Sci-fi audio drama podcasts galore

Radio drama is making a big comeback in the form of podcasts, with plenty of high quality science fiction to choose from. Here are some of my favourites.

I’ve been a science fiction fan since I first read John Wyndham’s The Chrysalids as a kid. I quickly graduated to the Hitchhiker’s Guide to the Galaxy books (I’m proudly sporting a “Vote Zaphod Beeblebrox 2016” t-shirt as I write this), Red Dwarf, and countless other books, TV shows, and films – some of them great, some of them terrible, some of them (my favourites, if I’m honest) somehow managing to be both.

I’ve also been a podcast fan for many years. Ironically, however, given the origins of my beloved Hitchhiker series as a radio programme, I’d never combined the two interests until very recently; my phone’s playlist was full of documentary series. But then CBC Vancouver ran a story on a locally made paranormal mockumentary podcast, The Black Tapes (The X-Files meets Serial), and I suddenly found myself in a whole new world of audio drama – and discovered some phenomenal new science fiction.

The podcast format is ideal for old-time radio drama-style productions, which are making a big comeback. There seem to be new shows launching every week, and unfortunately many of them just don’t work – even when the story’s decent the characters’ voices sometimes all sound too similar, the actors haven’t rehearsed properly and are obviously reading from a script, or it’s not clear what’s going on in the big action sequences (apart from an awful lot of banging and shouting, usually). But when it’s done well, it’s a truly immersive experience and a wonderful way to enjoy some quality sci-fi while you commute, exercise, or plot galactic domination at the head of an army of evil robots.

My all-time favourite sci-fi podcast has to be Sayer (miraculously resurrected recently for a fourth season). The story of a colony established by a private company on an artificial moon is told almost entirely in one voice, that of the eponymous AI entity who runs the operation. The first few episodes focused largely on a single new member of the colony, and were fairly light in tone. However, the series got darker, more thoughtful (downright philosophical at times), and a lot more intricate as it went on to explore the origins and likely fate of the colony, and I was completely absorbed by the extremely clever use of sound and music (I almost missed my bus stop several times). They even managed to pull off an extremely satisfying ending to the original three-season arc, which is all too rare for a much beloved series. Very cleverly done, and highly recommended. I shall be listening to the whole thing all over again in anticipation of the new episodes.

Back on Earth, The Bright Sessions is also excellent. Imagine if Professor X ran a psychiatry practice instead of a school for gifted youngsters, and you’ve got the premise – Dr. Bright specializes in counselling young people with extraordinary powers, including time travel and telepathy. The early episodes each comprise a single session with seemingly unconnected patients, but as the story progresses the dots begin to connect into a larger conspiracy.

To The Manor Borne (By Robots) rounds out my top three. This utterly charming podcast consists of stand-alone stories, as told to placate a Beast, Destroyer of Worlds. The episodes are held together by an ongoing swashbuckling, time-travelling, body-swapping tale about the quest for the Beast’s origins and the means to its downfall. It’s enormously good fun, and I only wish the episodes came out more frequently.

I also enjoy ars PARADOXICA (time travel shenanigans), Limetown, (mockumentary about a mysterious town and its scientific shenanigans)and The Message (another mockumentary – the format works well on audio podcasts – about scientists figuring out a mysterious signal)Away from the strictly sci-fi genre, I highly recommend Greater Boston (if you like Wes Anderson movies, you will like this), Hello from the Magic Tavern (silly), The Lift (spooky), The Magnus Archive (creepy), and Uncanny County (quirky). If you’re still looking for more radio drama content, there’s a good list of paranormal and sci-fi podcasts on Reddit, and you can find additional shows on Twitter via the #audiodramasunday hashtag.

Whole new worlds are waiting for you on your phone!

originally posted on my personal blog


“Introducing Epigenetics: A Graphic Guide” now available in the UK!

I’m delighted to announce that my book was published today in the UK!

I received a few advance copies on Tuesday, and I’m really pleased with how it’s turned out.




This is one of my favourite illustrations (although it’s hard to choose! Oliver Pugh did a fantastic job). I did my postdoctoral research on repetitive DNA, and I think RNA is one of the most interesting molecules of all time, so I might be a bit biased though.

I’ve also set up my author profile page on Goodreads.

