CHFR gene is neither mutated nor hypermethylated in ovarian cancer

• Published in: Cancer detection and prevention 2007-01, Vol.31 (3), p.257-261
• Main Authors: Ludwig, Agnieszka H., MSc, Bujko, Mateusz, MSc, Bidzinski, Mariusz, MD, PhD, Kupryjańczyk, Jolanta, MD, PhD
• Format: Article
• Language: English
• Subjects: Antineoplastic Agents - pharmacology; Antineoplastic Agents - therapeutic use; Cancer; Carcinoma - drug therapy; Carcinoma - genetics; Carcinoma - pathology; Cell Cycle Proteins - genetics; DNA Methylation; Drug Resistance, Neoplasm; Epidemiology; Exons; Female; Genes; Hematology, Oncology and Palliative Medicine; Humans; Mutation; Neoplasm Proteins - genetics; Ovarian cancer; Ovarian Neoplasms - drug therapy; Ovarian Neoplasms - genetics; Ovarian Neoplasms - pathology; Poly-ADP-Ribose Binding Proteins; Polymerase Chain Reaction; Polymorphism, Single Nucleotide; Polymorphism, Single-Stranded Conformational; Promoter Regions, Genetic; Sequence Analysis, DNA; Taxoids; Taxoids - pharmacology; Taxoids - therapeutic use; Tumors; Ubiquitin-Protein Ligases
• ISSN: 0361-090X; 1877-7821; 1873-443X; 1877-783X
• DOI: 10.1016/j.cdp.2006.04.005

Abstract Background : CHFR is a mitotic checkpoint protein that under mitotic stress (caused also by taxanes) delays progression into mitosis. Methods : We looked for CHFR gene (605209) alterations and its promoter hypermethylation in 48 ovarian carcinomas either sensitive or resistant to taxane treatment. We used single-strand conformation polymorphism analysis, sequencing and methylation-specific polymerase chain reaction. Results : Neither mutations in the CHFR gene nor hypermethylation of its promoter region were found. A novel single nucleotide polymorphism (Val154Val) was identified in exon 5 of alternatively spliced transcript. Conclusions : Our results indicate that CHFR gene status cannot serve as a molecular predictor of ovarian cancer sensitivity to taxanes.