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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1755-1760
Mutation of the p53 Gene Is Not a Typical Feature of Hodgkin and
Reed-Sternberg Cells in Hodgkin's Disease
Manuel Montesinos-Rongen,
Axel Roers,
Ralf Küppers,
Klaus Rajewsky, and
Martin-Leo Hansmann
From the Institute for Genetics, University of Cologne, Cologne; and
the Institute for Pathology, University of Frankfurt, Frankfurt,
Germany.
Point mutations of the p53 tumor suppressor gene are a frequent
finding in human carcinomas and are thought to be an important oncogenic event. In non-Hodgkin lymphomas, p53 mutations occur in a
minor fraction of cases. However, conclusive data are still lacking for
Hodgkin's disease (HD) where the analysis meets technical problems.
The neoplastic tumor cell clone in HD is represented by the large
Hodgkin and Reed-Sternberg (HRS) cells, which account for only a
minority of all cells in the tumor tissue (often <1%). To identify
putative HRS cell-specific mutations, single HRS cells were
micromanipulated from frozen tissue sections of HD biopsy specimens.
Exons 4 to 8 of the p53 gene (in which more than 90% of p53 mutations
associated with human neoplasms occur) were amplified from these single
cells and sequenced. Mutations of p53 were not found in HRS cells of
any of 8 cases of HD analyzed. We conclude that mutation of the p53
gene is only rarely, if at all, involved in the pathogenesis of HD.
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