Max Perutz Science Writing Award 2016

I remember, a couple of years ago, seeing an advert by the Medical Research Council (MRC) for a science writing competition and subsequently being bitterly disappointed when I found out it was only for PhD students. Luckily, it’s an annual competition and even more fortunately, The Francis Crick Institute is partly funded by the MRC so that I was eligible to enter.

Now – spoiler alert – before this post ends with an absolute anti-climax, I’ll tell you straight away that I didn’t win. However, I enjoyed answering the question why my research matters in the 800-word essayNot all cancer cells are equal“. The judges used three main criteria to evaluate the essays: 1) Does the essay convincingly explain why the research matters? 2) Is it easy to understand for a public audience? 3) Is the essay well written?

Although I didn’t win, I was shortlisted together with thirteen other entrants and got to attend a science writing masterclass led by Jon Copley, the co-founder of SciConnect, a company that provides science communication training to scientists. The News and Features producer at the MRC was live-tweeting from this course – how cool is that?

The class was really helpful. For instance, I learnt that when writing short to medium length articles (up to 1000 words maximum) the most common structure is the “inverted triangle”. The most important information goes first, i.e. my research matters because it may lead to the development of new anti-cancer drugs. This is different from a research article because there the discussion and conclusion are arguably the most important and come last. I think most essays, including mine, had introductions that were too long. Another handy tip was to think about when/at what age I last shared a class with my target audience. For these essays we could probably assume that interested readers would have had a science education until GCSE level – so we were supposed to write in a way that a fifteen year old might understand.

inverted-triangle

Inverted triangle essay structure for short to medium length articles – copied directly from Wikipedia

When I looked around the room during the writing class – and you might notice it in the photo – I realised that everyone else was probably British and definitely white. At first I was a little bit confused by this since, surely, there is no correlation between skin colour and English writing skills; of last year’s six Man Booker Prize nominees only two were white. But it all made sense when I looked up the MRC’s PhD student funding policy: students need to be eligible to reside in the UK without restrictions and therefore this skews the demographic. [Why higher education in the UK is not more widely accessed is a whole different kettle of fish.]

all-shortlisters

The fourteen shortlisters together with two of the judges, Chris van Tulleken and Donald Brydon, and Robin Perutz, the son of Max Perutz – image copied directly from the MRC website

To round off the day we were all invited to the ceremony at the Royal Institution that evening. In addition to the actual prize-giving, both Donald Drydon, chairman of the MRC, and Robin Perutz, Max Perutz’s son, gave good speeches. The former emphasised that science communication with the public is more important than ever for securing support and funding, since Brexit probably means there will be less money from the government.

Your ability to explain your science allows us, as a country, to carry on being curious. – Donald Brydon

Robin Perutz told a story, also very topical, about how his father and mother met due to an organisation called the Society for the Protection of Science and Learning (SPSL, founded in 1933), which had the mandate of supporting refugee scientists in the UK. Among others, the SPSL helped sixteen future Nobel Prize winners, among which were Max Perutz, Max Born and Hans Krebs. Other prominent academics included Nikolaus Pevsner and Karl Popper. Robin Perutz, currently a professor of inorganic chemistry at the University of York, explained that his lab is taking/has taken in a scientist from Syria who is being funded by the Council for At-Risk Academics (Cara). And it turns out that Cara is none other than SPSL under a new name.

Lastly, we received a copy of The Oxford Book of Modern Science Writing. Who can say no to a book. Overall, from the actual essay writing to the writing class and the ceremony this was an enjoyable experience, which I would highly recommend. Thanks to all the judges and the MRC staff who organised the award. Congratulations to the winners and other almost winners!

modern-science-writing


Now that I think about it, I’ve actually already written a few things relating to Max Perutz, including about his biography, his optimism in research and a symposium in honour of his 100th birthday. It seems I’m quite the fan.

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Not all cancer cells are equal

This is the essay I submitted to the Max Perutz Writing Award 2016.

Look at yourself in the nearest mirror and, if you aren’t too squeamish, visualise the inside of your body. It’s obvious that not all your cells are the same. We are made of many different tissues that perform different tasks: skin cells protect us from the environment, white blood cells defend us against infections, nerve cells allow us to move and think. Cancer – the uncontrolled growth of cells – can arise from virtually any type of tissue. We hear about new treatments for skin cancers, about raising money for childhood leukaemias, about inoperable brain tumours. We know that there are different types of cancer.