The book is available for pre-order everywhere, and will be published on March 14th in the USA and March 20th in Canada and elsewhere. Links to all major vendors can be found here – or ask your friendly local independent bookstore!

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Posted by on 2017/02/02 in Books, epigenetics


Announcing “Introducing Epigenetics: A Graphic Guide” – coming in early 2017!

INTRODUCING-EPIGENETICS-14mm new1I’m very excited to officially announce that I have a new book coming out next year!

“Introducing Epigenetics” is part of the Graphic Guides series by Icon Books. I’ve written the text, and artist Oliver Pugh is currently working on the illustrations. He’s done great work on earlier books in the series, and I can’t wait to see his artwork for Introducing Epigenetics!

The book covers all aspects of the exciting field of epigenetics, from the basics of gene regulation and embryonic development to the role of epigenetic modifications in diseases and their treatment, evolution, and the controversial field of epigenetic inheritance. I had a ton of fun writing it, even though it didn’t leave me with much time to do anything else last year!

The book will be available on February 2nd in the UK and March 14th in Canada, Australia, and the US. Other countries TBD.

More details, including links to online vendors, available here.


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Posted by on 2016/08/13 in Books, epigenetics


Quora activity for January 2015 – August 2016

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!


Would it be possible to avoid cancer by modifying our DNA?

Is whole genome sequencing of any use in cancer diagnostics?

If our body can detect cancerous cells, why do people still get cancer? Does it mean that we can improve our body’s defenses against cancer before even getting sick?

If 2/3 of cancers are caused by chance mutations, why should I work to help prevent cancer?

Is it possible that cancer is not actually a disease to be “cured”, but it is actually an inherent defect of genetics?

Is cancer an intrinsic feature of life?

Is worrying about cancer the biggest cause of cancer?

What are the chances (if any), that a blind person getting cancer in the eye would allow them to see again?

What cure would be most beneficial to discover: HIV/AIDS or cancer?

Can Ebola be treated with cancer drugs?


If two people have identical DNA fingerprints, what other molecular evidence does forensics use to distinguish between biological samples?

Can a methylation pattern be sequenced?

What could potentially be the most exciting application of epigenetic research?

Why hasn’t Lamarck been acknowledged in the face of the burgeoning advances made in the science of epigenetics?

In what way does histone methylation prevent transcription?

Is the epigenetic system of a person heritable?

Is there a meaningful way to diagnostically test a patient for epigenetic changes caused by long term use of medications?

Other Scientific Subjects

Is it a possibility that parents of genotype AA have an offspring with AS?

What is the reason that viruses are inactive when not inside any organism? What is the mechanism?

Will the final solution to HIV be to just accept it as part of the human genome?

What can you tell about a gene based on its tissue expression patterns?

What are some interesting examples of people becoming infected with typically fatal diseases (e.g. Ebola, HIV/AIDS, rabies, anthrax) through unusual means or at long odds?

Could cellular environment (pH, temperature, molecular crowding, redox state) affect a cell’s interactome?

What causes mutation in viruses?

Which (multicellular) animal is most deadly to humans?

What would happen if all the DNA in my body suddenly disappeared?

What are the most useful lab hacks, tips and tricks for molecular biology/biochemistry?

Do viruses have nutritional value for any organism?

What will next-generation sequencing be called a generation from now?

When will we be able to sequence the genome of every living vertebrate on Earth?

What are the oddest organisms?

Biochemistry: Why does the yeast two-hybrid system system have low specificity?

About Scientific Research and Careers

What does a principal investigator at a molecular biology lab spend time doing during the day?

How common is it for scientists to hire people to write their grant proposals?

How do I improve my grant writing?

I want to apply for a grant for a project, but I have no idea how to write a proper grant proposal. How can I go about this?

What is your favorite annual scientific conference?

Does a biochemist/biologist have to know all the reactions of cellular respiration or other general topics by heart after graduating?


Is there racism in Canada? Why?

What’s the best story about “fighting fire with fire”?

What are some of the best moments while taking exams?

Why do people believe in the ancient aliens theory?

If cloning of people was legal, whom would you choose and why?

What are some great optical illusions?

Which is the best way to pass the PMP exam?

Why do some people choose to use Quora over writing a blog?


Quora activity for June – December 2014

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!

