Prostate cancer – piecing together the jigsaw

At Cancer Research UK, we regularly get asked why we spend different amounts on different types of cancer.

Most commonly, people want to know why we spend more on breast cancer than on prostate cancer, despite the fact that there are similar numbers of cases of each per year.

These queries often contain the accusation, implied or explicit, that there is some prejudice against men, or male cancers, amongst the cancer research community.

This is absolutely not the case. Although there has been a deficit in prostate cancer funding in the past, there’s been a substantial effort to remedy this, and with the creation of organisations like the Prostate Cancer Charter for Action, we’re now seeing some focused, concerted action on this front.

But nevertheless, there’s still a discrepancy in the research spend. And ultimately, this has much more to do with the science and biology of prostate cancer than the politics of research funding.

The simple fact is, we know much, much less about prostate cancer than we do about any other cancer in the ‘big four’ (i.e. lung, breast, bowel and prostate cancer, which account for nearly 45 per cent of all cancers diagnosed in the UK).

“But surely,” you ask, “if you don’t know much about prostate cancer then you should spend more money on finding out?”

Sadly, its not quite that simple.

The causes of cancer

As we know now, cancer occurs when ‘things in the environment’ interact with our genes. Some people get dealt a ‘bad genetic hand’ – they inherit genes from their parents that make them more susceptible to the effects of these environmental factors.

So understanding the causes of cancer means working out two things: the genes involved, and the identity of these mysterious ‘things in the environment’. As Ed wrote about last week, gene-environment interactions are the key to understanding cancer.

Breast cancer & hormones

In the case of breast cancer, we’re pretty advanced in our understanding. We know that the ‘environmental factors’ are, essentially, variations in woman’s hormone levels caused by pregnancy, menopause, the Pill, HRT etc.

And we know about many of the genes involved, what they do, and how they can go wrong.

So its relatively easy to carry out research on breast cancer. We know a lot about it, so scientists can ask lots of sensible questions and carry out lots of research into different aspects of the disease.

Bowel cancer & diet

Bowel cancer, as you might expect, is linked to diet. What you eat has an effect on how your bowel cells grow and divide. The disease appears less common among people who eat a lot of fibre, and more common among people who eat a lot of red and processed meat. Alcohol too seems to be linked to higher rates. And exercise helps, possibly by working any nasties out of your system quickly.

Genetically speaking, however, we’re still feeling our way. We know a fair bit about a few of the genes involved, and how gut cells can develop into polyps, and then into cancer cells. But there’s still a long way to go.

Lung cancer & smoking

With lung cancer it’s even more simple. Smoking is so horrifically damaging to your DNA that you don’t even need ‘bad genes’ – nine-out-of ten lung cancers are caused by smoking. Interestingly, as smoking rates fall, we’re starting to find out more about the genetics of the disease, but that’s a story for another day. Given the starkness and strength of this one single environmental risk factor, its unsurprising that millions have been spent on anti-smoking strategies.

Prostate cancer & …?

But with prostate cancer, we’re much less advanced in our understanding.

We know there’s definitely an environmental effect, because rates are rising in the West and vary from country to country. There are suggestions that bodyweight, for example, can affect the risk of aggressive forms of the disease.

And we know there’s a genetic component because it can run in families, because different ethnicities have different rates of the disease, and because different men get different ‘types’ of prostate cancer.

But beyond that, we don’t know an awful lot for sure. And as a result, we still don’t really know the best way to treat men with prostate cancer, or who best to offer PSA screening. And ultimately, its difficult to push forward with the sort of research effort we see in breast cancer, when we know so little.

The way forward

But things are changing. Last week saw the publication of three papers in Nature Genetics that look set to kick-start prostate cancer research. The papers reported the discovery of a whole host of new genetic markers for the disease. One the papers reported the first results from a huge 13-year £multi-million gene-hunting study led by Cancer Research UK-funded scientists Ros Eeles and Doug Easton. The other two papers reported similar results from groups in Iceland and the US.

Taken together, these papers represent a huge step forward. Now we can, for example, start looking at the lifestyles of men who have several of these markers – that ‘bad hand’ we mentioned earlier – see which of them get cancer and which don’t. This should in turn allow us to pinpoint the environmental factors that affect cancer risk.

These findings also allow us to look at which markers are linked to aggressive cancers. We can think about offering screening to men whose markers tell us they’re at high risk. We have a starting point to develop new drugs. We can even, potentially, find out which men to exclude from testing, saving men from unnecessary worry, and saving vital healthcare resources.

In short, we’ve found some key pieces of the jigsaw puzzle, and now some of the other bits should start falling into place.

These findings won’t – yet – have any direct consequence for men who currently have prostate cancer. But as a result of these discoveries, hopefully the future will be a brighter place for prostate cancer research and, ultimately, for men diagnosed with the disease.

Henry