Researchers at The Jackson Laboratory have identified a molecule that
prevents repair of some cancer cells, providing a potential new "genetic
chemotherapy" approach to cancer treatment that could significantly reduce
side effects and the development of treatment resistance compared with
traditional chemotherapy. In the process of antibody production, white blood
cells turn on the gene known as activation-induced cytidine deaminase (AID),
which acts as a sort of molecular scissors that cut the chromosomes within
the white blood cells. This is needed to rearrange pieces of the white blood
cells chromosomes and produce different "flavors" of antibodies that do
different jobs. But in some cancers this process goes wrong, with AID acting
out of control and creating mutations and chromosome rearrangements that
make the tumor more aggressive. Although the process of homologous
recombination (HR) helps repair such cells and help them grow, researchers in
the laboratory of Associate Professor Kevin Mills, Ph.D., identified a molecule
called DIDS (for 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid) that blocks
the DNA repair action in chronic lymphocytic leukemia (CLL), causing the
cancer cells to die. With the help of this new treatment, it is possible to stop
cancer before it becomes too serious and even deadly.