t(14; 14)(q11;q32) in Biphenotypic Blastic Phase of Chronic Myeloid Leukemia

A blastic crisis of chronic myeloid leukemia without a detectable chronic phase is reported. At diagnosis, blast cells present t(9;22)(q34;q11 ),t(14;14)(q11 ;q32) transloca-tions and early B cell phenotype (DR + , TdT +, B4 + , BA1 +, J5 +). At relapse, the malignant clone evolves to a biphenotypic...

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Bibliographic Details
Published in:Blood 1986-10, Vol.68 (4), p.949-953
Main Authors: Dastugue, Nicole, Kuhlein, Emilienne, Duchayne, Eliane, Roubinet, Francis, Bourrouillou, Georges, Attal, Michel, Pris, Jacques, Colombies, Pierre
Format: Article
Language:English
Subjects:
Aged
Antibodies, Monoclonal
Antigens, Neoplasm - analysis
Antigens, Surface - analysis
B-Lymphocytes - pathology
Biological and medical sciences
Blast Crisis - genetics
Cell Differentiation
Chromosome Banding
Chromosomes, Human, Pair 14
Chromosomes, Human, Pair 22
Chromosomes, Human, Pair 9
Female
Hematologic and hematopoietic diseases
Humans
Leukemia, Myeloid - genetics
Leukemia, Myeloid - pathology
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Medical sciences
Phenotype
Translocation, Genetic
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Summary:A blastic crisis of chronic myeloid leukemia without a detectable chronic phase is reported. At diagnosis, blast cells present t(9;22)(q34;q11 ),t(14;14)(q11 ;q32) transloca-tions and early B cell phenotype (DR + , TdT +, B4 + , BA1 +, J5 +). At relapse, the malignant clone evolves to a biphenotypic expression, the initial markers remain unchanged, and two myeloid antigens (My 7, My 9) appear. The wide overlap in percentages of blast cells displaying lymphoid and myeloid markers shows that a single clone bears antigens of both lineages. Simultaneous occurrence of a t(14;14)(q11 ;q32) translocation, usually found in T cell malignancies, and of a B cell phenotype raises the question of the relationship between chromosomal changes and surface marker expression. The malignant cell is assumed to be a progenitor cell, already committed to lymphoid lineage and retaining the potential to switch to myeloid lineage.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V68.4.949.949