This is reported by Dr. Daniel Peeper and his colleagues from the Netherlands Cancer Institute - Antoni van Leeuwenhoek Hospital (NKI-AVL) in the June 13 issue of the prominent scientific journal Cell.
The cells in our body are exposed to numerous factors that can inflict damage to the genetic material (DNA). Usually, these errors are repaired. Sometimes, however, a change is incorporated into the DNA. If such a mutation localises to a so-called oncogene, a cell can be stimulated to divide, and a benign tumour can arise. Previously, the research group of Dr. Peeper showed that this does not necessarily result in the generation of a malignant tumour. They discovered that benign tumours can activate a permanent growth arrest, such that they enter a hibernation-like state (Nature, Aug 4th 2005). This hibernation represents a natural barrier against cancer.
In the present follow-up study, Thomas Kuilman, a PhD student in Dr. Peeper’s research laboratory, delineated the mechanism behind this hibernation in benign tumours. He compared the activity of thousands of genes in dividing and dormant tumour cells and discovered a specific DNA fingerprint. Unexpectedly, this revealed that in non-dividing tumour cells, dozens of genes that normally play a role in inflammatory reactions of the body, are activated.
In collaboration with Dr. Lucien Aarden (Sanquin), the researchers subsequently used advanced techniques to show that inflammatory proteins are essential to keep benign tumour cells in a non-proliferating state. Finally, together with Dr. Wolter Mooi (VUmc) the researchers showed that these inflammatory proteins are likely to play an important role in the natural defence against colon cancer.
Frederique Melman | alfa
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