Oral cancer - UK incidence statistics

Oral cancer - UK incidence statistics

This page presents oral cancer incidence statistics by type, age and sex,geographical variation, socio-economic deprivation , and trends over time The ICD codes for oral cancer are ICD9 140, 141, 143-146, 148 and 149, and ICD10 C00-06, C09, C10, C12-14.

Oral cancer incidence by sex

In the UK in 2006, 5,325 persons were diagnosed with an oral cancer. Across countries, the highest incidence, for both males and females, is in Scotland. ( Table 1.1)

Table showing the number of new cases and rates of oral cancer in the UK

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Types of oral cancer

Oral cancers are made up of:

  • cancer of the lip
  • cancer of the tongue
  • cancer of the mouth
  • cancer of the oropharynx
  • cancer of piriform sinus
  • cancer of the hypopharynx
  • other and ill-defined sites
Table 1.2 shows the number of new cases of these types of oral cancer.

Around one third (31%) of oral cancers are diagnosed in the mouth cavity and a slightly lower proportion (29%) on the tongue. Cancers of the oropharynx, piriform sinus and hypopharynx together account for a further quarter (28%) of cases while lip, the least frequent type of oral cancer, accounts only for 6%. 1-4. More than 90% of oral malignancies are squamous cell carcinomas. 5

Table showing the number of new cases of oral cancer by type, in the UK

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Oral cancer incidence by age and sex

In the UK and most other countries, oral cancer is more common in men than women. However, the sex ratio in the UK has decreased rapidly from around 5:1 fifty years ago to less than 2:1 today ( Table 1.2). The risk of developing oral cancer increases with age and in the UK the majority of cases (86%) occur in people aged 50 or over ( Figure 1.1). 1-4 However, in some high prevalence areas in the developing world, oral cancer is relatively common in younger people.

Figure showing the number of new cases and age-specific incidence rates for oral cancer in the UK

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Geographical variation in oral cancer incidence

As Table 1.1 shows, oral cancer incidence rates in Scotland are significantly higher than in other parts of the UK. 1-4, 6 This result correlates with the higher rates of tobacco and alcohol consumption in Scotland than in other parts of the UK.

Studies of oral cancer incidence in minority ethnic populations in Britain have reported high rates in south Asian and Chinese populations in which the habit of areca nut or betel quid chewing is still prevalent (see Risk factors section). 7

Worldwide an estimated 405,000 new cases of oral cancer (oral cavity and pharynx excluding nasopharynx) are diagnosed each year with two-thirds of these cases occur in developing countries. 8 Each year an estimated 66,650 new oral cancer cases are diagnosed in the countries of the European Union (EU). 8

Oral cancer incidence varies strikingly around the world ( Figure 1.2). 8

Figure 1.2: World age standardised male incidence rates for oral cancers, selected countries of the world,

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The highest age standardised rates (over 20 per 100,000 population) of oral cancer are reported in parts of Europe and south central Asia. In high-risk countries such as Sri Lanka, India, Pakistan and Bangladesh, oral cancer is the most common cancer in men and may account for up to 30% of all new cases of cancer compared to 3% in the UK and 6% in France.

Within the EU the highest oral cancer incidence rates for males are found in France and Hungary and the lowest rates in Greece and Cyprus ( Figure 1.3). 8

Figure 1.3: European age standardised incidence rates, by sex, oral and pharyngeal cancer, EU countries,

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The female oral cancer incidence rates are much lower and show less variation. The highest rates are in Hungary, Luxembourg and Germany. Oral cancer incidence rates in UK males are significantly lower than the EU average and rank 22nd out of the 25 EU countries: the oral cancer incidence rates in UK females are also lower than the EU average but rank higher at 12th.

Cancer of the lip has a different geographical distribution from other oral cancers and the highest incidence rates are reported in white populations in Canada and Australia. Cancer of the lip is rare in non-white populations. Lip cancer is particularly linked to outdoor occupations such as farming and fishing and there are twice as many male as female cases. As well as occupational differences, it is thought that the use of cosmetics helps to protect the female lip from damaging UV light.

Oral cancer incidence and socio-economic deprivation

Oral cancer incidence is strongly related to social and economic deprivation, with the highest rates occurring in the most disadvantaged sections of the population. The association is particularly strong for men.

