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Immunophenotypic Classification of Acute Lymphoblastic Leukemia

Learn about the immunophenotypic classification of ALL, including precursor B-cell ALL, mature B-cell ALL, and pre-B ALL, with detailed marker expressions and disease characteristics.

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Immunophenotypic Classification of Acute Lymphoblastic Leukemia

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    6. Flow cytometry of normal myeloid lineage differentiation

    7. Acute B-cell leukemias

    8. Common chromosomal abnormalities

    9. Genetic profiling in Diffuse large B-cell lymphoma (DLBCL)

    12. 2007 ?"? ??? ?????, ????? ????? ????? ????-?????????, ???? ?????? Primary antibody panel

    13. 2007 ?"? ??? ?????, ????? ????? ????? ????-?????????, ???? ?????? M1 Myeloid Leukemia

    14. 2007 ?"? ??? ?????, ????? ????? ????? ????-?????????, ???? ?????? Mutations & Gene-Expression Changes in AML with Normal Cytogenetics ITD of FLT-3 gene – poor prognosis Mutations in NPM1 gene – favorable prognosis PTD of MLL gene – poor prognosis High expression of BAALC gene - poor prognosis Mutations in CEBPA gene – favorable prognosis

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    18. 2007 ?"? ??? ?????, ????? ????? ????? ????-?????????, ???? ?????? ALL is classified immunophenotypically by expression of specific markers. Precursor B-cell ALL is the most frequent form in both children and adults. The immunophenotypic classification of ALL is based on the expression of key antigenic markers on lymphoblasts. These markers indicate which precursor cell stage is affected by the disease. This approach classifies lymphoblasts into three main groups: precursor B-cell ALL, mature B-cell ALL, and pre-B ALL.1,2 The precursor B-cell types express CD19, cytoplasmic CD22, and terminal deoxynucleotidyl transferase (TdT) . They are further subdivided by the presence or absence of other markers, such as CD10 and cytoplasmic immunoglobulin (cIg). Pro-B ALL is CD10–, cIg–; common ALL is CD10+, cIg–; and pre-B ALL is cIg+. Common ALL is the most frequent immunophenotype; combined with pro-B ALL, it comprises 65%-70% of childhood cases and 50%-60% of adult.1,2 Mature B-cell ALL is distinguished by the expression of surface Ig (sIg+), usually IgM, and the absence of TdT. It accounts for fewer than 5% of ALL cases.1,2 T-cell ALL is distinguished by the expression of cytoplasmic CD3 and CD7; more mature forms also express surface CD3, CD2, and either CD4 or CD8. T-cell ALL accounts for 10%-15% of cases in children and 20%-25% in adults.1,2 1. Cortes JE, Kantarjian HM. Acute lymphoblastic leukemia. A comprehensive review with emphasis on biology and therapy. Cancer. 1995;76:2393-2417. 2. Faderl S, Jeha S, Kantarjian HM. The biology and therapy of acute lymphoblastic leukemia. Cancer. 2003;98:1337-1354.ALL is classified immunophenotypically by expression of specific markers. Precursor B-cell ALL is the most frequent form in both children and adults. The immunophenotypic classification of ALL is based on the expression of key antigenic markers on lymphoblasts. These markers indicate which precursor cell stage is affected by the disease. This approach classifies lymphoblasts into three main groups: precursor B-cell ALL, mature B-cell ALL, and pre-B ALL.1,2 The precursor B-cell types express CD19, cytoplasmic CD22, and terminal deoxynucleotidyl transferase (TdT) . They are further subdivided by the presence or absence of other markers, such as CD10 and cytoplasmic immunoglobulin (cIg). Pro-B ALL is CD10–, cIg–; common ALL is CD10+, cIg–; and pre-B ALL is cIg+. Common ALL is the most frequent immunophenotype; combined with pro-B ALL, it comprises 65%-70% of childhood cases and 50%-60% of adult.1,2 Mature B-cell ALL is distinguished by the expression of surface Ig (sIg+), usually IgM, and the absence of TdT. It accounts for fewer than 5% of ALL cases.1,2 T-cell ALL is distinguished by the expression of cytoplasmic CD3 and CD7; more mature forms also express surface CD3, CD2, and either CD4 or CD8. T-cell ALL accounts for 10%-15% of cases in children and 20%-25% in adults.1,2 1. Cortes JE, Kantarjian HM. Acute lymphoblastic leukemia. A comprehensive review with emphasis on biology and therapy. Cancer. 1995;76:2393-2417. 2. Faderl S, Jeha S, Kantarjian HM. The biology and therapy of acute lymphoblastic leukemia. Cancer. 2003;98:1337-1354.

