The development of leukemia occurs from a single progenitor cells that has the capacity to duplicate indefinitely. This may occur in lymphocytes of B or T cells. This gives rise to ALL subtypes. 80% of cases of ALL have a precursor B cell marker. 1 to 2% has a mature B cell marker. 15 to 25% of cases are T cell (Medscape Today, 2005).
The chromosomal abnormalities in ALL include the TEL-AML1 fusion gene. The bcr-abl gene translocation with a high WBC count is responsible for 3 to 5% of all childhood cases. In infants the rearrangement of the MLL gene at chromosome band 11q23 is found in 80% of all cases (Medscape Today, 2005).
In AML there is a leukemogenic event that occurs in the stem cell. This may be due to a transformation of a primitive stem cell or the transformation of different blood cells. In the stem cell theory the transformation of the oncogene determines the specific form of AML. While class I and class II mutations collaborating are the actual cause of acute leukemia.
The identification of specific chromosomal abnormalities is essential in determining the treatment plan. The common abnormalities include AML1-ETO in 12% of cases, MLL gene rearrangement and PML-RAR-alpha both in 7% of all cases (Medscape Today, 2005).
In CML there is evidence of circulation of premature blood cells which can lead to their abnormal proliferation.
70% of all cases present with the acute lymphoblastic leukemia antigen (CALLA, CD-10). Almost all are also CD 19 positive and terminal deoxynucleotidyl transferase positive (Casciato & Territo, 2008).