It is always interesting to see what kids think about science and scientists. How their vision is affected by environment. A 7 year old boy drew a scientist in a funny but positive way. The scientist’s heart has a form of chemical flask.
Three years later, the same boy participated in the RDS Primary Science Fair which runs side by side with the BT Young Scientist and Technology Exhibition. The idea of this exhibition is very simple. It is a non-competitive event, showcasing STEM research projects (science, technology, engineering and maths) carried out by primary school classes across Ireland. The research projects encourage children’s native curiosity to explore the science behind the everyday.
His class presented a research project ‘Are We Living in the Dark Ages?’ The bunch of 4th class students were exploring the importance of sun light and electricity in our every day life.A colleague of mine was ‘Head Judge’ at this Fair and pointed out the overall enthusiasm and positivity coming from these young children about the research undertaken. I personally was stopped by every school team. Children wanted to share their findings. The project and its presentation were very important for them.
Children are natural explorers and when their ability can be encouraged by the events like the RDS Primary Science Fair, then we, adults, can feel reassured that research can make dreams come true. Dreams about new effective therapies, spaceflights to new stars and planets and many more.
This post is dedicated to parents of children with neuroblastoma. Some parents asked about DFMO – a re-purposing drug. In this post, I tried to collect and summarize information available from academic sources.
Q1: What is DFMO?
Difluoromethylornithine (DFMO, Eflornithine) is an anti-protozoan drug. It was originally developed and FDA approved for the treatment of Trypanosoma brucei gambiense encephalitis (“African sleeping sickness”). DFMO permanently binds to ornithine decarboxylase (ODC), an important enzyme in polyamine metabolism, and prevents the natural substrate ornithine from entering the active site.
By inhibiting ODC, DFMO reduces cellular polyamines and inhibits cell growth and proliferation of actively dividing cells, thus making DFMO an attractive candidate for cancer therapy. In neuroblastoma, a positive regulation of all aspects of polyamine metabolism by MYCN was reported (revived by Bassiri 2015, Gamble 2012). So, it is believed that MYCN amplified neuroblastomas would most benefit of the drug.
Q2: How intense is basic science behind DFMO in neuroblastoma?
To find out the intensity of basic science on DFMO in neuroblastoma search for ‘difluoromethylornithine/DFMO/Eflornithine’ and ‘neuroblastoma’ was run in PubMed, a web-based resource with 26 million citations for biomedical literature from MEDLINE, life science journals, and online books. The search returned 23 papers including 3 reviews and 20 primary research reports published from 1980 to present.
In comparison, I did another search for a novel drug Unituxin (dinutuximab) approved by FDA in 2015. It is monoclonal antibody against the glycolipid disialoganglioside GD2, a biomarker specific for neuroblastoma. Search for ‘anti-GD2 antibody’ and ‘neuroblastoma’ returned 181 papers including 25 reviews and 156 primary articles for the same period.
Q3: Is DFMO in cancer clinical trials?
“ClinicalTrials.gov is a Web-based resource that provides patients, their family members, health care professionals, researchers, and the public with easy access to information on publicly and privately supported clinical studies on a wide range of diseases and conditions. The Web site is maintained by the National Library of Medicine (NLM) at the National Institutes of Health (NIH).
Search for ‘difluoromethylornithine/DFMO/Eflornithine’ in ClinicalTrials.gov returned 36 registered trials across different health conditions.Two of these were withdrawn, the breakdown for the rest 34 is as follows: Adenomatous Polyp (1), Anaplastic Astrocytoma/Recurrent Anaplastic Astrocytoma (1), Bladder Cancer (1), Cervical Cancer/Precancerous Condition (1), Colorectal Cancer (3), Esophageal Cancer (1), Familial Adenomatous Polyposis (1), Gastric Cancer/Gastric Intestinal Metaplasia (1), Hirsutism (2), Human African Trypanosomiasis (5), Neuroblastoma (7), Non-melanomatous Skin Cancer/Precancerous/Nonmalignant Condition (4), Post-solid Organ Transplant/Skin Neoplasms (1), Precancerous Condition (1), Prostate Cancer (2), Pseudofolliculitis Barbae (1), Type 1 Diabetes (1) (Fig. 2). To see full details of 34 trials please click at this Table.