But an individual tumour in a tissue is also complex. Researchers realised decades ago that, like our healthy bodies, tumours aren’t simply lumps of identical cells; that within each tumour there are different cell types. For instance, some tumour cells divide indefinitely to keep the cancer alive, others invade into surrounding tissue and spread to other sites of the body, while yet others stimulate blood vessels to grow. Some cancer cells even combine several of these properties.

In our laboratory we study the pancreas, an organ of the digestive system, which aids digestion and controls metabolism throughout the body by secreting hormones such as insulin. In particular, we investigate variations among cell types in the most common kind of pancreatic cancer called pancreatic ductal adenocarcinoma (PDAC for short). PDACs are among the most deadly cancers with only about three per cent of patients diagnosed with PDAC in the UK surviving for longer than five years. One of the reasons for this gruelling statistic is that PDACs are often diagnosed late, when the cancer cells have already spread to and wreaked havoc in other internal organs. Previously, several labs, including ours, noticed that some PDAC cells are more aggressive than others, more capable of re-growing new tumours from scratch. Now, we aim to understand what makes the more aggressive PDAC cells different from the rest of the cancer cells and how they contribute to the deadliness of this cancer. With that knowledge in hand, the broader aim will be to find anti-cancer drugs to target and kill the most dangerous cells that lie at the heart of PDAC.

A previous PhD student in our lab discovered that the more aggressive PDAC cells make and display large amounts of a certain protein – let’s call it protein X – on their cell surfaces. We say that the more aggressive cells are “marked” by protein X. This realisation was my gateway into finding out exactly how these two cell types, the more and less aggressive cells, differ.

First, I wanted to know whether protein X not only marks the more aggressive cells but whether it is directly responsible for making those cells more dangerous. Therefore I experimentally reduced or elevated the levels of protein X in PDAC cells we grow in the lab. Then I assessed whether the PDAC cells grew more or fewer, larger or smaller “organoids”, miniature replicas of pancreatic tumours. Astonishingly, the cancer cells actually grew less well when I removed most of protein X, or they divided and proliferated much more when they had more of protein X. This is a good indication that, in future, drugs might be delivered directly to protein X to eliminate the aggressive cells or convert them into tamer cells.

In the meantime, I am on the lookout for other characteristics that might distinguish between the more and less aggressive cells. From one of my experiments I have data hinting that the two cell types might in fact have different physical properties. However, until I’ve repeated these experiments I can’t be certain that this difference in appearance contributes to the more aggressive cells’ behaviour. But it is thinkable, for example, that the more aggressive cells can attach to other cells or blood vessels more easily, aiding their movement to the lungs or liver. These secondary tumours, also known as metastases, are the tumours that PDAC patients usually die from. Next, I need to determine whether there is a direct connection between protein X and the variations among the physical properties of the PDAC cells.

We really want to pin down the differences between the more and less aggressive cells so that hopefully researchers and pharmaceutical companies will be able to design and develop more effective drugs to tackle PDAC. In a few years, once we know more precisely what protein X is doing in the more aggressive cells, our findings might matter a great deal to patients. For the moment I am simply trying to find out more about how PDAC cells work and I know that can sound theoretical. However, I am certain that knowing why and how some cancer cells, clearly, are more equal than others will help patients in the future.

 

New Scientist Live

This weekend the ExCeL centre in London hosted an event called New Scientist Live, which was aimed at the general public and invited speakers across various fields, including Brain & Body, Technology, Earth and Cosmos. Additionally, there were stands and interactive stations run by various scientific institutions from across the UK and Europe, including The Francis Crick Institute, the Royal Society of Biology and the European Space Agency, to name a few.

But, to be honest, I was already sold when I saw the giant bacterium (precise species is still a matter of debate; could be E. coli) hanging from the ceiling:

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Apart from this excellent demonstration of how cool cells are I want to write about two highlights.

  1. The talk by Molly Crockett on “What makes us moral?”
    Molly Crockett has a lab at the Department of Experimental Psychology, University of Oxford (but will be moving to Yale next year) where she and her research group study the neuroscience of “morality”. Dr Crockett’s talk was all-round excellent: from the clarity of her speaking, to the information on the slides, the science simplified enough to be understandable, yet retaining the references on the slides so that one can look up the original research (Crockett et al., 2014 and 2015, both open access!). The main finding of the 2014 paper was that people tend to be “hyperaltruistic”: when deciding whether to inflict painful electric shocks to oneself or another anonymous human being, the person deciding needed to be offered/paid more money to hurt another person. People also decided more slowly when the effects were to be felt by the other person rather than oneself. Importantly, and Dr Crockett emphasised this in her talk, these studies were conducted with real people and real electric shocks so that the results from their experiments might give us information about real life situations, as opposed to hypothetical ethical dilemmas. Possibly one of the most famous of these dilemmas is one in which a person needs to decide whether to save five people by actively sacrificing one, or to passively let five people die:moral-dilemmaIn the 2015 paper the authors then go on to test whether various drugs  – the antidepressant Citalopram, a selective serotonin re-uptake inhibitor and Levodopa, a dopamine precursor – can alter this moral decision making. Interestingly, the antidepressant reduced the overall number of electric shocks the deciders were giving out, both to themselves and to others. The hyperaltruism was preserved since deciders still gave fewer shocks to the receivers for the same amount of money. Levodopa, on the other hand abolished this hyperaltruistic effect:

