'Full genetics of cancer mapped'

Many newspapers have reported that scientists have "cracked the code" of cancer with the analysis of the entire genetic sequence of malignant melanoma skin cancer and an aggressive form of lung cancer.

In the past, researchers were only able to look at smaller sections of DNA, as sequencing the entire DNA of a cell would have taken a very long time. Recent advances in technology have allowed the analysis of the entire sequence of DNA within a cell much more quickly.

However, cancer is a complex disease and not all individuals with cancer will have exactly the same mutations found in this research. Equally, not all of the mutations identified will be contributing to the cancerous nature of the cells. Therefore, future research is needed to look at DNA from many other individuals to pinpoint which mutations are likely to cause these cancers.

These types of advances may mean that, eventually, each patient will routinely have their entire cancer genome sequenced. However, this is not likely to happen in the near future and we do not yet know enough to be able to use this knowledge to help tailor indviduals’ treatments, as some newspapers have claimed.

Where did the story come from?

This research was conducted by Dr Erin D Pleasance and colleagues from Wellcome Trust Sanger Institute and other research centres in the UK and the US. It was published as two papers in the peer-reviewed scientific journal Nature. One study was funded by the Wellcome Trust, sources of funding were not stated for the other.

These studies are part of a larger ongoing project called The International Cancer Genome Consortium that is attempting to genetically analyse 50 different tumour types.

What kind of research was this?

This was laboratory research looking at the genetic sequence of various human cancer cells grown in the laboratory. The researchers wanted to identify genetic mutations that might cause cancer.
Previous studies have mostly looked at mutations in small numbers of genes or in small sections of DNA, but this research aimed to read the entire sequence genetic sequence of these cancerous cells. Advances in DNA technology have now made it possible to perform this type of analysis much more quickly and easily than before.
The researchers hope that looking at the entire genetic sequence will help them to further understand factors such as how DNA is affected by known cancer risks such as UV rays and tobacco smoke, as well as which mutations might be behind the formation of cancers and how the cells attempt to repair mutated DNA.

What did the research involve?

The researchers used cancer cells that had been removed from people with cancer and grown in a laboratory. They looked at the overall pattern of mutations that the cancer cells contained. The cells examined were malignant melanoma cells taken from one person and small cell lung cancer cells (SCLC – a particularly aggressive form of lung cancer) taken from another person. The researchers also analysed the DNA of normal cells from these patients to help identify the mutations in the DNA of the cancerous cells.
The SCLC cells came from a site where the lung cancer had metastasised (spread) to the bone of a 55-year-old man before he received chemotherapy. It was not known whether this man had smoked. The melanoma cells came from a metastasis in a 43-year-old man with malignant melanoma before he received chemotherapy.
The researchers used special techniques that can rapidly read the sequence of letters that make up the code of the DNA in the cells, a technique called sequencing. Advances in DNA technology have made it easier and quicker to sequence the entire genetic code of a cell, called the genome.
The researchers then compared the sequences in the cancer cells to those in normal cells to identify any changes (mutations) in their DNA. These changes can range from changing a single letter in the code to rearranging whole sections of DNA. They looked at the characteristics of these mutations to see whether they were typical of the effects of UV exposure (a known risk factor for skin cancer), or of the 60 chemicals that are found in tobacco smoke (a known risk factor for lung cancer) that might potentially cause mutations. They also looked at what genes (sequences which carry instructions for making proteins) were affected, and whether the mutations were spread evenly throughout the DNA.

What were the basic results?