All of them have various statuses (Fig. 3) as well as study design. Importantly, 30 out of 34 studies are focused on safety and efficacy of this drug. Vast majority of studies of DFMO in adult cancers/benign conditions are randomized (16/18 or 89%). Randomization in assignment of patients in studied groups (control and new drug/combination) helps minimize researcher’s bias when comparing effect of the new treatment vs current/no treatment. All trials of DFMO in neuroblastoma are not randomized. Instead, studies use a single group assignment.
Three trails have been either completed/terminated and published results are available at ClinicalTrials.gov (NCT01059071, NCT00033371. NCT00118365).
Q4: What about clinical trials of DFMO in neuroblastoma?
The trial NCT01059071 was a Phase 1 clinical trial. A phase I clinical trial tries to find out whether a new treatment/drug is safe, what its side effects are, the best dose of the new treatment, if the treatment shrinks the cancer.
Twenty one patients were enrolled and eligible for treatment with DFMO and DFMO + etoposide. These patients were assigned into 4 groups of different DFMO doses (Fig. 4). The treatment was in cycles of 21 days. Cycle 1 – DFMO only followed by cycle 2 – combined treatment of DFMO+etoposide (14 days) and DFMO only (the last 7 days).
According to results of the trial: 14 patients did not complete the treatment due to different reasons. It was not clear what stage/cycle they left the trial.
As mentioned earlier this study used a single group assignment and a design called ‘3+3’. This design is straightforward and safe. Briefly, it means that for a dose (X) of the drug, 6 patients are selected. Of these, 3 receive the dose X and are monitored for a period of time. If no adverse effects are registered in these 3, then another new 3 patients start the same treatment. The effect of the drug is evaluated on the patent’s health condition before-, during – the treatment and after its completion. This approach is often used in vaccine tests and dose escalation methods in Phase I cancer clinical trials. This type of study can answer mainly two questions: 1) whether the tested drug is safe to use and 2) what doses are safe? The main drawbacks of this design are
Many patients treated at doses below therapeutic effect
Slow dose increase
Uncertainty about the recommended phase II dose (RP2D)
Only the result from the current dose is used for determining the dose of next cohort of patients. Information on other doses is ignored
Q6: What are main findings of the clinical trial NCT01059071?
The overflow of the study is presented in Fig 5 providing additional information on those who did not complete the trial. Out of 14 participants, disease has progressed in 11 patients – it is 52% of the enrolled participants. Authors highlighted that this phase I study was not designed to evaluateanti-tumour efficacy of DFMO. But tumour response and clinical response were monitored during the study.
According to the paper, 21 patients received at least one dose of DFMO only (Cycle 1, 21 days). During this cycle, 3 patients were withdrawn. All of them were assessed for safety of DFMO.
Eighteen of them completed cycle 1 and continued treatment with DFMO+etoposide for another 4 cycles followed with DFMO only therapy for a number of cycles. Their clinical response data were examined for efficacy of DFMO alone.
Three out of 21 participating patients in this clinical trial remain alive and disease free between 2–4.5 years after starting DFMO.
Authors concluded that
DFMO doses of 500-1500mg/m2/day are safe and well tolerated in children with relapsed NB
Research and review papers covering DFMO in neuroblastoma:
Evageliou NF, Haber M, Vu A, Laetsch TW, Murray J, Gamble LD, Cheng NC, Liu K, Reese M, Corrigan KA, Ziegler DS, Webber H, Hayes CS, Pawel B, Marshall GM, Zhao H, Gilmour SK, Norris MD, Hogarty MD. Polyamine Antagonist Therapies Inhibit Neuroblastoma Initiation and Progression. Clin Cancer Res. 2016 Sep 1;22(17):4391-404. doi: 10.1158/1078-0432.CCR-15-2539.
