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p16/INK4a and p15/INK4b Gene Methylation and Absence of p16/INK4a
mRNA and Protein Expression in Burkitt's Lymphoma
Ulf Klangby,
Ismail Okan,
Kristinn P. Magnusson,
Martin Wendland,
Peter Lind, and
Klas G. Wiman
From the Microbiology & Tumor Biology Center, Karolinska Institute;
and Pharmacia & Upjohn, Stockholm, Sweden.
The fact that the p16/INK4a and p15/INK4b genes are frequently
inactivated in human malignancies and that p16/INK4a null mice spontaneously develop B-cell lymphomas prompted us to examine the
status of both genes in Burkitt's Lymphoma (BL). We found a low
frequency of p16/INK4a and p15/INK4b deletions and mutations in BL cell
lines and biopsies. However, p16/INK4a exon 1 was methylated in 17 out
of 19 BL lines (89.5%) and in 8 out of 19 BL biopsies (42%) analyzed.
p15/INK4b Exon 1 was also methylated, although at a lower frequency.
p16/INK4a mRNA was readily detected in BL lines carrying unmethylated
p16/INK4a, but not in those carrying methylated p16/INK4a. No p16/INK4a
protein was detected in any of the BL lines and biopsies examined. In
contrast, only one out of seven lymphoblastoid cell lines (LCLs)
examined was methylated in p16/INK4a exon 1, and three out of the six
LCLs with unmethylated p16/INK4a expressed detectable levels of
p16/INK4a protein. Thus, the frequent p16/INK4a methylation in BL lines
correlates with downregulation of p16/INK4a expression, suggesting that
exon 1 methylation is responsible for silencing the p16/INK4a gene in BL.
Blood, Vol. 91 No. 5 (March 1), 1998:
pp. 1680-1687
© 1998 by The American Society of Hematology.
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