Discussion about this post

User's avatar
R Tyler's avatar

Obligatory context: I was skeptical at first, coming from cancer bioinformatics and somatic mutation research. However, I turned around quickly and this is quite an excellent concept.

I think oncologists will find utility from incorporating phylostratigraphy during somatic mutation profiling.

Is the atavistic reversion happening at the single-gene level or systems level?

Many of the ubiquitous drivers (oncogenes and tumor suppressor genes, TSGs) are very ancestral genes. So perhaps the oncogenic mutant states are a primitive, less-regulated form. And perhaps the TSGs are younger overall?

Would love to see PPI and GRN systems diagrams arranged by evolutionary age and overlaid with mutation frequency. And how this relates to 3D genome architecture, epigenetics, and replication timing.

Expand full comment

No posts