I haven’t been as active as usual over the last few months; I took a break over the summer, and then entered the busiest few months of my professional life (as well as doing my usual full-time job I also helped organise and run the 2014 Joint Annual Meeting of the International Human Epigenome Consortium and the Canadian Epigenetics, Environment, and Health Research Consortium, then studied intensively for my Project Management Professional exam, which I passed just before Christmas). I still managed to write a few answers though!


Which cancer strains are contagious among humans and how can they be contracted?

Do you think the government knows the cure for many illnesses like cancer but hides the information to make more money off the unsuspecting general public?

What types of cancer are affected by epigenetics?


How difficult is epigenome sequencing, as compared to genome sequencing?

What are all the elements of an epigenome?

What are some great resources to teach epigenetics to a class?

Does DNA methylation and histone acetylation add to the amino acids of the histone or nucleotide?

Other Scientific Subjects

Why isn’t there a cure for Ebola yet? Is it as mysterious as HIV?

What does it mean to have a genetic predisposition to a disease?

Why are longer DNA sequencing read lengths preferred over shorter read lengths?

What are the most amusing figures or images from academic journals and articles?

Do siblings who share the same set of parents each have the same distribution of parental DNA? Can one sibling have more of one parent’s DNA or would the parental DNA distribution be equal?

Does a chromosome contain a thousand genes, or is it gene pairs (i.e. 2000 genes in all)?

About Scientific Research and Careers

Why are biologists so secretive of their data?

What happens to old scientific grant applications?

What’s competitive research funding?


What has been the toughest decision of your life? Did it turn out to be the right one?

What is the wittiest thing a child has ever said to you?

Is the term “agnostic atheist” a double negative?

What are the best examples of people “gaming the system”?

What’s the worst logo failure you have ever seen?

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Posted by on 2015/01/03 in Quora


The epigenetics of The X-Files

(Originally published on Occam’s Corner at Guardian Science, in December 2014)

Epigenetics is helping us to solve DNA mysteries that cannot be explained by genetics alone. It might even help explain some of the spooky phenomena described in the 1990s science documentary series The X-Files

Epigenetics has the power to open up possibilities beyond those offered by genetics alone – including the occasional triple word score Photograph: Cath Ennis

Dana Scully was a scientist, always looking for a perfectly rational explanation for the strange phenomena encountered each week. Many of these explanations were based on genetics, especially in the “monster-of-the-week” episodes featuring assorted freaks and other abominations not part of the main alien conspiracy storyline. Memorable monsters included such delights as a sewer-dwelling fluke man, and a charming creature possessing the lethal combination of an ability to squeeze through any gap and a taste for human liver.

It was easy enough to explain some of these freaks as genetic mutants – the man with a tail and an unusual muscle structure allowing him to mimic facial features surely had some kind of mutation in a muscle fibre gene – but the scientific basis of many other cases remained unknown. This shouldn’t be surprising: science moves quickly, and we’ve learned a lot about genetics since the ‘90s. One of the major advances made since then is in the field of epigenetics – a field that I believe has the power to resolve some X-Files cold cases.

X chromosome inactivation can definitely be explained by epigenetics. X-Files? Less certain. Image from Reinius et al., BMC Genomics 2010, 11, 614.

Epigenetic modifications include the addition of a methyl molecule to the DNA itself (could this be the mysterious fifth letter that Scully found in a segment of alien DNA?), and changes to the histone proteins around which the double helix coils itself. This molecular highlighting affects how the DNA text is read in that region, helping to determine which genes are switched on or off in each cell.

Many unresolved X-Files cases that might be accounted for by a genetic mutation could just as easily be explained by an epigenetic modification of the same gene.

For example, in cancer (where the cell’s epigenetic patterns go just as awry as everything else), the same tumour suppressor genes that are often lost by mutation or deletion can also be eliminated by abnormal methylation patterns in that part of the DNA. If there’s also a “psychic abilities suppressor gene” lurking in our genome, then we can provide a perfectly rational explanation for multiple cold cases in one fell swoop.

But let’s move on to something a little more challenging.

