Shlomi Constantini

TL;DR: The findings here suggest that neuronal stem/progenitor cells may be involved in gliomagenesis and provide the first example of a donor-derived brain tumor complicating neural stem cell therapy.

TL;DR: This report of initial and durable responses of recurrent GBM to immune checkpoint inhibition may have implications for GBM in general and other hypermutant cancers arising from primary (genetic predisposition) or secondary MMRD.

TL;DR: An extensive assessment of mutation burden through sequencing analysis of >81,000 tumors from pediatric and adult patients, including tumors with hypermutation caused by chemotherapy, carcinogens, or germline alterations, uncovered new driver mutations in the replication-repair-associated DNA polymerases and a distinct impact of microsatellite instability and replication repair deficiency on the scale of mutation load.

TL;DR: It is suggested that A-to-I RNA editing may serve as an additional epigenetic mechanism relevant to cancer development and progression, and altered epigenetic control was recently shown to play a central role in oncogenesis.

TL;DR: A new mechanism of cancer progression is suggested in which mutations develop in a rapid burst after ablation of replication repair, which implies a threshold compatible with cancer-cell survival.