Marek Wanior

TL;DR: A series of chemical degraders (PROTACs) are developed by connecting a clinical kinase inhibitor of AURORA-A to E3 ligase-binding molecules (for example, thalidomide) and induces the fast and specific degradation of this kinase in cancer cell lines, which enables targeting of non-catalytic, oncogenic functions of Aurora-A resulting in S-phase arrest and rampant apoptosis.

TL;DR: In this article, the authors reviewed the importance of SWI/SNF chromatin remodellers in gene regulation as well as mechanisms leading to assembly defects and their role in cancer development.

TL;DR: Development of a selective ligand of the fifth BRD of polybromo protein-1 related to switch/sucrose nonfermenting (SWI/SNF) chromatin remodeling complexes is presented and the most potent analogue demonstrated high affinity and an excellent selectivity profile.

TL;DR: Co-targeting of histone acetylation by concomitant inhibition of HDAC and BET proteins synergistically induces mitochondrial apoptosis by shifting the ratio of pro- and antiapoptotic BCL-2 proteins towards apoptosis.

TL;DR: It is found that JQ1 treatment decreases the numbers of pre-, immature and mature B cells while numbers of early pro-B cells remain constant, and increases apoptosis in T cells, all together leading to reduced cellularity in thymus, bone marrow and spleen.