Cells have two different protection programs to safeguard them from getting out of control under stress and from dividing without stopping and developing cancer. Until now, researchers assumed that these protective systems were prompted separately from each other. Now for the first time, using an animal model for lymphoma, cancer researchers of the Max Delbrck Center (MDC) Berlin-Buch and the Charit University Hospital Berlin in Germany have shown that these two protection programs work together through an interaction with normal immune cells to prevent tumors. The findings of Dr. Maurice Reimann and his colleagues in the research group led by Professor Clemens Schmitt may be of fundamental importance in the fight against cancer (Cancer Cell, Vol. 17, Issue 3, 16 March 2010, pp. 262-272; DOI 10.1016/j.ccr.2009.12.043)*.
Researchers have known for some time that paradoxically oncogenes themselves can activate these cell protection programs in an early developmental stage of the disease. This may explain why some tumors take decades to develop until the outbreak of the disease. The Myc oncogene triggers apoptosis (programmed cell death), inducing damaged cells to commit suicide in order to protect the organism as a whole. By means of chemotherapy, physicians activate this protection program to treat cancer.
The second protection program not as well understood as apoptosis is senescence (biological aging). This program is triggered by another oncogene, the ras gene. Senescence stops the cell cycle, and the cell can no longer divide. But in contrast to apoptosis the cell continues to live and is still metabolically active. Professor Schmitt, physician at Charit University Hospital and research group leader at the MDC, was able to show on an animal model for lymphoma that senescence can block the development of early-stage malignant tumors.
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|Contact: Barbara Bachtler|
Helmholtz Association of German Research Centres