Cardenasgarcia7523

Cancer is a widespread disease that affects most of the metazoans. However, cancer development is a slow process and, long before causing the death of the individual, may weaken organisms' capacities and impair their interactions with other species. Yet, the impact of cancer development on biotic interactions, and over the dynamics of the whole ecosystem, is still largely unexplored. As well, the feedback of altered biotic interactions on the evolution of resistance against cancer in the context of community ecology has not been investigated. From this new perspective, we theoretically investigate how cancer can challenge expected interaction outcomes in a predator-prey model system, and how, in return, these altered interaction outcomes could affect evolution of resistance mechanism against cancer. First, we demonstrate a clear difference between prey and predator vulnerability to cancer, with cancer having a limited impact on prey populations. Second, we show that biotic interactions can surprisingly lead to a null or positive effect of cancer on population densities. Finally, our evolutionary analysis sheds light on how biotic interactions can lead to diverse resistance levels in predator populations. While its role in ecosystems is mostly unknown, we demonstrate that cancer in wildlife is an important ecological and evolutionary force to consider.Ecological and evolutionary concepts have been widely adopted to understand host-pathogen dynamics, and more recently, integrated into wildlife disease management. Cancer is a ubiquitous disease that affects most metazoan species; however, the role of oncogenic phenomena in eco-evolutionary processes and its implications for wildlife management and conservation remains undeveloped. Despite the pervasive nature of cancer across taxa, our ability to detect its occurrence, progression and prevalence in wildlife populations is constrained due to logistic and diagnostic limitations, which suggests that most cancers in the wild are unreported and understudied. Nevertheless, an increasing number of virus-associated and directly transmissible cancers in terrestrial and aquatic environments have been detected. Furthermore, anthropogenic activities and sudden environmental changes are increasingly associated with cancer incidence in wildlife. This highlights the need to upscale surveillance efforts, collection of critirategies for screening cancer incidence in wildlife and discuss how to integrate ecological and evolutionary concepts in the management of current and future cancer epizootics.Studies of model animals like mice and rats have led to great advances in our understanding of the process of tumorigenesis, but this line of study has less to offer for understanding the mechanisms of cancer resistance. Increasing the diversity of nonmodel species from the perspective of molecular mechanisms of natural cancer resistance can lead to new insights into the evolution of protective mechanisms against neoplastic processes and to a wider understanding of natural cancer defense mechanisms. Such knowledge could then eventually be harnessed for the development of human cancer therapies. We suggest here that seabirds are promising, albeit currently completely ignored candidates for studying cancer defense mechanisms, as they have a longer maximum life span than expected from their body size and rates of energy metabolism and may have thus evolved mechanisms to limit neoplasia progression, especially at older ages. We here apply a novel, intraspecific approach of comparing old and young seabirds for improving our understanding of aging and neoplastic processes in natural settings. We used the long-lived common gulls (Larus canus) for studying the age-related pattern of expression of cancer-related genes, based on transcriptome analysis and databases of orthologues of human cancer genes. The analysis of differently expressed cancer-related genes between young and old gulls indicated that similarly to humans, age is potentially affecting cancer risk in this species. Protein Tyrosine Kinase inhibitor Out of eleven differentially expressed cancer-related genes between the groups, three were likely artifactually linked to cancer. The remaining eight were downregulated in old gulls compared to young ones. The downregulation of five of them could be interpreted as a mechanism suppressing neoplasia risk and three as increasing the risk. Based on these results, we suggest that old gulls differ from young ones both from the aspect of cancer susceptibility and tumor suppression at the genetic level.It is increasingly suggested that ecological and evolutionary sciences could inspire novel therapies against cancer but medical evidence of this remains scarce at the moment. The Achilles heel of conventional and targeted anticancer treatments is intrinsic or acquired resistance following Darwinian selection; that is, treatment toxicity places the surviving cells under intense evolutionary selective pressure to develop resistance. Here, we review a set of data that demonstrate that Darwinian principles derived from the "smoke detector" principle can instead drive the evolution of malignant cells toward a different trajectory. Specifically, long-term exposure of cancer cells to a strong alarm signal, generated by the DNA repair inhibitor AsiDNA, induces a stable new state characterized by a down-regulation of the targeted pathways and does not generate resistant clones. This property is due to the original mechanism of action of AsiDNA, which acts by overactivating a "false" signaling of DNA damage through DNA-PK and PARP enzymes, and is not observed with classical DNA repair inhibitors such as the PARP inhibitors. Long-term treatment with AsiDNA induces a new "alarm down" state in the tumor cells with decrease in NAD level and reactiveness to it. These results suggest that agonist drugs such as AsiDNA could promote a state-dependent tumor cell evolution by lowering their ability to respond to high "danger" signal. This analysis provides a compelling argument that evolutionary ecology could help drug design development in overcoming fundamental limitation of novel therapies against cancer due to the modification of the targeted tumor cell population during treatment.