Prostate cancer drug abiraterone has been given the thumbs up by NICE

Regular readers will know that we’ve been keenly following the story of abiraterone – a prostate cancer drug developed by British scientists – since 2008.

So we hope you share our delight over this morning’s news, that NICE and pharma company Janssen have finally reached an agreement, and the drug will now be available to suitable men on the NHS in England, Wales and Northern Ireland.

NICE say they were able to reach their decision after Janssen gave them additional data about the number of men the drug will be suitable for, which men it will benefit most, and – crucially – offered the NHS a better deal on the drug’s price.

This is fantastic news.

All suitable men in these three countries will be now able to easily access the drug, which can dramatically improve quality of life, and offers men with advanced prostate cancer extra time with their families and friends.

But let’s be clear. Abiraterone was licensed in the EU in September 2011. It is now May 2012. In the eight months it took for the regulatory horse-trading to run its course, depending on where they live, some men with advanced prostate cancer in the UK have been able to get it easily, whereas others have had to get their doctors to apply for access on an individual basis.

On top of this, since the Scottish NHS has a separate system, until we hear the results of an appeal, Scottish doctors continue to have to jump through similar bureaucratic hoops to get the drug for their patients.

So our joy is tempered with yet more frustration that, despite recent political focus, the UK’s drug approval systems still aren’t working nearly as efficiently as they should.

And while the high cost of new drugs is a fundamental issue here, we also need reform, so that the UK’s cancer patients aren’t left stranded and without options available to their counterparts in other countries.

Abiraterone – a homegrown success story

Abiraterone was developed by UK researchers

In the past, we’ve devoted a considerable amount of space to our involvement in abiraterone’s development, so we won’t labour the point – but here’s a very quick recap for new readers.

Abiraterone was developed as a result of fundamental lab research that took place at The Institute of Cancer Research in the 1980s, which we helped fund.

This led to the development of a chemical that could, with exquisite precision, stop a man’s body from producing testosterone – a hormone that can fuel prostate cancer’s growth.

The chemical was developed into a drug by Cancer Research UK scientists, and we helped support the first-in-man trials that showed such initial promise. From there, the rights to develop the drug were licensed to the pharma industry (which has the financial firepower to run the large trials necessary to prove a drug’s effectiveness and safety).

And Janssen pharmaceuticals then took the drug all the way to market, driven by the researchers and doctors at The Institute of Cancer Research.

This part of the story is as clear-cut an example as you could wish for of how basic molecular studies, followed by collaborations between researchers, doctors and industry, can lead to drugs that can transform lives. It’s a story we hope will inspire people to continue to support medical research charities like Cancer Research UK.

Hitting the buffers

But – as is the case with drug approval in general in UK – the story began to get more complex.

Shortly after Janssen were given a license to sell the drug in Europe, eligible patients in England began to receive the drug if their local NHS trust had decided to pay for it under England’s Cancer Drugs Fund – a scheme set up by the coalition government to fast-track drugs to patients.

But patients in Wales, Northern Ireland and Scotland faced a more difficult situation.

Wales and Northern Ireland aren’t covered by the Fund, so while NICE assessed the drug’s cost-effectiveness, patients in these countries had to apply individually through so-called ‘exceptional case committees’ in order to get it.

And men in Scotland had to do similar, while they waited for their own country’s body – the Scottish Medicines Consortium – to reach a decision too.

Being told by your doctor that he or she has to ‘apply’ to get a treatment that could help you, must be the last thing a man with advanced prostate cancer wants to hear.

In February, NICE announced that they were minded to reject the drug on cost grounds unless more data were forthcoming, or a better price was offered.

But they failed to use their own, more lenient ‘end-of-life’ criteria to assess the drug (which allow a higher price to be accepted) – something we said at the time made ‘no sense’. And so we had to wait for their final decision, in the hope that they’d be able to strike a deal with Janssen.

Just a few days later, in a decision that surprised many, Wales’s drug approval body, the All Wales Medicines Strategy Group decided to give abiraterone the green light, having used the ‘end-of-life’ criteria – a decision that could only be overturned by a final ‘no’ from NICE.

But a month later, Scotland said the opposite – they didn’t think the drug was cost-effective – a decision that is currently open to consultation (a final decision is expected in September, according to the Daily Express).

This left a ridiculous situation. By March this year, eligible English prostate cancer patients had had access to the drug since December, but through a temporary and finite pot of money (the Cancer Drugs Fund).

All eligible men in Wales were now getting the drug on the NHS, but this situation was temporary, and could change if NICE said ‘no’.

But no-one in Scotland or Northern Ireland was able to receive abiraterone routinely on the NHS – they had to apply for it individually.

And so to today’s news. Janssen ultimately decided they were able to lower their price further, NICE decided to use their end-of-life criteria, and as of today the drug is now available on the English, Welsh and Northern Irish NHS.

If you’ve managed to make sense of all of that on first reading – well done. It truly is a complex and frustrating situation. But what next? This debacle highlights two key issues – process and price.

Process

Firstly, process. We need to re-think how the drug approval systems work together across the UK.

