FANCF methylation contributes to chemoselectivity in ovarian cancer.
A new model of ovarian cancer tumor progression implicates aberrant FANCF promoter methylation that is associated with gene silencing and disruption of the Fanconi-anemia-BRCA pathway. Disruption of the pathway occurs de novo in ovarian cancers and may contribute to selective sensitivity to platinum salts.
Olopade
Olufunmilayo I
OI
Center for Clinical Cancer Genetics, Department of Medicine, University of Chicago Medical Center, IL 60637, USA. folopade@medicine.bsd.uchicago.edu
Wei
Minjie
M
D000483:Alleles; D019313:BRCA1 Protein / Q000235:genetics; D019175:DNA Methylation; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm; D005091:Exons; D052219:Fanconi Anemia Complementation Group F Protein; D005260:Female; D006801:Humans; D008957:Models, Genetic; D020411:Oligonucleotide Array Sequence Analysis; D010051:Ovarian Neoplasms / Q000188:drug therapy* / Q000235:genetics*; D011401:Promoter Regions, Genetic; D016601:RNA-Binding Proteins / Q000235:genetics*; D015398:Signal Transduction
D019313:BRCA1 Protein; C499901:FANCF protein, human; D052219:Fanconi Anemia Complementation Group F Protein; D016601:RNA-Binding Proteins