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Human non-Hodgkin's lymphomas overexpress a wild-type form of p53 which is
a functional transcriptional activator of the cyclin-dependent kinase
inhibitor p21
R Maestro, A Gloghini, C Doglioni, S Piccinin, T Vukosavljevic, D Gasparotto, A Carbone and M Boiocchi
Department of Experimental Oncology 1, Centro di Riferimento Oncologico,
Aviano, Italy.
A large fraction of non-Hodgkin's lymphomas (NHLs) accumulate a wild- type
form of the p53 tumor suppressor protein at the nuclear level. In normal
cells, p53 induction is associated with a temporary cell growth arrest at
the G1-S boundary of the cell cycle. This activity of p53 as a G1
checkpoint molecule is strictly dependent on its ability to induce the
transcription of the inhibitor of the cyclin dependent kinase, p21. To
verify the functionality of the wild-type p53 protein accumulated in NHL
cells, 70 cases were comparatively analyzed for p53 and p21 expression and
status of the respective genes. Overexpression of the wt p53 protein was
associated with the accumulation of p21, indicating that p53 is functional
with respect to p21 induction in these tumors. The coaccumulation of p53
with Ki-67 antigen indicates that wt p53- positive cells and p21-positive
cells, as well, are actively proliferative elements, supporting the notion
that p53-induced, p21- mediated growth arrest is somehow overridden in NHL
cells. No p21 mutation or particular allele variant was shown to correlate
with p21 protein accumulation, thus excluding a role for p21 structural
abnormalities. Taken together, our data suggest the existence in NHL of a
peculiar mechanism of functional inactivation of the p53 G1 checkpoint
pathway occurring downstream of the CDK inhibitor p21.
Volume 89,
Issue 7,
pp. 2523-2528,
04/01/1997
Copyright © 1997 by The American Society of Hematology
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