The Presidential Symposium begins at 10:30 a.m.
Unstable Genes, DNA, and the Maytag
Repair Man

Today is the final day of the 46th ASH Annual Meeting. From 10:30 a.m. – 12:30 p.m. today, Dr. Stanley Schrier will host this year’s Presidential Symposium on “Genomic Instability and DNA Repair in Hematology.” In keeping with the rich tradition of ASH Presidential Symposia, today’s session promises to deliver a thorough and lucid overview of the mechanisms of genomic instability and the mechanisms by which DNA is repaired.

Dr. Michael Kastan of St. Jude Children’s Research Hospital will lead off the speakers with an in-depth discussion of “DNA Damage Responses in Cancer Development and Treatment.” It is now clear that central to the DNA damage response are the ataxia-telangiectasia mutated (ATM) and the ataxia-telangiectasia and Rad-3 related (ATR) phosphoinositide 3-kinase related kinases which modulate cell cycle progression, DNA repair, and sometimes apoptosis. Recent work by Dr. Kastan and associates has included a demonstration that the human telomere-associated protein TRF2 is an inhibitor of the ATM kinase and may thus regulate ATM-dependent DNA damage responses. Now, if that isn’t crystal clear to you then you need to attend this symposium.

Dr. Fred Alt from Children’s Hospital at Harvard Medical School has a number of different research interests including immunoglobulin class-switch recombination and allelic exclusion mechanisms. In his talk he will focus on the roles that histones and chromatin play in suppressing DNA breaks. We can likely look forward to hearing about how H2AX anchors broken chromosomal DNA ends in close proximity as well as other chromosomal stability/instability mechanisms.

Finally, Dr. Alan D’Andrea of the Dana-Farber Cancer Institute will update us on the ongoing brilliant path of exploration that started out examining Fanconi Anemia (FA) and led to a link to breast cancer. Eleven FA complementation groups have been identified and eight FA genes have been cloned. It turns out that the FANCD1 gene is identical to the breast cancer susceptibility gene, BRCA2. Dr. D’Andrea’s more recent investigations have revolved around the monoubiquitinated FANCD2 gene and its interaction with FANCD1/BRCA2 in chromatin. I know you’re all getting (or already are) burned out from multiple sessions and talks, but trust me, you need to muster up the energy and attention to make it to the last special session.