It's not all in a gene

Our rush to find a quick-fix way of preventing cancer may well blind us to the real solution when it comes

WITH typical coyness, Americans call it the "C-word", for the diagnosis is one of the most terrifying: cancer. It kills so many, so viciously; but last week you might have thought the tide had turned. "Anti-cancer gene found", yelled the front page of the Daily Mail on Tuesday. The previous evening ITN's News At Ten had run the news about the gene as its third item; and the BBC Nine O'Clock News broke a worldwide embargo by an hour to announce the latest results of the research.

The promises were fulsome: scientists had found a gene that protects smokers against lung cancer; you might be able in future to get a pill that would detoxify your body from all those environmental pollutants. The implication was that the end of the long "war on cancer", announced by Richard Nixon in the 1960s, might be in sight. Might this be exaggerated? To find a dissenting voice on the coverage, one didn't have to go far: indeed only to the man who carried out the principal experiment.

Ken Brown at the University of Glasgow found the coverage surprising on two fronts. First, because as a co-author of the paper summing up 18 months' work, he had seen it returned to him by the two main science journals, Nature and Science, neither of which had thought it worth pursuing. "I wasn't that surprised," Dr Brown says. "It wasn't a major enough discovery for them. To really rate being published there it has to have general significance, not just for one area."

Second, Dr Brown doesn't think that the experiment he conducted tells us that one gene decides whether humans get lung cancer. "It's just one gene that's involved in detoxifying," he says. "You have to remember that there are probably many genes playing a role in the whole cancer issue. If there are 20 or 30 genes involved, each might contribute 5 per cent to your susceptibility, and each could work at different levels. It's difficult to draw firm conclusions."

The way that this paper - submitted in January to the American-based Proceedings of the National Academy of Sciences (PNAS) - touched off a minor media earthquake is a modern morality tale, in which the key players are cancer, genes and us, the scientifically confused public.

What was the experiment, though? At the suggestion of Roland Wolf, of the University of Dundee, a Scottish team produced mice which lacked a particular gene that codes for an enzyme called glutathione S-transferase (GtSp). When Dr Brown treated the skins of both those mice and a group of normal mice with a known cancer-causing chemical, the mice without the gene developed significantly more skin cancers than the normal ones.

A SMALL step for a mouse, a giant leap for the media. Why? Because cancer is the second-biggest killer (after heart disease) in the developed world. Most people know someone who has or has had cancer. Nixon's war on cancer was about as effective as that on the Vietcong, but it did attract similar funding. We now know much more about how cancer starts, and what it is.

Cancer stems from errors in DNA - the "blueprint" - which mean that cells grow without stopping, instead of dividing when they should and then running normally. Cells multiply out of control, swallowing the body's resources. The immune system does not react until it is too late because the cells are the body's own. Carcinogens - chemicals that cause cancer - lead to the DNA damage which leads in turn to cancer. But the cell has three principal defence mechanisms against that. The first identifies potentially dangerous damage to the cell's DNA. The second brings repair mechanisms to damaged DNA sections. If those fail, the third and final defence is the equivalent of the secret agent's "suicide pill". The cell realises that something is wrong and kills itself. Scientists call this "apoptosis", or programmed cell death. Only when all three defences fail does cancer have a chance to start.

Cancer is big business. Two years ago shares in British Biotech soared when it showed promising early results from Marimastat, its treatment for pancreatic cancer. Marimastat is forecast to be worth pounds 800m a year if it passes all its clinical trials.

Meanwhile, cancer charities flourish: the UK alone has more than 600, which led Professor Gordon McVie, head of the Cancer Research Campaign (CRC), to say last week that the area was "oversubscribed" with competing charities. MPs joined him in saying that too much was being put into the hire of PR consultants and fundraisers.

