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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dastugue, N. Articles by Colombies, P. Search for Related Content PubMed PubMed Citation Articles by Dastugue, N. Articles by Colombies, P. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  t(14;14)(q11;q32) in biphenotypic blastic phase of chronic myeloid leukemia N Dastugue, E Kuhlein, E Duchayne, F Roubinet, G Bourrouillou, M Attal, J Pris and P Colombies 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. Volume 68, Issue 4, pp. 949-953, 10/01/1986 Copyright © 1986 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

	Copyright © 1986 by American Society of Hematology         Online ISSN: 1528-0020