Despite deep cuts in federal research spending due to sequestration, Associate Professor Muhammad Zaman (BME, MSE) has secured a five-year grant of more than $3 million from the National Institutes of Health to develop mathematical and computational models of how breast cancer cells move and communicate as they migrate from tumors, invade nearby tissue and proliferate.
By mapping this process from the molecular to the cellular level through detailed, comprehensive multiscale models based on strong experimental and computational data, Zaman and his collaborators—MIT Professors Frank Gertler, Roger Kamm and Douglas Lauffenberger, and a computational modeling team in Singapore—aim to uncover new pathways to control tumor development and metastasis in the breast, lung, and other organs.
Complex biochemical and biomechanical interactions govern how cancer cells spread from tumors and metastasize in nearby tissue. Much is known about the mechanics of how cancer cells migrate, but how biochemical signaling within and among the cells drives that motion remains elusive.
“Imagine we know a car needs fuel for its engine to run, and we want to figure out how that fuel interacts with the engine to make it run,” said Zaman. “Similarly, we’re trying to find out how biomechanical and biochemical components of a cancer cell interact to propel that cell from a tumor to surrounding tissue.”
Through their unprecedented effort to develop three-dimensional, multiscale models of the biomechanical motion and biochemical signaling of cellular proteins associated with breast cancer, the researchers hope to establish how these two phenomena work together to drive cancer cell migration, invasion and metastasis.
“The goal is to understand how specific signaling proteins which may be responsible for cancer—in this case breast cancer—are playing a role interacting with mechanical components of the cell in regulating its behavior,” said Zaman, who has developed several three-dimensional models of the mechanics of cancer cell migration. “Understanding this may allow us to develop specific therapies that can block that process, and thus give us a bigger repertoire of targets to stop cancer cells in their tracks,” he said.