Once cells became strong citrate utilizers, the initial gltA mutation became deleterious driving the evolution of a diversity of secondary mutations to compensate for its cost.
The mutation became relatively widespread amongst the current population.
Also, most QTL segregated in only one subspecies, suggesting that many mutations that affect the traits studied occurred after divergence of the subspecies or the mutation became fixed or was lost in one of the subspecies.
The tumor-specific mutation became undetectable prior to the second cycle of neoadjuvant chemotherapy and remained undetectable at nine subsequent time-points spanning12 months of follow-up (Fig. 5, Table 1), consistent with the absence of clinical recurrence.
When the mutation was associated with a mitochondrial genome that had a strong drive towards replication, the mutation became more widespread over time, and in most cases, this eventually resulted in the mutation killing the flies.
Indeed, by monitoring CTCs the acquisition of the recurrent T790M-EGFR drug resistance mutation became evident and coincided with the development of clinically refractory disease [ 55].
We also found that SOD1 protein bearing the G85R mutation became misfolded without increasing oxidative stress, showing the previously reported unstable nature of this mutant protein (24).
As a result, the mutation became more prevalent over time.
After 1956, however, a mutation became prevalent such that the recent sequences starting from A/Beijing/1/56 terminate after 57 codons.
Patient 16 acquired the F359V mutation on imatinib, and subsequently received an autologous HSCT and the mutation became undetectable by Sanger-sequencing.
