Can species be genetically doomed? Watch Jay’s video assignment for honours 2018 @ Deakin University

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“.

French president signs off on new cancer research collaboration with Deakin

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.

4th International Biannual Evolution & Cancer Conference(Resistance, resilience and robustness: can we target cancer’s evolutionary and ecological nature?)

Authors: Benjamin Roche, Beata Ujvari & Frédéric Thomas

SourceEvolutionary Applications (21 February 2018)

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.

Cross-talk between EGFR and IL-6 drives oncogenic signaling and offers therapeutic opportunities in cancer

Authors: Kriti Ray, Beata Ujvari, Venkata Ramana & John Donald

Source: Cytokine & Growth Factor Reviews (Available online 7 April 2018)

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.

Genetic diversity, inbreeding and cancer

Authors: Beata Ujvari, Marcel Klaassen, Nynke Raven, Tracey Russell, Marion Vittecoq, Rodrigo Hamede, Frédéric Thomas, Thomas Madsen

SourceProceedings of the royal society B, Volume 285, issue 1875, 28 March 2018

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.

The importance of cancer cells for animal evolutionary ecology

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

Source: Nature Ecology & Evolution, Vol 1, Nov 2017

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.

Oncogenesis as a Selective Force: Adaptive Evolution in the Face of a Transmissible Cancer

Nynke R., Thomas M. and Beata U.

Authors: Tracey Russell, Thomas Madsen, Frédéric Thomas, Nynke Raven, Rodrigo Hamede & Beata Ujvari

Source: BioEssays, Volume 40, Issue 3, March 2018

Brief summary of the paper: Similar to parasites, malignant cells exploit the host for energy, resources and protection, thereby impairing host health and fitness. Although cancer is widespread in the animal kingdom, its impact on life history traits and strategies have rarely been documented.

Devil facial tumour disease (DFTD), a transmissible cancer, afflicting Tasmanian devils (Sarcophilus harrisii), provides an ideal model system to monitor the impact of cancer on host life‐history, and to elucidate the evolutionary arms‐race between malignant cells and their hosts.

Here we provide an overview of parasite‐induced host life history (LH) adaptations, then both phenotypic plasticity of LH responses and changes in allele frequencies that affect LH traits of Tasmanian devils in response to DFTD are discussed.

We conclude that akin to parasites, cancer can directly and indirectly affect devil LH traits and trigger host evolutionary responses. Consequently, it is important to consider oncogenic processes as a selective force in wildlife.

Faced with extinction, the devils fight back

Devil with DFTD

The researchers looked at animals at risk of catching transmissible cancer, known as devil facial tumour disease (DFTD), which has been driving the species toward possible extinction over the past two decades, and found unexpected signs of immunity, including elevated levels of certain immune system molecules which reduce their likelihood of getting the disease.

Active immune responses to DFTD and even tumour regression have recently been observed in several animals, showing a very promising sign that could be exploited for the management of the species,” says lead author Beata Ujvari from Deakin University’s School of Life and Environmental Sciences in Melbourne, Australia.

Read all about it: Research finds clues that Tasmanian devils are adapting to the cancer that threatens their existence by Andrew P Street @ Cosmos – The Science of Everything.

Evolved Dependence in Response to Cancer

Authors: Frédéric Thomas, Irina Kareva, Nynke Raven, Rodrigo Hamede, Pascal Pujol, Benjamin Roche & Beata Ujvari

Source: Trends in Ecology and Evolution (Available online 20 February 2018)

Brief summary of the paper: Evolved dependence is frequent in evolutionary interactions between hosts and parasites. Similar to pathogens, oncogenic manifestations drive host adaptive responses. Multicellular organisms display evolved dependence in response to oncogenic processes. Evolved dependence in response to cancer has implications for prevention and treatment.


















Evolved dependence is a process through which one species becomes ‘dependent’ on another following a long evolutionary history of interaction. This happens when adaptations selected in the first species for interacting lead to fitness costs when the second species is not encountered.

Evolved dependence is frequent in host–parasite interactions, where hosts may achieve a higher fitness in the presence of the parasite than in its absence. Since oncogenic manifestations are (i) ubiquitous across multicellular life, (ii) involved in parasitic-like interactions with their hosts, and (iii) have effectively driven the selection of numerous adaptations, it is possible that multicellular organisms display evolved dependence in response to oncogenic processes.

We provide a comprehensive overview of the topic, including the implications for cancer prevention and treatment.