Posts Tagged ‘Cancer’

Science that’s only skin deep

// December 3rd, 2010 // 2 Comments » // How Things Work, Recent Research, Science Communication, Sex and Reproduction

I’m a guest blogger for the RiAus, and this post also appeared on their fancy website. To tell the truth, I really wanted to call this post “Hormonally Yours” in homage to the Shakespeare Sisters (anyone?) but I’ll save it for another post.

Recently I was in Arnhem Land, visiting some Indigenous communities with a couple of friends. While I was there, I got pretty jealous of everybody’s darker skin. “It’s so well suited for Australia,” one of my friends lamented. “I should be in Norway or something.”

Pale skin like mine is not great for Australia. I tan pretty easily, but only after being burned bright red. While I was in the NT I slathered sunscreen religiously, but still managed to get a highly embarrassing burn on my lower back when I was building a sandcastle (an epic sand turtle, actually. Totally worth it.)

Anyway, enough about me and my weirdly tanned lower back (it’s been months! Why won’t it go away?) Let’s talk about Nina Jablonski, an anthropologist. In 2000 she suggested a new reason why skin colour varies so much. It’s not an adaptation to protect against skin cancer and sunburn, like I always thought it was.

It’s real job is to keep us highly fertile by maintaining a delicate balance between two key vitamins: Vitamin D and Folic acid.

Pica's skin tone matched her UVB exposure like her scarf matched her dress. Image by Monja Con Patines

Vitamin D is obtained through some foods, but mostly from drinking in sunshine. UV light turns cholesterol into Vitamin D, which then goes to either your liver or kidneys to be converted to an active form.

Once active it helps white blood cells like macrophages kill bacteria, and helps control levels of calcium and phosphate – important for building healthy bones.

Deficiency in Vitamin D causes rickets, a disease resulting in soft, easily broken bones and deformity which can lead to early death.

So getting enough UV (specifically UVB light) is important to not dying, and therefore having reproductive success later in life. It’s been backed up by Yuen, A. (Vitamin D: In the evolution of human skin colour DOI: 10.1016/j.mehy.2009.08.007)

Natural selection favours soaking up UV.

Penny stayed under foliage at noon to protect her folic acid. Image by Monja Con Patines

Folic acid is obtained in leafy vegetables and fortified cereals. Rather than being made by UV, the light can destroy folic acid by literally breaking it apart. (Jablonski, N. The evolution of human skin coloration DOI: 10.1006/jhev.2000.0403)

Critical for DNA synthesis, folic acid is essential during pregnancy when a lot of new cells are being made.

Folic acid prevents against 70% of neural tube defects in embryos. Its destruction by UV is bad news.

Natural selection favours avoiding UV.

So there’s an ideal amount of UV light that needs to get through the skin – enough to produce Vitamin D, but not too much to destroy all the folic acid. Getting the balance right for the environment you’re in means higher fertility, which drives natural selection

This is what Nina Jablonski thinks caused the evolution of skin colour through the sepia spectrum we see today. Dark skin, with high melanin, stops more UV light. That’s exactly what you want if you live in a place with a lot of sun, like places near the equator. Light skin lets more UV in, which is great if you live somewhere overcast and not very high on UV.

Understanding how your skin colour (NOT your race) influences these two vitamins is important in being healthy. It’s more important now than ever, because we humans travel a LOT.

Sadly, Australia is pretty high in UV and I am pretty white. Thank god for sunscreen.

Things are rarely that simple though, and I imagine there’s a few different things going on that connect UV light to skin colour.

On Tuesday the RiAus is holding an event called Skin Deep: Exploring human ancestry. They’ll be showing a preview of a new SBS documentary about skin colour scientific research, as well as results from the Genographic Project. Basically they took DNA samples from a lot of volunteers and some national identities, and now they’re giving us the goss on who’s related to who’s secret love child.

I’ll be there, I’d love to see you (though seats are limited.) I’ll be the one tweeting in the corner. Follow me @CaptainSkellett

Would love to hear from anyone who took part in the Genographic Project, and anyone who didn’t. Who would you most like to be related to? For me it’s David Attenborough, then I can dream of inheriting his voice.