The Cancer Drugs Fund in England is a welcome sticking-plaster – it gets new drugs to patients that need them, but it can throw up regional disparities. We need the Department of Health to ‘show its working’ on the new proposed system – Value-Based Pricing – so that the medical community can begin to help build something we hope will be better, fairer, and more transparent.

We also need to see urgent progress on an ‘early access’ scheme, promised in the Government’s life sciences strategy late last year. The idea is that where treatments show exceptional promise in early clinical trials, patients (under very close supervision) get early access to them.

This could benefit both patients and drug developers. Many cancer patients would be willing to try experimental treatments showing early promise where there are no alternatives. For the pharmaceutical companies, this scheme means speeding up the time it takes to get drugs to market, while collecting valuable ‘real world data’ about their effects.

We also need to make sure that the reorganisations taking place in the NHS are used to improve the drug approval process, rather than make it even more complex.

Price

Secondly, price. We fully appreciate that the pharmaceutical industry is facing considerable pressures, and not just from the current global financial crisis. As this must-read piece in the Financial Times outlines, as its patents expire, the pharma industry – a vital and necessary part of the drug development pathway – is facing a huge squeeze on its future profits.

But the financial crisis affects all of us, including governments and healthcare services. We need industry to be much more flexible and forthcoming in setting prices that governments can afford, particularly as populations age and diseases like cancer become more common.

We simply can’t afford to go on like this.

The story of abiraterone is, at its heart, a motivating, inspirational success story – and one day, it will likely be regarded as a turning point in the fight against prostate cancer. We are genuinely proud to see a drug that we helped develop being released, so to speak, into the wild.

But today, the story of the drug’s emergence leaves us here at Cancer Research UK with our pride tinged with frustration.

The British public supports medical research to a phenomenal degree, donating over £1bn to UK medical research charities every year. And around the UK, our researchers continue to make serious inroads in understanding cancer’s inner workings, and in translating that knowledge into treatments that can bring real benefits to patients.

So we worry when stories like abiraterone, which should be about scientific success and medical breakthrough, lead to headlines about financial constraints, red tape, and missed opportunities.

All of us – governments, funders, regulators and pharma companies – owe it to cancer patients, charity supporters and the wider public, to do better next time.

Henry

The fact is that the number of men and women in their 50s – whose lives were once all too often cut tragically short by cancer – have new hope as their chances of beating the disease has hugely improved.

In the early 70s more than 21,000 people in the prime of life died from cancer. Today that figure has dropped below 14,000.

The below graphic summarises the key statistics:

Click to enlarge

Quicker and more accurate diagnosis, better treatment such as improved chemotherapy and radiotherapy and – most importantly – falling smoking rates, are behind this growing trend.

Cancer has been around for centuries. But today – as we can expect to live longer than our grandparents – the number of people who will develop cancer is rising. More than 1 in 3 of us will face that diagnosis at some point in our lives. But survival rates have doubled since the 70s.

It’s now been more than 60 years since the landmark research that showed smoking caused lung cancer. And as the number of habitual smokers has dwindled so the shocking number of lung cancer deaths has begun to drop.

Sadly though, this trend is much slower in women and we’re still seeing rising lung cancer cases, reflecting smoking behaviour over a generation ago.

But although the number of deaths has dropped, too many people still lose their fight against the disease. Spotting cancer earlier will have a big effect on cutting cancer deaths.

On average people in the UK are diagnosed at a later stage than in Europe and late diagnosis cuts the chances of curing the disease. We need to boost awareness of the signs of symptoms of cancer among both the public and GPs because the earlier cancer is diagnosed, the greater the chance of survival.

There is still a lot of work to do, particularly in cancers that are difficult to diagnose and treat, such as ovarian and pancreatic cancers, and where survival rates are far too low.

But hope is on the horizon, and these are exciting times for cancer researchers. Huge progress is being made in unlocking the mysteries behind cancer and, ultimately, finding cures.

• An edited version of this article originally appeared in the Daily Express

What is it like to work as a lung cancer nurse?

Lung cancer is the most common cancer in the world. Over 1.6 million people across the globe were diagnosed with the disease in 2008 (the last comprehensive count). That’s more than 4,300 people every day.

But these chilling numbers aren’t the ones we think of, or are aware of, when we try that first tentative, rather unpleasant puff. A puff that, for some, is a step on the path to addiction. An addiction that can lead to death.

Tobacco is at the root of a whole variety of cancers. But the one most associated with it is lung cancer.

With this in mind, we’ve asked one of our cancer information nurses – Caroline – to share her experience of working as a lung cancer nurse, and describe what it’s like to care for cancer patients.

This post also comes after the government launched a public consultation on the the future of tobacco packaging, and whether all branding should be removed to help reduce the appeal of tobacco to young people. We believe this will be effective and we’ve launched The Answer is Plain campaign so the public can show their support. 

Please keep one simple statistic at the back of your mind when reading this – nine in ten lung cancer deaths are down to smoking.

I’ve been working at Cancer Research UK as a Cancer Information Nurse for about 18 months now. Working on the telephones, answering email enquiries about cancer and posting online replies on Cancer Chat and Yahoo.

These enquiries range from people worried they may have cancer, to people wanting to enter a clinical trial and to those who are trying to cope with a loved one being diagnosed with cancer.

