Genomic Instability

Course Information

Date: Anytime
Duration: 60 Minutes
Location: Virtual
Audience: ACVIM, ECEIM, ECVIM-CA and ECVN Diplomates and candidates
Specialty: Oncology
Type: On Demand
CE Hours: 1.0

Course Overview

DNA damage response mechanisms protect mammalian cells from genomic instability and phenotypes such as aging and cancer. In contrast to normal cells, tumors exhibit extreme genomic instability, which can occur at the level of DNA as well as at the chromosomal level. This course reviews the causes and consequences of genomic instability, including manifestations in DNA and chromosomes; the course also provides a thorough review of cellular DNA damage response mechanisms, including detection of damage, checkpoint signaling, and recruitment of repair factors.

Learning Objectives:

• List causes and consequences of genomic instability.
• Define the following and explain their significance in cancer: chromosomal deletion, chromosomal translocation, chromosomal inversion, aneuploidy, polyploidy, internal tandem duplication. Provide key examples. 
• Explain the difference between and the significance of somatic and germline mutations.
• Describe the differences between single strand and double strand DNA breaks in terms of impact on the cell and repair processes involved.
• Name the kinases involved in signaling for DNA damage.
• Explain the following: mismatch repair, nucleotide excision repair, base excision repair, microsatellite instability. Name cancers or cancer syndromes associated with deficiencies in these repair processes. 
• Recognize the key players in checkpoint signaling and DNA repair including the DNA damage response pathway components that are currently undergoing evaluation as therapeutic targets. 

RACE Application Status

This module has been submitted and approved for 1.0 hours of continuing education credit in jurisdictions which recognize AAVSB RACE approval.

For additional questions, please contact us at Learning@ACVIM.org.