Loss of Cell Acidity Is Enough for Dysplasia

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Further, we show lethality in invasive, primary tumor cell lines with inhibiting H+ efflux. Synthetic lethality with reduced H+ efflux and activated oncogene expression could be exploited therapeutically to restrain cancer progression while limiting off-target effects.

Increased H+ efflux is sufficient to induce dysplasia and necessary for viability with oncogene expression