Poster prizes at ‘Defining and defeating metastasis’ – meet the winners!

We are excited to present the poster prizes awarded at the recent EMBO | EMBL Symposium  ‘Defining and defeating metastasis’,  hosted at the Advanced Training Centre in Heidelberg and bringing together researchers from diverse fields to enhance our understanding of the dissemination and metastatic colonisation of tumour cells. It provided a unique opportunity for interdisciplinary exchange on current approaches and future collaborations on metastasis and its therapeutic challenges. As with most events this year, for many participants this was the first onsite meeting that they attended since early 2020 which made it very special. It was a fantastic opportunity to meet in person for the three days full of exciting science, exchanging ideas, presenting latest research, catching up with old friends and making new ones. There were two live poster sessions during which the presenters could discuss their research– their work was then voted for by other attendees and speakers. We are pleased to be able to share with you the research from four out of six winners of the conference prizes: congratulations to all!

Jagged-1 promotes breast cancer metastasis through the lymphatic system

Presenter: Benjamin Gordon

Benjamin Gordon – University of Illinois at Chicago College of Medicine, USA

While early detection of breast cancer (BC) has improved prognoses, there is an urgent need to improve outcomes for patients with distant metastatic disease. Higher expression of the Notch ligand JAG1 in primary BC tumors is strongly associated with lymph node metastasis and patient mortality, but causality is unclear. We show that JAG1 expression is higher in metastatic BC cells colonizing lymph nodes than in primary tumors, suggesting that tumor cells with high JAG1 are preferentially able to metastasize to lymph nodes. JAG1 expression is higher in a derivative of BC line MDA MB 231 selected for tropism to lymph nodes (MDA231 LN) than in the parental line or derivatives with other tropisms. To determine the mechanism(s) of JAG1 mediated metastasis, we generated clonal JAG1 knockout cell lines from MDA231 LN cells with corresponding JAG1 rescue lines. We investigated the role of JAG1 in spontaneous metastasis under clinically relevant conditions by orthotopically implanting JAG1 knockout and expressing cells, resecting the primary tumor, and following long term metastatic spread in a mouse model. Quantification of tumor cells in blood showed that survival, metastatic burden, and JAG1 expression did not correlate with the number of circulating tumor cells. Conversely, JAG1 expression drove an increase in lymph node and body wide metastatic burden and a trend toward decreased survival. In this model, metastatic cells were abundant throughout lymph vessels, suggesting lymphatics are the primarily route of dissemination. Preliminary transcriptional analysis suggests that JAG1 alters interactions with lymphatic endothelial cells (LEC), leading us to examine downstream events in co cultures of LEC with lymphatically invasive BC lines. Deciphering tumor lymphatic endothelial signaling events may open new avenues to target BC metastasis.

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Poster Prize from the EMBO Journal

Biphasic contribution of platelets to metastasis

Presenter: María J. García-León

Maria J. Garcia-Leon – INSERM UMR_S1109, Tumor Biomechanics, Université de Strasbourg, France

Metastasis still remains elusive to treatment, with an overwhelming mortality rate of 90%. Accumulating evidence indicates that metastatic potential of circulating tumor cells (CTCs) can be tuned by intravascular components, including platelets. Platelet depletion impairs metastasis, which can be rescued upon platelet transfusion. Mechanistically, CTCs rapidly bind, activate and aggregate platelets, events that are crucial for the arrest, survival, and extravasation of the former. The current dogma states that platelets tune metastasis by impacting CTCs behaviour at early stages of metastatic seeding. However, whether platelets can regulate metastasis at later stage and which receptors may be involved remains unknown. In this study, we first documented the efficiency of platelet binding to a large panel of metastatic TCs and observed that not all recruit or aggregate platelets with the same efficiency. Interestingly, such binding impacts their intravascular fate by favoring their arrest, as observed in a combination of experimental metastasis models in thrombocytopenic (TCP) mice and zebrafish embryo. Using longitudinal imaging of metastatic seeding and growth in TCP mice at unprecedented spatial and temporal resolution, we demonstrated that binding and aggregation correlates with their metastatic potential in vivo. Additionally, by the dynamic in vivo tracking of TCs in the lungs of fully TCP mice, and the quantification of platelets depositions around arrested CTCs at seeding and late metastatic outgrowth, we showed that early platelet binding, aggregation, clot formation, and the subsequent increased adhesion and survival at lung microvessels, are capital but not exclusive factors increasing TC metastatic fitness. We observed that platelets contribute to late steps of metastatic outgrowth by experimentally interfering with platelet counts in animals already carrying metastatic foci. Doing so, we observed that platelets tune the growth of established foci, independently of their early intravascular interaction with CTCs. Finally, we have identified the platelet collagen receptor GPVI as key in this late modulation of metastatic outgrowth, suggesting its targeting in specific cancer types as a promising adjuvant therapy in oncologic patients to stop the metastatic progression.

