Baker and colleagues develop GRITIC, a novel Bayesian method for timing complex tumor events. It estimates the timing of clonal gains, accounting for whole genome doublings, using single-sample bulk whole genome sequencing data. Applied to 6,091 primary and metastatic tumors, it revealed that complex copy number states in genomedoubled tumors often arise through non-parsimonious histories. The authors found that genome doublings have a greater impact on the landscape of losses than gains, although late doublings often lead to an increased rate of copy number gains.

See article, p. 1810.

The etiology of meningiomas, the most common type of intracranial tumor, is poorly understood, as are mechanisms of resistance to standard treatment such as radiotherapy in high-grade tumors. Choudhury, Cady, and colleagues show that NOTCH3+ cells are conserved in the perivascular stem cell niche across vertebrate meningiomas and use single-cell transcriptomic profiling and lineage tracing in mouse models of...

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