Within a few years, girls will be vaccinated against cancer. Not every cancer — at least, not yet. But the cervical cancer jab is well on its way. A couple of shots in the arm, perhaps, and young women may never have to think about it again.
That is possible because cervical cancer is spread by a virus called human papilloma virus (HPV). You can catch it by sleeping with somebody who has it, so women with more sexual partners are more likely to get it.
The vaccine does not act against cancer per se, but protects against the virus that causes it. Which makes cervical cancer, effectively, an infectious disease.
Can you really catch cancer? And if cervical cancer is caused by an infection, is it remotely possible that we might also catch breast cancer, or prostate cancer, or bowel cancer? The answer is yes and no. Certainly, catching cancers is not the same as catching a cold. HPV may trigger cervical cancer, but many women infected with it will never develop the disease. There must also be other factors.
Where a virus is involved in cancer, it appears, it is one of many causes — a trigger in a chain of triggers. Along with the virus, there may have to be something in your genes that tips your chances of getting this particular cancer. Diet affects some cancers, alcohol and smoking others, and air pollution is under suspicion. But the remarkable thing about the involvement of viruses in cancer is that they are a switch that can potentially be turned off. This is not a bad news story; quite the opposite. If an infection is involved in the onset of some cancers, then there is a way to stop them developing. Potentially, we could invent a vaccine. That is exactly what has happened in cervical cancer.
We do not know to what extent viruses are implicated yet, nor in which cancers, but the estimate is that they may play a part in up to 20% of cases. The evidence is slowly accumulating. A paper recently appeared from Newcastle University that offered new evidence that minor viral infections such as colds, respiratory problems and mild flu might trigger childhood cancer.
Richard McNally, an epidemiologist, had mapped outbreaks of two cancers — forms of leukaemia and brain tumours — in children younger than 15 over a period of 45 years from a tumour database in Manchester. He discovered clusters of children who were born around the same time and in the same place — and went on to develop cancer.
Whenever clusters of childhood cancers have been spotted, parents have understandably ascribed them to the man-made environment, assuming that fallout from a power station or radiation from a phone mast must be to blame. But McNally and colleagues have identified a pattern that is exactly like is seen in infectious diseases.
”We found that place of birth was particularly significant, which suggests that an infection in the mother while she is carrying her baby, or in a child’s early years, could be a trigger factor for the cancer,” says McNally. ”These could be minor common illnesses that are not even reported to the doctor, such as a cold, mild flu or a respiratory virus.” But no, he hastens to say, you cannot catch cancer. His research suggests that infection is one of the factors in its onset, but it is not the only cause.
Instead, the hypothesis his research helps to support is a double-whammy theory. Firstly, babies are born with a propensity to leukaemia. Mel Greaves, a professor at the Institute of Cancer Research in London, analysed the blood taken by midwives from the heel-pricks of newborns and found that many already have cell damage that could lead to the disease. But it is now clear that a second thing has to go wrong before a possibility becomes a likelihood. And that could be a viral infection.
This fits with the work of Leo Kinlen at Oxford University, who has been lambasted by anti-nuclear campaigners for his theory, first mooted in 1988, that childhood leukaemia is not the result of radioactive fallout and waste but caused by ”population mixing”. Cancer clusters occur where whole groups from towns and cities have arrived to live and work in a remotish rural setting, he observed. The incomers bring with them new viral infections, which could spark cancers among the native local population.
In fact, infections associated with cancer have been known for some time. The neatest example of infection as a significant cause is in stomach cancer. This is not triggered by a virus, but by a bacterium called Helicobacter pylori. That discovery netted a recent Nobel prize. ”Fifteen to 20 years ago,” says Heather Dickenson, principal research associate at Newcastle University’s centre for health services research, ”nobody would have taken seriously the theory that stomach cancer was the result of infection.”
Helicobacter pylori is a bacterium that enters the stomach in food and drink, but does not get destroyed by the acid there. Around 30% to 40% of us are thought to be infected with it, and it can cause inflammation of the stomach lining, known as gastritis. In a small number of cases, that progresses to stomach cancer. But now we know that H. pylori is one of the guilty parties, many of these cancers (though not all) can be prevented.
Research into the links between cancer and viruses began around the start of the last century. In 1908, Wilhelm Ellermann and Oluf Bang identified a virus which they found spread leukaemia between chickens. In 1911, Peyton Rous in the United States found another chicken virus that caused sarcoma.
