B-cell acute lymphocytic leukemia

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An aggressive type of leukemia  in which too many B-cell lymphoblasts (immature white blood cells) are found in the bone marrow and blood. It is the most common type of acute lymphoblastic leukemia (ALL). Also called B-cell acute lymphocytic leukemia and precursor B-lymphoblastic leukemia.

B-ALL with BCR/ABL1 ,MLL-associated, and other recurrent chromosomal abnormalities. Several cases showed rare aberrancies such as coexistent IGH/BCL2 and MYC rearrangements and raised issues in classification.

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Immunophenotype:

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B-ALL is subdivided into:

Pro B-ALL: TdT+, CD19+, CD10-

common ALL: CD19+,  CD10+/CALLA+

pre B ALL: CD10+/-, CD19+,  HLA Dr+, cytoplasmic IgM+  

mature B ALL: CD10+, CD19+, CD20+, CD22+, surface IgM+   

 

B-ALL positive for HLA-DR+, TdT+, CD19+  CD79a+  CD22+, BCR-ABL positive B-ALL is usually CD13 or CD33 positive.

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Example :

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Above is a case of B-ALL, which shows (Blast-green and lymphocytes-red) positivity of CD19, CD34, CD10, cCD79a, CD58, CD38, CD81 and negative for MPO, cCD3, CD3, CD7, CD13, CD33, CD44, CD117

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Reference:

• Borowitz MJ, Chan JKC. B lymphoblastic leukaemia/lymphoma, not otherwise specified. In: SwerdlowSH, Campo E, Harris NL, et al, eds.World Health

• Organization Classification of Tumours of Haematopoieticand Lymphoid Tissues.4th ed. Lyon, France: IARC Press;2008:168-170.

• Preti HA, O’Brien S, Giralt S, et al. Philadelphia-chromosome–positive adult acute lymphocytic leukemia:characteristics, treatment results, and prognosis in41patients.Am J Med.1994;97:60-65.

• Faderl S, Kantarjian HM, Talpaz M, et al. Clinicalsignificance of cytogenetic abnormalities in adult acutelymphoblastic leukemia.Blood.1998;91:3995-4019.

• Moorman AV, Harrison CJ, Buck GA, et al. Karyotype is anindependent prognostic factor in adult acute lymphoblasticleukemia (ALL): analysis of cytogenetic data frompatients treated on the Medical Research Council (MRC)UKALLXII/Eastern Cooperative Oncology Group (ECOG)2993 trial.Blood.2007;109:3189-3197.

• Ottmann OG, Wassmann B, Hoelzer D. Imatinib for relapsedBCR/ABL positive leukemias.Ann Hematol.2002;81(suppl2):S36-S37.

• Wassmann B, Pfeifer H, Scheuring U, et al. Therapy withimatinib mesylate (Glivec) preceding allogeneic stem celltransplantation (SCT) in relapsed or refractory Philadelphia-positive acute lymphoblastic leukemia (Ph+ALL).Leukemia.2002;16:2358-2365.

• Schultz KR, Bowman WP, Aledo A, et al. Improvedearly event-free survival with imatinib in Philadelphiachromosome–positive acute lymphoblastic leukemia:
  a Children’s Oncology Group study.J Clin Oncol.2009;27:5175-5181.

• Ravandi F, O’Brien S, Thomas D, et al. First report of phase2 study of dasatinib with hyper-CVAD for the frontlinetreatment of patients with Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia.Blood.2010;116:2070-2077.

• Pfeifer H, Wassmann B, Pavlova A, et al. Kinase domainmutations of BCR-ABL frequently precede imatinib-basedtherapy and give rise to relapse in patients with de novoPhiladelphia-positive acute lymphoblastic leukemia (Ph+ALL).Blood.2007;110:727-734.

• Iacobucci I, Ferrari A, Lonetti A, et al. CDKN2A/Balterations impair prognosis in adult BCR-ABL1–positiveacute lymphoblastic leukemia patients.Clin Cancer Res.2011;17:7413-7423.

• Hu Y, Liu Y, Pelletier S, et al. Requirement of Src kinasesLyn, Hck and Fgr for BCR-ABL1–induced B-lymphoblasticleukemia but not chronic myeloid leukemia.Nat Genet.2004;36:453-461