It is the most common type of cancer in children, and treatment results in a good chance for a cure. The disease is characterized by the accumulation of lymphoblasts in the marrow or in various extramedullary sites, frequently accompanied by suppression of normal hematopoiesis.
B- and T-cell lymphoblastic leukemia cells express surface antigens that parallel their respective lineage developments.
Diagnostic confusion with AML, hairy cell leukemia, and malignant lymphoma is not uncommon.
Treatment is divided into the following three phases: The average length of treatment for ALL varies between 1.5 and 3 years in the effort to eradicate the leukemic cell population.
Younger adults with ALL may be eligible for selected clinical trials for childhood ALL.
Many patients who have molecular evidence of the fusion gene because many patients have a different fusion protein from the one found in CML (p190 vs. Using heteroantisera and monoclonal antibodies, ALL cells can be divided into several subtypes (see Table 1).[1,4-6] About 95% of all types of ALL (except Burkitt, which usually has an L3 morphology by the FAB classification) have elevated terminal deoxynucleotidyl transferase (Td T) expression.
This elevation is extremely useful in diagnosis; if concentrations of the enzyme are not elevated, the diagnosis of ALL is suspect.
Immunophenotypic analysis is essential because leukemias that do not express myeloperoxidase include M0 AML, M7 AML, and ALL.