1. t(14;14)(q11;q32) in biphenotypic blastic phase of chronic myeloid leukemia
- Author
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Emilienne Kuhlein, Francis Roubinet, Pierre Colombies, Michel Attal, Jacques Pris, Nicole Dastugue, Georges Bourrouillou, and Eliane Duchayne
- Subjects
Myeloid ,T cell ,Chromosomes, Human, Pair 22 ,Immunology ,Clone (cell biology) ,Biology ,Blastic Phase ,Biochemistry ,Translocation, Genetic ,Antigens, Neoplasm ,Precursor cell ,hemic and lymphatic diseases ,medicine ,Humans ,Progenitor cell ,B cell ,Aged ,Chromosomes, Human, Pair 14 ,B-Lymphocytes ,Myeloid leukemia ,Antibodies, Monoclonal ,Cell Differentiation ,Cell Biology ,Hematology ,Chromosome Banding ,medicine.anatomical_structure ,Phenotype ,Leukemia, Myeloid ,Antigens, Surface ,Cancer research ,Female ,Blast Crisis ,Chromosomes, Human, Pair 9 - Abstract
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) translocations 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.
- Published
- 1986
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