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Aberrant p15 gene promoter methylation in therapy‐related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations
Author(s) -
Au W. Y.,
Fung A.,
Man C.,
Ma S. K.,
Wan T. S.,
Liang R.,
Kwong Y. L.
Publication year - 2003
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2003.04194.x
Subject(s) - myelodysplastic syndromes , methylation , cdkn2b , myeloid leukemia , myeloid , cancer research , bone marrow , cytogenetics , chromosome 7 (human) , medicine , monosomy , dna methylation , leukemia , biology , oncology , pathology , immunology , gene , karyotype , chromosome , genetics , cancer , gene expression , cdkn2a
Summary. Seventeen patients with therapy‐related myelodysplastic syndrome/acute myeloid leukaemia (t‐MDS/AML) were examined for aberrant p15 gene methylation by methylation‐specific polymerase chain reaction. Ten patients (58%) showed p15 methylation, which was significantly related to monosomy/deletion of chromosome 7q, but not to antecedent chemotherapy, blast count, leukaemic evolution or survival. In three of six patients with marrow samples obtained prior to the diagnosis of t‐MDS/AML, p15 methylation predated disease development by up to 2 years. Bone marrow transplantation led to the disappearance of p15 methylation in one patient. These results showed that p15 methylation was an early event in the evolution of some t‐MDS/AML patients.