Hooray to our team!!! See below for full details:
In case you’ve missed it, here is a short summary of what we discussed about in our recent “Cancer mosaic, traits, stratigies and adaptations” workshop – Cancer mosaic workshop photos (PDF).
Authors: Erika H. Dawson, Tiphaine P. M. Bailly, Julie Dos Santos, Céline Moreno, Maëlle Devilliers, Brigitte Maroni, Cédric Sueur, Andreu Casali, Beata Ujvari, Frederic Thomas, Jacques Montagne & Frederic Mery
Brief summary of the paper: The influence of oncogenic phenomena on the ecology and evolution of animal species is becoming an important research topic.
Similar to host–pathogen interactions, cancer negatively affects host fitness, which should lead to the selection of host control mechanisms, including behavioral traits that best minimize the proliferation of malignant cells. Social behavior is suggested to influence tumor progression. While the ecological benefits of sociality in gregarious species are widely acknowledged, only limited data are available on the role of the social environment on cancer progression.
Here, we exposed adult Drosophila, with colorectal-like tumors, to different social environments. We show how subtle variations in social structure have dramatic effects on the progression of tumor growth.
Finally, we reveal that flies can discriminate between individuals at different stages of tumor development and selectively choose their social environment accordingly. Our study demonstrates the reciprocal links between cancer and social interactions and how sociality may impact health and fitness in animals and its potential implications for disease ecology.
We are happy to share Jay Fitzpatrick‘s video assignment for honours 2018 @ Deakin University, exploring a scientific paper that discovered that thylacines were genetically doomed before human settlement in Australia.
Jay Fitzpatrick – Honours student, co-supervised with Dr Rodrigo Hamede from University of Tasmania.
Topic of research – “the role of the innate immune system in DFTD progression and epidemiology“.
Deakin University will collaborate with a group of French research institutions and the University of Tasmania on a new international cancer research laboratory, after a special agreement signed by French President Emmanuel Macron and Australian Prime Minister Malcolm Turnbull (May 2nd, 2018).
The collaboration will include formation of a Laboratoire International Associé – a ‘laboratory without walls’ – and will be part of a world-leading program established by France’s National Research Institute, the Centre National de la Recherche Scientifique (CNRS).
The laboratory project was spearheaded by Dr Beata Ujvari (leader of the Wild Genes Group), a Senior Lecturer in Bioinformatics and Genomics at Deakin’s Centre for Integrative Ecology within the School of Life and Environmental Sciences, and CNRS Research Director Frederic Thomas, both of whom will be Scientific Coordinators of the LIA.
According to Dr Ujvari the laboratory would reshape the conceptual landscape of cancer biology, evolutionary ecology and biology, breaking new ground in its transdisciplinary approach.
More details available @ Deakin Media Releases.
On behalf of all of us here with the Wild Genes Group, we would like to congratulate Beata Ujvari for being part of a successful project in the latest round of Linkage Projects announced by the Australia Research Council (ARC).
Project: Natural selection and the Tasmanian devil
Led by: Dr Rodrigo Hamede at University of Tasmania
Award amount: $300,000
Authors: Benjamin Roche, Beata Ujvari & Frédéric Thomas
Brief summary of the paper: Many biological systems are resilient to shock and have the ability to return to a previous state following a disturbance. In the case of cancer, this resilience may jeopardize our understanding of tumerous cell proliferation and presents many clinical problems, including therapeutic resistance.
Indeed, during progression and treatment, cancer has the capacity to exhibit resistance, resilience, and robustness, making its dynamics very challenging to forecast. Furthermore, organisms have evolved defenses that increase the robustness to mutations and other perturbations that can increase cancer susceptibility.
Authors: Kriti Ray, Beata Ujvari, Venkata Ramana & John Donald
Brief summary of the paper: Epidermal growth factor receptor (EGFR) is a known target in cancer therapy and targeting the receptor has proven to be extremely successful in treating cancers that are dependent on EGFR signaling.
To that effect, targeted therapies to EGFR such as Cetuximab, Panitumumab-monoclonal antibodies and Gefitinib, Erlotinib-tyrosine kinase inhibitors have had success in therapeutic scenarios. However, the development of resistance to these drugs makes it necessary to combine anti- EGFR therapies with other inhibitors, so that resistance can be overcome by the targeting of alternate signaling pathways.
On the other hand, components of the inflammatory pathway, within and around a tumor, provide a conducive environment for tumor growth by supplying numerous cytokines and chemokines that foster carcinogenesis. Interleukin 6 (IL-6) is one such cytokine that is found to be associated with inflammation-driven cancers and which also plays a crucial role in acquired resistance to anti-EGFR drugs. The EGFR and IL-6 signaling pathways crosstalk in multiple ways, through various mediators and downstream signaling pathways driving resistance and hence co-targeting them has potential for future cancer treatments.
Here we provide an overview on the crosstalk between the EGFR and IL-6 pathways, and discuss how co-targeting these two pathways could be a promising combination therapy of the future.
Brief summary of the paper: Genetic diversity is essential for adaptive capacities, providing organisms with the potential of successfully responding to intrinsic and extrinsic challenges. Although a clear reciprocal link between genetic diversity and resistance to parasites and pathogens has been established across taxa, the impact of loss of genetic diversity by inbreeding on the emergence and progression of non-communicable diseases, such as cancer, has been overlooked.
Here we provide an overview of such associations and show that low genetic diversity and inbreeding associate with an increased risk of cancer in both humans and animals. Cancer being a multifaceted disease, loss of genetic diversity can directly (via accumulation of oncogenic homozygous mutations) and indirectly (via increased susceptibility to oncogenic pathogens) impact abnormal cell emergence and escape of immune surveillance.
The observed link between reduced genetic diversity and cancer in wildlife may further imperil the long-term survival of numerous endangered species, highlighting the need to consider the impact of cancer in conservation biology.
Finally, the somewhat incongruent data originating from human studies suggest that the association between genetic diversity and cancer development is multifactorial and may be tumour specific. Further studies are therefore crucial in order to elucidate the underpinnings of the interactions between genetic diversity, inbreeding and cancer.
Authors: Frédéric Thomas, Camille Jacqueline, Tazzio Tissot, Morgane Henard, Simon Blanchet, Géraldine Loot, Erika Dawson, Frédéric Mery, François Renaud, Jacques Montagne, Christa Beckmann, Peter A. Biro, Rodrigo Hamede & Beata Ujvari
Brief summary of the paper: Reciprocal interactions between hosts, their symbionts and their oncobiota (cancer cell communities) are yet to be studied in detail. Considering malignant cells in addition to the holobiont perspective allows greater understanding of the processes governing both host phenotypes and cancer dynamics.