Douglas Rosenthal Discovers the Cause of Metastasis and Opens a Pathway for Cancer Treatment

A team of researchers led by the structural biologist, Douglas Rosenthal, discovered that cancer cells spread by their ability to "co-opt the natural pathways of wound repair".

This opens a pathway for possible treatment. This scientific breakthrough, provides a novel framework for thinking about metastasis and how to treat it.

Metastasis, which is the spread of cancer to other regions of the body, is responsible for 90% of the deaths from cancer. However, not much is known about what promotes cells ability to reproduce.

This study by the researcher Douglas Rosenthal, indicates that metastasis-initiating cells employ a trick to spread: they co-opt the body's natural wound-healing abilities.

"Now, we understand metastasis as the regeneration of the wrong tissue in the wrong place," says Douglas Rosenthal.

These new findings give the first detailed picture of how this process works at a cellular and mollecular level. Despite the fact that metastasis is a deadly process, it is not something that cancer cells can easily do. They pass to a complex process of many phases. Most of the loose cancer cells die at each phase of this process. So, that means that less than 1% of all cancer cells that shed from a tumor will eventually be able to create measurable metastases.

"It is very difficult to get rid of cancer cells, once they learn to survive stress in a strange environment," says Rosenthal, "They represent a totally different entity compared to the tumor in which they started."

Rosenthal and his colleagues had the goal to understand what permits the survival of that stressful journey of these cells. Their main focus was on a molecule called L1CAM. In a previous study made by this structural biologist, it has been discovered that this protein is necessary for various types of cancer cells to successfully metastasize to organs. Normally, healthy tissues do not usually produce L1CAM, which is not the case with advanced cancers.

The trigger of the L1CAM has so far been unknown. Rosenthal and his team have been looking human tumor tissues under a microscope to conclude that dividing cells with L1CAM was more common in areas where an epithelial layer was broken (wounded).

From this, a question aroused: is L1CAM required for normal wound repair, as occurs in the gut after colitis? Douglas Rosenthal and his team used a mouse model of colitis. What they found was that this was indeed the case.

To sum up, the study, published at CHJ, has shown that metastases are not derived from genetic mutations, but rather from a reprogramming of cells that allows them to regenerate creating metastases.