That’s only a snap shot of what we get asked about – it’s astonishing what one subject can generate in terms of feelings, questions and worry.

But before joining Cancer Research UK I was a Lung Cancer Nurse Specialist working at different hospitals across London. This involved being part of the team who diagnosed, treated and supported people with lung cancer and their families.

It’s difficult for me to think about all the people I’ve met who’ve been affected by lung cancer – not just those who have been diagnosed with the disease, but their families too. The overriding desire for me is to tell you about all the people I helped to treat who eventually died from their disease.

Because unfortunately, this is my main memory.

Some people are cured: usually those who are diagnosed at an early stage and can have surgery. These are the people who I used to see in follow up clinics for up to five years.

But – despite some progress in treating lung cancer – they are still in the minority. Most people go through treatment that will not cure them but that may help them to live for a few extra weeks or months, and in some cases a few years.

Having cared for and frequently talked to people with lung cancer and their families, I can honestly say it has a devastating effect. Both physically and emotionally.

Treating people with cancer can often be hugely rewarding, but also tremendously tough. One particularly vivid memory is of the moment a woman was told she had lung cancer. She was in her 40s and had smoked about 20 cigarettes a day since she was in teenager, when the dangers of smoking were less well-known.

Because of a cough she’d had for a few weeks her GP arranged for her to have a chest x-ray. This was reviewed by a specialist chest doctor who saw a suspicious shadow on her lung. A CT scan and biopsy were done and she was now back to the lung clinic with her family, her doctor and I to get the results.

She was told she had ‘small cell’ lung cancer, an aggressive and fast-growing form mostly caused by cigarette smoking. The doctor showed her the CT scan on the computer screen and pointed out the cancer in her lung. This scan also showed that she had severe damage to the bones in her spine, which explained why she had so much pain in her back that she was finding it difficult to walk when she first came in.This was likely to be caused by the lung cancer spreading and the reason for the pain in her back.

I can still remember the despair on their faces, the crying of the children, the pain they all must have felt. As a mother myself, I knew she was not only worried for herself but for her children. I wondered how she would possibly cope.

Sadly, she died six months after finishing six months of radiotherapy and chemotherapy.

I’ve met countless men and women with similar stories. Of course, some non-smokers get lung cancer too, but more often than not the people I looked after during my time as a lung cancer specialist were smokers. And almost all the people I looked after told me that they were sorry they smoked.

This is why it’s so important to help smokers to quit and to prevent young people from starting in the first place.

I’m proud to work for Cancer Research UK. And my experience of trying to help lung cancer patients is why I think our new campaign, to persuade the government to force the tobacco industry to sell their deadly products in standardised packaging, has my full support.

Tobacco still takes the lives of far too many fathers, mothers, husbands, wives, grandparents, uncles, aunts and children. We need to end the packet racket – to keep smoking rates on a downward trend, and lower the number of people who have to hear those devastating words: ‘you have lung cancer’.

Caroline

• To support the campaign to put tobacco in plain packaging and end the packet racket, sign our petition.

It's news time

• We launched a clinical trial (press release) to test whether curcumin – an extract from the curry spice turmeric – could improve treatment for advanced bowel cancer. This doesn’t mean curry cures cancer (as we pointed out here), or that people with bowel cancer should take curcumin supplements. But this early-stage trial could help us find out whether curcumin’s promise in the lab could be translated into patient benefit.

• Around one in six worldwide cancers – two million new cases every year – are caused by infections, according to a French study published on Wednesday and covered on our news feed and the BBC. Eighty per cent of these cases occur in less developed parts of the world, where measures to prevent and treat infections are not always widely available. (On a related note, it’s worth reading Olly’s post on the ‘blame game’, and this post by Ed Yong, on why we need to be careful about how such stats are explained).

• Measuring a type of genetic variation in the blood of men with prostate cancer could help predict how their disease will develop, according to US research published on Tuesday (covered here). If confirmed, the work might help towards the development of a test to distinguish slow growing prostate cancers from more aggressive ones – something we urgently need to improve to help men diagnosed with the disease.

• Wednesday brought news from the US, where researchers have discovered that a gene called PREX2 is faulty in some people with malignant melanoma, the most deadly form of skin cancer. The discovery of the mutated BRAF gene by our scientists led to the development of a new melanoma drug that targets these faults, so this work could be a step towards more new drugs for people with this hard-to-treat disease.

• We were pleased to find out on Thursday that a new drug for non-small cell lung cancer (NSCLC) is to be made available on the NHS. Erlotinib (Tarceva) is suitable for a small but significant proportion of NSCLC patients whose cancer is caused by mutations in a gene called EFGR (which our scientists first linked to cancer in 1984). While it’s neither a cure nor the only option for these patients, it’s great that there’s now another potentially life-extending treatment option.

• US scientists have developed a new way to help patients with a type of brain tumour called glioblastoma better tolerate the effects of chemotherapy. The “stem cell shielding” (BBC) technique involves using genetically modified stem cells to protect healthy bone marrow from the cell-killing effects of treatment. A lot more work is needed, but these are interesting and encouraging results that could boost the effectiveness of temozolomide, a drug Cancer Research UK discovered and developed.