Have a nap and let your computer cure cancer

// October 18th, 2010 // 2 Comments » // Drugs, How Things Work, Recent Research, Science Communication

computer doing science

Image by John Watson

While waiting for inspiration to strike a solid introduction into my head, my computer screen went blank. Good ol’ MacBook conserving energy! But letting your computer go idle doesn’t mean you have to waste its processing power. Why not cure cancer with grid computing?

It’s a kind of parallel computing, which breaks up complex problems into smaller calculations and then solves them at the same time. Instead of one processor working on one calculation a time, a group of processors work on different calculations together. Dual-core computers is one way to do it. Grid computing is another.

Grid computing is like a massive virtual computer whose processors are computers linked by a central software.

World Community Grid is one group which utilises the personal computers of over half a million volunteers around the globe. Their software switches on when the computer is idle and runs virtual experiments, calculating and number crunching its way through chemical simulations. They provide this public grid to humanitarian research projects.

Childhood cancer
One of the projects they are running is helping to solve childhood cancer by finding potential new drugs for neuroblastoma, one of the most common solid tumors in children. In some people the tumors do not respond well to chemotherapy. This research is hoping to turn this around by targeting three proteins which are important to the cancer’s survival. Knock out those proteins and the cancer will in turn be knocked out by chemo.

Good plan, but how to knock out the proteins? That’s where the grid comes in.

There are three million potential drug candidates who MIGHT bind to one of the proteins and knock them out. Of course, that’s a lot of laboratory time right there. A computer would be better, but to run these nine million virtual experiments would take 8000 years. By working with the public grid they expect the project to be finished in just two years. Possibly less.

That’s a big saving on time and grant money. It’s rational based drug design (which I blogged about here) taken to a crowd sourcing extreme. They are trying a similar thing to discover dengue fever drugs.

Carbon Nanotubes

Image by Mstroeck

Clean Water
Drug design isn’t the only industry using the World Community Grid. Last month universities in Australia and China announced they are running simulations through the grid to find out how to filter water using nanotubes.

Nanotubes are small tubes that only water molecules can fit through. Not bacteria, not even viruses. It’s a great way to get rid of water dwelling nasties and desalinate sea water. But with such small pores you would expect the pressure and energy needed to force water through the filter to be incredible. And incredibly expensive. But in 2005 experiments showed that actually the water flowed pretty fast through the filters.

Why? Possibly the water molecules touching the nanotubes act more like ice and reduce friction. But who knows? To find out exactly what’s happening they’re running realistic simulations using the grid. The outcome could lead to huge improvements in water availability, potentially saving millions of lives a year in the developing world.

Like the idea of grid computing? Sign up to the World Community Grid here, and let your down time make a difference.

Meet telomerase, the enzyme that won a Nobel Prize

// February 18th, 2010 // 20 Comments » // Recent Research

As a pirate I am rarely afforded the luxury of meeting the rich and famous, but today I met Elizabeth Blackburn. She was awarded the 2009 Nobel Prize in Physiology or Medicine, making her the first first FEMALE Australian born scientist to win a Nobel Prize. (I also met the PM and Senator Kim Carr, just to round out my VIP day.)

Sadly the story didn’t make the news on TV… further evidence that science just doesn’t rate to the media.

Well, it rates to ME. So I’m dedicating this post to the research that nabbed the Nobel Prize, the discovery of telomerase, builder of telomeres, protector of chromosomes.

WTF is a telomere? Inside your cell you have 46 chromosomes, long strands of DNA that have ends. Chromosomes have telomeres for the same reason we shipfolk dip the ends of rope in wax – so the ends don’t fray. Instead of wax, we have the same sequence of DNA bases (TTAGGG) that repeat over and over and wrap around some special proteins to make a nice neat little end.

When it comes to that special time in a cells life when the mommy cell loves itself very much, it needs to make a copy of all its DNA so it can split into two new cells. Because of how the machinery works it needs some DNA at to hold onto before it can start copying, which means some DNA at each end is lost every time the cell splits. That’s another good reason to have telomeres, you can lose a bit of them each time and it doesn’t hurt your genes.

However you’ve only got a certain amount of telomeres, and once they run out two things can happen. One: the cell stops dividing. Two: Something bad.