    crockett-2015

    Bar charts showing the effects of citalopram and levodopa on harm aversion – copied directly from Crockett et al., 2015

    Obviously the talk and the papers go into much more detail, especially with the statistics used to evaluate these admittedly small effects. Lastly, it’s important to note that, as Dr Crockett pointed out, none of this means that researchers are working on, or should be working on, developing a “morality drug”…

  2. The science magazine Nautilus published by the MIT Press.
    Nautilus starts where the New Scientist stops, namely, where things get really interesting. To me, the New Scientist poses similar questions to the ones I might ask, but often fails to really answer them or provide a satisfactory explanation as to why there is no answer (yet). When I do read its articles they often leave me with more questions than before, which, of course, isn’t a bad thing. However, after reading a few articles of Nautilus it seems that this magazine is more thought-provoking: the articles are longer and maybe more on the creative side, but retain the references at the end, and the style of writing is more enjoyable to me. For instance, an article called “The Wisdom of the Aging Brain” by Anil Ananthaswamy discusses the possibility that there are neural circuits, or certain regions of the brain, that, with training and age, allow us to become wiser.
    So if any of my few readers is feeling particularly generous today then why not consider getting me the Sep/Oct edition…?

References:

Crockett MJ, Kurth-Nelson Z, Siegel JZ, Dayan P, Dolan RJ (2014) Harm to others outweighs harm to self in moral decision making. Proceedings of the National Academy of Sciences 111: 17320-17325

Crockett Molly J, Siegel Jenifer Z, Kurth-Nelson Z, Ousdal Olga T, Story G, Frieband C, Grosse-Rueskamp Johanna M, Dayan P, Dolan Raymond J (2015) Dissociable Effects of Serotonin and Dopamine on the Valuation of Harm in Moral Decision Making. Current Biology 25: 1852-1859

Still digesting…

… the outcome of the Brexit referendum, yes. Or the fact that Austrian presidential elections need to be repeated, yes. But also, and on a more positive and scientific note, still digesting articles at eLife. It’s almost exactly a year since I did a short internship with their Features Editorial team, at the end of which my boss, Peter Rodgers, asked whether I would consider continue writing as a freelancer. Consider it? Of course. Yes, no consideration needed. I don’t think I could conceal quite how pleased I was with the offer. So for almost a year now I have been writing one digest a week (about two hours worth of work) and here I’d just like to highlight a few of the most interesting ones.

Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation

This was the second paper that landed in my inbox to digest. When I read the subject line I was a bit baffled by the coincidence, because it surely had to be a coincidence. The lead author of this paper was none other than my current PhD supervisor with whom I was scheduled to start a month later.
The main finding of this paper was a little bit counter-intuitive. The first author, Sophia Blake, studied glioblastomas, the most aggressive form of brain cancer, iand found that when she deleted a tumour suppressor gene called p53 in mice, the animals developed these tumours. So far so good. However, when she deleted a second tumour suppressor called ATMIN at the same time, fewer mice got fewer and smaller tumours.  The paper then goes into some mechanistic detail of how this happens and finishes by showing that there are probably similar processes at play in human glioblastomas.

Ebola virus disease in the Democratic Republic of the Congo, 1976-2014

Most often the papers I read and digest are about cancer, stem cells or molecular biology. Here, however, I got to take a look at an epidemiology study: the authors compiled data for seven Ebola outbreaks in the Democratic Republic of the Congo. To me the most interesting observation was that outbreaks that had, at the outset, a high “reproduction number” – the number of people a single infected person transmits the disease to – were caught and contained early. However, when this reproduction number was smaller than about three the outbreaks seemed to be dealt with less quickly, leading to an overall greater negative effect.