• Last week we reached 100,000 people with our hard-hitting plain packaging video, and this week we doubled that figure. This is an important video behind an important campaign. Will you help us make it 300k or more next week? Please share it with your friends and family.

• And in related news, we published this post in response to several media stories about plain packaging, that weren’t as balanced as they could have been.

And finally… there were a couple ‘scare’ stories in the media this week, which on closer look, shouldn’t be a cause for concern:

• This Daily Mail headline about “new breast cancer fears” is unfounded. The story is about research on a chemical called bisphenol A, which is present in some food packaging, and its effects on breast tissue in monkeys. But the study didn’t gather enough data to be certain its findings weren’t down to chance. Even if bisphenol A affects the development of breast tissue in other primates, that’s a long way from showing that it might be responsible for cases of breast cancer in humans.
• Along with our other SunSmart advice, our recommendation is to stick to the sunscreen, despite some dodgy headlines this week claiming that a key ingredient in such products causes skin damage. The researchers themselves say their work isn’t confirmed and is at a very early stage, so shouldn’t inspire anyone to sideline the sun cream. And, a crucial point, the full research hasn’t even been published yet.

We separate fact from fiction about plain cigarette packaging

Since we launched our campaign to put tobacco products in plain packs, it’s been interesting to read some of the reactions in the media – particularly those of the tobacco industry.

Several points stand out that are worth discussing.

Firstly, in an interview in the Telegraph, the chief executive of Imperial Tobacco, Alison Cooper confirmed that her company would mount a legal challenge if the UK government was to force tobacco to be sold in standardised packets.

Fiction: The tobacco industry claims that plain packaging is confiscating the property of tobacco companies and could result in significant legal and compensation costs for governments.

Fact: The trademarks are not being ‘acquired’ by anyone – it is just their use that is being restricted. International treaties on intellectual property have opt-outs for public health .

On top of this, the Telegraph article goes on to say: “The industry calculates one in four cigarettes smoked in the UK is bought from smugglers or counterfeiters – a figure that is expected to rise if the industry is regulated more tightly.”

The tobacco industry exaggerates the scale of smuggling. While still a problem, it has halved  [pdf] since its peak, to one in ten cigarettes. This is due to better enforcement by government agencies and strict curbs on the tobacco industry’s own activities as they have a poor record on smuggling. For example, in the late 1990s and early 2000s, most illicit cigarettes were genuine products manufactured in the UK, exported to continental Europe and then smuggled back to the UK.

Fiction: Plain packs are easier to forge, so smuggling will rise.

Fact: The existing packs are already so easy to forge that they have covert markings to enable enforcement officials to distinguish illicit cigarettes. With these markings and large pictorial warnings, standardised packs will not be easier to forge.

In a second article in the Financial Times Alison Cooper goes on to say: “The so-called evidence supporting plain packaging is purely put together by anti-tobacco lobby groups…[so] we need to push here to make sure we get a genuine consultation with the health department. Maybe it should be overseen by someone like business instead, because I’m concerned it won’t be genuine otherwise.”

It’s no great surprise to see the tobacco industry’s concern over plain packaging. With advertising bans in place, tobacco manufacturers have increasingly focused on packaging design to make their products more appealing [pdf].

A leading industry analyst has estimated that plain packaging will halve tobacco industry profit margins so it is not surprising that Philip Morris has stated “we don’t want to see plain packaging introduced anywhere regardless of the size and importance of the market.”

It’s important to remember that this is a health measure, designed to protect children from tobacco marketing and ultimately reduce the number of deaths caused by tobacco. More than 100,000 cancer deaths are caused by tobacco in the UK every year. It’s for this reason that the Department of Health are overseeing the consultation.

And finally, a third article in the Daily Mail also caused us some concern, since it only looked at the industry view and didn’t appear terribly balanced.

To try to address this, we sent the Mail a letter for publication. It didn’t appear in the newspaper, so we have also tried to post it online in the comment section of the website. It wasn’t published either, and we doubt it will be at this stage. This is what we wrote:

Dear Sir

It’s no surprise to see the Adam Smith Institute, the Institute of Economic Affairs and Imperial Tobacco all seriously opposed to an effective measure that protects young people from tobacco marketing and helps prevent the next generation from starting to smoke. Imperial Tobacco sells tobacco and the other organisations have received funding from the tobacco industry.

What is disappointing is to see such a complete lack of balance in the article. It fails to mention the evidence – not just from UK researchers but from around the world – showing the impact of packaging in helping recruit new smokers and the importance of the pack to an industry trying to disguise a lethal product with glitzy and distracting designs.

Tobacco kills half of all long term smokers. In the UK, smoking kills five times more people than road accidents, overdoses, murder, suicide and HIV all put together. Around 157,000 children between 11 and 15 start smoking in the UK every year. We know that plain packaging won’t stop them all from starting to smoke, but it will give millions of children one less reason to start.

Sarah Woolnough

Director of policy

Cancer Research UK

We’ll be keeping an eye on more media commentary on plain packaging. In the mean time, you can sign up and support our campaign: “The answer is plain”.

Cancer Research UK has launched “The Answer is Plain” campaign to raise awareness of the issue, alongside a hard-hitting short film that illustrates children’s attraction to the slickly designed cigarette packs.

