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Missing Receptor Molecule Causes Tumor Growth

A missing receptor molecule contributes to the growth of tumors in human ovaries. This surprisingly evident connection has now been proven by a team at the Medical University of Vienna, who published their data in the science journal Molecular Cancer Research. The team, who is supported by funding from the Austrian Science Fund FWF, also discovered the possible genetic reason why the receptor molecule, which is an important factor in regulating cell growth, is missing.

In healthy tissue, cells grow and divide - this is also true of cancerous tumors. The difference between the two lies in the regulation, which functions well in healthy tissue, but not in tumors. An important mechanism of this regulation is programmed cell death, known as apoptosis. It causes the controlled death of single cells, if this is to the advantage of the whole organism. If this process of self-protection does not work then the destructive cells can proliferate uncontrollably.

Signal Without Effect
Prof. Michael Krainer and his team from the Medical University of Vienna have now been able to prove that programmed cell death does not function in cells of certain tumors in the ovaries. Not because the starting signal is missing, but because this signal cannot be received by the cell.

This finding, published today in the American science journal Molecular Cancer Research, shows that these cells lack a receptor molecule called DR4. DR4 is responsible for receiving the signal molecule TRAIL, which initiates apoptosis in these cells.

Prof. Krainer explains: "To begin with it was not evident what was missing in the signal transmission. The signal or the receptor molecule? To answer this question, we examined ten different ovarian cancer cell lines. In doing this we found out that 40% of these specimens contained none or only a few DR4 receptor molecules." It was proven in further tests that these cells react particularly badly to TRAIL. This proves that the missi
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Source:Medical University of Vienna


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