But the two biggest British cancer charities, the Imperial Cancer Research Fund (ICRF) and the CRC (which together have funding of almost pounds 160m) are hardly shy about promoting findings that emerge from their research efforts. When Professor Wolf, who is funded by the ICRF, described the research results to the ICRF's press officer - Geoff Watts, an experienced journalist - the focus shifted away from skin cancer in mice and towards lung cancer in humans. "The title of the paper meant nothing to me," Mr Watts says, "but the more we talked about it, the more encouraging it seemed." The press release was headlined "Researchers find single gene playing important role in protection against cancer". It began: "Some people who smoke develop cancer, while others do not." Cancer and genes: a science media hit.

A FEW decades ago scientists held us agog with exotic subatomic particles such as the quark. Now it's the gene. You could almost rewrite its definition as "the smallest biological element comprehensible by a member of the public".

A gene provides the instruction for a cell to make a single, particular protein. It does not determine how much of, or when, the cell makes that protein. But in the mouths of some exponents, genes become magical things that decide if you're homosexual, likely to be depressive, develop Alzheimer's Disease, or even be lucky.

Wolf's and Brown's research is far more sound. But, even so, it is a big leap from one gene that helps clean up the cell to "a single gene [that] could be profoundly important in protecting us against cancer", as Professor Wolf was quoted as saying in the ICRF's press release. Genetic determinism - that you are what your genes make you - is becoming a dangerously popular concept. Dangerous because it is patently untrue, as the mathematician Ian Stewart points out in Life's Other Secret, published this month. After a detailed examination of animal behaviour, he concludes: "You'll never solve the problem of animal behaviour just by sequencing DNA, looking for proteins, or otherwise focusing solely on molecular mechanisms."

What Professor Stewart says about animal behaviour can also be applied at the fundamental, cellular level. We really don't know what GtSp does; only that it plays a role in the huge, complicated process of the cell's survival. We can see the bricks, but not the building.

However, genes play well with the public, and news bulletins and newspapers are increasingly aware that people like to know about science. ITV, ITN's paymaster, is understood to be applying pressure to it to run health and consumer stories that are directly relevant to viewers, in contrast to the BBC's approach of "the news you ought to be interested in". The suggestion that your genes might save you even if you puff 60 a day fits sweetly into that category.

The trouble is, though, that the scientists themselves don't see it that way, and aren't sure if they want others to. Professor Wolf says: "The only way to bridge the gap between the laboratory and the public is to tell the public about what's going on

"This isn't the only gene that will protect against cancer," he says. "There will be many more." The trouble is that those won't ultimately save us from cancer either. What is needed is some way to step back from the tiny details to look at the broader picture. But where are the headlines, the TV news bulletins in that?

What's genetic and what's not

CYSTIC FIBROSIS: YES. Fatal disease caused by a single inherited gene.

HAEMOPHILIA: YES. Caused by a flawed single gene on the female (X) chromosome, which is not masked by a functioning gene on the shorter male (Y) chromosome.

HOMOSEXUALITY: NO. Despite claims that area Xq28 of the X chromosome contains a gene giving a "tendency" to homosexuality, scientists dismiss the idea.

BREAST CANCER: YES AND NO. Two genes have been identified which can be inherited and cause breast cancer but many cases arise every year with no apparent genetic cause.

BALDNESS: NO. Though researchers identified a gene earlier this year which instructs hair to grow, but that does not tell the whole story of why some men go bald.

DEPRESSION: NO. No single influencing gene has been found.

LUCK: NO. Even if there was a way to define "luck" (lottery winners? happy families?) no single gene could affect a life in that way.

CJD (Creutzfeldt-Jakob Disease): YES AND NO. A number of mutations of one gene have been identified that give rise to this fatal disease. But many more cases occur without any apparent genetic cause. (These are not linked to BSE, which causes another form of CJD in humans.)

ALZHEIMER'S DISEASE: NO. Many genes are involved, but no single one decides whether you will get Alzheimer's.

FEMALE INTUITION: YES. British researchers last year identified a gene that appears to have influence in distinguishing boys' and girls' behaviour. They studied girls with behavioural disorders and the gene was faulty in all of them.