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Bi‐allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia
Author(s) -
Tischkowitz Marc,
Ameziane Najim,
Waisfisz Quinten,
De Winter Johan P.,
Harris Richard,
Taniguchi Toshiyasu,
D'Andrea Alan,
Hodgson Shirley V.,
Mathew Christopher G.,
Joenje Hans
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.1365-2141.2003.04640.x
Subject(s) - fanconi anemia , cancer research , gene silencing , chromosome instability , carcinogenesis , biology , medicine , gene , genetics , dna repair , chromosome
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.