Bassiri H, Benavides A, Haber M, Gilmour SK, Norris MD, Hogarty MD. Translational development of difluoromethylornithine (DFMO) for the treatment of neuroblastoma. Transl Pediatr. 2015 Jul;4(3):226-38. doi: 10.3978/j.issn.2224-4336.2015.04.06. Review.
Saulnier Sholler GL, Gerner EW, Bergendahl G, MacArthur RB, VanderWerff A, Ashikaga T, Bond JP, Ferguson W, Roberts W, Wada RK, Eslin D, Kraveka JM, Kaplan J, Mitchell D, Parikh NS, Neville K, Sender L, Higgins T, Kawakita M, Hiramatsu K, Moriya SS, Bachmann AS. A Phase I Trial of DFMO Targeting Polyamine Addiction in Patients with Relapsed/Refractory Neuroblastoma. PLoS One. 2015 May 27;10(5):e0127246. doi: 10.1371/journal.pone.0127246.
Lozier AM, Rich ME, Grawe AP, Peck AS, Zhao P, Chang AT, Bond JP, Sholler GS Targeting ornithine decarboxylase reverses the LIN28/Let-7 axis and inhibits glycolytic metabolism in neuroblastoma. Oncotarget. 2015 Jan 1;6(1):196-206.
Samal K, Zhao P, Kendzicky A, Yco LP, McClung H, Gerner E, Burns M, Bachmann AS, Sholler G. AMXT-1501, a novel polyamine transport inhibitor, synergizes with DFMO in inhibiting neuroblastoma cell proliferation by targeting both ornithine decarboxylase and polyamine transport. Int J Cancer. 2013 Sep 15;133(6):1323-33. doi: 10.1002/ijc.28139.
Koomoa DL, Geerts D, Lange I, Koster J, Pegg AE, Feith DJ, Bachmann AS. DFMO/eflornithine inhibits migration and invasion downstream of MYCN and involves p27Kip1 activity in neuroblastoma. Int J Oncol. 2013 Apr;42(4):1219-28. doi: 10.3892/ijo.2013.1835.
Gamble LD, Hogarty MD, Liu X, Ziegler DS, Marshall G, Norris MD, Haber M. Polyamine pathway inhibition as a novel therapeutic approach to treating neuroblastoma. Front Oncol. 2012 Nov 16;2:162. doi: 10.3389/fonc.2012.00162. Review
Passariello CL, Gottardi D, Cetrullo S, Zini M, Campana G, Tantini B, Pignatti C, Flamigni F, Guarnieri C, Caldarera CM, Stefanelli C. Evidence that AMP-activated protein kinase can negatively modulate ornithine decarboxylase activity in cardiac myoblasts. Biochim Biophys Acta. 2012 Apr;1823(4):800-7. doi: 10.1016/j.bbamcr.2011.12.013.
Rounbehler RJ, Li W, Hall MA, Yang C, Fallahi M, Cleveland JL. Targeting ornithine decarboxylase impairs development of MYCN-amplified neuroblastoma. Cancer Res. 2009 Jan 15;69(2):547-53. doi: 10.1158/0008-5472.CAN-08-2968.
Koomoa DL, Yco LP, Borsics T, Wallick CJ, Bachmann AS. Ornithine decarboxylase inhibition by alpha-difluoromethylornithine activates opposing signaling pathways via phosphorylation of both Akt/protein kinase B and p27Kip1 in neuroblastoma. Cancer Res. 2008 Dec 1;68(23):9825-31. doi: 10.1158/0008-5472.CAN-08-1865.
Hogarty MD, Norris MD, Davis K, Liu X, Evageliou NF, Hayes CS, Pawel B, Guo R, Zhao H, Sekyere E, Keating J, Thomas W, Cheng NC, Murray J, Smith J, Sutton R, Venn N, London WB, Buxton A, Gilmour SK, Marshall GM, Haber M. ODC1 is a critical determinant of MYCN oncogenesis and a therapeutic target in neuroblastoma. Cancer Res. 2008 Dec 1;68(23):9735-45. doi: 10.1158/0008-5472.CAN-07-6866.
