Leukemic cell characteristics including morphological features, cytochemistry, immunologic cell surface and biochemical markers, and cytogenetic characteristics are important. In adults, FAB L1 morphology (more mature appearing lymphoblasts) is present in fewer than 50% of patients and L2 histology (more immature and pleomorphic) predominates.[1] Chromosomal abnormalities including aneuploidy and translocations have been described and may correlate with prognosis.[2] In particular, patients with Philadelphia chromosome (Ph1)-positive t(9;22) acute lymphoblastic leukemia (ALL) have a poor prognosis and represent more than 30% of adult cases. The bcr-abl fusion gene resulting from the breakpoint in the Ph1 may, on occasion, be detectable only by pulse-field gel electrophoresis or reverse-transcriptase polymerase chain reaction. Bcr-abl-rearranged leukemias that do not demonstrate the classical Ph1 carry a poor prognosis that is similar to those that are Ph1-positive.

Using heteroantisera and monoclonal antibodies, ALL cells can be divided into early B-cell lineage (80% approximate frequency), T cells (10%–15% approximate frequency), B cells (with surface immunoglobulins), (<5% approximate frequency), and CALLA+ (common ALL antigen), 50% approximate frequency.[1,3-5]

About 95% of all types of ALL except B cell, which usually has an L3 morphology by the FAB classification, have elevated terminal deoxynucleotidyl transferase (TdT) expression. This elevation is extremely useful in diagnosis; if concentrations of the enzyme are not elevated, the diagnosis of ALL is suspect. However, 20% of cases of acute myeloid leukemia (AML) may express TdT; therefore, its usefulness as a lineage marker is limited. Because B-cell leukemias are treated according to different algorithms, it is important to specifically identify these cases prospectively by their L3 morphology, absence of TdT, and expression of surface immunoglobulin. These patients will typically have one of three chromosomal translocations: t(8;14), t(2;8), or t(8;22).

References

1. Brearley RL, Johnson SA, Lister TA: Acute lymphoblastic leukaemia in adults: clinicopathological correlations with the French-American-British (FAB) co-operative group classification. Eur J Cancer 15 (6): 909-14, 1979.  [PUBMED Abstract]
   
   
2. Chromosomal abnormalities and their clinical significance in acute lymphoblastic leukemia. Third International Workshop on Chromosomes in Leukemia. Cancer Res 43 (2): 868-73, 1983.  [PUBMED Abstract]
   
   
3. Hoelzer D, Thiel E, Löffler H, et al.: Prognostic factors in a multicenter study for treatment of acute lymphoblastic leukemia in adults. Blood 71 (1): 123-31, 1988.  [PUBMED Abstract]
   
   
4. Sobol RE, Royston I, LeBien TW, et al.: Adult acute lymphoblastic leukemia phenotypes defined by monoclonal antibodies. Blood 65 (3): 730-5, 1985.  [PUBMED Abstract]
   
   
5. Foon KA, Billing RJ, Terasaki PI, et al.: Immunologic classification of acute lymphoblastic leukemia. Implications for normal lymphoid differentiation. Blood 56 (6): 1120-6, 1980.  [PUBMED Abstract]
   
   

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