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Br J Haematol. 2003 Nov;123(3):469-71.

Bi-allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia.

Author information

1
Department of Medical and Molecular Genetics, Division of Genetics and Development Guy's, King's and St Thomas's School of Medicine, King's College London, Guy's Hospital, London, UK.

Abstract

Fanconi anaemia (FA) is a chromosomal instability disorder associated with a high risk of acute myeloid leukaemia (AML). Previous work has shown that the AML cell line CHRF-288, derived from a sporadic AML-M7 patient, does not express FANCF protein and exhibits a cellular FA phenotype. We show that this phenotype is corrected by a FANCF-expressing plasmid and that the absence of FANCF protein is explained by hypermethylation of the promoter region of the FANCF gene. As FANCF is localized in a hot-spot region for somatic hypermethylation (11p15), FANCF silencing might be an early step in sporadic carcinogenesis, including leukaemogenesis.

PMID:
14617007
[Indexed for MEDLINE]

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