Wallick CJ, Gamper I, Thorne M, Feith DJ, Takasaki KY, Wilson SM, Seki JA, Pegg AE, Byus CV, Bachmann AS. Key role for p27Kip1, retinoblastoma protein Rb, and MYCN in polyamine inhibitor-induced G1 cell cycle arrest in MYCN-amplified human neuroblastoma cells. Oncogene. 2005 Aug 25;24(36):5606-18.
Bachmann AS. The role of polyamines in human cancer: prospects for drug combination therapies. Hawaii Med J. 2004 Dec;63(12):371-4. Review
Chen ZP, Chen KY. Differentiation of a mouse neuroblastoma variant cell line whose ornithine decarboxylase gene has been amplified. Biochim Biophys Acta. 1991 Dec 3;1133(1):1-8.
Piacentini M, Fesus L, Farrace MG, Ghibelli L, Piredda L, Melino G. The expression of “tissue” transglutaminase in two human cancer cell lines is related with the programmed cell death (apoptosis). Eur J Cell Biol. 1991 Apr;54(2):246-54.
Melino G, Piacentini M, Patel K, Annicchiarico-Petruzzelli M, Piredda L, Kemshead JT. Retinoic acid and alpha-difluoromethylornithine induce different expression of neural-specific cell adhesion molecules in differentiating neuroblastoma cells. Prog Clin Biol Res. 1991;366:283-91.
Stephanou A, Knight RA, De Laurenzi V, Melino G, Lightman SL.Expression of pre-opiomelanocortin (POMC) mRNA in undifferentiated and in vitro differentiated human neuroblastoma cell lines. Prog Clin Biol Res. 1991;366:173-80.
Melino G, Farrace MG, Ceru’ MP, Piacentini M. Correlation between transglutaminase activity and polyamine levels in human neuroblastoma cells. Effect of retinoic acid and alpha-difluoromethylornithine. Exp Cell Res. 1988 Dec;179(2):429-45.
Chen KY, Dou QP. NAD+ stimulated the spermidine-dependent hypusine formation on the 18 kDa protein in cytosolic lysates derived from NB-15 mouse neuroblastoma cells. FEBS Lett. 1988 Mar 14;229(2):325-8.
Karvonen E, Andersson LC, Pösö H. A human neuroblastoma cell line with a stable ornithine decarboxylase in vivo and in vitro. Biochem Biophys Res Commun. 1985 Jan 16;126(1):96-102.
Pösö H, Karvonen E, Suomalainen H, Andersson LC. A human neuroblastoma cell line with an altered ornithine decarboxylase. J Biol Chem. 1984 Oct 25;259(20):12307-10.
Chen KY, Nau D, Liu AY. Effects of inhibitors of ornithine decarboxylase on the differentiation of mouse neuroblastoma cells. Cancer Res. 1983 Jun;43(6):2812-8.
Chapman SK. Antitumor effects of vitamin A and inhibitors of ornithine decarboxylase in cultured neuroblastoma and glioma cells. Life Sci. 1980 Apr 21;26(16):1359-66. No abstract available.
I continue to share the meaning of research for non-science students. Zaki was a summer medical student in 2015.
“I am a final year Malaysian medical student studying at RCSI. I had the opportunity to join RCSI Research Summer School (RSS) by assisting in research with Cancer Genetics, Molecular and Cellular Therapeutics Department of RCSI. My mentor was Dr Olga Piskareva. My research project investigated the role of chromogranin A as a biomarker in drug-resistant neuroblastoma by analysing its expression in different neuroblastoma samples of murine models.
