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Clonal studies of CD3- lymphoproliferative disease of granular lymphocytes
R Nash, P McSweeney, R Zambello, G Semenzato and TP Loughran
Fred Hutchinson Cancer Research Center, Seattle, WA.
The lymphoproliferative disease of granular lymphocytes (LDGL) results from
chronic proliferation of either CD3- or CD3+ large granular lymphocytes
(LGLs). Most CD3+ LGLs have been well characterized as clonal LGL
proliferations (LGL leukemia). In contrast, the clonal nature and clinical
features of patients with CD3- LDGL have not been defined. In this study,
we analyzed seven female patients with CD3- LDGL who were heterozygous at
certain X-linked gene loci. Neutrophils and CD3- granular lymphocytes were
isolated from peripheral blood. Clonal analysis was performed on genomic
DNA from these cell fractions on six patients by conventional Southern
techniques using probes to the X-linked genes, PGK and DXS255 (M27 beta).
In four patients, three of whom were already studied by Southern analyses
of genomic DNA and one in whom there were insufficient amounts of DNA,
polymerase chain reaction (PCR)-based clonal analysis was performed with
primer pairs flanking the BstXI polymorphism on the PGK gene. In six
patients, a polyclonal expansion of CD3- granular lymphocytes was
demonstrated and in one the result was indeterminate. In contrast to
patients with CD3+ LDGL (LGL leukemia), a clonal disease could not be
demonstrated with X- linked markers in patients with CD3- LDGL, suggesting
a reactive rather than a neoplastic origin of the lymphocytes in these
cases.
Volume 81,
Issue 9,
pp. 2363-2368,
05/01/1993
Copyright © 1993 by The American Society of Hematology

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