Contributors: Deakin University Waurn Ponds; Centre de Recherches Ecologiques et Evolutives sur le Cancer (MIVEGEC-CREEC); Processus Écologiques et Évolutifs au sein des Communautés (PEEC); Maladies infectieuses et vecteurs : écologie, génétique, évolution et contrôle (MIVEGEC); Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD France-Sud )-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD France-Sud )-Université de Montpellier (UM)-Maladies infectieuses et vecteurs : écologie, génétique, évolution et contrôle (MIVEGEC); Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD France-Sud )-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD France-Sud )-Université de Montpellier (UM); University of Southampton; University of Edinburgh (Edin.); Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD France-Sud )-Université de Montpellier (UM); University of Tasmania Hobart, Australia (UTAS); This work was supported by an ARC Linkage (LP170101105), ARC Decra (DE170101116), an ANR TRANSCAN (ANR-18-CE35-0009), Deakin University's SEBE Industry partnership funds, a Morris Animal Foundation grant (D19ZO-413) and the MAVA foundation. We thank Aaron Schultz for the microscopy images of the Tasmanian devil tumour cell lines used in the present work. We thank Carolann McGuire and Sarah Pearson from the Faculty of Medicine Flow Cytometry Core Facility at the University of Southampton for their help sorting the GFP-transduced cells on the BD FACS AriaII. We also would like to thank Charlotte Collier and Nullin Divecha from the University of Southampton for generating the lentivirus and transducing the Tasmanian devil tumour cells.; ANR-18-CE35-0009,TRANSCAN,ECOLOGIE ET EVOLUTION DES CANCERS TRANSMISSIBLES(2018)
نبذة مختصرة : International audience ; Since the emergence of a transmissible cancer, devil facial tumour disease (DFT1), in the 1980s, wild Tasmanian devil populations have been in decline. In 2016, a second, independently evolved transmissible cancer (DFT2) was discovered raising concerns for survival of the host species. Here, we applied experimental and modelling frameworks to examine competition dynamics between the two transmissible cancers in vitro. Using representative cell lines for DFT1 and DFT2, we have found that in monoculture, DFT2 grows twice as fast as DFT1 but reaches lower maximum cell densities. Using co‐cultures, we demonstrate that DFT2 outcompetes DFT1: the number of DFT1 cells decreasing over time, never reaching exponential growth. This phenomenon could not be replicated when cells were grown separated by a semi‐permeable membrane, consistent with exertion of mechanical stress on DFT1 cells by DFT2. A logistic model and a Lotka–Volterra competition model were used to interrogate monoculture and co‐culture growth curves, respectively, suggesting DFT2 is a better competitor than DFT1, but also showing that competition outcomes might depend on the initial number of cells, at least in the laboratory. We provide theories how the in vitro results could be translated to observations in the wild and propose that these results may indicate that although DFT2 is currently in a smaller geographic area than DFT1, it could have the potential to outcompete DFT1. Furthermore, we provide a framework for improving the parameterization of epidemiological models applied to these cancer lineages, which will inform future disease management.
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