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Abnormal methylation of the calcitonin gene marks progression of chronic
myelogenous leukemia
BD Nelkin, D Przepiorka, PJ Burke, ED Thomas and SB Baylin
Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD.
The clinical aspects of disease progression in chronic myelogenous leukemia
(CML) are well established, but the nature of the molecular events
responsible is not known. We have previously reported a consistent pattern
of novel sites of methylation in the 5' region of the calcitonin (CT) gene
and other chromosome 11p loci in acute myelogenous and and lymphoid
leukemias. In the present study, CT gene methylation patterns were
investigated in peripheral blood from 51 patients with CML. Abnormal
patterns were found in only 2 of 31 patients in chronic phase, but in 5 of
8 patients in accelerated phase, and in 11 of 12 patients in blast crisis
(P less than .005). For one patient studied in blast crisis, abnormal CT
gene methylation was found in the peripheral blast cells but not in the
granulocytes. In two of three patients studied with CML and having normal
peripheral cell patterns, abnormal patterns were found in marrow blast
cells. In one patient, only partial normalization of the CT gene
methylation pattern was seen after chemotherapy induction of a second
chronic phase and the patient relapsed 5 months later. Our findings
indicate that abnormal methylation of the 5' region of the CT gene is
regularly a marker of disease progression in CML which may prove clinically
useful. This abnormal methylation site is part of an imbalance in DNA
methylation that may play a role in the progressive genetic instability
which characterizes the advancing stages of CML.
Volume 77,
Issue 11,
pp. 2431-2434,
06/01/1991
Copyright © 1991 by The American Society of Hematology
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