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Poster Prize from EMBO Molecular Medicine

Colonic fibroblasts in tissue homeostasis and cancer

Presenter: Michael Brügger

Michael Brügger – University of Zürich, Switzerland

Colorectal cancer (CRC) is among the most prevalent cancers in Switzerland (2nd in women 3rd in men, BFS statistics 2013 2017) and worldwide (3rd in women and men). More than half of the patients diagnosed with CRC either harbour metastases or will develop metastatic disease, which is the primary cause of death for CRC patients. There is therefore a dire need for new therapies. These must be guided by a better understanding of the metastatic process. We are only now starting to appreciate the contribution of not only tumour cells themselves, but also the non tumour stromal cells of the tumour microenvironment (TME) to tumour growth, progression and metastasis. To understand how non tumour stromal cells are changed in CRC it is integral to first characterize their identity and functions during colonic homeostasis.
To describe the stromal cell populations in an unbiased manner, we carried out a single cell transcriptome analysis of the adult murine colon, producing a high quality atlas of matched colonic epithelium and mesenchyme. We identify two crypt associated colonic fibroblast populations that are demarcated by different strengths of platelet derived growth factor receptor A (Pdgfra) expression. Crypt bottom fibroblasts (CBFs), close to the intestinal stem cells, express low levels of Pdgfra and secrete canonical Wnt ligands, Wnt potentiators, and bone morphogenetic protein (Bmp) inhibitors. Crypt top fibroblasts (CTFs) exhibit high Pdgfra levels and secrete noncanonical Wnts and Bmp ligands. While the Pdgfralow cells maintain intestinal stem cell proliferation, the Pdgfrahigh cells induce differentiation of the epithelial cells. Notably, these cell populations are conserved in the human colon.
Recently, we established a murine model of metastatic colorectal cancer, based on the orthotopic endoscopy guided injection of cancer organoids (colonic organoids harbouring mutations in APC, Kras, Tp53 and Smad4). In this context we study how the abovementioned fibroblast populations are affected by the primary tumour and how they in turn affect tumour progression.

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Single cell transcriptomic profiling of brain metastatic founders in small cell lung cancer patient derived models to identify potential vulnerabilities

Presenter: Maria Peiris-Pagès

Maria Peiris Pages – Cancer Research UK Manchester Institute, UK

Background: Brain metastasis is a major cause of patient morbidity and mortality in small cell lung cancer (SCLC) with an ~80% incidence during disease progression, contributing to the dismal 5 year survival rate of <7%. Mechanisms underpinning SCLC brain metastasis are understudied due to scarcity of brain biopsies and preclinical models. We have developed a biobank of >60 circulating tumour cell (CTC) derived patient explant models of SCLC in immunodeficient mice (CDX) where brain metastasis is routinely observed upon resection of the subcutaneous (S.C) tumour
Methods: We developed an in vivo S.C tumour resection workflow in brain tropic CDX3P to isolate single CTCs, early brain founder tumour cells and subsequent established brain metastases. Following FACS of CDX cells from dissociated mouse brain (using a human CD147 antibody) we performed single cell RNA sequencing (scRNAseq) to reveal potential molecular regulators hypothesised to support brain metastatic founding and subsequent colonisation
Results: Brain metastases were detectable in CDX3P on average 195 days after S.C implantation (study length 174 230 days). We analysed 58 single CTCs (n=6 mice, 191 230 days) and 214 brain metastatic founder cells (n=2 mice, 205 218 days) by scRNAseq. Bioinformatics analyses defined transcriptomic features underpinning single cell heterogeneity and identified sub populations within CTCs and metastatic founders indicative of brain tropic CTC sub clones. We also characterised molecular features unique to brain founders as candidates that could serve as therapy targets
Future Tissue expression of candidate genes of brain metastatic founding will be validated in CDX and patient samples. Genetic manipulation of CDX cells ex vivo combined with pharmacological approaches will be used to explore their roles in metastatic seeding and to identify potential vulnerabilities. Transcriptomic analysis of cells from established brain metastases obtained from the above in vivo protocol will be conducted to explore molecular programs of brain colonisation. Combined, these data will contribute to our long term goal of identifying novel therapeutic strategies that may ultimately improve the quality of life for the significant number of patients with SCLC who present with or subsequently develop brain lesions.

