Bi‐allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia
Open Access
- 20 October 2003
- journal article
- Published by Wiley in British Journal of Haematology
- Vol. 123 (3) , 469-471
- https://doi.org/10.1046/j.1365-2141.2003.04640.x
Abstract
Summary. 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.Keywords
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