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Clonal analysis of myelodysplastic syndromes: evidence of multipotent stem
cell origin
JW Janssen, M Buschle, M Layton, HG Drexler, J Lyons, H van den Berghe, H Heimpel, B Kubanek, E Kleihauer and GJ Mufti
Department of Pediatrics II, University of Ulm, FRG.
Restriction fragment length polymorphisms (RFLPs) of the X-chromosome genes
hypoxanthine phosphoribosyl transferase (HPRT) and phosphoglycerate kinase
(PGK) were studied in 34 female patients with primary myelodysplastic
syndromes (MDS). Twelve patients (35%) were heterozygous at the HPRT or PGK
loci for BamHI or BglI RFLPs, respectively. In eight patients showing PGK
polymorphisms, clonality was determined by X-chromosome inactivation
analysis. These included patients from different morphologic subtypes: four
with refractory anemia (RA), two with RA and ring sideroblasts (RARS), one
patient with RA with excess of blasts (RAEB), and one with chronic
myelomonocytic leukemia (CMML). A monoclonal pattern of X-chromosome
inactivation was observed in seven cases. In a further case characterized
by bone marrow hypoplasia, peripheral blood (PB) leukocytes were polyclonal
in origin. Following low-dose cytarabine therapy, reversion to polyclonal
hematopoiesis was observed in a case of RAEB indicating the presence of
residual normal hematopoietic stem cells with the capacity for marrow
reconstitution. The clonal relation of lymphoid and granulocyte/monocyte
lineages was studied directly in two cases of CMML exhibiting somatic
mutations of N-ras or Ki-ras oncogenes. By selective oligonucleotide
hybridization to ras gene sequences amplified in vitro by the polymerase
chain reaction, a mutated ras allele was demonstrated in PB granulocytes,
monocytes, and B and T lymphocytes of both patients. We conclude that MDS
arise from a multipotent hematopoietic stem cell with the potential for
myeloid and lymphoid differentiation.
Volume 73,
Issue 1,
pp. 248-254,
01/01/1989
Copyright © 1989 by The American Society of Hematology
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