Due to the confidentiality of the unpublished data, we cannot share the poster.

Effective treatment of colorectal peritoneal metastases by exploiting a molecular subtype specific vulnerability

Presenter: Sanne Bootsma

Sanne Bootsma, Amsterdam UMC, The Netherlands

In colorectal cancer, peritoneal metastases (PMs) associate with severe morbidity and dismal prognosis. Given the incidence of this disease and the lack of adequate treatments currently available, PMs pose a large unmet clinical need. Although PMs can be accompanied by more widespread metastatic disease, it often occurs as the only sign of dissemination. This implies that the route of metastatic spread to the peritoneum differs from that to distant organs. PMs are thought to result from cancer cells that spill into the abdominal cavity, and are able to attach to the peritoneal lining and form tumor deposits. This cascade places specific demands on the cancer cells.
Here, we report that colorectal cancers that present with PMs almost universally classify as consensus molecular subtype 4 (CMS4). This previously recognized disease entity is characterized by mesenchymal features, poor prognosis, and resistance to therapies currently used against peritoneal metastases, which explains their limited efficacy. By leveraging disease models that capture CMS4 specific features, including the ability to form PMs in vivo, we identified elesclomol as a highly effective agent. Elesclomol kills cancer cells in a copper dependent fashion by targeting the oxidative phosphorylation machinery, which we found to be a specific vulnerability of CMS4 cancers. Elesclomol Cu2+ was effective following only minutes of exposure to CMS4 cell lines and organoids, supporting its use in intra abdominal treatment procedures. It is therefore a promising candidate for the local treatment of peritoneal metastases of colorectal cancer.

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Poster Prize from Metastasis Research Society


The remaining prize was:

Short talk Prize from Metastasis Research Society: Eric Rahrmann – University of Cambridge, UK


Congratulations to all six winners!

The EMBO | EMBL Symposium ‘Defining and defeating metastasis’ took place from 19 – 22 June 2022 at EMBL Heidelberg and was streamed online for virtual participants.

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How to get your abstract selected for a short talk

by Nicola Vegiopoulos, EMBL Alumna, marketing expert and pianist

So, you’ve registered for a conference – be it virtual or onsite – and you reeeeeally want to present your work? It’s got everything going for it – it’s a hot topic and you have some great results to show. There’s just one little problem – you haven’t made a name for yourself in the field yet, so of course you haven’t been invited as a speaker. Never fear! There are some short talk speaking slots available. But how are you going to make sure that the abstract you submit is selected for a short talk?

Follow these steps to give yourself an edge over the others, and increase the chances of your abstract being selected to present your work.

  1. Get to the point – quickly

Generally you will have a word limit for your abstract. Don’t waste valuable words making your abstract flowery – enter straight into the subject, your problem or research question. Scientific organisers have to read a lot of abstracts, so make sure you put the most important information at the beginning.

  1. Make sure you answer 4 important questions

– What problem are you addressing and why is it important?
– What methods are you using to research the problem?
– What data have you been able to produce or process?
– What (preliminary) findings will you be able to discuss?

  1. Make it clear why your work is important

Be sure to clearly emphasise the approach and importance of your findings and theorisation. Make a concise statement that outlines the purpose, context, approach and significance of your work.

  1. Clarity, clarity, clarity!

Make sure you give strong conclusions and clear outcomes. Don’t leave anything open to misinterpretation, and make it clear if the work is finished, or at least nearly finished.

  1. Make it relevant to the research field

Outline how your research has made steps forward in the field, and what impact it will have.

  1. Make it relevant to the conference topic

Take a look at the conference programme and relate your work to areas of interest covered at the conference, as well as session titles. Have an idea of which session your short talk could fit into.

  1. Avoid dull titles

Make sure the title is catchy and informative – it will be the first thing that anyone reading your abstract will see, and will also be the topic of your short talk should you be successful in your goal.

  1. Find the balance

It’s not the easiest thing to do, but try to bring across enthusiasm for the topic across whilst remaining professional. This is one of the hardest things to do, so take your time with it and don’t try to do it at the last minute.

  1. Get feedback before submitting

Ask others to read and review your abstract before submitting, for example your colleagues or PI. They can provide you with valuable feedback which you should take on board!

  1. Follow the guidelines

It sounds like a no-brainer, but it’s amazing how many people contact us to ask if they can submit their work after the deadline. Late submissions won’t get considered for a short talk, and there is a chance that they will not be accepted at all. In addition, stick to the word limit, and make sure you include all authors and co-authors in the correct format.

