Methylation status of the gene promoter of cyclin-dependent kinase inhibitor 2A (CDKN2A) in ovarian cancer.
Summary of "Methylation status of the gene promoter of cyclin-dependent kinase inhibitor 2A (CDKN2A) in ovarian cancer."
Abstract Objective. This study investigated the methylation status of the promoter of the tumor suppressor gene cyclin-dependent kinase inhibitor 2A (CDKN2A) in ovarian cancer. Design and methods. CDKN2A methylation was quantified by real-time PCR in ovarian biopsies of 52 patients with ovarian cancer, 43 patients with benign ovarian tumors and 40 patients with benign uterine pathology and healthy ovaries. Results. CDKN2A methylation was detected in the three groups. The methylation level was higher in the cancer patients than in the other two groups (p = 0.0003) but was not different between benign tumors and healthy ovarian tissue (p > 0.05). Using a cutoff threshold based on receiver-operating characteristic analysis, 21 patients with ovarian cancer and three patients with benign tumors were considered positive for CDKN2A methylation while all patients with healthy ovaries were considered negative. At the chosen cutoff, the diagnostic sensitivity was 40.4% and specificity 96.4%. CDKN2A methylation level and frequency were associated with high grade tumors (p = 0.0001 and p = 0.0005) but were not associated with disease stage or serum CA125 levels. However, it should be noted that most patients (92.3%) presented with advanced stage 3 or 4 disease. Conclusion. CDKN2A promoter methylation is common in ovarian cancer. Quantification of CDKN2A methylation may be useful in distinguishing malignant from benign ovarian tumors or healthy ovarian tissue.
Departments of Clinical Pathology.
This article was published in the following journal.
Name: Scandinavian journal of clinical and laboratory investigation
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21728901
- DOI: http://dx.doi.org/10.3109/00365513.2011.590224
Medical and Biotech [MESH] Definitions
Cyclin-dependent Kinase Inhibitor P27
A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2.
Cyclin-dependent Kinase 2
A key regulator of CELL CYCLE progression. It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. Its activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P27 and CYCLIN-DEPENDENT KINASE INHIBITOR P21.
Cyclin-dependent Kinase 4
Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. It partners with CYCLIN D to phosphorylate RETINOBLASTOMA PROTEIN. CDK4 activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P16.
Cyclin-dependent Kinase 6
Cyclin-dependent kinase 6 associates with CYCLIN D and phosphorylates RETINOBLASTOMA PROTEIN during G1 PHASE of the CELL CYCLE. It helps regulate the transition to S PHASE and its kinase activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P18.
Cyclin-dependent Kinase Inhibitor P21
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
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