Professor Simon Chapman is professor of public health at the University of Sydney

In the past 20 months, Australian news audiences have been exposed to some exotic, thought-to-be-extinct species on their screens and radios. After more than 15 years, the tobacco industry dodo is back and walking among us, attempting to fly.

Australia’s pioneering plain packaging legislation has brought them out into public, in a desperate effort to prevent the fall of a domino that promises to cascade globally, ending the industry’s centre-piece of tobacco promotion: the lure of the pack.

The University of California’s Stan Glantz once remarked that those who lead the tobacco industry are like cockroaches: “They love the dark and they spread disease.”

Ever since the magnesium glare unleashed by the public release of its internal private tobacco industry documents via the 1998 US Master Settlement Agreement, the industry has kept well out of public view, working behind the scenes to shore up its ebbing credibility.

The court of public opinion told them they were regarded as the most untrustworthy of all industries. Media appearances had become progressively humiliating as their spin was rejected.

But the truth serum contained in the millions of now public pages of court-ordered internal documents sealed their public fate. The industry always knew tobacco killed, but had lied about it for decades. Their marketing divisions had underlined the vital importance of recruiting youth, and their chemists had been busy working overtime to enhance the addictiveness of nicotine.

Australia’s historic plain cigarette packaging legislation is weapons-grade public health policy that is causing apoplexy in the international industry. It is likely to have little effect on heavily dependent smokers who tend to be brand loyal and less image conscious, but without branding, future generations will grow up never having seen category 1 carcinogens packaged in attractive packs.

Today’s Australian 20-year-olds have never seen local tobacco advertising, and youth smoking rates are at an all-time low. Plain packs will turbocharge this trend, making smoking history.

Tobacco is a dying market in nations like Australia which lead the world in comprehensive tobacco control. National data released in July show only 15.1 per cent are now smoking daily – the lowest ever recorded.

From the time that machine-manufactured cigarettes were first marketed at the beginning of the twentieth century, the advertising and packaging industries did all they could to portray cigarettes as a means of signaling personal identity to the young as they took up smoking. A callow youth who wouldn’t be seen dead with a menthol Alpine felt assured by the promise of masculinity in pulling out a packet of Marlboros.

Those not wanting the social opprobrium that can come with being showy had the iconic ordinariness of Winfield to clutch as their totem. Those wanting to affect retro stylishness have Peter Stuyvesant or Lucky Strike, and wannabes, any number of haute couture named brands – designer carcinogens.

But from December 1st 2012, all cigarettes will look the same, distinguished only by the brand and variant name in standard font.

The industry’s re-entry into policy debate has produced some high comedy. In advising government that plain packs will “not work”, it sought a role as a wise public health authority, when of course its fiduciary duty to its shareholders demands that it support policies which maximise use.

It has commissioned reports that purport to show that one in six cigarettes being smoked now are illicit, when the latest national survey reports that a mere 1.5 per cent of smokers use illegal tobacco more than half the time.

Most of all though, its blank cheque advertising campaigns, imploring the government to desist, say to anyone with half a brain that the industry knows plain packs will “kill their business”, as the cover story of a tobacco trade magazine put it in 2008. That’s precisely the plan.

Tobacco kills one in two of its long-term users. The tobacco industry’s current undisguised panic shows that plain packs will hit them very hard. If she were to do nothing else, Health Minister Nicola Roxon (now Attorney General) has marked her tenure with this historic legislation.

It will stand in public health history as a major chapter of how governments put the health of the population before the corporate interests of a pariah industry. Just one disease caused by smoking – lung cancer – was rare before 1930. Over the next 50 years, it rose to become the world’s leading cause of cancer death. In countries like Australia it is now on the wane.

Plain packaging will accelerate its eventual demise as a major cause of death.

You can sign up to support plain packs here.

Simon

• Professor Simon Chapman is Professor of Public Health at the University of Sydney

Could a spice extract help to treat bowel cancer? (image by Sanjay Acharya)

Headline writers take note: curry doesn’t cure cancer.

But over the years, several studies have given researchers a tantalising glimpse of the cancer-fighting potential of a chemical called curcumin, an extract of the yellow curry spice turmeric. This is the chemical that gives some drinks, sweets and foods – notably curries and Jaffa cakes – their bright colouring.

But it seems that as well as its culinary properties, curcumin can slow the growth of cancer cells in the lab.

Our scientists are now building on this early work by starting a clinical trial to find out if curcumin could help to treat people with advanced bowel cancer.

This doesn’t mean that a curry or Jaffa cake a day will keep the doctor away. In fact, taken to extremes, such a diet could increase your chances of being overweight, which ups the risk of developing cancer.

And the evidence just isn’t there yet to recommend anyone starts taking curcumin-containing supplements to ward off cancer.

But this small trial will answer some important questions about whether curcumin’s promise in the lab can be translated into an effective, standardised treatment for bowel cancer.

Treatments from nature

Tumeric is a member of the ginger family, and has been used for hundreds of years in many Indian, Persian and Thai dishes.

The idea that a plant extract could help fight disease isn’t a new one. Indeed, some of today’s cancer drugs came from the natural world. For example, the cancer drug paclitaxel (Taxol) originally came from the Pacific yew tree, while eribulin was discovered in sea sponges.

