Mechanism involved in breast cancer’s spread to bone uncovered
By ANIFriday, February 4, 2011
WASHINGTON - A team of Princeton University scientists has discovered a mechanism involved in breast cancer’s spread to bone, which may lead to a new treatment for the disease.
Cancer cells often travel throughout the body and cause new tumours in individuals with advanced breast cancer - a process called metastasis - commonly resulting in malignant bone tumours.
And what the new research has uncovered is the exact mechanism that lets the traveling tumour cells disrupt normal bone growth.
Breast cancer spreads to the bone in 70 to 80 percent of patients with advanced breast cancer, and it can also spread to the brain, lung and liver.
The team’s findings shows that breast tumour cells are able to give bone cells the wrong instructions through a process known as cell signaling -with disastrous effects for the patient.
The billions of cells in a living human body must communicate to develop, repair tissue, and effectively maintain normal physiological functions. Cell signaling is part of a complex system that enables them to do that.
But, in patients with cancer, the relationship between signaling molecules and the molecules that communicate with them has gone awry.
Signaling molecules are those that can be received and read by a cell through a receptor molecule on its surface. Once the signaling molecules connect with a receptor, their union sets off a process that leads to the receiving cell changing its behavior.
The sequence of events that follows involves a signaling pathway, which is a group of molecules that work together, one molecule activating the next until a specific function is carried out, such as renewing an organ’s cells. There are many such signaling pathways.
But in the case of metastatic breast cancer, a disruptive pathway is formed. The signaling molecule, also known as a ligand, connects with a receptor molecule on certain bone cells and activates a cellular pathway that ultimately disrupts healthy bone renewal.
Kang’s team identified the signaling molecule as Jagged1, and the receptor molecule as one that activates a cellular pathway known as the “Notch pathway.”
The study has been published online in the journal Cancer Cell. (ANI)
