Wim Ammerlaan

TL;DR: It is demonstrated that CLL-derived exosomes actively promote disease progression by modulating several functions of surrounding stromal cells that acquire features of cancer-associated fibroblasts, contributing to a tumor-supportive microenvironment.

TL;DR: The results suggest that the telomere maintenance mechanism of B‐CLL cells do not preferentially use telomerase or ALT, and that the rupture of the dissolvasome/resolvasite balance may increase telomeres shuffling that could homogenize telomerre length, slowing telomer erosion in this disease.

TL;DR: It is shown that CLL-exosomes efficiently transfer nucleic acids, including functional microRNAs, and proteins, including MHC-Class II molecules and B-cell specific proteins, to bone marrow mesenchymal stem cells and endothelial cells, and that gene expression is strongly modified indicating a switch towards a cancer-associated fibroblast phenotype.

TL;DR: As downregulation of h topoisomerase III alpha could increase recombination rate between sister chromatid, methylation of hTERT and hTopoIIIa promoter CpG islands may lead to telomere dysfunction and increased genetic instability in B-CLL.