An important feature of epigenetics is that the pattern of molecular highlighting isn’t fixed. The DNA sequence itself is essentially the same in every cell of the body and through all stages of life; in contrast, epigenetic modifications are different in different cells, change during processes such as metamorphosis (definitely in frogs, so probably also in shape-shifting extraterrestrial species), and can change in response to the environment.

Even identical twins (or, say, genetically engineered clones), who have identical DNA sequences, have different epigenetic patterns – and these differences increase as the twins get older. This helps to explain why identical twins aren’t actually identical, and also why some clones are evil and others are able to overcome their genetic programming to become productive members of society.

Experiences as diverse as chemical exposures, traumatic experiences, and exercise have been shown to cause epigenetic changes. I haven’t yet seen any published scientific papers documenting the epigenetic effects of exposure to alien abduction, alien virusesparasitic ice wormshallucinogenic fungal spores, or questionable tattoos, but I’m sure they would be spectacularly interesting and could account for the strange behaviour of some of the unfortunate people involved. They probably also explain Scully’s cancer; if carcinogens such as bisphenol A can operate at least partially via epigenetic mechanisms, I don’t see why alien experimentation techniques can’t do the same.

There’s even evidence that the epigenetic changes caused by some experiences, such as periods of starvation or drug use, can be passed on to future generations. Could epigenetic inheritance account for the supernatural abilities of Mulder and Scully’s son William? (Yes, William’s abilities were demonstrated in seasons eight and nine. Yes, I just said that I refuse to admit that these seasons ever happened. If Chris Carter doesn’t have to be internally consistent, then I don’t have to either). Some might even argue that epigenetic inheritance can also explain memories of past lives, but hey – that’s just silly.

In summary, the hypothesis that we can use epigenetics to finally close several X-Files cold cases seems to have some merit. (We can ascribe anything we can’t explain via epigenetics, such as invisibility and possibly the conception of baby William, to epic genie tricks instead). I hope the FBI are paying attention…

Add your own cold case explanations in the comments!

Cath Ennis is, like all the best X-Files episodes, based in Vancouver, Canada. She doesn’t really believe The X-Files was a documentary.

This article most definitely does not represent the official position of the International Human Epigenome Consortium. However, Cath and other consortium members did discuss some of the cold case explanations included in the article (on their own time and their own dime) during the 2014 Annual IHEC Meeting in Vancouver. Thank you Dena Procaccini and other participants for your contributions!

Cath is on Twitter as @enniscath, and on Words With Friends as Wonderbrit. The Truth is out there, and it’s worth at least eight points.


Can a trigger-happy immune system cause cancer after viral infection?

(Originally published on Occam’s Corner at Guardian Science, in June 2014)

Friendly fire: while the immune system tries to protect us from viruses, it could be causing cancer

The immune system is a fickle thing, both hero and villain.

The ability of our ancestors to survive plague and pestilence was one of the forces that shaped the evolution of the human species into its current form. But many of us now find ourselves in environments where many of the biggest infectious threats have been neutralised by a combination of vaccination programmes, improved hygiene, and (temporarily) effective treatments. With their usual duties cut back so drastically, our evolutionary superstar immune systems sometimes lash out at innocuous perceived threats. This can cause allergies, multiple sclerosis, and other auto-immune disorders in the process – sins of commission, if you will.

But at least our immune systems are still pretty good at protecting us from infections and most cancers, right?

Well, much of the time, yes. The importance of the immune system in protecting us from cancer is evident from the increased rates of the disease in people with reduced immunity due to HIV/Aids or followingorgan transplants. And yet the immune system’s sins of omission mean that far too many cancer cells slip through the net – and we still get colds and the dreaded norovirus, too.

This week, though, new research from University College London (UCL) suggests for the first time that the immune system also commits sins of commission when it comes to cancer.

The research, published in the journal Cell Reports on Thursday, concerns a class of genes called the APOBEC family. These genes code for proteins that attack invading viruses by mutating their DNA, a tactic that can stop or at least slow the replication and spread of the virus. The mutations caused by APOBEC proteins occur in a characteristic pattern – a pattern that also shows up in some types of cancer, including types that are often caused by infection with human papilloma viruses (HPV). Could the mutations in these cancers be caused by misfiring antiviral defences?

