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 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.]


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!


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.


A Short (Literary) Digression

Instead of bombarding you with too much text I thought I would share this YouTube channel with you, which is run by the journal Cell and features the authors of some of the papers published there as they explain their own research in a few minutes. Admittedly, some videos are more accessible than others, but browsing through is certainly a valid form of procrastination.

On the more literary front, I received a complimentary copy of this book in the post last week:


In fourteen chapters it outlines various career paths that biomedical scientists might take after doing a PhD and post-doc positions, ranging from science policy and patent law to science writing and publishing. Probably the three main take-home messages are that a) it is important to network (whatever that really means), b) one has to be somewhat daring in who one is willing to contact about potential jobs, and c) serendipity is usually involved in the process somewhere.

Moving from scientific self-help book to non-fiction/biography: I finally managed to finish Georgina Ferry’s biography of Max Perutz:


Perutz was a crystallographer and molecular biologist. Originally from Vienna, he went to Cambridge to do his PhD, where, apart from being deported to Canada during World War II as an “enemy alien”, he stayed until his death. Together with John Kendrew he won the Nobel prize in Chemistry in 1962 for “studies of the structures of globular proteins”. Undoubtedly a great researcher, and possibly an even greater mentor who founded and guided the prestigious Laboratory of Molecular Biology, he was certainly also a slightly difficult person to deal with. His constant psychosomatic illnesses, although certainly real ailments, drove some people up the wall. I wonder whether “great” and famous people become difficult as a result of their greatness and fame, or whether they have to be difficult in the first place to achieve greatness? If it’s the former then I’m not sure I want to become a great researcher, and if it’s the latter then by being quite “normal” (as I would like to believe) it seems unlikely that I ever will be a great researcher.

Although this is now moving from non-fiction to fiction, Candide by Voltaire is still in the realm of philosophy. If you are feeling strong and robust then I recommend this short 18th century novel for a rainy afternoon. But be prepared to be faced with the (irrefutable?) truth that we do not live in the best of all possible worlds, even if, like in this picture, it sometimes might seem that we do.

image1If, on the other hand, you are not feeling up to Voltaire, then why not go see Interstellar? It was valuable in that it taught me some poetry by Dylan Thomas:

Do not go gentle into that good night,
Old age should burn and rave at close of day;
Rage, rage against the dying of the light.

Though wise men at their end know dark is right,
Because their words had forked no lightning they
Do not go gentle into that good night.

Good men, the last wave by, crying how bright
Their frail deeds might have danced in a green bay,
Rage, rage against the dying of the light.

Wild men who caught and sang the sun in flight,
And learn, too late, they grieved it on its way,
Do not go gentle into that good night.

Grave men, near death, who see with blinding sight
Blind eyes could blaze like meteors and be gay,
Rage, rage against the dying of the light.

And you, my father, there on the sad height,
Curse, bless, me now with your fierce tears, I pray.
Do not go gentle into that good night.
Rage, rage against the dying of the light.

Ageing Research – A promise to “cure” all communicable diseases that plague our society?

Possibly one of the most up-and-coming yet controversial areas in biomedical science is the ever-growing field of ageing research. Last week Guy Brown gave introductory lectures on this topic, which were interesting and thought-provoking, especially because I previously had not given ageing much thought (neither as a thing that would affect me personally, nor as a topic of experimentation). His opening slide included this cartoon, which I copied from here:

Aging Researchers

As with most controversial topics, the controversy starts with the definition: currently there is no all-encompassing, universally accepted definition of ageing. However, most people would agree that ageing is a process that involves “progressive physical deterioration over time” (according to Prof. Brown). Furthermore, it is generally accepted that ageing is a major risk factor for a multitude of communicable late-onset diseases such as cancer, diabetes, cardiovascular disease and neurodegenerative diseases.

Therefore, if it were possible to reduce ageing – by which I mean to increase the human health span as opposed to the average/maximum human life span – then could we be preventing these diseases? In other words, should more (financial) efforts be put towards ageing research instead of cancer research, for example? A short and fairly straightforward review (Guarente (2014)) from a proponent of ageing research gives a good, if slightly biased, introduction to the area.

