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Blood, 1974, Vol. 43, No. 1, pp. 15-22.
© 1974 American Society of Hematology, Inc.
Evidence for the Clonal Origin of Chronic Myeloid
Leukemia From a Sex Chromosome Mosaic:
Clinical, Cytogenetic, and Marrow Culture Studies
M. A.S. Moore 1,
H. Ekert 1,
M. G. Fitzgerald 1, and
A. Carmichael 1
1 Cancer Research Unit, Walter and Eliza Hall Institute, Royal Melbourne Hospital,
Victoria, Australia, and the Department of Haematology, Royal Children’s Hospital, Parkville,
Victoria, Australia.
Cytogenetic studies on a 7 -yr-old child presenting with clinical and hematological features of chronic myeloid leukemia (CML) revealed a constitutional 46 XY/47 XYY
mosaicism in skin, blood, and marrow. A
third 46 XY, Ph1 cell line predominated in
the marrow on initial presentation and in
subsequent acute transformation. Assessment
of granulocytic colony-forming capacity in
agar culture revealed that colony-forming cells
(CFCs) were greatly increased in the circulation
and possessed the abnormal light buoyant
density and low susceptibility to tritiated thymidine killing which distinguishes leukemic
CFCs from normal. During acute transformation colony-forming capacity was lost but small,
poorly differentiated cell clusters persisted in
culture. Only 46 XY, Ph1 metaphase were obtained following cytogenetic analysis of in vitro
colonies and clusters displaying leukemic
growth characteristics in agar culture. The coexistence of CML and sex chromosome mosaicism in this patient provides further support for
the uniclonal origin of CML and indicates that
cytogenetic instability implicated in mosaicism
may carry an increased risk of further cytogenetic evolution with emergence of the Ph1
chromosome.
Submitted on April 2, 1973
Revised on June 23, 1973
Accepted on June 29, 1973
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