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uni'wissen 01-2016_ENG

find its weak spot. Brummer sees a personalized medicine that treats each patient individually as only achievable through interdisciplinary coop- eration. Tumor conferences hosted by members of the German Consortium for Translational Can- cer Research are one means of promoting such cooperation. Cancer typically begins with the mutation of a gene belonging to one of two classes: the onco- genes or the tumor suppressors. An oncogenic protein drives the growth of a cancer tumor. When the underlying gene is not mutated, it is referred to as a proto-oncogene. Its products are proteins that play an important part in the trans- mission of signals in the cell. In wound healing, for example, the Ras/B-Raf/MEK/ERK pathway interacts with several proto-oncogenes. Brum- mer is focusing on an important component of this signaling pathway, the protein B-Raf: He is conducting research to determine how the body of mammals regulates this protein, when a mutation appears in the BRAF gene, and which mechanisms enable a tumor to spread. For a wound to close, the skin cells must multiply and move toward each other. The blood platelets secrete so-called growth factors that switch on a receptor in cells in the wound. This receptor then activates the protein Ras to set the signaling chain in motion: Ras activates B-Raf, B-Raf activates MEK, and MEK activates ERK. ERK migrates to the cell nucleus and causes the cell to divide. This involves a series of steps: “The protein ERK controls hundreds of different processes in the human cell,” says Brummer. When the RAS or BRAF genes mutate and be- come oncogenes, the signaling pathway is always switched on, and the cells keep on multiplying: A cancerous ulcer develops. The Antagonist’s Blueprint Tumor suppressors are genes that provide the blueprint for the antagonist of the proto- oncogene proteins. The body uses the proteins transcribed from these genes to protect itself from mutated cancer cells. For example, they can initiate their cell death. “A tumor suppressor product is like the brakes of a car,” Brummer explains. “Proto-oncogenes, on the other hand, work like a gas pedal.” The car needs to increase its speed from time to time to keep moving, but it can’t keep on accelerating forever. “You might say an oncogenic mutation blocks the gas pedal. If the brakes don’t work either, you’ll soon have an accident.” A common mutation of the BRAF gene is the V600E mutation. When the cell fails to repair this modification, it assembles the protein in B-Raf Lung cancer cells with a so-called Ras mutation under the microscope. The cell nuclei are shown in blue, the cytoskeleton in green. Photos: Florian Weinberg/AG Brummer “A tumor suppressor product is like the brakes of a car.” 9