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Deletion variants within the NF-kappa B activation domain of the LMP1
oncogene prevail in acquired immunodeficiency syndrome-related large cell
lymphomas and human immunodeficiency virus-negative atypical
lymphoproliferations
H Knecht, M Raphael, C McQuain, S Rothenberger, G Pihan, S Camilleri-Broet, E Bachmann, GR Kershaw, S Ryan, EL Kittler, PJ Quesenberry, D Schlaifer, BA Woda and P Brousset
LINK Laboratories, University of Massachusetts Medical Center, Worcester
01655-0246, USA.
This sequencing study of 17 acquired immunodeficiency syndrome-related
lymphomas (9 primary brain, 8 systemic) and 8 human immunodeficiency
virus-negative atypical lymphoproliferations expressing large amounts of
the latent membrane protein 1 (LMP1) of Epstein-Barr virus was performed to
characterize the carboxy terminal NF-kappa B activation domain of LMP1 at
the molecular level in an immunocompromised host. In- frame deletions
within the NF-kappa B activation domain were identified in all but 2
primary brain lymphomas, 4 systemic lymphomas, and 4 atypical
lymphoproliferations, ie, in 60% of cases. In addition, non silent point
mutations (range 1 to 5, mean 3.3) were detected in all cases. Although all
changes occurred within the first 100 nucleotides of the carboxy terminal
NF-kappa B activation domain--a critical sequence for the protein
half-life--not a single point mutation was found in the remaining 62
nucleotides, necessary for malignant transformation. Such a clustering of
nonrandom sequence variations, associated with a high oncoprotein
expression in immunocompromised hosts, suggests that this part of the LMP1
oncogene behaves as a hypervariable region with natural selection of
growth-promoting variants through prolongation of the protein half-life.
Volume 87,
Issue 3,
pp. 876-881,
02/01/1996
Copyright © 1996 by The American Society of Hematology
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