In the malignant melanoma skin cancer cells, the researchers identified 33,345 single-letter changes in the DNA. The also identified various other mutations involving rearrangements, insertions and deletions of sections of DNA. Most of the mutations identified appeared to be caused by ultraviolet light exposure, which is known to be a risk factor for skin cancer. Mutations were found to be more common in areas where the genetic sequence did not contain any genes, suggesting that the cells’ DNA repair mechanisms had preferentially fixed mutations that affected genes.
In the SCLC line, the researchers identified 22,910 single-letter changes in the DNA. This included 134 changes within the pieces of genes that contained the instructions for making proteins. These genes with mutations included those known to play a role in cancer. As was the case in the melanoma cells, they also identified larger mutations involving rearrangements, insertions and deletions of chunks of DNA.
Most of the mutations they identified in the lung cancer cells did not appear to be giving them a ‘selective advantage’ that would help them to survive and divide. The mutations were of varying types, which indicated the effects of the many different cancer–causing chemicals found in cigarette smoke. Again, there was evidence that suggested that the cells’ DNA repair mechanisms had ‘fixed’ some of the mutations that affected genes.
The researchers identified one specific mutation that caused a duplication of a part of a gene called CHD7. Two other SCLC lines were also shown to have mutations that caused part of the CHD7 gene to be inappropriately joined to the PVT1 gene. This suggested that rearrangements in the CHD7 gene may be common in small cell lung cancer.
Based on their results and the average number of cigarettes needed to cause lung cancer, the researchers estimated that cells which eventually become cancerous, develop an average of one mutation for every 15 cigarettes smoked.

How did the researchers interpret the results?

The researchers concluded that their results “illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic”. They also say their findings “illustrate the potential for next-generation sequencing to provide unprecedented insights into mutational processes, cellular repair pathways and gene networks associated with cancer.”

Conclusion

This research has been made possible by advances in DNA sequencing technology, and understanding the mutations that lie behind cancer may have numerous implications for future research. However, cancer is a complex disease and not all of the mutations identified in these studies will be contributing to the cancerous nature of the cells. Equally, not all individuals with cancer will have exactly the same mutations. Therefore, future research will be needed to look at DNA from many other individuals to try to identify which mutations are likely to be causing the cancers.
Eventually, these and future advances may mean that sequencing the entire genome of cancer cells from each individual may eventually become a routine part of cancer care. However, this is not likely to be the case in the near future and currently, we do not know enough to be able to use this knowledge to help doctors to tailor treatment to the individual.

Links to the headlines

The bespoke cancer 'cure': Patients could get specially tailored drugs after British scientists decode damage to DNA. Daily Mail, December 17 2009

Just 15 cigs can give you cancer. Daily Mirror, December 17 2009

Scientists celebrate blueprint in battle with lung and skin cancers. Daily Mirror, December 17 2009

Cancer ‘maps’ pave way for tailored drugs. Financial Times, December 17 2009

Genetic map of tumours reveals thousands of mutations. The Times, December 17 2009

First cancer genome sequences reveal how mutations lead to disease. The Guardian, December 17 2009

Cancer treatment takes a giant step forward as scientists crack code. The Times, December 17 2009

Scientists crack 'entire genetic code' of cancer. BBC News, December 17 2009

Docs make Big C breakthrough. The Sun, December 17 2009

Links to the science

Pleasance ED, Keira Cheetham R, Stephens PJ. et al. A comprehensive catalogue of somatic mutations from a human cancer genome. Nature [advance online publication] December 16 2009

Pleasance ED, Stephens PJ, O’Meara S et al. A small-cell lung cancer genome with complex signatures of tobacco exposure.Nature [advance online publication] December 16 2009

Dentist

Today 94% dentistry score (Peter G dentist has 89% with 2 crowns). My previous score was 86%.

My first half marathon - New Forest

New Forest Half Marathon (13.1 miles) on 27 September 2009 from New Milton to Sway.

My first half marathon jogged in 2 hours 43 minutes (slower than top 97% of runners). 12.4 minutes per mile or 4.8 miles per hour. I came 5 runners who finished.

I'm listed & pdf

1820 3427 Jane Fergusson F 46 2:43:18 (Chiptime) 2:44:57 (Guntime)

The organisers obviously hadn't sorted out the transfer of race details from Jane to me!

I ran all the race with Jonathan:

1821 3426 Jonathan Ferguson M 48 2:43:17 (Chiptime) 2:44:58 (Guntime)

Apart from a very minor stomach twinge at 6 miles (which went by the 7th) and a minor blister on my foot - the race was great fun! Thanks Jonathan for your support.

