The evolution of resistance to diseases, from infectious illnesses to cancers, poses a formidable challenge.
Despite the expectation that resistance-conferring mutations would dwindle in the absence of treatment due to a reduced growth rate, preexisting resistance is pervasive across diseases that evolve—like cancer and pathogens—defying conventional wisdom.
In cancer, it is well known that small numbers of drug-resistant cells likely exist in tumors even before they’re treated. In something of a paradox, before treatment, these mutants have been repeatedly shown to have lower fitness than the surrounding ancestor cells from which they arose. It leads to a scenario that seems to break Darwin’s rules: Why do these least fit cells survive?
In a new study, researchers at Case Western Reserve University and Cleveland Clinic reveal a fascinating discovery: Interactions between these mutants and their ancestors, like two species in an ecosystem, may hold the key to understanding this paradox.
Their findings suggest these ecological interactions play a pivotal role in reducing the costs of resistance, providing a path to survival for preexisting resistance. And not just in lung cancer, but across various biomedical contexts where drug resistance is a challenge, including other cancers, pathogens and even parasites.