It feels like the geographically structured oral mucosa undergoes 100s of contingency-like seed/soil experiments, with almost no mutant able to break out from their local niche, while in "well-mixed" blood we see a winner (1st or most advantageous mutant) takes all situation. Food for thought!

Congrats Iñigo for a(nother) great article. Figure 4a is my personal favourite finding, because of what it reveals about the role of tissue organisation in keeping clonal expansions in check.

I'd suggest forking out the money for a new keyboard. But since it's a Mac, you may have to talk to your bank first.

Big thanks and congratulations to my wonderful colleagues @mariaouzounova.bsky.social, Lauriane Muller, Frédérique Fauvet, Anne-pierre Morel & @cyrildegletagne.bsky.social

Our results however suggest that plasticity fosters prospective phenotypic diversification, which facilitates the emergence of “pre-adapted” cells, that are by chance already able to adapt to a given environmental change that hasn’t occurred yet.

We could not see evidence of selection of genetic clones harbouring specific CNAs, but our short (3w) timeframe and the limitations of our purely scRNA-seq-based data do not allow us to fully and accurately characterise selection and genomic evolution.

We used two in vitro TNBC models, in which EMT-driven plasticity was either induced by ZEB1 expression, or spontaneously occurred upon oncogenic transformation. We used single-cell cloning experiments and scRNA-seq data pre and post doxorubicin treatment to investigate phenotype dynamics.

We were interested in the impact of EMT-driven plasticity on the dynamics of phenotypic diversity. And, in particular, whether plasticity-mediated resistance is a prospective or a reactive process.