Even ‘head and heart’ tablet aspirin, which is based on old remedies extracted from plants, has shown promise in preventing the disease.

Evidence, not anecdotes

But using the power of plants to beat cancer isn’t about brewing up herbal tea or collecting leaves from the wild. Scientists and doctors are a scrupulously accurate bunch, so when they notice that a particular plant extract might be helpful in treating disease they aim to find out exactly which molecule, at what dose, can actually help patients.

This process of testing and standardisation is absolutely vital – not only to make sure patients are protected from harmful side effects, but also to prove that the potential treatment really does offer clear benefits. Modern medicine is built on evidence – and anecdotes aren’t enough to go on.

Testing curcumin

So how can we investigate whether turmeric could help to treat bowel cancer? The scientific approach is to find the key ingredient – in this case curcumin – and test its effects against bowel cancer in the lab, and then in patients.

Professor Will Steward has been investigating curcumin, and in this latest trial (known as CUFOX) he’ll be finding out if it’s safe and acceptable to patients when taken alongside chemotherapy.

The researchers suspect that the curcumin may make bowel cancer cells more sensitive to the effects of the standard chemotherapy treatment offered to bowel cancer patients – a combination of drugs called FOLFOX. This could be extremely useful. At the moment, six in every 10 patients have to either be given a reduced dose or, in some cases, stop chemotherapy altogether because of serious side effects like nerve pain.

Anything that allows them to continue treatment for longer, or increases the effectiveness of lower doses, could mean treatment is more successful. And because we already know that curcumin is generally safe for consumption, it should be able to be taken long-term without causing severe side effects.

The CUFOX trial will involve around 40 patients with advanced bowel cancer. The first phase will help researchers to work out the best dose of curcumin, as higher levels can sometimes cause side effects like diarrhoea and nausea.

The next phase will involve two groups of patients – one group will receive the standard chemotherapy treatment, while the other group will be given chemotherapy and curcumin capsules. They will then be monitored for two years.

The results initially aim to show that adding curcumin to the standard FOLFOX treatment doesn’t have any negative effects, but the researchers will also be looking for any sign of beneficial effects. This is a small, early-stage trial, so by itself it can’t tell us if curcumin could help people with bowel cancer.

But if the results are promising, the research will ramp up to larger trials that will help to answer this question.

Curry doesn’t cure cancer

A few years ago, early reports of research into turmeric spawned a range of ‘curry cures cancer’ headlines – claims like this are misleading and not helpful for people coping with the disease.

We said it earlier, but it’s worth repeating, the evidence doesn’t justify eating more curry or taking turmeric supplements.

Curries aren’t always the healthiest of meals, and in general there isn’t any evidence that supplements can help to reduce the risk of cancer. And worryingly, there have been reports of contamination in certain turmeric supplements in the past.

Step by step towards better treatments

Our excitement at this new trial has to be tempered with patience. Better treatments for cancer can’t be developed overnight. Research advances our knowledge step by step, not through single breakthroughs.

But we’re making progress – bowel cancer survival rates have doubled in the last 40 years, and research like this will help to save more lives in the future. Researchers will be monitoring participants in this for years to come – and we’ll be awaiting the results.

Nell

Find out more

• 2008 post about Professor Will Steward’s work
• UK clinical trial investigating whether curcumin can help treat Barrett’s oesophagus (please note – this trial is no longer recruiting)
• The American Cancer Society’s page about turmeric and curcumin

Lots of cancer-related stories in the news this week

Here’s our weekly digest of all the main discoveries and developments this week.

We’re still playing around with the format of this digest – let us know what works for you.

News from Cancer Research UK

It’s been a busy week for our press office, who’ve had several prominent stories in the media.

On Sunday, our researchers in Cambridge published their discovery of a new pancreatic cancer gene which could lead to new treatments. “Study points to potential new treatment for deadly pancreatic cancer”, said our press release – and Kat covered the exciting implications in this blog post.

People don’t seem to know the symptoms of lung cancer, we warned on Monday, as we published results of a survey showing that “People fail to list persistent cough as a lung cancer warning”.

Results of a thyroid cancer trial we funded were published on Wednesday, which we summarised in this press release entitled “Trial transforms thyroid cancer treatment into safer and shorter session”.

And yesterday, we revealed news statistics showing that “Prostate cancer cases hit 40,000 for the first time”, most of the increase being driven by more widespread use of the PSA blood test. Our head nurse, Martin Ledwick, had this to say about prostate cancer symptoms:

News from elsewhere

Several other cancer charities had stories in the media this week.

On Monday, a survey by our friends at the Teenage Cancer Trust discovered the concerning news that “Many young cancer patients fail to get early diagnosis” (Guardian), while MacMillan Cancer Support’s survey found “’Too few’ women using sun cream” (BBC) – the consequences of which were dramatically highlighted by these shocking pictures in The Sun later in the week (although we loved the headline).

On Tuesday, Breast Cancer Campaign’s story about a “Way to spot breast cancer years in advance” (BBC) got widespread coverage in the papers, on TV and on the radio. We co-funded this research, and took a deeper look in this blog post. NHS Choices also had this useful breakdown.