Thanks for the cheers en route from my wife Sharon, Jane Fergusson and daughter Georgina ... and Jazzie my dog.

I wore the 'silver' medal all day at CRABS! Very proud to have done it!

• My first half marathon in 2 hours 43 mins: 1820/1875  (top 97% runners). 12.4 mins/mile, 4.8 miles/hr.

Next half marathon target? Based on the NFHM 2009 results:

• less than 2 hr 30 mins:  1724/1875 (top 92% runners), 11.4 mins/mile, 5.2 miles/hr (8% faster) 
• less than 2 hr 15 mins: 1468/1875 (top 78% runners), 10.3 mins/mile, 5.8 miles/hr (20% faster)
• less than 2 hr: 1000/1875 (top 53% runners), 9.1 mins/mile, 6.6 miles/hr (37% faster)
• 1 hr 15 mins: First place, 5.7 mins/mile, 10.5 miles/hr (118% faster)

Congratulations to First place runner:

1 3402 Steve Jeffery who is 40 from Basingstoke & Mid Hants AC  in 1:15:50.

and congrats to the oldest runner aged 88, Bruce Davidson from New Forest Runners in 3:05:23

and to 1086 3991 Scott Wareham M 44 2:01:30 2:01:54
and to 638 4311 Paula Barker F 41 1:50:46 1:51:30 (Sharon's cousin)

Middle age fat and life-span in women

Middle age fat and life-span

NHS ChoicesSep 30, 2009 18:31:00 GMT Share

“Middle-age spread can knock years off your life,” the Daily Mail has warned, saying that piling on weight in middle age can cut your chances of living to an old age by 80%.

This news is based on a well conducted study that had followed 121,700 nurses since 1976, carrying out regular and comprehensive assessments of them. It does suggest, as may be expected, that reduced weight and body fat is associated with good health and survival. The research team also adjusted to account for various social, demographic and lifestyle factors that may influence the association.

It should be noted that the study did not assess the chance of survival, but of ‘healthy survival’ at age 70 or over (the researchers’ own measure of disease-free living), which was seen in only 9.9% of participants. 

While there are some limitations to the study, its conclusions agree with traditional advice that the best way to aim for a healthy life is to eat a balanced diet, exercise regularly and avoid health risk behaviours such as smoking and excess alcohol.

Where did the story come from?

The story was published in the British Medical Journal and authored by Qi Sun and colleagues of Harvard School of Public Health and the University of Warwick. The study was funded by the National Institutes of Health in the US, and the Pilot and Feasibility Program sponsored by the Boston Obesity Nutrition Research Center.

What kind of scientific study was this?

This was a cohort study designed to examine the theory that mid-life “adiposity” (build up of fat) is linked to a reduced chance of maintaining optimal health in older age.

The study involved participants of the Nurses’ Health Study, which started in 1976 and enrolled 121,700 healthy women aged between 30 and 55. Questionnaires were sent to the participants upon entry into the study (baseline) and at various points during the follow-up period, asking questions on disease, lifestyle and medical risk factors. Food frequency questionnaires were used in 1980 and repeated every two to four years.

A 36-item health status survey was included on the 1992, 1996, and 2000 questionnaires, and included questions on physical activity and perception of health. Major chronic diseases (including coronary disease, cancer and diabetes) were self-reported and then confirmed through medical records. From 1995 onwards, 93% of nurses aged 70 or older had their cognitive function assessed.

Weight and height were collected during the baseline questionnaire, with further weight assessments every two years thereafter. Although weight was self-reported, a validity study was carried out in 184 women and showed a strong correlation between self-reported and measured weights.

In a 1986 assessment of central obesity, the participant’s BMI was calculated and measures of waist circumference, hip circumference, and waist-to-hip ratio were taken. The study population for this analysis was, however, only a subset of the primary study population (9512 for waist circumference; 9450 for hip circumference; 9438 for waist-hip ratio). When conducting analyses between these measures and survival, researchers adjusted for various social and demographic factors that might affect the relationship.