Papilloma Virus (HPV) EM
Human papilloma virus. Photograph: Laboratory of Tumor Virus Biology/Wikimedia Commons

Drs Stephen Henderson, Tim Fenton and their teams at UCL have now demonstrated that there is indeed an association between the presence of HPV in some cancer cells, elevated activity of the APOBEC proteins in those cells, and the presence of the characteristic APOBEC-mediated mutation pattern. These findings support the idea that HPV infection triggers an anti-viral attack that not only hits the intended target – the viral genes –but also the cell’s own DNA. The UCL team also found that mutations caused by APOBEC have a strong tendency to hit genes such as PIK3CA that help to regulate the growth and division of the cell, and whose mutation is associated with the development of cancer.

“It is not clear why HPV infection causes the APOBEC genes to misbehave and mutate PIK3CA,”says Dr Henderson. “It could be that the body responds to HPV infection with increased ABOBEC activity, simply making ‘friendly fire’ more likely. Alternatively, there may well be something about the virus that causes the APOBEC response to wrongly target the body’s own genes for mutation.”

The good news is that these new findings open up new avenues for researchers working on diverse aspects of the cancer problem: there are known inherited variations in a member of the APOBEC family that have been linked with an elevated risk of developing breast cancer; other viral infections may also be associated with cancer, possibly via the same mechanism; and drugs that target mutated versions of the PIK3CA protein are already being developed.

Meanwhile, if you don’t want to give your trigger-happy immune system a shot at the human papilloma virus, effective vaccines are now available.

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Posted by on 2014/09/14 in cancer, genetics, viruses


Epigenetics part 2: cancer, chaos and chemo

(Originally published on Occam’s Corner at Guardian Science, in June 2014)

As explained in part 1, epigenetics — chemical modifications to DNA and proteins – can profoundly affect gene activity. But epigenetics also plays an important role in cancer, and research in this field may be opening up potential new treatment options.

There are many different types of cell in the body. With very few exceptions, our cells contain identical DNA, but have different levels of activity of each of the genes encoded in that DNA. A gene that’s switched on at low levels in the intestine might be highly active in the brain and completely silent in the liver. Epigenetic marks (chemical modifications of the DNA or of the histone proteins that bind it — see part 1) help to set and maintain the appropriate levels of gene activity for each cell.

Histone modifications are very dynamic, allowing for rapid changes to the activity of specific genes in response to outside stimuli; in contrast DNA modifications, primarily a mark called DNA methylation, are much more stable. The epigenetic mechanisms that regulate both kinds of marks are like cogs in a well-oiled machine, working together with other parts of the cellular apparatus to keep everything running smoothly.

Cells affected by diseases have abnormal levels of gene activity. For example, the activity of the various tumour suppressor genes that usually inhibit cell growth and division might be lost in a cancer cell, while pro-division genes might be hyperactive. The epigenetic marks and mechanisms found in such cells also look very different to those present in their healthy counterparts. In cancer cellsfor instance, the overall amount of DNA methylation decreases as the disease progresses, even while specific parts of the DNA near important genes experience abnormally high levels of methylation; the patterns of histone modification observed in cancer cells also deviate more and more from the normal baseline over time.

There are also characteristic epigenetic changes in many inflammatory and autoimmune disorders, conditions associated with ageing, and many others. However, I’m going to focus on cancer in the rest of this article, since that’s the field I know best.

Epigenetic changes in disease: cause or effect?

A cancer cell is a chaotic beast. Freed from the multiple layers of regulation that usually control its growth and division, everything from its molecules to its movements is abnormal. Teasing apart the abnormalities that contribute to the chaos from those that are just collateral damagecaused by the chaos has proven to be a difficult problem to solve, and epigenetic abnormalities are no exception to this general rule.

It’s likely that many of the altered epigenetic patterns observed in cancer cells are just noise, a response to the chaos caused by other, earlier, changes. However, there’s evidence that in some cases epigenetic changes can actively contribute to the progression of the disease, and are sometimes even the very first event that sets a cell off on its path to malignancy:

  • Changes to the activity of specific genes that are usually involved in controlling cell growth can sometimes be attributed at least in part to epigenetic changes. The BReast CAncer (BRCA) genes, and other examples of the tumour suppressor genes that usually control cell growth, are often silenced by DNA methylation in cancer cells; conversely, the epigenetic marks that usually keep pro-growth genes silent in normal cells can be removed in cancer cells.
  • Mutations in proteins that create, remove, or bind to specific epigenetic marks have also been found in malignant cells; some of these mutations may even be the first alteration to occur in some types of cancers. For example, researchers (including some of my former and current colleagues) have identified a mutation in an epigenetic regulator protein called EZH2 in some types of lymphoma. The mutation changes the activity of EZH2, making it create more of a type of histone modification that’s associated with gene silencing. This seems to be a very early event in the development of these types of cancer. Mutations in other genes that are involved in forming, removing, or recognising specific epigenetic marks are also quite common in additional forms oflymphoma and other cancers.

