Cancer needs blood. In fact, some cancer medications work solely to slow or prevent cancer cells from creating new capillaries, choking off their much-needed blood and nutrient supply to halt the growth of tumors.
In a paper published online Aug. 8 in the Proceedings of the National Academy of Sciences, researchers at Stanford University describe the creation of a new type of engineered protein that is significantly more effective at preventing the formation of blood vessels by targeting not one, but two of the chemical receptors that control the creation of new capillaries - a process known as angiogenesis. The study shows that the new protein blocks both receptors.
"Chemical receptors and their protein ligands control many cellular functions, but the protein must fit the receptor exactly. It's like a molecular jigsaw puzzle," said lead researcher Jennifer Cochran, PhD, assistant professor of bioengineering. "When the right proteins come along and engage their matching receptors, things begin to happen at the cellular level. In this case, we looked at the chemical signaling and cellular machinery responsible for producing new blood vessels."
Existing cancer treatments block the activity of specific receptors that control capillary creation. Some of these drugs act like a cork in a bottle, occupying the receptor and thus preventing capillary-inducing proteins from activating cell signaling and biochemical processes, while others attach to the capillary-inducing proteins and shield the receptor from them.
Complicating matters for cancer researchers, however, is the fact that angiogenesis is often controlled by multiple receptors working together. "Cell-signaling pathways are analogous to a safe-deposit box requiring many keys to open," said Cochran.
Cochran's team including postdoctoral scholars Niv Papo, PhD, Adam Silverman, PhD, and Jennifer Lahti, PhD, who was a graduate student at the time of the research
|Contact: Andrew Myers|
Stanford School of Engineering