October 13, 2010
A recent Research Scholar Grant from the American Cancer Society acknowledges the potential of Rensselaer researcher Lee Ligon’s work on breast cancer. Ligon is investigating interactions between cells as breast cancer spreads within the body.
“We’re trying to figure out how cancerous and non-cancerous cells communicate with each other, how they bind to each other, and what the consequences of those interactions are,” Ligon said.
The Research Scholar Grant from the American Cancer Society includes a four-year $720,000 award to support this research.
“The Research Scholar Grant is a highly prestigious award for junior faculty. This grant acknowledges the importance of Dr. Ligon’s work in the field of cancer research and heralds a promising future of valuable insights and discoveries,” said Susan Gilbert, a Rensselaer professor and head of the department of biology.
Ligon studies cadherins, proteins that cause cells to adhere to one another, allowing cells to form organs and other structures. Different cadherins are expressed by different cells, each for its proper function.
“Cells have to stick together appropriately and if they express the same cadherin they will,” Ligon said. “But that only works in the normal situation when cells are sticking to cells that they’re supposed to stick to. We’re interested in the situation in tumors.”
More than 90 percent of all cancers, Ligon said, originate in epithelial cells – cells that form barriers between the inside and outside of the body, like skin cells, or the cells that line the intestines, or milk ducts in the breasts.
Because epithelial cells form a barrier between the inside and outside of the body, they must renew themselves more frequently than many other kinds of cells – like muscle or nerve cells. That presents more opportunity for abnormal cell division and cancer.
Most breast cancers originate in the epithelial cells that line milk ducts. In the early stages of the disease, the epithelial cells begin to grow abnormally, but are still confined within the lining of the milk ducts. At that point, the cancerous growth can still be excised with a surgeon’s knife.
But with continued growth, the cancerous cells break through the barrier between the lining and the surrounding tissue – the stroma – at which point they come into contact with a different type of cell called fibroblasts. Now the cancer is progressing into the body. Unchecked, it will reach the bloodstream at which point it becomes far more difficult to treat.
“Normally fibroblasts live in stroma, epithelial cells live in ducts, and they never make physical contact. They don’t come into contact with one another until there is pathological situation – cancerous cells have broken the membrane, and invaded the stroma,” Ligon said. “When that happens, they run into each other and we don’t know much about the consequences of that contact between epithelial cells and fibroblasts.”
In an earlier study, Ligon found that cancerous epithelial cells and fibroblasts do adhere to one another, despite expressing different cadherins.
“Everyone thought they wouldn’t stick together, but when we introduced mildly invasive cancerous epithelial cells to normal fibroblasts, a certain percentage stick together,” Ligon said.
“What we don’t know is whether that will happen with normal epithelial cells or more invasive cancerous epithelial cells and fibroblasts,” Ligon said. Those questions will form the basis for her next series of experiments, in which Ligon will introduce cancerous epithelial cells of varying invasiveness to healthy fibroblasts and observe the outcome.
Ligon said the results of her experiments could shed light on another puzzle: Whether her early results – in which the cancerous epithelial cells and healthy fibroblasts did adhere – bode ill or good for the patient.
“It is possible that this adhesion to these local cells is a good thing, in that it may be a barrier to stop metastasis. It’s also possible that it will cause these cells to be more invasive,” Ligon said.
Contact: Mary L. Martialay
Phone: (518) 276-2146
E-mail: martim12@rpi.edu