Epigenetic therapies

There are two main targets when trying to reverse the epigenetic changes that contribute to the initiation and progression of cancer: the altered epigenetic marks themselves, and the abnormal proteins (such as mutated EZH2) responsible for initiating and maintaining these changes. In my last article, I compared the patterns of epigenetic marks found in different parts of the genome to using a pack of highlighters to mark up different parts of a text for different kinds of follow-up; to extend this analogy, epigenetic therapies try to either erase any coloured ink that has ended up on the wrong part of the text, or to fix the broken highlighter pen itself.

Given how hard it can be to distinguish epigenetic signal from noise in a cancer cell, and how critical epigenetic marks are to the normal function of healthy cells, the first of these two approaches – targeting the altered epigenetic marks found in cancer cells – is a more complicated and risky approach. Removing an epigenetic mark that’s present at abnormally high levels in cancer cells, but only as a reaction to the processes that are actually driving the progression of the disease, won’t effectively treat the cancer; decreasing the overall level of an epigenetic mark across the whole genome when only its effects on a couple of genes are actually important runs the risk of causing a lot of new collateral damage.

However, despite these difficulties it has been possible to design drugs that function by reversing global changes to DNA and histone modifications. Some of them are already in use, with many more in development.

The first such epigenetic-based cancer therapies to be approved are from a class known as histone deacetylase (HDAC) inhibitors. These drugs increase the overall level of a specific type of histone modification, and can reactivate some of the tumour suppressor genes that are silenced in certain cancer cells. The details of exactly how these drugs work are still being investigated (interestingly, their epigenetic effects may not represent the full story), but HDAC inhibitors have been shown to have a beneficial effect against some cancers, especially in combination with other therapies.

Drugs that reverse the gene silencing caused by DNA methylation in cancer cells are also in development, although at an earlier stage of the testing process. The benefits of these drugs are accompanied by the same kinds of side effects seen with other chemotherapy agents, but as the field matures and new classes of drugs enter the development pipeline, there is hope that these problems can be mitigated.

The second approach to epigenetic therapies – targeting the “broken highlighters” directly – mirrors a general trend in cancer therapy to develop drugs that target a specific protein. The goal is to drastically reduce the number and severity of side effects compared to those caused by traditional chemotherapy drugs, which are less precisely targeted and cause more collateral damage to the body’s healthy cells.

When a rogue protein (such as the form of mutated EZH2 seen in some lymphomas) is spreading epigenetic chaos in the cell, and when there’s good evidence that the resulting changes contribute to the progression of the disease, then inhibiting that protein would be expected to be an effective anti-cancer therapy.

Indeed, drugs that specifically block the function of the mutated EZH2 protein are in development. In early tests in cultured cancer cells and in mouse models, the EZH2 inhibitor reversed the altered pattern of epigenetic marks, restored the activity of the genes silenced by these marks, and slowed the growth of the lymphoma cells (NB my institution was not involved in this study).

Similar work is being done with the other “highlighter pens” that are known to often malfunction in cancer cells.

Given how long the drug development and testing process is, and how many potential drugs fail along the way, I’d call this a field with a lot of promise – in the long term. Researchers are still working out the details of how hundreds of proteins work together to set and maintain the patterns of epigenetic marks needed in a healthy cell, and the ability to tweak this complex machinery to turn a specific gene on or off at will is still a long way away. However, the ability to target and reverse the epigenetic chaos caused by mutations in specific epigenetic regulators is certainly a good place to start, and it’s encouraging to see such a relatively new field of basic research already reaching the clinic.

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Posted by on 2014/09/14 in cancer, epigenetics


Quora activity for May 2014

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!


