note to self, incase I forget why I put this in Mendeley: people keep using the word "induce" in tumour evolution stories, when one event tends to follow another, and I'm not entirely convinced that it's being used correctly. But I need to think about it some more.
In addition, emerging evidence that loss of RB1 function can induce genomic instability has raised the tantalizing possibility that RB1-deficient retinal cells might be predisposed to accumulating many additional mutations…
also, looks like there should be a story worth telling here:
The researchers found that RB1 was the only known cancer-related gene consistently mutated, and that the retinoblastomas had 15-fold fewer total mutations than other types of solid tumour whose genomes have been sequenced.
…
Low mutation frequency has also been observed in medulloblastoma (a type of brain tumour that affects children), suggesting that it could be a general feature of childhood cancers. A possible explanation for this difference between the cancers of children and adults is that childhood tumours arise in cells that are naturally undergoing rapid developmental growth, with fewer brakes on their proliferation than cells in adults. An alternative explanation is that, in children, these cells are negotiating crucial developmental checkpoints that are susceptible to corruption, leading to incomplete or abnormal maturation. In both cases, only a few mutations would be needed to trigger the cellular changes associated with cancer.