The final follow-up for the purposes of this study was in 2000, when 95% of the cohort could be contacted. Deaths were identified by reports from next of kin, postal authorities, or through the national death index and almost all of those who had died could be identified. The researchers defined healthy survivors as women who survived to age 70 or older and were at that point free from 11 major chronic diseases, had no major limitations of physical function, had intact cognitive function and were in good mental health.

What were the results of the study?

Only 1686 (9.9%) of the surviving cohort met the criteria for a “healthy survivor”. A total of 15,379 (90.1%) were “usual survivors”, who had various impairments of either chronic disease, cognitive function or mental health, physical health, or a combination of these. In comparison, healthy survivors were typically healthier at baseline, and were more likely to have better diet and greater education. They were also less likely to have overall or central obesity in 1986, to have gained less weight since age 18, and to smoke.

After adjusting for various lifestyle and dietary variables, there was a significant trend of a reduced chance of healthy survival in those women with a higher BMI at baseline or greater waist circumference, hip circumference or hip-to-waist ratio in 1986. Compared with women of BMI 18.5 to 22.9, obese women (BMI ≥30) had a 79% decreased risk of healthy survival (odds ratio 0.21, 95% confidence interval 0.15 to 0.29).

The chance of healthy survival after age 70 was also decreased with weight gained from age 18 until middle age. For women who were both overweight (BMI ≥25) and had gained at least 10kg since age 18, there was an 82% decreased risk of being a healthy survivor compared to women of lean BMI and who had remained at a relatively stable weight.

What interpretations did the researchers draw from these results?

The researchers say that their findings give evidence that adiposity in middle-aged women is strongly related to a reduced risk of healthy survival into older age.

What does the NHS Knowledge Service make of this study?

This is a very well conducted study that has followed a large group of women over a considerable period of time using regular and comprehensive assessments. It does suggest, as one might expect, that reduced weight and adiposity is associated with healthy survival. In their analyses they also adjusted for various social, demographic and lifestyle factors that may affect the association. However, there are still related issues to consider:

• 
  

  Although the news highlights that “middle-age spread” reduces your chance of surviving by 80%, it is not survival that is being assessed, it is healthy survival. 
  

  
  
• This measure was designed by the study authors to mean absence of any of 11 major chronic diseases, physical limitations, cognitive impairment or mental health issues at age 70. Very few people in this cohort met these full criteria, and it may be expected that a comparatively low proportion of the general population aged 70 or over would be able to meet all of them. Outside of this study context, there is no validated definition of a healthy survivor in general use.
• Most women were under 75 at the study’s end-point, and so survival rates into older ages cannot be accurately determined.
• The adiposity measures were conducted at one time point in 1986, and the women may have changed over time.
• Weight and measurements were self-reported, which may introduce inaccuracies, although the researchers did make efforts to account for this through their validation assessment.
• 
  

  Although some news reports feature photographs of men, this was a study of women only. Results from this study may not be generalised as applying to men. 
  

  
  
• Additionally, all participants were nurses, a specific social group that may not be comparable to all other populations. The women were also primarily of white ethnicity.

The researchers say that their study “emphasises the importance of maintaining a healthy weight from early adulthood”. Despite the limitations, their conclusions agree with traditional advice that, although all genetic and medical predispositions to disease may not be controllable, the best way to aim for a healthy life is to eat a balanced diet, exercise regularly and to avoid health risk behaviours as much as possible such as smoking and excess alcohol.

Links To The Headlines

How middle-age spread can knock years off your life. Daily Mail, September 30 2009

Gaining weight in middle age cuts chances of healthy long life. The Daily Telegraph, September 30 2009

Links To Science

Sun Q, Townsend MK, Okereke IO et al. Adiposity and weight change in mid-life in relation to healthy survival after age 70 in women: prospective cohort study. BMJ 2009;339:b3796

Today's babies will live a century

Today's babies will live a century

NHS ChoicesOct 02, 2009 17:20:00 GMT Share

“Most babies born in the past few years in the UK will live to be 100 if current trends continue,” The Guardian has today reported. The newspaper said that despite the elderly having more long-term illnesses, such as cancers and heart conditions, people will survive them because they will receive earlier diagnosis and better treatment.

