, it consists of four members: JAK1, JAK2, JAK3 and TYK2.6 Janus kinases Janus was named after Janus or the r mix mythology was the god of gates, beginning length and purpose. It is as two-faced or K Designed heads before directions.7 Indeed, Janus kinases are just below the cell receptors for embroidered l downstream signaling and seven areas, including two Hnlicher structure. One of them is ne one Aktivierungsdom, W While the other seems to exert an inhibitory effect. After binding of a ligand to its specific receptor of the JAK protein is activated, and it is then downstream. Rts phosphorylate STAT signaling molecules such as, which is actively transported into the cell nucleus, where it activates transcription factors Abnormalities have been reported in JAK1 in ALL T-cell type Haupt Chlich where it is used in almost 20% of the F Found lle, 8 JAK2 in myeloproliferative neoplasms Rearranged and rarely in the ALL has reported 6 JAK3 in more mylopo 50% of the transition period abnormal ESR