Cascade which Activates Cell Protection Programs (IMAGE)
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Researchers have known for some time that -- paradoxically -- oncogenes themselves can activate 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 the first program called 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 Clemens Schmitt, physician at Charité University Hospital Berlin, Germany and research group leader at the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, was able to show on an animal model for lymphoma that senescence can block the development of early-stage malignant tumors. Now, for the first time, Professor Schmitt and his team have provided evidence that the Myc oncogene plays a key role in the activation of both protection programs -- without the presence of the ras oncogene. "What is remarkable about this finding is that an oncogene can first trigger apoptosis and interact with the tumor stroma -- the tissue that surrounds the tumor which also contains healthy cells -- and with the immune system and then is able to switch on signals which lead to tumor senescence," Professor Schmitt said, summarizing how the interaction works.
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Clemens Schmitt
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