Chemotherapy for metastatic cancer commonly fails due to evolution of drug resistance in tumor cells. Here, we view cancer treatment as a game in which the oncologists choose a therapy and tumors “choose” an adaptive strategy. We propose the oncologist can gain an upper hand in the game by choosing treatment strategies that anticipate the adaptations of the tumor. In particular, we examine the potential benefit of exploiting evolutionary tradeoffs in tumor adaptations to therapy. We analyze a math model where cancer cells face tradeoffs in allocation of resistance to two drugs. The tumor “chooses” its strategy by natural selection and the oncologist chooses her strategy by solving a control problem. We find that when tumor cells perform best by investing resources to maximize response to one drug the optimal therapy is a time-invariant delivery of both drugs simultaneously. However, if cancer cells perform better using a generalist strategy allowing resistance to both drugs simultaneously, then the optimal protocol is a time varying solution in which the two drug concentrations negatively covary. However, drug interactions can significantly alter these results. We conclude that knowledge of both evolutionary tradeoffs and drug interactions is crucial in planning optimal chemotherapy schedules for individual patients.

Our results indicate that the elimination of HR HPV through vaccines may alter the evolutionary trajectory of the remaining types and promote evolution of new HR HPV types.

We apply competition colonization tradeoff models to tumor growth and invasion dynamics to explore the hypothesis that varying selection forces will result in predictable phenotypic differences in cells at the tumor invasive front compared to those in the core. Spatially, ecologically, and evolutionarily explicit partial differential equation models of tumor growth confirm that spatial invasion produces selection pressure for motile phenotypes. The effects of the invasive phenotype on normal adjacent tissue determine the patterns of growth and phenotype distribution. If tumor cells do not destroy their environment, colonizer and competitive phenotypes coexist with the former localized at the invasion front and the latter, to the tumor interior. If tumors cells do destroy their environment, then cell motility is strongly selected resulting in accelerated invasion speed with time. Our results suggest that the widely observed genetic heterogeneity within cancers may not be the stochastic effect of random mutations. Rather, it may be the consequence of predictable variations in environmental selection forces and corresponding phenotypic adaptations.

Summary1. Plants defend and predators attack, provoking the foraging dilemma faced by herbivores and frugivores of how to eat enough without being eaten. High toxin concentration in leaves and fruits inhibits consumption, while predation risk reduces feeding opportunities, as prey forage to avoid encountering predators. Thus, both factors vary and define the quality of the landscape. How foraging animals directly quantify, compare and respond to these two costs has rarely been tested. 2. We show that free-ranging bushbabies -small, frugivorous primates -change their behaviour and use of artificial food patches based on the interplay between toxin concentration in food and patch safety. Using a titration experiment, we demonstrate that bushbabies quantify the relative costs of toxin and fear. We pinpoint where these costs are equivalent and show that animals seek food patches with the lower net cost. 3. We conclude that the ecological effectiveness of plant toxins as defence against consumers needs to be considered in the context of a landscape of fear -and the relative impact of antipredator tactics and plant defence is strongly shaped by the concentration of these defences. 4. A corollary is that plants may benefit from fear as a substitute for their own chemical defence, adding a new dimension to the concept of indirect plant defence. Whether, from the plant's perspective, the benefits derived from fear can be considered evolutionarily adaptive rather than simply ecologically serendipitous remains to be tested.

Should parasites stabilize or destabilize consumer–resource dynamics? Recent theory suggests that parasite‐enhanced mortality may confer underappreciated stability to their hosts. We tested this hypothesis using disease in zooplankton. Across both natural and experimental epidemics, bigger epidemics correlated with larger—not smaller—host fluctuations. Thus, we tested two mechanistic hypotheses to explain destabilization or apparent destabilization by parasites. First, enrichment could, in principle, simultaneously enhance both instability and disease prevalence. In natural epidemics, destabilization was correlated with enrichment (indexed by total phosphorous). However, an in situ (lake enclosure) experiment did not support these links. Instead, field and experimental results point to a novel destabilizing mechanism involving host stage structure. Epidemics pushed hosts from relatively more stable host dynamics with less‐synchronized juveniles and adults to less stable dynamics with more‐synchronized juveniles and adults. Our results demonstrate how links between host stage structure and disease can shape host/consumer–resource stability.