Also on Tuesday, Action on Bladder Cancer published a survey of bladder cancer awareness, which we covered on our news feed (“Low awareness of bladder cancer is ‘disappointing’”), along with some interesting US research on B-cell lymphoma: “B-cell lymphoma discovery could lead to new treatments,” said the headline.

“How Do Brain Cancer Cells Spread? New Study Finds Clues”, wrote Medical News Today after researchers at Johns Hopkins University made an intriguing discovery about how the cells of a form of brain tumour called glioblastoma can spread.

“Minimally Invasive Procedure For Oesophageal Cancer Shows Promise” (Medical News Today), according to new research in Lancet Oncology, comparing traditional open surgery with a new, less intensive form of surgery – this could be good news for oesophageal cancer patients in future.

And finally, there was continued talk and chatter about our plain packaging campaign, The Answer Is Plain. Lots of people continued to tweet about it using the hashtag #packetracket, resulting in our video getting more than 100,000 views:

#ff big well done to @CR_UK who's #packetracket video has just had 100k views please RT. http://t.co/IBgqCtFM

May 4, 2012 4:05 pm via Twitter for iPadReplyRetweetFavorite

@camtia

David Collins

…while our director of tobacco control wrote this thoughtful piece for the Speaker’s Chair blog, and we spotted this on Sifting The Evidence: “Tobacco Control, Plain Packaging, and Media Misinformation”. Clearly, the debate is building up steam – you can sign the petition here.

That’s all for this week, see you next time.

Henry

Mammography is currently used to detect breast cancer

Earlier this week, the news was full of stories about a ‘blood test’ that can apparently predict a woman’s risk of breast cancer, years before she develops the disease.

This sounds exciting. Being able to work out someone’s risk of cancer well in advance of developing the disease could be incredibly powerful.

People at higher risk could take extra steps to change their lifestyle, be offered extra screening or other monitoring, or even take drugs to prevent the disease.

But how valid are these claims? How would such a test work? What’s the science behind it? And how does it fit into the bigger picture of breast cancer prevention and detection?

We’ve been poring over the research paper that led to the headlines, and spoke to Imperial College’s Dr James Flanagan, the researcher who led the study together with Cancer Research UK’s Professor Robert Brown – to get his take on it.

The bottom line is the ‘test’ reported here is more of a proof-of-concept than a fully developed ‘cancer blood test’.

The principles that underpin the research are definitely promising, and suggest that in future the way we understand a person’s cancer risk (and what we do with this info) will be much more sophisticated.

But there’s a long way to go before a clinically useful test can be built from these findings.

Let’s take a look at how it all fits together.

Cancer risk, gene faults, and genetic variation

Cancer is ultimately caused by faults in the genes in our DNA that cause cells to multiply out of control.

For much of the last half-century, cancer researchers have been trying to understand how these faulty genes cause cancer, and how to use this knowledge to prevent and detect the disease.

Because of this research, people with multiple cases of cancer in their family can now be tested for rare faults in genes like BRCA1, BRCA2 and APC – faults that are known to substantially increase a person’s chances of cancer. Carriers can be offered extra screening or other treatments, and this has undoubtedly saved many lives.

But, crucially, only a small proportion of people who develop cancer do so because of an inherited gene fault. So researchers have been looking for common, more subtle genetic differences that explain why some people are more likely to develop cancer.

These efforts have borne fruit, and researchers are now beginning to paint a detailed picture of scores of tiny, common, genetic variations between individuals, each of which seems to cause a small change in risk, but which can add up to something more significant.

All of us carry some of these variations – precisely which ones we carry, and how many, plays a role in our chances of developing cancer later in life.

But this is very much work in progress, and this picture isn’t yet complete. And we don’t fully understand precisely how these variations influence a person’s risk, how they interact with lifestyle factors like smoking or obesity, or why some variations are linked to certain types of cancer.

And unlike testing for faulty genes, tests that can accurately predict a person’s cancer risk based on genetic variation are still some years away.

On top of this, researchers are still trying to work out whether offering people more or less screening, monitoring, or other treatments, based on these subtle variations in their DNA, actually saves lives.

Nevertheless, both these types of test look for changes in our DNA sequence – the code that contains information about how to make proteins.

But over the last few decades, it’s become apparent that on top of our DNA lies a whole extra layer of information – so-called ‘epigenetic’ information. And it’s this that Dr Flanagan’s team – in particular, PhD student Kevin Brennan – has been studying

DNA molecules are like a twisted ladder

Beyond our DNA

DNA molecules are long, twisted ladder-like molecules that live in the nucleus of each of our cells. Before a gene in our DNA can be activated, (i.e. the information on the ‘rungs’ of the ladder are ‘read’), one or more proteins first needs to stick to the outside of the DNA ladder to physically untwist it.

Cells carefully control which genes are active (i.e. which bits of the ladder are ‘untwisted’) at any given point in time by adding tiny chemical ‘tags’ to the DNA, known as epigenetic markers.

Some tags – called methyl groups – attract clusters of proteins that keep the DNA ladder tightly closed, meaning that genes can’t be switched on. The process of adding these methyl groups is known as methylation.

Scientists studying DNA methylation have discovered that it tends to occur in clumps along the length our DNA, and that these patterns are copied from cell to cell as they divide.