Something bad is that the cell, keeps dividing and starts cutting into the rest of its DNA. Suddenly you have lose ends of DNA whipping around the cell like untied ropes in a storm. The cell freaks out and thinks “eep, my DNA strand has been cut! Must sew it back together!” and then attaches one end to another end, probably to another chromosome altogether. That’s actually okay, until it comes time to divide again. The chromosomes need to separate so they can go into the daughter cells, and oh noes they are attached to each other! Solution? Rip them apart, then sew two bits back together… somewhere… Oh dear…

Soon you have DNA that has been stitched together a bit like Frankenstein’s monster. Most of the cells will die (for obvious reasons), but some will survive, will become stronger, better, faster than before, will become the cancer.

So telomeres protect your cells, but usually run out over the life of the cell. Fortunately there’s an enzyme that makes more of those TTAGGG repeats, so you have more telomeres! That’s what Elizabeth Blackburn helped discover – the superdooper trooper enzyme TELOMERASE.

Most of your cells don’t make telomerase, but stem cells do – that’s why they can survive for your whole life. Having an active version of telomerase can help protect against that split/stitch cycle and prevent cancer forming… mice often have more telomerase in their cells, and longer telomeres – as a result they get different kinds of cancers to us.

Pretty nifty enzyme, hey. Don’t know why the media wouldn’t be interested in that… you know, protects against cancer, important part of stem cells… no, don’t put THAT on the news. Let’s have some hardcore sport and a weather feature or two. GORDAMMIT!!!

HeLa, the first immortal human cells and a tale of immorality

// January 12th, 2010 // Comments Off on HeLa, the first immortal human cells and a tale of immorality // Science Communication, Unethics

When we work with cell lines in the lab, we often work with HeLa cells. They can live in a vial of nutrients, and from a small sample you can grow a large quantity to use in cancer research, in vitro fertilisation research, stem cell research, virus research, pretty much any kind of human biology research actually. They’re a biologist’s wet dream.

HeLa cells come from an aggressive cervical cancer that attacked, and eventually killed, a women called Henrietta Lacks.

She has been dead for over 60 years but those cancer cells are still going strong. Which is pretty amazing! Usually when you take some cells out of a person they die pretty soon after, or they might live for a few months, but not 60 years. That’s rare. Cancer emerges after a lot of severe mutations and a Darwinian baptism by fire, only strong, successful mutants emerge from the ashes of their brothers who died from lethal mutations. The survivors are bad-ass.

They are also very weird looking. HeLa DNA has been extremely mutated, instead of 46 chromosomes it has 82, and it has several versions of human papilloma virus (HPV) DNA, which is found in pretty much every case of cervical cancer. So research with HeLa cells is NOT research with a normal human cell.

That strange DNA makes it do some pretty amazing things: It replicates abnormally fast, even for cancer cells, and it has an active copy of telomerase which means it can replicate indefinitely. Most other cells age as they divide until they reach the Hayflick Limit, then they don’t divide no more. Not HeLa. Neither do stem cells actually, but that’s a tale for another day.

HeLa cells revolutionised our understanding of human biology, but the family of Henrietta have yet to see a cent of it. In fact, those cells were taken from her without her knowledge. Dodgy, dodgy stuff. I’m placing this story firmly in the unethics basket just for that. HT to Ed Yong for telling us about a book soon to be released about the lady herself.

The Immortal Life of Henrietta Lacks” comes out next month, written about the woman and the cells which should have made her famous. Rebecca Skloot been researching it for something like 10 years and it’s got some great reviews. I’m going to pre-order a copy, and if you’d like to know more about HeLa cells and Henrietta Lacks, do the same! It’s a story that deserves to be heard, and if there are enough pre-orders, Amazon will help promote the book. Plus it’s 30% off at the moment. What more could you want? Here’s the blurb.

Her name was Henrietta Lacks, but scientists know her as HeLa. She was a poor Southern tobacco farmer who worked the same land as her slave ancestors, yet her cells—taken without her knowledge—became one of the most important tools in medicine. The first “immortal” human cells grown in culture, they are still alive today, though she has been dead for more than sixty years. If you could pile all HeLa cells ever grown onto a scale, they’d weigh more than 50 million metric tons—as much as a hundred Empire State Buildings. HeLa cells were vital for developing the polio vaccine; uncovered secrets of cancer, viruses, and the atom bomb’s effects; helped lead to important advances like in vitro fertilization, cloning, and gene mapping; and have been bought and sold by the billions.

Yet Henrietta Lacks remains virtually unknown, buried in an unmarked grave.

