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Biphenotype acute leukemia is an uncommon type of leukemia which arises in multipotent progenitor cells which have the ability differentiating into both myeloid and lymphoid lineages. The direct reason lead BAL is still not clear. BAL can be de novo or secondary to previous cytotoxic therapy. Many factors, such as virus, hereditary factors, radiation, might have relationship with BAL. BAL is hard to treat, usually the chemotherapy is chosen according to the morphology of the blast (ALL or AML). The stem cell transplantation is highly recommened. About 5% of acute leukaemia cases are BAL. BAL could occur in all the age of the people, but more in adults than in children. == Mechanisms == The mechanism of BAL is related to several mutations. The most common abnormalities are t(9;22) and MLL gene rearrangement at 11q23. T(9;22) affect the ABL gene at 9q34 and BCR at 22q11. The hybrid gene product ABL/BCR is an oncogene which could lead several types of leukemia including BAL. ABL/BCR could active several molecular pathways: # RAS signaling could be activated by BCR/ABL by GRB2 adaptor which interact with Y177 of BCR. # Through AKT/PKB, PI3-K pathway could also be activated. # STAT5, 1, and 6 has been reported that is a major molecular signaling event activated by BCR/ABL. # Some focal adhesion complex (PAXILLIN, FAK0 could be activated by BCR/ABL with adaptor molecule CRK-L. # BCR/ABL could inactivate negative regulatory molecules PTP1B and Abi-1. Their inactivation is related with progression into blast crisis. # BCR/ABL pathway could also active PI64K/Akt/STAT5 pathway which has anti-apoptotic activity. # BCR/ABL induce cell adhesive and migratory abnormalities because the mutation will lead an abnormal response to chemokine SDF-1〔(【引用サイトリンク】first=Jean-Loup )〕 Philadelphia Chromosom Figure 1. T(9,22) translocation MLL gene encode Histone-lysine N-methyltransferase (HRX), which is a histone methyltransferase. It is a positive regulator for gene transcription. It has been shown that associates with Host cell facor C1, CREB binding protein, WDR5, CTBP, MEN1, etc. The rearrangement of MLL are related with different kinds of aggressive acute leukemias. Most of biphenotypic leukemia in children is due to the rearrangement of MLL Besides them, other gene abnormalities has been reported. Such as t(8;21), t(15;17),del(6q), del(12p), t(x;12) and t(14;19). In BAL patients, it is prone to bruising, spotting, which is due to megakaryocytes that could produce platelets decrease, resulting in a lack of platelets. Anemia: reduction metrocytes that could produce red blood cells, resulting in a lack of red blood cells. Patients are prone to asthma and dizziness in walking or exercise. Persistent fever, infection prolonged healing: Most of the white blood cells are leukemia cells, no normal function, leading to decreased immunity, susceptible to infection. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Biphenotype acute leukemia」の詳細全文を読む スポンサード リンク
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