The more strategies we adopt in the war on cancer, the more opportunities we will have to develop new medicines. Here’s how Sanford-Burnham scientists approach the fight…Tumor Development
Cancer is caused by changes in our DNA sequences or how those sequences are expressed. These changes can be caused by genetic mutations or by epigenetic alterations (changes that do not alter the genome, but affect its function). Understanding how genetic and epigenetic changes arise, the significance of these specific changes and the consequences of inappropriate gene regulation (when genes are turned on or off) can reveal new strategies for drug discovery.
We now know that the growth and spread of cancer involves not just tumor cells, but also other host cells in the tumor microenvironment—cancer’s cellular neighborhood. For example, angiogenesis (blood vessel growth) requires the tumor to recruit surrounding blood vessel-building cells to enlarge its blood supply. This mechanism provides oxygen and nutrients to tumors so they can grow, and allows cancer cells to escape their primary site and metastasize. Learning how to alter the microenvironment could lead to new approaches against cancer.
Our cells are constantly receiving signals to grow, divide and perform many other functions. But when these signals get crossed, cells can no longer perform the jobs they’ve been assigned. In cancer, cells may ignore the instructions they’re receiving or accept entirely new instructions—to divide unchecked or migrate to another part of the body. If we can learn how these complex signals work, we can figure out ways to correct them when they go wrong.
Finding ways to trigger apoptosis, a mechanism that tells cells to self-destruct, holds great promise for new treatments that target cancer and other diseases. Sanford-Burnham research has led to a synthetic DNA-based drug that shuts off an anti-apoptosis gene in cancer cells, making them easier to kill with conventional chemotherapy. Numerous other possible therapies are under development. But it all comes down to one question: How do we convince errant cells to do the right thing and die?