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Genomic instability of microsatellite repeats and its association with the
evolution of chronic myelogenous leukemia [see comments]
C Wada, S Shionoya, Y Fujino, H Tokuhiro, T Akahoshi, T Uchida and H Ohtani
Department of Clinical Pathology, School of Medicine, Kitasato University,
Kanagawa, Japan.
Tumorigenesis has been shown to proceed through a series of genetic
alterations involving protooncogenes and tumor-suppressor genes.
Investigation of genomic instability of microsatellites has indicated a new
mechanism for human carcinogenesis in hereditary nonpolyposis colorectal
cancer and sporadic cancer and this instability has been shown to be
related to inherited predisposition to cancer. This study was conducted to
determine whether such microsatellite instability is associated with the
evolution of chronic myelogenous leukemia (CML) to the blast crisis.
Nineteen CML patients clinically progressing from the chronic phase to
accelerated phase or blast crisis and 20 other patients in the CML chronic
phase were studied. By polymerase chain reaction assay, DNAs for genomic
instability in five separate microsatellites in chromosome arms 5q (Mfd27),
17p (Mfd41), 18q (DCC), 3p (CI3-9), and 8p (LPL) were examined. Differences
in unrelated microsatellites of chronic and blastic phase DNAs in 14 of 19
patients (73.7%) were demonstrated. Somatic instability in five
microsatellites, Mfd27, Mfd41, DCC, CI3-9, and LPL, was detected in 2 of 19
(10.5%), 8 of 19 (42.1%), 11 of 19 (57.9%), 4 of 17 (23.5%), and 4 of 17
(23.5%) cases. In 10 of 19 cases (52.6%), genetic instability in at least
two of five microsatellites was observed and was categorized as replication
error (RER+) phenotype. CML evolution cases with myeloid, lymphoid, and
mixed phenotypes and the blast crisis and accelerated phase showed somatic
instability in a number of microsatellites. No alterations in leukemic
cells at the chronic phase could be detected in any microsatellites. These
data indicate instability of microsatellites (RER+) but not familial
predisposition to possibly be a late genetic event in the evolution of CML
to blast crisis. In the microsatellite of the DCC gene, complicated
alterations in band patterns caused by instability as well as loss of
heterozygosity (LOH) were observed in 13 of 19 cases (68.4%): instability
in 9 cases, instability plus LOH in 2 cases, and only LOH in 2 cases. These
highly frequent alterations in microsatellites, including instability and
LOH, suggesting that secondary events due possibly to loss of fidelity in
replication and repair machinery may be significantly associated with CML
evolution.
Volume 83,
Issue 12,
pp. 3449-3456,
06/15/1994
Copyright © 1994 by The American Society of Hematology
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