We still don’t know everything about cancer, but a new NYU study discovered just one more piece of the puzzle on our way to understanding tumor formation.
Cancer experts have established how cancer cells compete amongst themselves for resources. But there are still unanswered questions about how cancer cells turn into tumors that lead to diagnosis.
A new study published in Nature in February looks at the way cancer cells cooperate with each other to eventually form tumors. It was conducted by New York University (NYU) and its findings lit up the scientific world, as it might lead to ways experts can interrupt the life cycle of a tumor before it becomes aggressive. It’s especially remarkable because cooperation among cancer cells hasn’t been given a lot of attention.
Current Understanding of Cancer
Cancer is caused by human cells that essentially go renegade, according to Dr. Adeel Khan, MD. He explains, “A cancerous cell has stopped responding to the normal signals of growth and death. It abnormally grows and divides, so if a cell becomes carcinogenic, it doesn’t stop changing.”
Per Dr. Khan, the formation of tumors is still a mystery. Some tumors have more structure to them than others.
“This article looked at something called the Allee effect, in which there’s a minimum number of cells that is needed for a self-sustaining environment or else they’ll die off,” he says.
Cooperation Among Cancer Cells
Nature’s published study was conducted by Dr. Carlos Carmona Fontaine and involved adding cancer cells into test tubes, adding a variety of nutrients in their environment, and looking at their reactions in specialized equipment, including a robotic microscope. This created opportunities to look at various tumors at a time in a controlled environment and more easily track and compare their growth. Special software allowed researchers to more accurately track their findings.
NYU’s study isolated the CNDP2 enzyme, which cancer cells leave behind after they digest amino acids.
According to Nature, the drug bestatin was effective in preventing the CNDP2 to continue its course, and prevented tumor cells from working together.
Essentially, this means that by stopping tumor cells from cooperating within their own systems, scientists might have found a way to force cancer cells to stop competing with each other for nutrients, creating ecosystems that allow them to thrive, and essentially cause malignant cells to die.
Since these results were gathered from test tubes, applying the lessons learned from these studies might still be a challenge. These findings are bound to provide a new direction for scientists who want to find ways to interrupt the formation of certain tumors before they become fully grown.
Dr. Khan explains, “In a given small population of cancer cells there’s a lot of heterogeneity because these cells don’t stop mutating. They acquire more abnormalities as time goes on. So I am sure that even if we then block this pathway more enzymes could come up.”
In the field, Dr. Khan likens these changes to drug resistance in tumors that might force oncologists to change or switch therapies as they deal with patients because tumors continue to evolve as cells replicate.
Even so, finding even one key enzyme and monitoring how different cancer cell lines react created excitement about the possibility to interrupt the growth cycle of tumors.
