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Simultaneous demonstration of the Philadelphia chromosome in T, B, and myeloid cells
Author(s) -
Mackinney Archie A.,
Clark Steven S.,
Borcherding Wayne,
Fizzotti Marco,
Hong Richard
Publication year - 1993
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830440110
Subject(s) - chromosomal translocation , biology , breakpoint cluster region , lymphoma , bone marrow , microbiology and biotechnology , leukemia , myeloid leukemia , cd34 , interleukin 21 , immunology , stem cell , gene rearrangement , myeloid , cancer research , t cell , immune system , gene , genetics
A patient presented with lymphoblastic lymphoma in lymph‐nodes and chronic myeloge‐nous leukemia (CML) in marrow and peripheral blood. All marrow and unstimulated peripheral blood cells contained the Philadelphia chromosome{t(9:22)}. Lymphoma cells were analyzed by flow cytometry and were identified as T cells (CD2+CD5+CD7+CD34+). All fresh lymphoma cells contained the t(9:22) translocation. Cultures of purified peripheral blood T and B cells and specifically stimulated NK cells revealed that 59% of the B cells, 10% of the NK cells, and none of the normal T cells contained the translocation. The lack of translocation in normal peripheral T cells is attributed to their long lifespan. No rearrangement of immunoglobulin or T cell receptor beta or gamma genes was found in either the leukemia or lymphoma cells. Analysis of the DNA from cryopreserved lymphoma biopsy showed clonal rearrangement within the common breakpoint cluster region of the bcr gene identical to the bcr rearrangement in DNA from leukemia blood cells. The data support the concept that T and B cells originate in the patient's totipotent stem cell from which the CML is also derived. © 1993 Wiley‐Liss, Inc.