The scientific review behind this story builds on a large body of ongoing research from the past five years. Its authors pose the question asked by policy makers about whether expected increases in life expectancy will actually be accompanied by a better quality of life. They believe that because aspects of the ageing processes have become more controllable, people are currently living longer without severe disability. However, whether these quality of life benefits will extend to future elderly generations remains uncertain.

One finding from this well conducted research is that more than half of the babies born in developed countries since 2000 will potentially celebrate their 100th birthday. However, to predict what this will mean for the ageing population’s quality of life will need more study.

Where did the story come from?

This research was carried out by Professor Kaare Christensen from the Danish Ageing Research Centre at the University of Southern Denmark and colleagues from Germany. The study was supported by grants from the National Institutes of Health and of Ageing in the US, and published in the peer-reviewed medical journal, The Lancet.

What kind of scientific study was this?

This was a systematic review of several pieces of previous research, which were then used to create a narrative report on predicted life expectancy and the rates of disease or disability (quality of life).   The review section mainly included studies conducted since 2005, mathematical modelling was included to predict the length and quality of life of people through to 2050 and beyond.

The researchers searched a variety of sources for information, including the International Network on Health Expectancies and Disability Process, the TRENDS network, and reports that were identified through published research databases such as PubMed. The researchers looked for reports published after 2005, also searching through their reference lists to find cited, older reports for inclusion if relevant. To ensure the most recent demographic data was used, they extracted data from a source called the Human Mortality Database. The researchers present their findings in sections that cover mortality projections, trends in the complex notions of health, and issues of disease and disability.

What were the projections for mortality?

The researchers say the data on life expectancy from selected developed countries shows that between 1840 and 2007 life expectancy has lengthened almost linearly, with no sign of any deceleration. Importantly, the researchers claim the data suggests that a limit to human lifespan is not yet near. The researchers also assess the probability of dying before the ages of 80 and 90 years, showing that this too had fallen between 1950 to 2003.

The predictions out to the year 2050 are based on German statistics and show increases in the proportion of elderly and retirement age groups compared to working and younger age groups. The calculations assume a constant total fertility rate of 1.4 babies per pregnant woman and a yearly net migration of 100, 000 people.

Life expectancy is predicted to reach 83.5 years for men, and 88.0 years for women by 2050.

What were the trends in health and disease?

The researchers explain that studies of health trends are complex due to a number of reasons. For example, the measures of disease, of any functional limitations or of disability are not consisted across the research. Also, the individual studies are not directly comparable as their designs or questions have also changed over time, and often the elderly in institutions are excluded from surveys despite the fact they are an important group to study.

Despite these limitations, the researchers are able to say that there have been rises in many long-term diseases among the elderly including heart disease, arthritis and diabetes. In addition there have also been increases in pain-related and psychological distress, general fatigue, dizziness, leg ulcers, heart problems, hypertension, asthma, osteoarthritis, and lower-back complaints. In other reports, several diseases have decreased or improved: cardiac disease, asthma, osteoarthritis, depression, and lower-back complaints were found to be less in a Dutch study. The data was based on registers of activity and diagnoses from family doctors.

The researchers say that total cancer incidence has been rising, but deaths from heart attack have fallen more than rates of new heart disease. Obesity is also increasing.

What were the trends in disability?

The researchers analysed changes in disability over time using measures such as the restrictions in the ability to perform the activities of daily living and the need for assistance in daily life. These, they say, provide increasing evidence that the prevalence of disability has been falling since the 1980s and 1990s. Reductions in disability have been reported as fall of 0.4—2.7% every year.

What are the implications for a healthy and long life?

