Abstract A02: Investigating the contribution of RAD51 paralog mutations to cancer development

• Published in: Clinical cancer research Vol. 24; no. 15_Supplement; p. A02
• Main Authors: Baldock, Robert A., Pressimone, Catherine A., Bernstein, Kara A.
• Format: Journal Article
• Language: English
• Published: 01-08-2018
• ISSN: 1078-0432; 1557-3265
• DOI: 10.1158/1557-3265.OVCA17-A02

Homologous recombination (HR) is a high-fidelity DNA repair mechanism that utilizes a homologous template to repair double-strand breaks (DSBs). The defining step of HR is the formation of a RAD51 nucleoprotein filament, which performs the homology search and strand invasion steps. RAD51 filament formation is aided by the RAD51 paralogs, which structurally resemble RAD51. The RAD51 paralogs form sub-complexes including CX3 (RAD51C and XRCC3) and BCDX2 (RAD51B, RAD51C, RAD51D, and XRCC2).
Here we use a use a Yeast 3-hybrid assay to determine which patient-identified mutations in RAD51D impair the interaction with RAD51C and XRCC2. We further validate this interaction data in mammalian cells. Lastly, we are going to complement RAD51D and XRCC2-depleted cells with mutant versions of the proteins to determine their impact on HR as well as sensitivity to specific chemotherapeutic agents.
Citation Format: Robert A. Baldock, Catherine A. Pressimone, Kara A. Bernstein. Investigating the contribution of RAD51 paralog mutations to cancer development. [abstract]. In: Proceedings of the AACR Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; Oct 1-4, 2017; Pittsburgh, PA. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(15_Suppl):Abstract nr A02.