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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1773-1781
Frequent Methylation Silencing of p15INK4b
(MTS2) and p16INK4a (MTS1)
in B-Cell and T-Cell Lymphomas
Audrey S. Baur,
Phil Shaw,
Nathalie Burri,
Françoise Delacrétaz,
Fred T. Bosman, and
Pascal Chaubert
From Institut Universitaire de Pathologie, Lausanne, Switzerland.
The methylation status of p15INK4b
(MTS2), p16INK4a (MTS1) and
p14ARF (p16 ) was
analyzed in 56 lymphomas by restriction-enzyme related polymerase chain
reaction (PCR) (REP), methylation-specific PCR (MSP), and bisulfite
genomic sequencing (BGS). Methylation of the p15 and
p16 genes was detected, respectively, in 64% and 32% of the
B-cell lymphomas, in 44% and 22% of the T-cell lymphomas, and in none
of the 5 reactive lymph nodes analyzed. Both p15 and p16 genes were methylated more often in the high-grade (78%
and 50%, respectively) than in the low-grade B-cell lymphomas (55% and 21%, respectively). For 5 cases, mapping of the methylated CpGs of
the p16 promoter region confirmed the results of REP and MSP.
In addition, a large variation in the methylation patterns of
p16 exon 1 was observed, not only from one lymphoma to another, but also within a given tumor. Methylation of p15 and
p16 was associated with an absence of gene expression, as
assessed by reverse transcription-PCR. The p14 gene was
unmethylated and normally expressed in all 56 tumors. We found no
mutations of p15, p16, or p14 in any of the 56 lymphomas. Our results suggest a role for p15 and p16
gene methylation during lymphomagenesis and a possible association
between p15 and p16 inactivation and aggressive transformation in B-cell and T-cell lymphomas.
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