Thymidine Kinase 1 in Risk Assessment for Hereditary Breast /Ovarian Cancer
Recruitment status was: Recruiting
|Study Design:||Observational Model: Family-Based
Time Perspective: Prospective
|Official Title:||Thymidine Kinase 1 in Risk Assessment for Hereditary Breast /Ovarian Cancer|
|Study Start Date:||March 2009|
|Estimated Study Completion Date:||March 2011|
|Estimated Primary Completion Date:||March 2010 (Final data collection date for primary outcome measure)|
With BRCA1 or BRCA2 mutations
Without BRCA1 or BRCA2 mutations
Hereditary breast/ovarian cancer syndrome is associated with mutations in tumor suppressor BRCA1 and BRCA2 genes. Products of these genes play an important role in the repair of DNA double-strand breaks. Mutations in BRCA1 and BRCA2 genes could impair DNA repair. In resting or G1 cells, where the de novo synthesis of DNA precursors is absent, the salvage pathway is the sole provider of deoxyribonucleotides to be used in DNA repair. For this process a sufficient supply of deoxynucleotides and activity of Thymidine Kinase 1 are essential. TK1 is an important component of adaptive response of cells to DNA damage. Mutations in genes directly engaged in the DNA repair process could lead to the accumulation of DNA damage and in turn cause an adaptive cell reaction manifesting as permanently increased Thymidine Kinase 1 activity.
A recently developed new high-sensitive assay DiviTum® allows to investigate the contribution of this enzyme to DNA repair processes and to make a comparison of Thymidine kinase 1 activity in women with normal and impared DNA repair system.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00855998
|Hadassah Medical Organization|
|Jerusalem, Israel, 91120|