Frankly speaking, I had zero experience in clinical research (apart from basic science project I did at high school) before the placement started. The reading materials that Dr Piskareva handed to me felt like an alien language that had to be deciphered, let alone doing experiment with western blotting and ELISA. I remembered my first day at the lab, staring enthusiastically at every apparatus and machines but not knowing how to run them.
Fortunately, Dr Piskareva and other lab buddies were very experienced and helpful enough with my insufficiency. Their perseverance and willingness to share knowledge and tip built my confidence and understanding to finish my research project. I never had any difficulty to discuss and ask for help any time I needed it from them in the lab. They were also very warm and friendly not just inside the lab but also outside of the lab.
I felt like we were one big multinational family in one small lab. Imagine researchers coming from Russia, Ireland, Italy, Netherlands and myself from Malaysia working hand-in-hand, together. Over time, we bonded very close especially with our weekly breakfast getaway at Gerry’s and my friend Mei Rin and I even prepared our Malaysian cuisine for everyone in the lab in our last days. Even though most of my friends went home for the summer break, never did I felt lonely during my time in the lab. I am very grateful to have them in the lab and to call them my ‘keluarga’ (means family in Malay language).
After the research, I had the opportunity to do poster presentation at RCSI Research Day 2016 and International Conference for Healthcare and Medical Students (ICHAMS) 2016 at RCSI. These were great platforms for me to share my findings with other researchers. Above all, these were made possible with the help of Dr Piskareva and my lab buddies in preparing the poster and full report of the research. Additionally, the findings also provided me with extra information about neuroblastoma in line with my medicine study in paediatrics.
I would cherish every moment in the lab and indeed it was a very priceless experience. I would very much do it all over again in the lab if I had the chance because of the craving for knowledge and warmth of the lab buddies.
One of my classmates shared a funny image of the Upturned Microscope and I could not agree more… That week was exactly 12 months since I have started to apply for funding to carry out neuroblastoma research. Seven applications were submitted to various national and European funding bodies. Some were for a PhD student project, other were for PostDoc or both, Four came back with nothing. Two – decision pending and another one was shortlisted but not funded in the first round. A possibility existed that it could be funded at some day in 2017. So, this pic illustrated my feelings very well..
However, either my efforts were paid off or some Christmas miracle has happened, and I have received a note informing on the green light to funding my application. The funding comes from the National Children’s Research Centre and covers a PostDoc position and research consumables over 3 years. It was the very Christmasy news! I was over the moon.
The conditions of the award states:
Finally, the applicants must indicate how the investment in this research will be measured and communicated, not only to the academic community but also to the hospital, the fundraisers, to parents and patients and to the wider public.
This place will be my research diary to share ups and downs of the ongoing work. Please join me in this exciting journey!
Continue research into 3D neuroblastoma models, we imaged cells growing on collagen based scaffolds using confocal microscopy. This technique is very popular in cell biology providing depth in cell imaging.
Here you can see cells growing on scaffolds: white dots – cells, irregular fibers – collagen containing scaffold.
The results are fascinating! Cell nucleus is in blue (DAPI), cell actin is in red (phalloidin). You will be able also to see how two cells ‘having a handshake’. It is happening just in the middle.
My RSS project investigated the role of VDAC-1 protein on chemotherapy resistance in neuroblastoma. The only research focus of this lab is to find key players in neuroblastoma pathogenesis and to advance anti-cancer therapy.
I was entrusted with the task of splitting cells. I would plate them onto 96-well plates, add cisplatin drug and measure their viability afterwards. It may sound simple here, but the whole process required passion and hard-work.
Prior to this, I did not have any experience in the medical research field. During my first two weeks, everything seemed so tough; however, they became easier as the weeks flew by. My mentor, Olga, and the other staff and PhD students (Garret, John and Ross) were helpful and always guided me to explore my potentials. This programme taught me various new things which I would not have acquired on a normal day-to-day basis in school.
