Bi‐allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia
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...
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Veröffentlicht in: | British journal of haematology 2003-11, Vol.123 (3), p.469-471 |
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Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 0007-1048 1365-2141 |
DOI: | 10.1046/j.1365-2141.2003.04640.x |