How would you explain to a layperson why cancer has been such a difficult medical problem to solve?

Are cancer cells organisms?

Can you name some practices that cause cancer that people do without knowing?

Is chemotherapy effective in late-stage cancers?

Why is nausea often a side effect of receiving chemotherapy?

Other Scientific Subjects

What non-standard model organisms are currently used in experimental biology?

Should genetic engineering be banned?

Is AIDS a virus or cancer of the human blood?

Do human beings have unique toe prints, similar to unique fingerprints?

Doesn’t a person’s body reject embryonic stem cells from another person?

When will HDAC inhibitors be available for humans?

About Scientific Research and Careers

Writing Grant Applications: How do funders measure their grant’s impact?

What is the most annoying thing people have asked you after you told them your decision to do a Ph.D.?


What are some funny stories you have about your name being mispronounced or misspelled?

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Posted by on 2014/06/07 in Quora


Epigenetics 101: a beginner’s guide to explaining everything

[Originally published on Occam’s Corner at Guardian Science, in April 2014]

The word ‘epigenetics’ is everywhere these days, from academic journals and popular science articles to ads touting miracle cures. But what is epigenetics, and why is it so important?

Epigenetics is one of the hottest fields in the life sciences. It’s a phenomenon with wide-ranging, powerful effects on many aspects of biology, and enormous potential in human medicine. As such, its ability to fill in some of the gaps in our scientific knowledge is mentioned everywhere from academic journals to the mainstream media to some of the less scientifically rigorous corners of the Internet.

  • Wondering why identical twins aren’t actually, well, identical?Epigenetics!
  • Want to blame your parents for something that doesn’t seem to be genetic? Epigenetics!
  • Got a weird result from an experiment that doesn’t seem to make sense? Epigenetics!
  • Want to think yourself healthy? That’s not epigenetics! (Sorry ‘bout that).

But what exactly is epigenetics – and does the reality live up to the hype?

Screen Shot 2014-05-04 at 5.37.45 PM

The incidence of the word ‘epigenetics’ in published books, 1800-2008, via Google ngrams. Bringing this graph up to date and including other publication types would send that line right off the top of your screen.

Epigenetics is essentially additional information layered on top of the sequence of letters (strings of molecules called A, C, G, and T) that makes up DNA.

If you consider a DNA sequence as the text of an instruction manual that explains how to make a human body, epigenetics is as if someone’s taken a pack of highlighters and used different colours to mark up different parts of the text in different ways. For example, someone might use a pink highlighter to mark parts of the text that need to be read the most carefully, and a blue highlighter to mark parts that aren’t as important.

There are different types of epigenetic marks, and each one tells the proteins in the cell to process those parts of the DNA in certain ways. For example, DNA can be tagged with tiny molecules called methyl groups that stick to some of its C letters. There are proteins that specifically seek out and bind to these methylated areas, and shut it down so that the genes in that region are inactivated in that cell. So methylation is like a blue highlighter telling the cell “you don’t need to know about this section right now.”

DNA doesn’t just float around the cell by itself; it wraps itself around a group of proteins called histones. There are some epigenetic marks that actually affect these histones, rather than the DNA itself.

The DNA double helix wrapped around four histone proteins, in a structure called a nucleosome. By Richard Wheeler (Zephyris) [CC-BY-SA-3.0]]/Wikimedia Commons

Methyl groups and other small molecular tags can attach to different locations on the histone proteins, each one having a different effect. Some tags in some locations loosen the attachment between the DNA and the histone, making the DNA more accessible to the proteins that are responsible for activating the genes in that region; this is like a pink highlighter telling the cell “hey, this part’s important”. Other tags in other locations do the opposite, or attract other proteins with other specific functions. There are epigenetic marks that cluster around the start points of genes; there are marks that cover long stretches of DNA, and others that affect much shorter regions; there are even epigenetic modifications of RNA, a whole new field that I’m simultaneously fascinated by and trying to ignore because it’s bound to create a lot of extra work for me in both the project manager and the grant writing parts of my role. There are no doubt many other marks we don’t even know about yet.

