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Homozygous deletions of the p16 tumor-suppressor gene are associated with
lymphoid transformation of chronic myeloid leukemia
H Sill, JM Goldman and NC Cross
LRF Centre for Adult Leukaemia, Royal Postgraduate Medical School,
Hammersmith Hospital, London, UK.
The p16 gene, also referred to as MTS1, INK4, CDK4I, or CDKN2, at
chromosome 9p21 has recently been described as a tumor suppressor that may
be involved in a wide range of tumors. We have used a semiquantitative
multiplex polymerase chain reaction assay to search for deletions of the
p16 gene in 34 patients with chronic myeloid leukemia in blast crisis (CML
BC), 19 patients with acute lymphoblastic leukemia (ALL), and 25 patients
with acute myeloid leukemia (AML). Homozygous deletions of p16 exons were
found in 5 of 10 (50%) patients with CML in lymphoid BC and in 5 (26%) ALL
patients, but in only 1 (2%) case with AML. No deletions were found in CML
BC of nonlymphoid phenotype. Comparison of chronic phase DNA or remission
DNA with acute leukemia DNA in 5 individuals showed that the p16 deletions
were acquired and not inherited, directly implicating these lesions in the
pathogenesis of the disease. We conclude that functional elimination of the
p16 gene, or a closely mapping gene, is involved in a significant number of
patients with CML in lymphoid transformation.
Volume 85,
Issue 8,
pp. 2013-2016,
04/15/1995
Copyright © 1995 by The American Society of Hematology
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