Health expectancies combine information about life expectancy and prevalence of good health. They can indicate if the period of disease or disability at the end of life is shortening or lengthening.  Several measures can be used and results differ depending on which is used (disease-free health expectancy, life expectancy in perceived good health, and disability-free life expectancy). While the trend has been improving for most measures, there has been a decrease for the most severe levels of disability at the same time as an increase for the least severe levels.

What interpretations did the researchers draw from these results?

The researchers conclude that people are living longer, but are not definite about whether this is accompanied by a better quality of life.

For people younger than 85 years today limitations and disabilities seem to occur later in life than in previous generations, despite an increase in chronic diseases and conditions.

The researchers explain this contradiction in four ways:

• There may be earlier diagnosis, improved treatment and better outcomes from prevalent diseases so that they are less disabling.
• An estimated 14—22% of the overall fall in disability can be attributed to reductions in disabilities associated with cardiovascular diseases. This has complicated the picture.
• The rising use of technology to help older people’s mobility, as well as improvements in housing standards and accessibility of buildings. might have made some diseases less of a functional limitation or disability.
• Finally, socioeconomic changes such as increasing levels of educational attainment and income in elderly people and improved living and workplace conditions, might have contributed to the fall in disability.

The authors say that people younger than 85 years today are living longer and are generally able to manage their own daily activities for longer than previous generations could.

What does the NHS Knowledge Service make of this study?

This is a complex and well-presented review, which has summarised a number of individual studies. The newspapers have focused on data on children that indicates that most born now will live beyond 100 years. While this may be true from the modelling contained in this report, the issue of how well they will be during their life still needs further research.

The researchers call for more research into this and discuss policy implications for issues such as retirement and the major challenges that health-care systems will come to face. They say that, “very long lives are not the distant privilege of remote future generations - very long lives are the probable destiny of most people alive now in developed countries.”

Links To The Headlines

Most babies born in Britain will live to 100, doctors predict. The Guardian, October 2 2009

Half of babies 'will live to 100'. BBC News, October 2 2009

Most babies born in Britain will live to 100. The Independent, October 2 2009

Links To Science

Christensen K, Doblhammer G, Rau R, Vaupel JW. Ageing populations: the challenges ahead. The Lancet, Volume 374, Issue 9696, Pages 1196 - 1208, 3 October 2009

HPV vaccine for Cervical Cancer, in the clear

HPV vaccine in the clear

NHS ChoicesOct 02, 2009 17:35:00 GMT Share

A pathologist has confirmed that the human papilloma virus (HPV) vaccine did not cause the death of Natalie Morton, the schoolgirl from Coventry.

Early media speculation suggested the anti-cancer jab could be responsible, but a post-mortem has found that she died from a large malignant tumour of the heart and lungs.

Dr Caron Grainger, joint director of public health for NHS Coventry and Coventry City Council, said, “The pathologist has confirmed today at the opening of the inquest into the death of Natalie Morton that she died from a large malignant tumour of unknown origin in the heart and lungs. There is no indication that the HPV vaccine, which she had received shortly before her death, was a contributing factor to the death, which could have arisen at any point”.

“We hope that this news will reassure parents that the vaccine is safe and that they should continue to encourage their daughters to be protected against cervical cancer. The HPV vaccination programme will continue as planned in the city from Monday.”

Why was a link made between the HPV vaccine and the girl’s death?

No link should ever have been made. However, the girl died on the same day as receiving her vaccination and this led to associations being drawn between the jab and her death.

This happens largely through misinterpretation of probabilities. Unfortunately, young people do die suddenly of natural causes. Although such events are rare, they are statistically much more common than fatal reactions to routine medical treatments.

Do people ever have severe adverse reactions to vaccinations?

They do, but it is much less common than many people think.

In very rare cases, it is possible for someone who is vaccinated to experience an allergic reaction, known as an anaphylactic reaction. These are extraordinarily rare, with a recent study showing that only one anaphylactic reaction is reported in about a million immunisations.

