Elisa ten Hacken

Abstract Ribosomal protein mutations are increasingly associated with cancer risk and thought to perturb ribosome function. At the same time, they reportedly activate p53, a critical anti-cancer barrier. To determine how these mutations overcome this protective block to enable tumorigenesis, we generate an in vivo model of the hotspot ribosomal protein RPS15-S138F mutation identified as a putative driver of chronic lymphocytic leukemia.

Addendum to: Nature Medicine https://doi.org/10.1038/nm.3562, published online 11 May 2014. The Editors would like to alert the readers that concerns have been raised regarding some of the data presented in the figures of this article, specifically: Fig. 1a: MM-001 and MM-003 appear to overlap with different brightness and magnification. Fig. 2a: WT MM.1S Nucleus p84 blot appears highly similar to Supplementary Fig. 3b Nucleolin (flipped horizontally). Fig.

Genome and Epigenome Anat Biran, Shanye Yin, Helene Kretzmer, Elisa ten Hacken, Salma Parvin, Fabienne Lucas, Mohamed Uduman, Catherine Gutierrez, Nathan Dangle, Leah Billington, Fara Faye Regis, Laura Z. Rassenti, Arman Mohammad, Gabriela Brunsting Hoffmann, Kristen Stevenson, Mei Zheng, Elizabeth Witten, Stacey M. Fernandes, Eugen Tausch, Clare Sun, Stephan Stilgenbauer, Jennifer R. Brown, Thomas J. Kipps, John C. Aster, Andreas Gnirke, Donna S. Neuberg, Anthony Letai, Lili Wang, Ruben D.