Researchers have also found evidence that exposure to various things over the course of our lives can influence our epigenetic patterns – things like tobacco smoke, radiation, alcohol and diet.

And they’ve also discovered that these patterns go completely, catastrophically awry in cancer. This allows cancer cells to turn on genes that should be off (and vice versa), and grow and divide out of control.

Putting all this together raises an interesting question. Can looking at these epigenetic patterns before cancer develops – and at differences in these patterns between individuals – yield any clues about a person’s chances of subsequently developing the disease?

Epigenetics and cancer risk

Several studies in recent years have suggested that the answer could be yes. For example, in 2008, blood samples from bladder cancer patients in a Spanish study were found to have different methylation patterns from people without the disease. And last year, a US study, also of bladder cancer, found a similar thing .

One important point about all these studies is that they looked at DNA from white blood cells – the cells of our immune systems. But although the immune system is heavily involved in cancer (as we’ve blogged about before), this wasn’t why researchers looked here. It was because they had no choice – the red cells in our blood don’t contain any DNA. In Dr Flanagan’s words, “they’re all we can get our hands on for this type of research”.

In 2009, Dr Flanagan’s team published results of a study of methylation patterns in the DNA from breast cancer patients’ white blood cells. They looked at epigenetic ‘tags’ on a whole range of genes involved in cancer, and found that one gene in particular seemed to be methylated in patients but not in women without the disease – a gene called ATM, which is known to be involved in several types of cancer.

But despite these tantalising results, a glaring weakness in all of the studies to date has been that they looked at the blood of people who already had cancer.

Cancer – and its treatment – can cause all sorts of changes to our bodies, so no-one could be sure that these epigenetic differences were caused by the cancer itself, or whether they’d existed before. So it wasn’t clear whether epigenetic markers could help predict a person’s risk.

Prospective studies

To try to address these flaws, with funding from Breast Cancer Campaign and Cancer Research UK, Dr Flanagan’s team turned to three large forward-looking (or ‘prospective’) studies – the European Prospective Investigation into Cancer (EPIC), the UK’s Breakthrough Generations Study, and the Australian KConFab study. These studies have been running for several years, collecting blood samples from healthy people, and following what subsequently happened to them.

This allowed Dr Flanagan’s team to identify women on these studies who had developed breast cancer, and then to go back and analyse blood samples taken many years before they were diagnosed.

The researchers identified 640 women who developed breast cancer in the three studies, and Brennan painstakingly measured whether the ATM gene in each of their blood samples was methylated.

They then repeated the process on a similar number of women on the studies who didn’t have breast cancer. And then, with the assistance of The Institute of Cancer Research’s genetic epidemiologist, Professor Montse Garcias-Closas, they put all their results into a computer to crunch the numbers.

They found that women who had the highest levels of methylation in the ATM gene in their white blood cells were nearly twice as likely to have subsequently developed breast cancer. And the effect was even more apparent in younger women. But it’s important to point out: not every women who had a methylated ATM gene developed breast cancer, and not every women who developed breast cancer had a methylated ATM gene.

What does all this mean?

According to Dr Flanagan, this is the first study with sufficient size and rigour to be able to find a definite link between an epigenetic marker in the blood and cancer risk.

“To be honest, most of the previous studies to try to look at this have been too small – we haven’t been able to measure this with any certainty,” he told us, adding “but this isn’t a ‘blood test’ yet. We need to look at how this fits in with other factors”.

How could this finding be used to help patients in future? Currently, people are offered cancer screening based on their age. But many researchers think that this ‘one-size-fits-all’ approach won’t last forever, and one day genetic testing will be used to offer people more tailored screening.

Dr Flanagan thinks that, in future, epigenetics could also help determine from what age, and how often, women should be offered screening. “That’s absolutely where we’re heading with this research,” he said, “but we’re not there yet.”

Next, Flanagan plans to look at how these epigenetic markers affect risk in people with different DNA variations, and he plans to collaborate with researchers at the Institute of Cancer Research to do so. Another plan is to look at the type of breast cancer women with methylated ATM genes develop, and to look in detail at the type of white blood cells that contain these modifications, to find clues as to how this marker actually increases risk.

So some of the media reports of an imminent ‘blood test’ that can “predict a woman’s breast cancer risk” were wide of the mark. Although it’s early days, this research suggests that epigenetic markers that can be measured in our blood – along with variations in our DNA – are a significant piece of the complex and fascinating jigsaw puzzle that is cancer risk.

Henry

Reference:

• Brennan, K. et al (2012). Intragenic ATM Methylation in Peripheral Blood DNA as a Biomarker of Breast Cancer Risk Cancer Research, 72 (9), 2304-2313 DOI: 10.1158/0008-5472.CAN-11-3157

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This month, we hear how a landmark study could revolutionise breast cancer treatment, and take a look at the growing evidence on aspirin and cancer.

We also hear how obesity may be driving rises in kidney and womb cancer rates, while smoking patterns of the past mean that lung cancer continue to rise in women.

Plus, scientists develop the first snap-shot of tiny brain tumours, and we talk to Stephanie Moore MBE about how treatment for bowel cancer has changed since her husband, footballer Bobby Moore, died from the disease.

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Kat