The people at Cancer Genetics were warm and wonderful. The hospitality, love and guidance cannot be quantified and words cannot express my immense gratitude towards them. It has been fascinating and I cherish every moment I spent there. We bonded over our weekly breakfast and tea sessions so well, and I am indeed grateful for being a part of this big family. It is my sincere wish that this positive spirit of togetherness will be preserved and will grow stronger in the future. This is something special, and I think ours is the best lab at RCSI!
I returned to Penang Medical College to further my studies in my clinical years. I took part in the PMC Research Day 2016 in which I was awarded the First Prize in Oral Presentation. I would like to dedicate this success to Olga and everyone who has been with me throughout my time at Cancer Genetics. Without all the guidance, I would not have made it this far.
I strongly urge students to take part in the research opportunities, because you gain invaluable experiences that you do not get elsewhere. May whatever we do at the lab today make a difference in another person’s life someday in the future.
It seems I have got a conference season. Three conferences within 2 months – no complains though. This time I went to the Matrix Biology Ireland Meeting in Galway. It was fantastic mix of topics and speakers ranging from new approaches in bone and heart repair to new matrixes in reconstruction of body tissues and diseases in the lab to minimise use of animals in pre-clinical studies.
My talk was focused on neuroblastoma microenvironment and cell-to-cell communication through exosomes. I wrote about it in October post. I talked about things that did work and did not as well as new directions. One of the new directions is reconstructing neuroblastoma by growing neuroblastoma cells on collagen based scaffolds in 3D. Collagen constitutes most of our tissues to keep it shape and strength. These scaffolds are sponge-like matrixes built from collagen and other components. Of course cells grow differently on these matrixes. They have a different shape and growing properties in 3D. Neuroblatoma cells look like water drops on the cotton wool-like collagen scaffolds. In contrast, when they grow on plastic in 2D, they are flat. Studies show that cells in 3D respond to cytotoxic stress in a similar pattern as if being within a body (details in recent reviews 1-4). It would be a great breakthrough once these models are optimised for neuroblstoma research field. It will help to test all new and known drugs in the environment close to clinical settings. It could be a step forward to personilised therapies for children with neuroblastoma by isolating cancer cells, growing them in 3D and testing how they respond to all therapies available. It will facilitate more efficient design of treatment for relapsed or poorly responding tumours, sparing patients unnecessary rounds of chemotherapy and ultimately increasing survival.
I’ve always felt that a selection of abstracts for an oral presentation is biased. The overall background and views of conference organisers would affect works selected for an oral presentation. The same abstract was not selected for an oral presentation by one committee, but was supported by the other. Never give up!
Schweiger PJ, Jensen KB.Modeling human disease using organotypic cultures. Curr Opin Cell Biol. 2016 43:22-29.
Salamanna F, Contartese D, Maglio M, Fini M. A systematic review on in vitro 3D bone metastases models: A new horizon to recapitulate the native clinical scenario? Oncotarget. 2016 7(28):44803-44820.
Picollet-D’hahan N, Dolega ME, Liguori L, Marquette C, Le Gac S, Gidrol X, Martin DK. A 3D Toolbox to Enhance Physiological Relevance of Human Tissue Models. Trends Biotechnol. 2016 34(9):757-69.
Nyga A, Neves J, Stamati K, Loizidou M, Emberton M, Cheema U. The next level of 3D tumour models: immunocompetence. Drug Discov Today. 2016 21(9):1421-8.
For children who do survive cancer, the battle is rarely over. Over 60% of long‐term childhood cancer survivors have a chronic illness as a consequence of the treatment they received; over 25% have a severe or life‐ threatening illness. How much do we know about quality of life of childhood cancer survivors?
Researchers in health- and illness-related social sciences understand that the there is a life after the treatment completed. The life is full if diverse levels and issues from health related to social adaptation in different shapes and forms. Children and teenagers may experience fear when returning to school due to temporary or permanent changes to their physical appearance (1,2). They worry about their ability to socialise with their friends due to lengthy absences (3–5). Treatment can result in the development of learning disabilities in children and thus marking school as a major source of frustration (1,2). These learning difficulties can affect a child’s confidence and self-esteem, if left without attention and care (1,3). All studies come to the same conclusion. Challenges in education of children with cancer are complex, however most can be tackled efficiently through planning and good communication (1–5).
