In here presented what-if analysis we substitute a unified therapy with a ' therapy species', which is the population of heterogeneous therapies evolving accordingly to evolutionary principles. Each therapy within the species may be, at any time, either free or in the exclusive complex with one cell. The therapy is allowed to create the complex with another cell only after its current host cell has died, playing the role of a catalyst. Regarding therapeutic context, the fitnesses of the therapies reflect their respective cytotoxicities in a way which conforms to evolutionary causation. Results of the minimalistic in silico modeling indicate that the resistant cells could bias the evolution of the therapies towards more toxic ones by inhibiting non-efficient therapies. In this way , not only  therapies govern the evolution of different  phenotypes, but variable resistances of cells govern the evolution of  therapies as well  . As the evolutionary causation of cancer drug resistance has been intensively studied for a few decades, we refer to cancer as a special case to illustrate purely theoretical analysis.
In here presented in silico study we suggest a way how to implement the evolutionary principles into anti-cancer therapy design. We hypothesize that instead of its ongoing supervised adaptation, the therapy may be constructed as a self-sustaining evolutionary process in a dynamic fitness landscape established implicitly by evolving cancer cells, microenvironment and the therapy itself. For these purposes, we replace a unified therapy with the ` therapy species', which is a population of heterogeneous elementary therapies, and propose a way how to turn the toxicity of the elementary therapy into its fitness in a way conforming to evolutionary causation. As a result , not only the therapies govern the evolution of different cell phenotypes, but the cells' resistances govern the evolution of the therapies as well . We illustrate the approach by the minimalistic ad hoc evolutionary model. Its results indicate that the resistant cells could bias the evolution towards more toxic elementary therapies by inhibiting the less toxic ones . As the evolutionary causation of cancer drug resistance has been intensively studied for a few decades, we refer to cancer as a special case to illustrate purely theoretical analysis.
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in silico study we suggest a way how to implement the evolutionary principles into anti-cancer therapy design. We hypothesize that instead of its ongoing supervised adaptation, the therapy may be constructed as a self-sustaining evolutionary process in a dynamic fitness landscape established implicitly by evolving cancer cells, microenvironment and the therapy itself. For these purposes, we replace a
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therapies evolving accordingly to evolutionary principles. Each therapy within the species may be, at any time, either free or in the exclusive complex with one cell. The therapy is allowed to create the complex with another cell only after its current host cell has died, playing the role of a catalyst. Regarding therapeutic context, the fitnesses of the therapies reflect their respective cytotoxicities
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Results of the minimalistic in silico modeling indicate that the resistant cells could bias the evolution of the therapies towards more toxic ones by inhibiting non-efficient therapies. In this way
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. We illustrate the approach by the minimalistic ad hoc evolutionary model. Its results indicate that the resistant cells could bias the evolution towards more toxic elementary therapies by inhibiting the less toxic ones