YB-1 elicits deficient cell division leading to genetic instability and tumorigenesis. Results generated in cooperation with scientists from the Heinrich Heine University, Düsseldorf, the Charité of the Humboldt University, Berlin, the Max Delbrück Center for Molecular Medicine, Berlin-Buch and the German Cancer Research Center, Heidelberg have been published in the current issue of renowned US science journal Cancer Research.
Researchers are convinced that the insights offer new approaches in breast cancer therapy. About five percent of breast cancer incidences are hereditary (mutations in the BRCA1 and BRCA2 genes). In contrast, the precise pathogenesis mechanism is mainly unknown in 95 percent of cases.
In previous studies, Dr. med. Hans-Dieter Royer's team of caesar scientists was able to demonstrate that YB-1, a stress inducible human protein, is aberrantly expressed in breast cancer cells and is related to resistance against chemotherapy. YB-1 regulates cell proliferation and further biological processes related to cellular defense against environmental stressors. Increased concentrations of YB-1 in breast tissue cells lead to cell division as demonstrated in transgenic mice.
However, cell division actuated by YB-1 is deficient and induces genetic instability: for example, surplus chromosomes, as discovered by the researchers. It is precisely this mechanism that provokes the development of breast cancer in transgenic animals.
In human cancer cells, the numbers and structures of chromosomes are frequently altered. It is a hotly debated issue whether genetic instability is a cause or consequence of tumorigenesis. The caesar researchers' results indicate that YB-1 induced genetic instability is a cause rather than a consequence of breast cancer development.
MEDICA.de; Source: Caesar