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Blood, Vol. 92 No. 3 (August 1), 1998:
pp. 952-958
Clonal Diversity of Ig and T-Cell-Receptor Gene Rearrangements
Identifies a Subset of Childhood B-Precursor Acute Lymphoblastic
Leukemia With Increased Risk of Relapse
Elaine Green,
Carmel M. McConville,
Judith E. Powell,
Jillian R. Mann,
Philip J. Darbyshire,
A. Malcolm R. Taylor, and
Tatjana Stankovic
From the Department of Haematology/Oncology, Birmingham Children's
Hospital NHS Trust, Ladywood Middleway, Birmingham; and the Division of
Medical Genetics, Department of Public Health and Epidemiology, and CRC
Institute for Cancer Studies, University of Birmingham, UK.
Current prognostic indicators such as age, sex, and white blood cell
count (WBC) fail to identify all children with more aggressive forms of
B-precursor acute lymphoblastic leukemia (ALL), and a proportion of
patients without poor prognostic indicators still relapse. Results
obtained from an analysis of 65 pediatic B-precursor ALL patients
indicated that subclone formation leading to clonal diversity, as
detected by Ig and T-cell receptor (TCR) gene rearrangements, may
represent a very useful prognostic indicator, independent of age, sex,
and WBC. Disease-free survival was significantly shorter in those
patients showing clonal diversity at presentation. Furthermore, clonal
diversity was detected not only in the majority of high-risk patients
who relapsed but was also associated with a high probability of relapse
in standard-risk patients. Sixty-five percent (13/20) of standard-risk
patients who also showed clonal diversity subsequently relapsed,
whereas the percentage of relapses among standard-risk patients without
clonal diversity was much lower at 19% (7/36). Continued clonal
evolution during disease progression is an important feature of
aggressive B-precursor ALL. All 5 patients with clonal diversity who
were followed up in our study showed a change in the pattern of
clonality between presentation and relapse. This implies an important
role for clonal diversity as a mechanism of disease progression through
the process of clonal variation and clonal selection.
© 1998 by The American Society of Hematology.
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