Now Rebecca Skloot takes us on an extraordinary journey, from the “colored” ward of Johns Hopkins Hospital in the 1950s to stark white laboratories with freezers full of HeLa cells; from Henrietta’s small, dying hometown of Clover, Virginia—a land of wooden slave quarters, faith healings, and voodoo—to East Baltimore today, where her children and grandchildren live and struggle with the legacy of her cells.

Henrietta’s family did not learn of her “immortality” until more than twenty years after her death, when scientists investigating HeLa began using her husband and children in research without informed consent. And though the cells had launched a multimillion-dollar industry that sells human biological materials, her family never saw any of the profits. As Rebecca Skloot so brilliantly shows, the story of the Lacks family—past and present—is inextricably connected to the dark history of experimentation on African Americans, the birth of bioethics, and the legal battles over whether we control the stuff we are made of.

Over the decade it took to uncover this story, Rebecca became enmeshed in the lives of the Lacks family—especially Henrietta’s daughter Deborah, who was devastated to learn about her mother’s cells. She was consumed with questions: Had scientists cloned her mother? Did it hurt her when researchers infected her cells with viruses and shot them into space? What happened to her sister, Elsie, who died in a mental institution at the age of fifteen? And if her mother was so important to medicine, why couldn’t her children afford health insurance?

Intimate in feeling, astonishing in scope, and impossible to put down, The Immortal Life of Henrietta Lacks captures the beauty and drama of scientific discovery, as well as its human consequences.

Catching cancer part two – HPV infection versus the face of Tasmanian Devils

// January 2nd, 2010 // 5 Comments » // How Things Work, Sex and Reproduction

Following on from yesterday’s post about the Tasmanian Devils, this is all about HPV – a highly infectious virus that can cause cancer (well, sort of. Read on.)

The Human Papillomavirus is crazy infectious – around three out of four women will have it at some time in their lives. That’s a LOT of people considering it’s transmitted sexually – ‘specially when you consider people who get married before sex and nuns and what not. It’s spread by skin to skin contact in the genital region, so a condom won’t completely protect you. Cling wrap all around the nether regions is what you need to stop this ninja virus. The stealthy, sneaky sonbich could be anywhere, including in your cells right now.

HPV infects the epidermis and can cause nothing, warts, or cancer. Most HPV just loiters around and is eventually cast out by your hard-core immune system, making you a lucky carrier! Some forms of HPV cause genital warts, an unpleasant and unattractive affliction which is nevertheless treatable. Other types are associated with cervical (and anal, vaginal and penile) cancers. Cervical cancer is the second most frequent cancer in women worldwide. 🙁

How does a virus cause cancer? Well, to put it simply, it messes with the cell cycle. Before your cell divides, it checks that things are okay – it checks the DNA for any mistakes (p53 is a protein involved in this) and it makes sure it has enough proteins to go ahead without making more mistakes (pRB is the man for this.) The virus produces two proteins – E6 and E7 that bind to p53 and pRB respectively, and inactivates them. This means your cell can replicate without the proper checks (good for the virus), leading to more cancerous changes. p53 in particular is a famous tumor suppressant, and messing with it can lead to out of control replication and chromosomal instability. In some cases, the virus DNA can insert itself into your normal DNA – then there’s no getting rid of it.

The journey to cancer takes around 10 years and a number of other cell mutations. Very different to the Tasmanian Devil face tumors in which the cancer is directly infectious. When I say “HPV causes cancer” I actually mean certain types of HPV can cause pre-cancerous changes in a cell which could one day lead to cancer. Think of it as the first mutation…

Freaked out? Well good news! There is a vaccine! Two actually, Cervarix and Gardasil protect against HPV types 16 and 18, which cause 70% of cervical cancers. Gardasil also protects against most genital warts by coinkidink. That doesn’t mean you can stop getting pap smears ladies. Still gotta do that. Sucks to be us.

This is a very cool vaccine though – in one generation of women (in the developed world they immunised at the age of 12, hope it’s available to developing countries as well), we could eliminate 70% of cervical cancer cases. That’s freaking fantastic! Oh, and HPV isn’t the only virus that can lead to cancer. Hepatitis can cause liver cancer, and Epstein-Barr Virus, lymphoma. We’ve got vaccines against Hepatitis viruses too!

A parting tip, swanky statistics available from WHO. And don’t type HPV into google images. Not cool guys… not cool.

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