Generally speaking, I would argue that there are two approaches one can take when researching the process of ageing. On the one hand, one can ask why animals (but also single-celled organisms) age, and on the other hand, one can ask how animals age.

As to the why there are a lot of theories, but the main arguments include the following (and it is worth bearing in mind that ageing does not generally occur in “the wild”, since most animals die from extrinsic causes (e.g. predation or infection) before they age):

  • Mutation accumulation theory (Medawar, 1952): as we age we accumulate damage in our cells, and as long as this happens after reproduction (i.e. after selection pressure has been removed to keep our DNA healthy) then this should not adversely affect our offspring’s fitness.
  • Antagonistic pleiotropy theory (Williams, 1957): this theory posits that some genes, which are beneficial early during life and may increase the chances of having healthy offspring, can have detrimental effects later in life.
  • Disposable soma theory (Kirkwood, 1977): after reproduction, which is costly to the individual and uses up a lot resources, an organism is less able to repair damage.

Although these theories may seem logical to a certain extent, it can be easy to start invoking teleological arguments: maybe we age (and die) in order to make space for our children? But how would that information be encoded in our genetic material if ageing (by definition, I would say) occurs after reproduction? Would Darwin be happy with this?

I dare say he might prefer to know how we age. Again, there are a slew of theories regarding the mechanism of (cellular) ageing. Lopez-Otin et al. (2013) attempted to summarise these into nine hallmarks of ageing (in analogy to Hanahan & Weinberg (2011), who have famously done this for cancer). The mechanisms proposed include the accumulation of damage to both DNA (e.g. in the form of mutations) and proteins (e.g. they might start to form toxic aggregates), the exhaustion of stem cell self-renewal capabilities, a deregulation of nutrient sensing and cellular metabolism, as well as chronic inflammation.

You might accuse me of having a pessimistic outlook on life, but from the little I have read about the process and mechanisms of ageing and the still developing area of ageing research, it seems unlikely that vastly different diseases such as cancer and diabetes can easily be tackled from this one approach. Until now (but of course who knows what the future will bring) no treatments have unequivocally been shown to increase human health span. Possibly the most promising to date is a calorie restriction regime. To me personally, however, that seems quite unappealing – do I want to live healthily but hungrily to the age of 100, or satiated but with greater probability of dying by the age of 80?


Guarente L (2014) Aging Research – Where Do We Stand and Where Are We Going? Cell 159: 15-19

Hanahan D, Weinberg RA (2011) Hallmarks of Cancer: The Next Generation. Cell 144: 646-674

Lopez-Otin C, Blasco MA, Partridge L, Serrano M, Kroemer G (2013) The Hallmarks of Aging. Cell 153: 1194-1217

Max Perutz Interviews

The Vega Science Trust – Max Perutz Interview 1 – watch the first 45 seconds to hear about Perutz’s motto, “in science, truth always wins”. And then maybe watch the rest, indulging yourself in productive procrastination.

The Vega Science Trust – Max Perutz Interview 2 – here Max Perutz talks about science (with an emphasis on crystallography of course) and other important topics, such as religious fundamentalism (9:30) and faith/atheism (42:40) and the problem of overpopulation, partly due to lack of birth control. I particularly agree with him that, as a scientist, one should take a stance against creationism, but also not go as far as people like Richard Dawkins who relentlessly attack religion, which, Perutz says, “discredits science” and “shows our arrogance”.

Also watch out for an instance of mouth pipetting at 4:45 in the video posted in the last entry ( – this would be unheard of today!

Lastly, Perutz made an interesting prediction about whether and when the protein structure of haemoglobin would be solved in a paper from 1949:


[from: Perutz MF (1949): Recent developments in the x-ray study of haemoglobinRoughton FJWKendrew JC, eds. Haemoglobin: A Symposium Based on a Conference Held at Cambridge in June 1948 in Memory of Sir Joseph BarcroftLondonButterworths Scientific Publications135147]

Funnily enough, the structure of haemoglobin was eventually solved in 1968 – a year before the Apollo 11 moon landing.