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Blood, Vol. 95 No. 10 (May 15), 2000:
pp. 3208-3213
Hypermethylation of E-cadherin in leukemia
John R. Melki,
Paul C. Vincent,
Ross D. Brown, and
Susan J. Clark
From Kanematsu Laboratories, Royal Prince Alfred Hospital,
Camperdown, NSW 2050, Australia; Faculty of Medicine, University of
Sydney, Sydney, NSW, 2006, Australia; Institute of Haematology, Royal
Prince Alfred Hospital, Camperdown, NSW 2050, Australia; CSIRO,
Molecular Science Sydney Laboratory, PO Box 184, North Ryde, SW 1670, Australia.
E-cadherin gene is often termed a "metastasis suppressor" gene
because the E-cadherin protein can suppress tumor cell invasion and
metastasis. Inactivation of the E-cadherin gene occurs in undifferentiated solid tumors by both genetic and epigenetic
mechanisms; however, the role of E-cadherin in hematologic malignancies
is only now being recognized. E-cadherin expression is essential for
erythroblast and normoblast maturation, yet expression is reduced or
absent in leukemic blast cells. This study examined the messenger RNA
(mRNA) and protein expression of the E-cadherin gene in bone
marrow and blood samples from normal donors and patients with leukemia.
We found that all normal donor samples expressed E-cadherin mRNA,
whereas both samples of acute myelogenous leukemia and chronic
lymphocytic leukemia had a significant reduction or absence of
expression. However, normal blast counterparts expressed only a low
level of E-cadherin surface protein. Sodium bisulphite genomic
sequencing was used to fully characterize the methylation patterns of
the CpG island associated with the E-cadherin gene promoter in
those samples with matched DNA. All of the normal control samples were
essentially unmethylated; however, 14 of 18 (78%) of the leukemia
samples had abnormal hypermethylation of the E-cadherin CpG island. In
fact both alleles of the E-cadherin gene were often
hypermethylated. We conclude the E-cadherin gene is a common
target for hypermethylation in hematologic malignancies.
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