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Molecular characterization of CD30+ anaplastic large-cell lymphoma: high
frequency of c-myc proto-oncogene activation
G Inghirami, L Macri, E Cesarman, A Chadburn, J Zhong and DM Knowles
Division of Surgical Pathology, College of Physicians and Surgeons of
Columbia University, New York, NY.
Anaplastic large-cell lymphoma (ALCL) represents a morphologically distinct
type of non-Hodgkin's lymphoma (NHL) characterized phenotypically by the
expression of the CD30 antigen, a new member of the nerve growth factor
gene family. The lymphoid origin of ALCL has been documented using
immunohistochemical and molecular genetic analyses. However, very little is
known so far regarding the precise pathogenetic mechanisms involved in its
development and progression. Therefore, we investigated bcl-2, p53, and
retinoblastoma gene (Rb) expression immunohistochemically; the occurrence
of bcl-2, c-myc, and Rb gene rearrangements using Southern blotting; and
the presence of ras and p53 gene somatic mutations by single-strand
conformation polymorphism assay in a panel of 18 well-characterized ALCLs.
In addition, the presence of Epstein-Barr (EBV) and human T-cell
lymphotropic virus type I (HTLV-I) genomes were investigated using
polymerase chain reaction. We identified abnormal c-myc gene products in 6
of 18 cases (33%) of ALCL. On the other hand, the bcl-2 and Rb genes were
not rearranged and K-, N-, and H-ras gene somatic mutations were not found.
Significant levels of p53 protein expression were found in more than 60% of
ALCLs, but only a single ALCL carried a p53 gene mutation (exon 5). Only 3
ALCL cases, all occurring in human immunodeficiency virus-infected
patients, were positive for EBV genomes. On the other hand, contrary to
previous findings, no HTLV-I products could be identified. Despite the fact
that the c-myc proto- oncogene appears to be frequently altered in ALCL, no
pathognomonic abnormality could be identified and therefore additional
studies and new strategies should be designed to identify the pathogenetic
mechanisms involved in the development of ALCL.
Volume 83,
Issue 12,
pp. 3581-3590,
06/15/1994
Copyright © 1994 by The American Society of Hematology
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