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Mutations prevent programmed cell death in lymphoma

is a mechanism that causes defective and potentially harmful cells to destroy themselves. It serves a number of purposes in the body, including the prevention of malignant tumor growth. Now, researchers at () have discovered a previously unknown mechanism for regulating . They have also shown that patients with lymphoma often carry mutations in this signal pathway.

[Fluorescence microscopy image showing the ubiquitin ligase FBXO25 (green) and the
Fluorescence microscopy image showing the ubiquitin ligase FBXO25 (green) and the “life-preserving” protein (red) in a cancer cell that is currently undergoing programmed cell death. The yellow signal indicates instances where both proteins are at the same location.
Credit: Picture / TUM


Original publication: Baumann U., Fernández-Sáiz V., Rudelius M., Lemeer S., Rad R., Knorn A.M., Slawska J., Engel K., Jeremias I., Li Z., Tomiatti V., Illert A.L., Targosz B.S., Braun M., Perner S., Leitges M., Klapper W., Dreyling M., Miething C., Lenz G., Rosenwald A., Peschel C., Keller U., Kuster B., and F. Bassermann, Disruption of the PRKCD–FBXO25–HAX-1 axis attenuates the apoptotic response and drives lymphomagenesis, Nature Medicine, 20, 1401-1409 (2014). DOI: 10.1038/nm.3740

Technische Universitaet Muenchen