In that same decade, the first definitive link between infection and a human cancer was established. A British scientist called Anthony Epstein, based at the Middlesex hospital, went to listen to a British surgeon called Denis Burkitt, who had identified what is now known to be the commonest childhood cancer in Africa. This was a tumour of the jaw that became known as Burkitt’s lymphoma.
In a remarkable piece of scientific detective work, Epstein mapped the incidence of the tumour across the wet, lowland areas of Central Africa and realised he was looking at the malarial belt. He hypothesised that the cancer was caused by an infectious agent, spread by the malarial mosquito.
He and his team had no luck until one tumour biopsy arrived from Uganda in an unfit state for microscopic examination. So Epstein cultured the cells instead. To everyone’s surprise, it grew a previously unknown form of herpes virus, which became known as Epstein-Barr. Epstein-Barr was later found in almost all samples of Burkitt’s lymphoma from Africa.
Almost everyone has this virus. ”Ninety-five per cent of us are infected by Epstein-Barr,” says Lawrence Young, professor of cancer biology at the institute of cancer research in Birmingham. ”It doesn’t cause us any effect at all. But with certain co-factors it could cause problems.” Malaria was the co-factor in Africa.
If you have Epstein-Barr and you catch malaria while on holiday, it does not mean you will develop Burkitt’s lymphoma. None of this is quite that simple. You would have two of the risk factors — two possible triggers — but because this is mostly an African cancer, there is probably a genetic component involved too. Too little is known about the causes of cancer, for all the noise made about diagnosis and treatment. But if scientists can nail down a particular virus as a risk, they can interrupt the process that can cause disease and death.
Young calls the virus ”a link in the chain of events. This is not like catching a cold. You can’t catch cancer as an acute disease. But if it is a vital link, you can break the chain.”
Epstein-Barr is also implicated in about half of Hodgkin’s lymphomas, but not the other half. In China, Epstein-Barr is in nasopharyngeal carcinoma — but fascinatingly, the extra link in the chain is the salted fish in the Cantonese diet.
Breast cancer, too, appears to have dietary links. The incidence in Japanese women who move to the US soars. ”Diet is a major contributory factor to cancer,” acknowledges Young.
Diet we can change. Viruses and bacteria we live with. Epstein-Barr does most of us no harm unless our immune system is suppressed. In the early days of heart transplants, for instance, most patients died not because the heart gave out or was rejected, but of Epstein-Barr-associated lymphomas. They were being given massive doses of immuno-suppressant drugs, which meant the virus was no longer kept in check, allowing the cancer to develop.
And, in the early Eighties, the first sign that we were in trouble from a new virus that would wreak havoc across the planet was the arrival of a new cancer in the US called Kaposi’s sarcoma. It had once been a very rare disease in elderly Jewish men from the Mediterranean. Suddenly, young gay men had it, as HIV knocked out their immune systems, allowing the Kaposi’s sarcoma herpes virus to flourish.
Viruses are now thought to be implicated in up to one in five cancers. As time goes on, we may find it is more. Finding any cause of cancer is very good news as it means prevention is possible. If a virus is involved, it opens up the possibility of a vaccine to disrupt the chain of events that leads to cancer. That is, in short, a holy grail. The revelations of the excellent results in trials of the cervical cancer vaccine were greeted with euphoria. Gardasil, manufactured by Merck, was 100% effective among the 12 000, mostly young, women who took part. It knocked out the two strains of HPV, 16 and 18, that are implicated in 70% of cervical cancers.
And the vaccine could prove even more useful. The trials showed that some of the other HPV types involved in a minority of cervical cancers were also stopped in their tracks. So cervical cancer could, in theory, be wiped out. This is only achievable if every girl and boy has the jab. The vaccine is expected to be offered in the United Kingdom to sexually inexperienced girls who will not have HPV, aged around 10 to 13, but suggesting a vaccination for a young girl that will protect her from a sexually transmitted disease has not gone down well with parents.
Cancer is the scourge of our times, the most feared disease of the 21st century. It appears to come from nowhere and kill at random. The more we know of the causes, the better we will be able to protect ourselves. Finding a silent trigger such as a virus that scientists may be able to knock out of the equation with a vaccine is not a reason to panic, but a cause for hope. — Â