Editor’s note: As National Cancer Prevention Month winds to a close, the folks over here at Health Talk thought they’d gather together some expert voices to break down the science of cancer prevention. Here’s the first post in the series. Stay tuned in the coming days for more!
It is widely accepted that tumors arise primarily as a result of DNA mutations that cause cells to multiply and grow abnormally.
However, even non-tumor cells located in or next to the growing tumor can contribute to tumor growth and metastasis, which is the spread of tumors.
The surrounding tissue and non-tumor cells have been termed the “tumor microenvironment” and extensive studies have demonstrated that the tumor microenvironment is an active contributor to tumor cell growth and escape to other organs.
While the majority of treatments used for eradicating tumors are designed to specifically target and kill tumor cells, there is a wealth of evidence demonstrating that targeting both the tumor cells and the microenvironment is more effective than targeting the tumor cells alone. One reason is that targeting only the tumor cells leaves behind a fertile environment in which tumor cells that have escaped treatment can develop into a tumor once more.
Interestingly, upon examination of a tumor and its environment, it is clear that there are many events common to the normal wound healing process and the process of tumor formation that also help tumors grow and spread.
Similar to how a cut on the skin heals, during which inflammatory cells help increase the amount of nutrients to the area and help create a large number of new skin cells to replace damaged ones, tumor cells also recruit inflammatory cells to perform similar functions. This leads to increased nutrients available to tumor cells and the creation of more tumor cells.
The large number of inflammatory cells in the area that were intended to heal, often contribute to a reoccurrence of cancer – another form of too many unwanted cells in one area. Recent studies have demonstrated that inflammatory cells can sometimes actually help the tumors grow and spread to other organs.
Researchers are focused on understanding the similarities and differences between the mechanisms that drive these processes in hopes of identifying anti-inflammatory strategies that can be used to treat cancer patients and find the perfect balance between new cells helping and harming.
One example of inflammatory cells harming rather than helping can be seen in the macrophage.
Macrophage literally means “big eater”, and during the normal wound healing process, these cells are capable of engulfing and destroying invading pathogens. If given the correct instructions, these cells are also highly effective at destroying tumor cells.
However, tumor cells have figured out ways to outsmart the macrophages. The tumor cells exploit the macrophage’s ability to promote blood vessel growth and remodeling during wound healing, and use it to help tumor cells grow.
If we can understand how the tumor cells tell the macrophages to help them grow and whether we can take advantage of the macrophages and direct these cells to destroy the tumor cells, rather than help them, our understanding might ultimately lead to treatments that do a better job of targeting both the tumor cells and their surrounding environment.