So, to sum it up, aim for precision, linearity of thought, and succinctness, and you‘re in with a good chance of getting selected for a short talk at your next conference.

Original video by EMBL Photolab and EMBL Events, EMBL Heidelberg

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How to present a memorable flash talk in 12 easy steps

Flash talks are a great way to give an introduction to your work, and whet people’s appetite for your research.

Generally flash talks last for 1 to 2 minutes, and presenters are normally allowed one simple PowerPoint slide or, in the case of virtual events, a 1 – 2 minute pre-recorded video. But is it really possible to present something really memorable within such limitations?

Here are some things to take into account when preparing your flash talk to make sure the audience remembers you, and contacts you after the session to find out more. Because that’s the goal, right?

1. Keep it brief

You should definitely start by giving a very brief introduction that makes people understand why your work is interesting, and ends by saying how people can contact you afterwards. Of course you can say where you’re from and your affiliation, but the critical thing is to attract to people’s attention.

2. Cover the basics

Answer the following questions:

  • Why is it interesting?
  • What is it about?
  • How did you do it?
  • With whom did you carry out the work?

3. Connect with the audience

For live events be sure to always look at the audience – don’t lose eye contact. Keep scanning the room for the duration of your talk, and definitely do not turn your back to them. In the case of a pre-recorded video, treat your camera like an audience and talk directly to it.

 4. Leave the audience asking for more

Try to build up the anticipation and attention of the people who are listening and watching– put out something you’ve investigated but don’t tell them the whole story. You want to leave them hanging and intrigued enough to want to find out more.

5. Be dynamic

Your flash talk is going to be short so your audience will generally be paying attention to you. Build up to something where you clearly emphasise one or two points. These are the sort of things that are going to bring their attention to the most important parts. Be enthusiastic – if you show that you’re really into your science people will come along and want to know more.

6. Don’t be afraid to use visual tools

If it’s relevant, there is no problem with using props in your flash talk. Alternatively, make your talk visually memorable by using dynamic diagrams, graphics and images. Videos will normally not be possible for live flash talks, so don’t rely on these.

7. Avoid special effects

It is possible to make something visually memorable without going overboard on big special effects such as PowerPoint animations. If your science is good it doesn’t need any fireworks.

8. Do the unexpected

If it fits with your character, you can try to make people laugh. Doing something that the audience is not expecting can be very effective. We’ve seen everything from interpretive dance to a guitar-accompanied talk – anything is possible! Just make sure it matches to who you are so that it appears natural.

9. Include your poster number

Definitely, definitely, definitely include your poster number during your flash talk! It will make it much easier for people to come and find you later on at the poster session.

10. Be a slide minimalist

As already mentioned, diagrams, graphs and images are great when you have only 1 or 2 slides at your disposal. Make sure though that there is a minimum of information on your slides to try to bring people into the main message – focus on the thing that you want them to remember.

11. Practise!

Like all talks, you need to practise beforehand! Even if you want to bring across that you’re relaxed and everything is quite informal there is no way around it – you’ve got to practise to be prepared.

12. Stick to the time limit

With a flash talk this is so important – the time limitations are extremely strict, and you will be moved off the stage when your time is up, or your video won’t be uploaded to a virtual event platform. So make sure you have condensed everything into the time provided, and don’t go over or you may be stopped mid-sentence!

Check out these examples of great flash talk slides!
Single-slide flash talk by Fariha Akter
Multi-slide flash talk by Pablo Gonzalez-Suarez

Original video with Dr. Cornelius Gross, EMBL Rome, and Dr. Francesca Peri, University of Zurich

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Best Poster Awards – The Non-Coding Genome

Taking place for the third time,  the EMBO|EMBL Symposium: The Non-Coding Genome (16 – 19 October 2019) brought together 305 RNA experts to discuss the roles of non-coding RNAs in both prokaryotes and eukaryotes, gene regulation and function. 

A total of 189 posters were presented, from which two were singled out as the winners by popular vote.

