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.

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.