It is important not only to recognise the problems but to start changing the situation. Apparently much more could be done more efficiently if patients are involved in setting up future research agenda.
Gurney JG, Krull KR, Kadan-Lottick N, Nicholson HS, Nathan PC, Zebrack B, et al. Social outcomes in the childhood cancer survivor study cohort. J Clin Oncol. 2009;27(14):2390–5.
McDougall J, Tsonis M. Quality of life in survivors of childhood cancer: A systematic review of the literature (2001-2008). Supportive Care in Cancer. 2009. p. 1231–46.
Barrera M, Shaw AK, Speechley KN, Maunsell E, Pogany L. Educational and social late effects of childhood cancer and related clinical, personal and familial characteristics. Cancer. 2005;104(8):1751–60.
Langeveld NE, Stam H, Grootenhuis MA, Last BF. Quality of life in young adult survivors of childhood cancer. Support Care Cancer. 2002;10(8):579–600.
Klassen AF, Anthony SJ, Khan A, Sung L, Klaassen R. Identifying determinants of quality of life of children with cancer and childhood cancer survivors: A systematic review. Support Care Cancer. 2011;19(9):1275–87.
Yeh JM, Hanmer J, Ward ZJ, Leisenring WM, Armstrong GT, Hudson MM, et al. Chronic Conditions and Utility-Based Health-Related Quality of Life in Adult Childhood Cancer Survivors. J Natl Cancer Inst [Internet]. 2016;108(9):4–7.
Armstrong GT, Chen Y, Yasui Y, Leisenring W, Gibson TM, Mertens AC, et al. Reduction in Late Mortality among 5-Year Survivors of Childhood Cancer. N Engl J Med. 2016;374(9):833–42.
Ok. Now, when the stress of the presentation is over, I am happy to share new technologies used during the SIOP2016. As I mentioned yesterday, my work was selected for e-poster presentation. It looked this way:
It is definitely a step forward. Anyone can look up any poster, listen to a commentary recorded by the author, zoom in and out and send a request/comment to the author. It looks cool and trendy. Though, you can feel invisible as no physical copy displayed in a designated area. No crowds of poster presenters and judges. No waiting faces desperate to share their study…
The actual Poster Discussion session was a traditional presentation when my poster was up on the big screen, I had 8 minutes to convince the audience navigating through figures. This session was late and no many attendees survived to come and challenge your statements. Nevertheless, it was enjoyable experience. 🙂
SIOP is the International Society of Paediatric Oncology. It is a global multidisciplinary society representing doctors, nurses, other health care professionals, scientists and patients or their relatives. The Society’s motto is ‘no child should die of cancer’. The meeting 2017 is being held in Dublin, the city where I live and work.
Indeed, it was appealing to attend the key meeting in childhood oncology field. As any participant, I had an opportunity to submit an abstract about my research. To no surprise at all, I received email notifying me on my work being selected for e-Poster presentation. Common stuff. The email also said that it would be displayed at designated stations, like big screens throughout the meeting. Very unusual format, but we are living in the digital technology era; things are changing all the time. So, I would not need to stay by the poster this time. Great – more time for networking and talks.
Then I received another email informing about a Poster Discussion session, which I assumed to be a standard procedure when a group of selected piers stand by your poster and ask Qs. None comes in majority cases. A participant stands and waits and waits till the session is over. So, of course I took it easy.
A day before the meeting, I downloaded the meeting app and started to browse along the content and features. Out of curiosity, I checked details of the Poster Discussion session. This was the moment of mental breakdown – I discovered being selected for an oral poster presentation! My chances were 1 in 1475 (the number of submitted abstracts). I should probably also buy a lottery ticket tonight. Could lucky things come together?
I will reflect on the new e-poster presentation experience later today…