Breast, lung and colorectal cancer diagnosed and treated early can be surgically removed with success, but if the cancerous cells have already entered the bloodstream at the time the tumor is surgically removed, the danger of a secondary tumor elsewhere in the body is a serious cause for worry.

But not all roaming cancer cells become a secondary tumor, which leaves the question as to what is happening to encourage or suppress additional cancer. According to University of Liverpool researchers, the answer is found in a large protein called MUC1.

MUC1 acts as a protective shield, thereby allowing our immune system a chance to destroy the rogue cancer cells. When the protein shield fails, cancerous cells can begin to develop into a new tumor.

University's School of Clinical Sciences Dr Lu-Gang Yu explains, "MUC1 on the cell surface prevents the cancer cells from attaching to the blood vessel wall which causes secondary tumors. We have discovered that a small protein called galectin-3, attacks MUC1 and breaks up its protective shield, forcing large areas of the cancer cell to become exposed. The exposed areas of the cell allow the cancer to attach to the blood vessel wall. The cancer cells then eventually penetrate the blood wall to form tumors at secondary sites."

As more scientific discoveries into the mechanisms and spread of cancer are revealed, the less mysterious it will be in determining ahead of time who is at most risk of cancer recurrence. More importantly, new treatments might be developed that stop the process in those most at risk for a secondary cancer.