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Structural and functional analysis of oncogenes and tumor suppressor genes
in adult T-cell leukemia/lymphoma shows frequent p53 mutations
E Cesarman, A Chadburn, G Inghirami, G Gaidano and DM Knowles
Department of Pathology, Columbia University, College of Physicians and
Surgeons, New York, NY.
The human T-cell lymphotropic virus type I (HTLV-I) is capable of inducing
adult T-cell leukemia/lymphoma (ATLL). However, the long latency period
between infection and development of ATLL, as well as the small fraction of
the infected population that actually develops this disease, suggest that
additional factors are involved in its pathogenesis. Therefore, we
performed a molecular analysis of 10 cases of ATLL presenting in a
nonendemic area that were shown to have HTLV-I sequences by polymerase
chain reaction as well as clonal T-cell receptor beta gene rearrangements.
We analyzed these cases for alterations in some of the oncogenes and tumor
suppressor genes frequently involved in hematopoietic neoplasia.
Specifically, we used a single-strand conformation polymorphism assay to
determine the presence of mutations in the p53 tumor suppressor gene, as
well as the K-RAS, N- RAS, H-RAS, and c-myc oncogenes. In addition, we
studied the c-myc gene for rearrangements by Southern blotting and assessed
expression of the retinoblastoma (Rb) and p53 genes by immunostaining.
Analysis of the c- myc gene and the RAS family of oncogenes did not show
any alterations. Also, the Rb gene was expressed in all cases analyzed.
However, we found mutations of the p53 gene in 3 of the 10 cases and these
results were confirmed by sequence analysis. In two of these cases, we
showed by restriction fragment length polymorphism analysis of chromosome
17p sequences that the p53 mutations were accompanied by a loss of
heterozygocity. Also, these mutations correlated with an altered pattern of
p53 expression. Thus, mutations in the p53 locus may be a cofactor for the
development of ATLL in some cases, whereas the c-myc, Rb, and RAS genes do
not appear to be involved in these neoplasms.
Volume 80,
Issue 12,
pp. 3205-3216,
12/15/1992
Copyright © 1992 by The American Society of Hematology
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