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Blood, 1 September 2002, Vol. 100, No. 5, pp. 1787-1794
NEOPLASIA
A high-resolution allelotype of B-cell chronic lymphocytic
leukemia (B-CLL)
Urban Novak,
Elisabeth Oppliger Leibundgut,
Jörg Hager,
Dominique Mühlematter,
Martine Jotterand,
Celine Besse,
Nicolas Leupin,
Daniel Ratschiller,
Jeanette Papp,
Gina Kearsey,
Stefan Aebi,
Hans Graber,
Rolf Jaggi,
Jean-Marc Lüthi,
Sandrine Meyer-Monard,
Mark Lathrop,
Andreas Tobler, and
Martin F. Fey
From the Department of Clinical Research and Medical
Oncology/Hematology, Inselspital (University Hospital), Bern,
Switzerland; the Centre National de Génotypage, Evry, France; the
Division of Medical Genetics, University Hospital, Lausanne,
Switzerland; the Department of Human Genetics, University of
California, Los Angeles; the Department of Medicine, Regionalspital,
Thun, Switzerland; and the Department of Hematology/Central
Laboratories, University Hospital, Basel, Switzerland.
The most frequent chromosomal aberrations in B-cell chronic
lymphocytic leukemia (B-CLL) are deletions on 13q, 11q, and 17p, and
trisomy 12, all of which are of prognostic significance. Conventional cytogenetic analysis and fluorescence in situ hybridization (FISH) are
used for their detection, but cytogenetic analysis is hampered by the
low mitotic index of B-CLL cells, and FISH depends on accurate information about candidate regions. We used a set of 400 highly informative microsatellite markers covering all chromosomal arms (allelotyping) and automated polymerase chain reaction (PCR)
protocols to screen 46 patients with typical B-CLL for
chromosomal aberrations. For validation, we compared data with our
conventional karyotype results and fine mapping with
conventional single-site PCR. All clonal cytogenetic abnormalities
potentially detectable by our microsatellite PCR (eg, del13q14 and
trisomy 12) were picked up. Allelotyping revealed additional complex
aberrations in patients with both normal and abnormal B-CLL karyotypes.
Aberrations detectable in the samples with our microsatellite panel
were found on almost all chromosomal arms. We detected new aberrant
loci in typical B-CLL, such as allelic losses on 1q, 9q, and 22q in up
to 25% of our patients, and allelic imbalances mirroring chromosomal duplications, amplifications, or aneuploidies on 2q, 10p, and 22q in up
to 27% of our patients. We conclude that allelotyping with our battery
of informative microsatellites is suitable for molecular screening of
B-CLL. The technique is well suited for analyses in clinical trials, it
provides a comprehensive view of genetic alterations, and it may
identify new loci with candidate genes relevant in the molecular
biology of B-CLL.
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