Biphenotype acute leukemia

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 recommended. 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.

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:

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

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