Fig. 8: Model describing how rapid, non-genetic drug adaptation can lead to bona fide drug resistance. | Nature Communications

Fig. 8: Model describing how rapid, non-genetic drug adaptation can lead to bona fide drug resistance.

From: Melanoma subpopulations that rapidly escape MAPK pathway inhibition incur DNA damage and rely on stress signalling

Fig. 8

Dabrafenib-treated melanoma cells initially use non-genetic mechanisms, such as ATF4 stress signalling, to adapt to and escape from drug-induced quiescence. These early drug-adapted escapees incur DNA damage while cycling in drug, yet out-proliferate non-escapees over extended drug treatment. Thus, escapees are more likely than non-escapees to acquire the genetic mutations that lead to permanent drug resistance.

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