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 Delbrück Center (MDC) Berlin-Buch and the Charité - University Hospital Berlin in Germany have shown that these two protection programs work together through an interaction with normal immune cells to prevent tumors. Their findings may be of fundamental importance in the fight against cancer (Cancer Cell, 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 Charité 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.
"Our findings promise to have fundamental significance for elucidating the pathogenesis not only of lymphoma cancers, but of cancer in general. Our results indicate that senescence triggered by the immune system's messenger molecules may be a further important active principle, apart from apoptosis induced by chemotherapy."
At present the researchers in Professor Schmitt's group are focusing intensively on chemotherapy-mediated senescence. "If by inducing senescence we could obtain a sustained suppression of the cancer cells we can no longer destroy, this would mean exciting new possibilities for therapy," Professor Schmitt said.
*Tumor Stroma-Derived TGF-? Limits Myc-Driven Lymphomagenesis via Suv39h1-Dependent Senescence
Maurice Reimann1,6, Soyoung Lee1,2,6, Christoph Loddenkemper3,6, Jan R. Dörr1,6, Vedrana Tabor2,6, Peter Aichele4, Harald Stein3, Bernd Dörken1,2, Thomas Jenuwein5, and Clemens A. Schmitt1,21Charité - Universitätsmedizin Berlin/Molekulares Krebsforschungszentrum der Charité - MKFZ, Berlin, Germany
Barbara Bachtler | Max-Delbrück-Centrum
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