Even though every cell in your body starts off with the same DNA sequence, give or take a couple of letters here and there, the text has different patterns of highlighting in different types of cell – a liver cell doesn’t need to follow the same parts of the instruction manual as a brain cell. But the really interesting thing about epigenetics is that the marks aren’t fixed in the same way the DNA sequence is: some of them can change throughout your lifetime, and in response to outside influences. Some can even be inherited, just like some highlighting still shows up when text is photocopied.

Epigenetics and our experiences

Any outside stimulus that can be detected by the body has the potential to cause epigenetic modifications. It’s not yet clear exactly which exposures affect which epigenetic marks, nor what the mechanisms and downstream effects are, but there are a number of quite well characterized examples, from chemicals to lifestyle factors to lived experiences:

  • Bisphenol A (BPA) is an additive in some plastics that has been linked to cancer and other diseases and has already been removed from consumer products in some countries. BPA seems to exert its effects through a number of mechanisms, including epigenetic modification.
  • The beneficial effects of exercise have been known for generations, but the mechanisms are still surprisingly hazy. However, there’s mounting evidence that changes to the pattern of epigenetic marks in muscle and fatty tissue are involved.
  • Childhood abuse and other forms of early trauma also seem toaffect DNA methylation patterns, which may help to explain the poor health that many victims of such abuse face throughout adulthood.

Epigenetic inheritance

This is an area where the hype has advanced faster and further than the actual science. There have been some fascinating early studies on the inheritance of epigenetic marks, but most of the strongest evidence so far comes from research done on mice. There have been hints that some of these findings also apply to human inheritance, but we’ve only just started to untangle this phenomenon.

  • We’ve known for some time that certain environmental factors experienced by adult mice can be passed on to their offspring via epigenetic mechanisms. The best example is a gene called agouti, which is methylated in normal brown mice. However, mice with an unmethylated agouti gene are yellow and obese, despite beinggenetically essentially identical to their skinny brown relatives. Altering the pregnant mother’s diet can modify the ratio of brown to yellow offspring: folic acid results in more brown pups, while BPAresults in more yellow pups.
  • Research on the epigenetic inheritance of addictive behavior is less advanced, but does look quite promising. Studies in rats recently demonstrated that exposure to THC (the active compound in cannabis) during adolescence can prime future offspring to display signs of predisposition to heroin addiction.
  • Studies of humans whose ancestors survived through periods ofstarvation in Sweden and the Netherlands suggest that the effects of famine on epigenetics and health can pass through at least three generations. Nutrient deprivation in a recent ancestor seems to prime the body for diabetes and cardiovascular problems, a response that may have evolved to mitigate the effects of any future famines in the same geographic area.

“More research is needed”

Epigenetics research continues apace in labs investigating a dazzling variety of topics. One interesting direction is the application of high-throughput sequencing technologies to the characterization of hundreds of ‘epigenomes’ (epigenetic marks across the entire genome). I manage a project that’s part of the International Human Epigenomics Consortium (IHEC), and am also a member of a couple of the consortium’s working groups, so I see for myself every day how fast this field is progressing. The goal of IHEC is to generate at least 1,000 publicly available ‘reference’ epigenomes (patterns of DNA methylation, six histone modifications, and gene activation) from various normal and diseased cell types. These references will serve as a baseline in other studies, in the same way that the original human genome project sequenced a reference genome to which scientists can now compare their own results to identify changes associated with specific diseases.

This is a field that’s guaranteed to keep generating headlines and catching the public’s interest. The apparent ability of epigenetics to fill some pretty diverse gaps in our understanding of human health and disease, and to provide scientific mechanisms for so many of our lived experiences, makes it very compelling, but we do need to be careful not to over-interpret the evidence we’ve collected so far. And we certainly need to be highly sceptical of anyone claiming that we can consciously change our epigenomes in specific ways through the power of thought.

Now that I’ve piqued your interest in this fascinating field (and maybe that of your unborn children. Epigenetics!), in my next piece I’ll explore the role of epigenetic changes in the onset of cancer and other diseases, and what this means for the development of new treatment options.

There are links to videos and other resources about epigenetics on the IHEC website. There’s also a free Massive Open Online Course (MOOC) in epigenetics offered by the University of Melbourne on the Coursera site; I just started the April 2014 session so I can vet it for work-related purposes and it’s great so far, although a pretty solid background in genetics is required.

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Posted by on 2014/05/04 in epigenetics, genetics