Pericytes are progenitors for coronary artery smooth muscle

In this paper Volz et al. used fluorescent imaging to track the progression of epicardial cells (on the surface of the heart) deep into the muscle tissue of the heart. Using these microscopy techniques, the authors could follow how the epicardial cells become smooth muscle cells, cells that contract and relax, in the coronary arteries. Clicking on the image below will take you to a video consisting of snapshots taken from the outside of a mouse heart to further within. The epicardial cells first become so-called pericytes, cells that normally support blood vessels, and then eventually turn into smooth muscle cells.

pericytes

Snapshot from the first video in Volz et al.

Secretion of protein disulphide isomerase AGR2 confers tumorigenic properties

This last paper I want to mention briefly because it is on a subject that is similar to my project. Fessart et al. studied what can make lung and breast cancer cells more aggressive, more tumorigenic. They noticed that a protein called AGR2, which is normally found within cells where it helps to fold other proteins correctly, can also be secreted outside cells. When this happens AGR2 can make healthy lung cells cancerous.

Almost one year of PhD is already over, three more to go. I think we can count ourselves lucky if, by the end of it, we have a nice story to publish…

References:

Blake SM, Stricker SH, Halavach H, Poetsch AR, Cresswell G, Kelly G, Kanu N, Marino S, Luscombe NM, Pollard SM, Behrens A (2016) Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation. eLife 5: e08711

Fessart D, Domblides C, Avril T, Eriksson LA, Begueret H, Pineau R, Malrieux C, Dugot-Senant N, Lucchesi C, Chevet E, Delom F (2016) Secretion of protein disulphide isomerase AGR2 confers tumorigenic properties. eLife 5: e13887

Rosello A, Mossoko M, Flasche S, Van Hoek AJ, Mbala P, Camacho A, Funk S, Kucharski A, Ilunga BK, Edmunds WJ, Piot P, Baguelin M, Muyembe Tamfum J-J (2015) Ebola virus disease in the Democratic Republic of the Congo, 1976-2014. eLife 4: e09015

Volz KS, Jacobs AH, Chen HI, Poduri A, McKay AS, Riordan DP, Kofler N, Kitajewski J, Weissman I, Red-Horse K (2015) Pericytes are progenitors for coronary artery smooth muscle. eLife 4: e10036

Righting wrongs & reading writings

Now this story is not invented, and reality is always more complex than invention: less kempt, cruder, less rounded out. It rarely lies on one level. – The Periodic Table by Primo Levi

Today I would like to firstly share a book recommendation: The Periodic Table by Primo Levi. Levi, born in Turin, Italy in 1919, was a chemist by training and a writer by necessity. He also happened to be Jewish. The Periodic Table (1975) contains, chapter by chapter – each named after an element that featured in Levi’s life, work or imagination – short stories, memories and anecdotes: ranging from the history and ancestry of his own family, to the story of a lone lead miner, the attempts at finding closure after surviving the concentration camp at Auschwitz, all the way to the life-affirming story of a single atom of carbon. You don’t have to be a chemist (although you can be) to enjoy the humour, the writing style and the humanity of this collection. It would make a good pairing with the psychologist Viktor Frankl’s book Man’s Search for Meaning (1946; the original German title …trotzdem Ja zum Leben sagen more literally means “Yes to Life despite it all”), a different survivor’s account of Auschwitz.

primo-levi

Primo Levi – image copied from Nature


And on another more literary than scientific note: I had the opportunity to attend a talk by Brett Benedetti, an Associate Editor at Nature Medicine. He explained the processes that manuscripts go through when they are received by the journal’s editorial team and what “tricks” authors can use to give their manuscripts a better chance. Among these were so-called “pre-submission enquiries”, which are letters (i.e. e-mails) that potential authors can send in advance of their manuscript to double check whether their work will be appropriate to the journal. In many cases this may save a lot of time if the answer to the enquiry is a resounding “no”: the work can be revised or immediately sent to a different journal instead, without going through the time-consuming process of submitting the entire manuscript.

The most common reason that papers are rejected from leading journals such as Nature, Science or Cell is that they are not “novel” enough. After this talk I think I have understood a little better what exactly is meant by novel: if you imagine knowledge in a scientific field as a two-dimensional line or arrow, it is never a smooth line. There are always gaps and, maybe more often than not, branches that come to a sudden halt. So something that is novel and publishable in high-impact journals contains work that pushes this arrow further and does not merely fill in the preceding gaps. This kind of work, of course, is no less important and needs to be done rigorously, perhaps even more so than those types of experiments that are novel.

Lastly, when asked by the audience about his own career path into scientific editing/publishing, Benedetti replied that he had had no experience in this field whatsoever (apart from the scientific prerequisites of a PhD and post-doc as a neuroscientist). I found this surprising but also highly encouraging.