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

TY - JOUR

T1 - Bi-allelic silencing of the Fanconi anaemia gene FANCF in acute myeloid leukaemia

AU - Tischkowitz, M

AU - Ameziane, N

AU - Waisfisz, Q

AU - De Winter, J P

AU - Harris, R

AU - Taniguchi, T

AU - D'Andrea, A

AU - Hodgson, S V

AU - Mathew, C G

AU - Joenje, H

PY - 2003/11

Y1 - 2003/11

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0242298162&partnerID=8YFLogxK

U2 - 10.1046/j.1365-2141.2003.04640.x

DO - 10.1046/j.1365-2141.2003.04640.x

M3 - Article

SN - 1365-2141

VL - 123

SP - 469

EP - 471

JO - British Journal of Haematology

JF - British Journal of Haematology

IS - 3

ER -