Nagesh Kalakonda

TL;DR: It is demonstrated that the malignant-brain-tumor protein L3MBTL1 is in a complex with core histones, histone H1b, HP1gamma, and Rb, and the MBT domain is structurally related to protein domains that directly bind methylated histone residues.

TL;DR: Tafasitamab in combination with lenalidomide was well tolerated and resulted in a high proportion of patients with relapsed or refractory diffuse large B-cell lymphoma having an objective response according to the 2007 International Working Group response criteria for malignant lymphoma.

TL;DR: Single-drug oral selinexor induced durable responses and had a manageable adverse events profile in patients with relapsed or refractory DLBCL who received at least two lines of previous chemoimmunotherapy, and could be considered a new oral, non-cytotoxic treatment option in this setting.

TL;DR: It is shown that transcriptional repression by L3MBTL1 is enhanced by the H4K20 monomethyltransferase PR-SET7 (to which it binds) but not SUV420H1 or G9a (an H3K9 dimethylase) and knockdown of PR- SET7 decreases H 4K20me1 levels and the chromatin association of L3 MBTL1.

TL;DR: It is demonstrated that CLL cells secrete exosomes that are nanovesicles originating from the fusion of multivesicular bodies with the plasma membrane, to shuttle proteins, lipids, microRNAs (miR) and mRNAs to recipient cells, and it is suggested that specific packaging of miR-202-3p into exosome results in enhanced expression of ‘suppressor of fused’ (Sufu), a Hedgehog signalling intermediate, in the parental