Mechanisms That Cause DNA Damage and Related Diseases

Cells are under constant threat of DNA damage from both internal and external sources, including reactive oxygen species (ROS) produced during normal cellular metabolism and environmental stresses like ultraviolet (UV) radiation from the sun. Failure to correct genome damage can have a variety of negative consequences, ranging from cell death to uncontrolled oncogenic proliferation. Consequently, eukaryotic cells employ a variety of evolutionarily-conserved mechanisms to protect genomic integrity. Inherited defects in these genome protection mechanisms are responsible for a variety of human diseases, such as Ataxia Telangiectasia, Fanconi Anemia, Bloom’s syndrome, Cockayne syndrome, Xeroderma pigmentosum, Nijmegen breakage syndrome, and Werner syndrome, which are associated with premature aging and dramatically increased risk for age-related diseases, such as cancer.

The 2014 Conference on Genomic Instability seeks to bring together a diverse group of participants to comprehensively address the primary topics in the field, including mechanisms of DNA damage signaling, replication fidelity, DNA recombination and chromosome segregation, as well as the physiological significance of these processes in aging and age-related diseases. The proposed meeting is distinct in providing broader coverage to the entire field of Genomic Instability and integrating basic and applied elements. Broader topics include programmed genome rearrangements during development of the immune system and of ciliates, as well as conflicts between the replication and transcription machineries. To date, most meetings on this topic focus either on the mechanisms that cause genetic instability or the diseases that stem from it. This conference covers both ends of this topic and aims to promote dialog that bridges the gulf between the causes and consequences of genomic instability.