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LAZ3 rearrangements in non-Hodgkin's lymphoma: correlation with histology,
immunophenotype, karyotype, and clinical outcome in 217 patients
C Bastard, C Deweindt, JP Kerckaert, B Lenormand, A Rossi, F Pezzella, C Fruchart, C Duval, M Monconduit and H Tilly
Department of Cytogenetics, Centre Regional de Transfusion Sanguine et de
Genetique Humaine, Bois Guillaume, France.
We have recently shown that an evolutionary conserved gene LAZ3, encoding a
zinc finger protein, is disrupted and overexpressed in some B-cell
lymphomas (mainly with a large cell component) that show chromosomal
rearrangements involving 3q27. Because the breakpoints involved in these
rearrangements are focused in a narrow major translocation cluster (MTC) on
chromosome 3, we used genomic probes from this region to study the
molecular rearrangements of LAZ3 in a large series of patients (217) with
non-Hodgkin's lymphoma (NHL). Southern blot analysis showed LAZ3
rearrangement in 43 patients (19.8%). Rearrangement was found in 11 of the
84 patients (13%) with follicular lymphoma but was most frequent in
aggressive lymphoma (diffuse mixed, diffuse large cell, and large cell
immunoblastic subtypes), in which 31 of the 114 patients (27%) were
affected. The highest proportion of LAZ3 alteration was observed in B-cell
aggressive lymphoma (26 of 71 cases, 37%). Eleven of the 32 patients with
3q27 chromosomal abnormality had no LAZ3 rearrangement, suggesting the
possibility of LAZ3 involvement outside the MTC. On the other hand, 18 of
the 39 patients with LAZ3 rearrangement and available cytogenetic results
did not have visible chromosomal break at 3q27, suggesting that almost a
half of the rearrangements are not detectable by cytogenetic methods. No
statistical association could be found between LAZ3 status and initial
features of the disease or clinical outcome in either follicular or
aggressive lymphomas. We conclude that LAZ3 alteration is a relatively
frequent event in B-cell lymphoma, especially in those of aggressive
histology. It could be used as a genomic marker of the disease, and further
studies are needed to clarify clinical implications of these alterations.
Volume 83,
Issue 9,
pp. 2423-2427,
05/01/1994
Copyright © 1994 by The American Society of Hematology
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