Moreover, most anaphylactic reactions to vaccines do not result in death. According to data from the Office for National Statistics, there has not been a single recorded death due to anaphylactic shock following a vaccination for at least 10 years. This covers all recorded incidents between 1997 and 2007, the last year for which data are available.

What are the benefits of the HPV jab?

It’s been calculated that the UK HPV vaccination programme will ultimately save 400 lives a year. Around 3,000 women a year are currently diagnosed with cervical cancer, and the disease kills more than 1,000 women a year in the UK.

Half of all sexually active women will be infected by a strain of HPV in their lifetime. These infections cause more than 99% of cervical cancer cases and a range of other cancers.

The HPV vaccine protects against two types of HPV: strains 16 and 18. Together these cause around 70% of cervical cancers.

Have any side effects been reported?

Yes. All drugs have side effects and the HPV vaccine is no different.

Very common side effects include:

• pain or discomfort at the injection site,
• redness or swelling at the injection site,
• headache,
• aching muscles, muscle tenderness or weakness (not caused by exercise), and
• tiredness.

Common side effects include:

• gastrointestinal symptoms including nausea, vomiting, diarrhoea and abdominal pain,
• itching, red skin rash, hives (urticaria),
• joint pain, and
• fever (≥38°C).

Uncommon side effects (occurring in less than one per 100 but more than one per 1,000 doses of vaccine):

• upper respiratory tract infection (infection of the nose, throat or trachea),
• dizziness, and
• other injection site reactions such as hard lump, tingling or numbness.

For more on the vaccine’s known side effects go to Health A-Z: side effects.

Does the vaccine have a good safety record?

The vaccine’s safety record is excellent and it has passed the rigorous safety tests needed for it to be used in the UK and other European countries.

It underwent safety testing as part of the licensing process, with over 70,000 doses used in clinical trials here before a licence was granted (it’s now licensed in more than 90 other countries).

In total, more than 1.4 million doses of the vaccine have since been given in Britain, and millions more worldwide.

Who should have the vaccine?

The HPV vaccine is being offered to all girls aged 12-13 as part of a national vaccination programme that aims to cut deaths and serious illness from cervical cancer. The vaccination programme began in September 2008. By 2011, all girls under 18 in Britain will have been offered the jab. The vaccine is given in three injections over six months. A catch-up programme also started in September 2008 and offers the vaccine to other older girls up to the age of 18.

How does the vaccine work?

Virtually all cases of cervical cancer are caused by a virus called human papilloma virus (HPV), which is passed on during sex (although sexual intercourse isn’t always necessary to pass on the virus).

The vaccine, Cervarix, which is used in the NHS national programme protects against two types of HPV, strains 16 and 18, which together cause around 70% of cervical cancers.

What is HPV?

HPV is a virus that infects the deepest layer of the skin or genital surfaces. There are over 100 different types of HPV, 13 of which are known to cause cervical cancer. The others are harmless or cause genital warts. The virus is transmitted through sexual contact and is very common, with over half of all women becoming infected at some point in their lifetime.

How does HPV cause cancer?

Most HPV infections clear up by themselves, but in some people the infection can last a long time.

HPV infects the cells of the surface of the cervix (the neck of the womb), where it can stay for years without anyone knowing.

HPV can damage these cells, causing changes in their appearance. Over time, these changes can develop into cervical cancer.

Will the cervical cancer programme be suspended?

No. There are no plans to suspend the vaccination programme.

As with any vaccine, Cervarix is associated with side effects, but overall this is a well tested vaccine that’s been introduced to tackle a serious health problem.

The MHRA has reviewed all reported side effects related to Cervarix and concluded there is no evidence to suggest that the vaccine carries any long-term side effects.

The independent Expert Advisory Group of the Commission on Human Medicines has reviewed the data and endorses the MHRA’s view that no new or serious risks have been identified and the balance of risks and benefits remains overwhelmingly favourable.

Should I let my daughter have the cervical cancer jab?

Yes. The established risks of getting cervical cancer are far, far greater than any risk from the HPV vaccine.