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Amplification of genomic DNA demonstrates the presence of the t(2;5)
(p23;q35) in anaplastic large cell lymphoma, but not in other non-
Hodgkin's lymphomas, Hodgkin's disease, or lymphomatoid papulosis
AH Sarris, R Luthra, V Papadimitracopoulou, M Waasdorp, MA Dimopoulos, JA McBride, F Cabanillas, M Duvic, A Deisseroth, SW Morris and WC Pugh
Department of Hematology, University of Texas M.D. Anderson Cancer Center,
Houston 77030, USA.
Anaplastic large cell lymphoma (ALCL) is a distinct clinicopathologic
variant of intermediate grade non-Hodgkin's lymphomas (NHL) composed of
large pleomorphic cells that usually express the CD30 antigen and
interleukin (IL)-2 receptors, and is characterized by frequent cutaneous
and extranodal involvement. With variable frequency ALCL bear the
t(2;5)(p23;q35) chromosomal translocation that fuses the nucleophosmin
(NPM) gene on chromosome 5q35 to a novel protein kinase gene, Anaplastic
Lymphoma Kinase (ALK), on chromosome 2p23. We determined the frequency of
this translocation with a novel DNA polymerase chain reaction (PCR)
technique using 0.5 microgram of genomic DNA, 5'-primers derived from the
NPM gene and 3'-primers derived from the ALK gene and hybridization with
internal probes. The presence of amplifiable DNA in the samples was tested
with the inclusion in the PCR reaction of oligonucleotide primers designed
to amplify a 3016-bp fragment from the beta-globin locus. NMP-ALK fusion
amplicons were detected using DNA isolated either from all three ALCL cell
lines tested, or from all four primary ALCL tumors known to contain the
t(2;5)(p23;q35) translocation. Nested amplicons were detected by
hybridization in 100% of specimens diluted 10(4)-fold and in 20% of those
diluted 10(5)-fold. We subsequently examined archival genomic DNA from 20
patients with ALCL, 39 with diffuse large cell, 2 with mantle cell, 20 with
peripheral T cell, 13 with low-grade NHL, 31 with Hodgkin's disease (HD),
and 6 with lymphomatoid papulosis. Fusion of the NPM and ALK genes was
detected in three of 18 patients with ALCL who had amplifiable DNA (17%,
95% confidence intervals 4% to 41%), but not in any patients with other
NHL, HD, or lymphomatoid papulosis. The amplicon sizes were different in
all cell lines and patients reflecting unique genomic DNA breakpoints. We
conclude that with genomic DNA-PCR the rearrangement of the NPM and ALK
loci is restricted to patients with ALCL. Further studies are needed to
determine the prognostic significance of the NPM-ALK rearrangement, to
determine whether its detection can aid in the differential diagnosis
between ALCL. Hodgkin's disease, and lymphomatoid papulosis, and to
establish the usefulness of the genomic DNA PCR in the monitoring of
minimal residual disease in those patients whose tumors bear the t(2;5).
Volume 88,
Issue 5,
pp. 1771-1779,
09/01/1996
Copyright © 1996 by The American Society of Hematology
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