Emodin is a bioactive compound isolated from the root and rhizomes of Rheum plamatum L. (polygenaceae), which is known as a traditional Chinese and Japanese medicine. In the present study, the effect of emodin on YD-15 mucoepidermoid carcinoma cells and its molecular mechanism were investigated. This study shows that emodin significantly inhibits the growth of YD-15 cells. Activation of caspase-3 and PARP is triggered by emodin and it increases sub-G1 population and the number of YD-15 cells with nuclear condensation and fragmentation. In addition, we found that emodin significantly decreases myeloid cell leukemia 1(MCL-1). These results suggest that MCl-1 is an important molecule for emodin-induced apoptosis. Taken together, emodin inhibits cell viability and induces apoptosis via down-regulation of MCL-1 and it can be a new potent anticancer drug candidate for the treatment of mucoepidermoid carcinoma

Chronic myeloid leukemia (CML) was a well-known myeloproliferative neoplasm and a disease of haemopoietic stem cells due to BCR-ABL fusion protein arising from a translocation t(9;22), known as the Philadelphia chromosome. Imatinib (Gleevec), a selective small molecule inhibitor of Bcr-Abl kinase, has been confirmed as the standard drug therapy for CML. Discovery of imatinib led to the availability of a molecular-targeted therapy as a new model of cancer treatment and challenged the molecular target cancer treatment trend from non-targeted cytotoxic chemotherapy. We reviewed the advancement of chronic myeloid leukemia treatment in the area of imatinib.

JAK2 V617F mutation is a common event in chronic myeloproliferative disorders. However, de novo acute myeloid leukemia with JAK2 V617F is rarely encountered. The authors report the case of a 74-year-old male with de novo acute myeloblastic leukemia without maturation (AML M1) and a JAk2 V617F heterozygotic mutation. Despite treatment with standard AML regimens, the patient died 2 months after a diagnosis of acute leukemia. This case of an AML patient with a JAK2 V617F mutation with a poor prognosis suggests that despite its rarity, a JAK2 V617F mutational study be considered for prognostic purposes in AML.