Healthy Cells A Culprit For Poor Chemo Results
(Ivanhoe Newswire) — It is natural to blame chemo therapy failure on the malignant cancer cells themselves, but an unlikely antagonist has recently been identified: healthy stress response cells. These cells protect our organs in times of crisis, but new research shows that they may also be protecting cancer cells during chemo therapy.
In the process of organ homeostasis, the organ responds to stressful conditions by producing a stress signal that solicits help from protective molecules. When observing mice with thymus gland lymphoma, researchers reporting in the Cell Press Publication Cell found that the mice’s healthy cell response to the stress of chemo therapy protected both healthy cells and some surrounding cancer cells.
The stress signal is sent as a molecule called IL-6, and was found to permit the existence of cancer cells in the thymus. Since IL-6 is emitted by human liver cells during chemotherapy, the researchers combined the treatment with an IL-6 signal-blocking treatment, and found that the harmful cancer cells tended to die.
“Our data suggests that a combination of DNA damaging chemotherapy or radiation plus treatments designed to block pro-survival pathways would be the most potent therapy” researcher Michael Hemann of the Massachusetts Institute of Technology was quoted as saying. The researchers believe that their data provides hope for the future of chemotherapy, which they view as an unreliable treatment which ultimately fails to cure cancer victims.
Instead of only looking at changes within individual cancer cells when treating cancer patients, the Cell researchers want to look more at the external environment of the cells. In other words, immune stimulating molecules and growth factors within the specific location of the tumor’s microenvironment should now be considered when predicting the outcome of chemotherapy. Hemann points out that some locations are more protective than others, but that IL-6 exists in many of the body’s microenvironments.
SOURCE: Cell, October 2010