Characterization of the genomic and splicing features of long non-coding RNAs using bioinformatics approaches

Monah Abou Alezz is a Ph.D student in genetics, molecular and cellular biology at the University of Pavia, Italy. PHOTO: Monah Abou Alezz

Authors: Monah Abou Alezz, Ludovica Celli, Giulia Belotti, Silvia Bione, Institute of Molecular Genetics L. L Cavalli-Sforza – National Research Council, Italy

Recent developments in deep sequencing approaches have simulated the continuous discovery of a significantly large number of novel long non-coding RNA (lncRNA) genes loci in the genomes. Long non-coding RNAs are recognized as a new class of regulatory molecules despite very little is known about their functions in the cellular processes. Due to their overall low expression level and tissue-specificity, the identification and annotation of lncRNA genes still remains challenging. The characterization of lncRNAs’ features is crucial to understand and get functional insights on their mechanisms of action. We exploited recent annotations by the GENCODE compendium to characterize the genomic and splicing features of long non-coding genes, in comparison to protein-coding ones, in the human and mouse genome by using bioinformatics approaches. Our analysis highlighted differences between the two classes of genes in terms of gene architecture regarding exons and introns length, GC-content, and the combinatorial patterns of chromatin marks and states. Moreover, significant differences in the splice sites usage were observed between long non-coding and protein-coding genes. While the frequency of non-canonical GC-AG splice junctions represents about 0.8% of total splice sites in protein-coding genes, we identified a remarkable enrichment of the GC-AG splice sites in long non-coding genes, both in human (3.0%) and mouse (1.9%). In addition, we identified peculiar characteristics of the GC-AG introns in terms of donor and acceptor splice sites strength, poly-pyrimidine tract, intron length, and a positional bias of GC-AG junctions being enriched in the first intron. Genes containing at least one GC-AG intron were found conserved in many species across large evolutionary distances, more prone to alternative splicing and a functional analysis pointed toward their enrichment in specific biological processes such as
DNA repair.

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MirGeneDB 2.0: The metazoan microRNA complement

Bastian Fromm is a Senior Researcher at Science for Life Laboratory, Stockholm University, Sweden. PHOTO: Bastian Fromm

Authors: Bastian Fromm (1), Diana Domanska (2), Eirik Hoye (3), Vladimir Ovchinnikov (4), Wenjing Kang (5), Ernesto Aparicio-Puerta (6), Morten Johansen (7), Kjersti Flatmark (3), Anthony Mathelier (8), Hovig
Eivind (3), Michael Hackenberg (6), Marc Friedländer (5), Kevin Peterson (9)

Non-coding RNAs (ncRNA) have gained substantial attention due to their roles in human disorders and animal development. microRNAs (miRNAs) are unique within this class as they are the only ncRNAs with individual gene sequences conserved across the animal kingdom. Bona fide miRNAs can be clearly distinguished from the myriad small RNAs generated in cells by a set of unique criteria. Unfortunately, recognition and utilization of these clear and mechanistically well understood features is not a  common practice. We addressed this by extensively expanding our curated miRNA gene database MirGeneDB to 45 organisms that represent the breadth of Metazoa. By consistently annotating and naming more than 11,000 miRNA genes in these organisms, we show that previous miRNA annotations contained not only many false positives, but surprisingly many false negatives as well. Indeed, curated miRNA complements of closely related organisms are very similar and can be used to reconstruct evolution of miRNA genes, families and biogenesis across more than 1 billion years of evolution. MirGeneDB represents a robust platform for providing deeper and more significant insights into the biology of miRNAs, possible sources of mis-regulation, and evolutionary mechanisms. MirGeneDB is publicly and freely available under

View PDF Poster

Fromm, B. et al. MirGeneDB 2.0: the metazoan microRNA complement. Nucleic Acids Research, gkz885, (2019),

(1) Science for Life Laboratory, Sweden
(2) Department of Informatics, University of Oslo, Oslo, Norway
(3) Department of Tumor Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
(4) School of Life Sciences, Faculty of Health and Life Sciences, University of Nottingham, United Kingdom
(5) Stockholm University, SciLifeLab, Sweden
(6) Department of Genetics, Faculty of Sciences, University of Granada, Granada, Spain
(7) Institute for Medical Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
(8) Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo, Oslo, Norway
(9) Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire, United States of America

Working on your own conference poster? Then check out 10 tips to create a scientific poster people want to stop by .

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No more browser restrictions!

For those of you who have been coming to EMBL for scientific training over the years, you may have noticed that we recently (finally?!) have a new and improved registration and abstract submission software, with a brand new look and feel.

We have moved to an HTML5 software solution, which offers an enhanced customer experience, meaning that we now no longer have browser restrictions or preferred browsers. The interface is fully responsive for submitters and evaluators alike, and is user-friendly on all devices. YAAAAAAY!!!!

The new software is pretty self-explanatory, but just in case you get stuck, here are a couple of how-to videos for abstract and motivation letter submission.

How to submit an abstract – for EMBL conferences and symposia


How to submit a motivation letter – for EMBL courses


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