    19. 2007 ?"? ??? ?????, ????? ????? ????? ????-?????????, ???? ??????

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    29. RBC Size as a Classification of Anemia

    30. Changes in iron stores and distribution

    31. Lab tests of iron deficiency of increased severity

    32. Differentiation of anemia of chronic disease and iron deficiency anemia by laboratory measures

    33. Homocysteine & MMA Tests Can Distinguish Between Cbl & FA Deficiency

    36. Immunohistochemistry TdT = Terminal Deoxy Transferase B cell: CD34, CD19, CD10, CD79A, CD20, cytoplasmic-IgM T cell : CD34, CD2, CD5, CD7, cCD3, CD1a, CD4, CD8

    37. Translocations: t(12:21) t(9:22)Philadelphia chromosome t(4:11) Hyperdiploidy (>50 chromosomes)

    38. Peripheral (mature) B cell lymphomas Small lymphocytic lymphoma / * / chronic lymphocytic leukemia (CLL) Follicular lymphoma * Diffuse large cell lymphoma * Burkitt’s lymphoma * Plasma cell neoplasms Lymphoplasmacytic lymphoma (Waldenstrom) Mantle cell lymphoma * Marginal zone lymphoma * Hairy cell leukemia

    39. Small lymphocytic lymphoma / chronic lymphocytic leukemia SLL/CLL Indolent (Low grade) immunophenotype CD20+, CD5+, CD23+, IgM+, IgD+

    40. Mantle cell lymphoma Small mature lymphocytes Immunophenotype CD20+, CD5+, CD23-, IgM+, IgD+,

    41. Follicular lymphoma Indolent (Low grade) Germinal center B mature lymphocytes CD20+, BCL6+, CD10+

    42. Mature germinal center B cell: CD20, BCL6, CD10 Translocation oncogene c-myc (chrom 8) Heavy chains: t(8:14) Light chains: t(2:8), t(8:22) c-myc gene and protein: proliferation

    43. Diffuse large B cell lymphoma Aggressive (High grade) Cell origin ? B cell: CD20+ BCL6 and CD10 heterogeneous

    44. International Prognostic Index (IPI) Patients of all ages Risk Factors Age >60 years Stage (Ann Arbor) III-IV Extranodal involvement >1 site PS 2-4 LDH level Elevated To identify prognostic factors for survival, an international study involving >2000 patients with aggressive NHL was conducted between the years 1982 and 1987.56 Objective characteristics independently associated with survival included age, PS, serum LDH level, number of extranodal disease sites, and disease stage (Ann Arbor). For younger patients (?60 years), clinical features predictive of survival were PS, LDH, and stage.To identify prognostic factors for survival, an international study involving >2000 patients with aggressive NHL was conducted between the years 1982 and 1987.56 Objective characteristics independently associated with survival included age, PS, serum LDH level, number of extranodal disease sites, and disease stage (Ann Arbor). For younger patients (?60 years), clinical features predictive of survival were PS, LDH, and stage.

    45. Age <60 vs ?60 Haemoglobin ³12g/dL vs <12g/dL Serum LDH level £ULN vs >ULN Ann Arbor stage I–II vs III–IV Number of nodal sites involved £4 vs >4 The Follicular Lymphoma International Prognostic Index (FLIPI)

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