Research on Oral Cancer

Pre-cancer cells (in deep purple) penetrating the underneath stroma (light blue) under the effect of some stimulating molecules.

Written by Amani Hamza Ali Osman

It is widely accepted that oral cancer is caused by genetic aberrations (mutations) that occur in the cells that are lining the mouth cavity or in the cells of the salivary glands. However, it is now increasingly recognized that the other normal cells around the mutated cells have a large effect on the progression of cancer in terms of helping it to grow bigger and to invade other surrounding parts of the body.

How does oral cancer develop?

One fact about the cells lining the mouth, in which most of the genetic aberrations leading to oral cancer occur, is that they are rather compact and stationary, forming a membrane that works as a protective layer. To ensure this protective function they are tightly connected to each other. Another essential feature that allows this barrier to be effective all the time is that these cells proliferate and die at constant rates that balance each other. When cancer occurs, these cells that harbor genetic aberrations start growing nonstop, avoid dying, and some of them split apart from the mouth lining membrane and start invading and penetrating the close-by organs and the blood vessels so they can settle in new locations in the body and start new tumors there.

Bergen Oral Cancer Research Group

Part of the research we do at the Bergen Oral Cancer Group at The Gade Institute is to study the interactions between the mutated oral cells and the surrounding tissues in oral cancers.  Through this we are trying to understand how the mutated cells manage to transform themselves from cells that are tightly connected to the cells around them to free cells that can move around and find their way through barriers of the body defenses.

One theory explaining this change in behavior of cancer cells is that it is caused by stimulation from the normal cells surrounding the mutated cancer cells. There are various proposals on how this stimulation occurs, but most of them suggest that it occurs through the synthesis of some particular molecules of the activated, but normal surrounding host cells, which then influence and change the behavior of mutated cells.  Thus, what we do is to test some of the factors known to influence the motility of other cell types on oral cells with various degrees of genetic aberrations (normal cells, pre-cancer cells, cancer cells).  We harvest oral cells from volunteer patients and healthy volunteers, grow them in the lab, then add certain stimulating molecules to them and assess the possible effects of these molecules by looking at the way/speed the cells move, their pattern of growth, their renewal potential, and their expression of various molecules known to be important in cancer progression.

Challenges

This research outlined above is not as simple as it may seem, though. We are working with live cells from different patients and they are as different from each other as individuals are different from each other.  Thus, sometimes it is difficult to find a common clue for the changes we see in the cells’ behavior when exposed to a certain molecule. One way to overcome this is to gather cells from as many patients as possible so that a common trend is identified. Another way is to identify a set of trends and describe each of them in more detail, in the hope that the mechanisms discovered by us can be used in the future for individualized treatment of cancer. Any of these alternatives demands hard work, but if our efforts would succeed in recognizing essential factors responsible for this transformation, how they function, and how they can be impaired, then our work will open the door for new cancer treatment strategies.