For patients diagnosed in 1991-95 in Scotland, incidence rates for cancer of the head and neck were twice as high for those in the most disadvantaged category compared with the least disadvantaged. 2 This reflects the higher tobacco consumption in the more disadvantaged groups.

Oral cancer incidence trends over time

The age standardised incidence of oral cancer in British males stayed at around 7 per 100,000 males between 1975 and 1989, but since then, the rate has steadily increased to reach 11 per 100,000 in 2006, an increase of 51% since 1989. While female oral cancer rates have remained significantly lower than male rates, their incidence trends have been similar with an average increase of 2.7% each year since 1989.

Trends are shown in Figure 1.4. 6

Chart showing the age standardised (European) incidence rates for oral cancer in Great Britain, 2005

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When the oral cancer incidence trends are analysed by age group, differing patterns emerge as Figures 1.5 and 1.6 illustrate. 6

Figure showing the age-specific incidence rates for oral cancer in males in GB

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Figure showing the percentage change in incidence rates for oral cancer in British men

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For men over 80, the incidence of oral cancer has more than halved since 1975, while rates for men in their 70's have remained relatively stable. However, there have been large increases in the incidence of oral cancer diagnosed in men in their 40s and 50s whose rates have more than doubled from 3.6 to 10.0 per 100,000 for men aged 40-49 and from 11.5 to 27.2 for men aged 50-59.

Rising trends of oral cancer in young and middle-aged men, particularly of cancer of the tongue, have been reported in other European countries and the USA. 9-15 This increase in a cancer that is often difficult to treat and sometimes debilitating and disfiguring, is alarming -see last section under Risk factors.

The oral cancer incidence trends for the UK are shown in figure 1.7

oral cancer incidence trend in the UK since 1993

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Updated: 10/08/2009 0:00

Oral cancer - UK mortality statistics

This page presents oral cancer mortality statistics including by age and sex and trends over time.

Oral cancer mortality by age and sex

In 2007 there were 1,851 deaths from oral cancer in the UK ( Table 2.1). 1-3

Table 2.1: Number of deaths and mortality rates, oral cancer, UK

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Oral cancer mortality rates are highest for Scottish men reflecting their high incidence rates.

The predominance of male over female deaths from oral cancer at the young and middle ages is shown clearly on Figure 2.1. 1-3

Figure 2.1: Number of deaths and age-specific mortality rates, by sex, oral cancer, UK

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Oral cancer mortality trends over time

The overall age standardised mortality rate has remained fairly stable between 1971 and 2007 at around 3.5 and 1.4 per 100,000 for males and females respectively ( Figure 2.2). 1-3

Figure 2.2: Age-standardised (European) mortality rates, oral cancer, by sex, UK

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As with the incidence trends, the all-ages oral cancer mortality figure masks the variation in age-specific trends seen in Figure 2.3. Mortality rates among men aged 85+ have fallen by 60%, while rates in those aged 75-84 have also fallen by 52% since 1971. On the contrary, for men aged 45-64 there has been an increase of 90%. For younger men the rate has remained stable.

Figure 2.3: Oral cancer mortality rates, by age, males, UK

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Updated: 18/05/2009 0:00

Oral cancer - survival statistics for England and Wales

This page presents oral cancer survival statistics including by stage at diagnosis, trends in cancer survival, by age, and by deprivation group.

Many patients who are treated for oral cancer have to cope with the devastating consequences of their treatment. 1 These may affect the patient’s appearance and how they function. For example, eating, drinking and speaking may become difficult and these can lead to other problems such as depression and nutritional deficiency. Quality of life issues are therefore especially important for this group of patients.

Oral cancer survival by stage at diagnosis

Many oral cancers present at a late stage as illustrated in Table 3.1 using data from the south and west of England for patients diagnosed in 1996-2000. 2 Patients with early disease can be cured, but for those with metastatic disease, the aim is to contain the disease and maximise quality of life. The survival statistics shown here, unless otherwise stated, include all types of cases of the disease, early and late, and should be used as a general guide only.

Table 3.1: Stage and two-year crude survival, cancers of the oral cavity and pharynx, South and West of England, 1996-2000

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Oral cancer survival trends over time

Five-year survival rates for cancers of the lip, oral cavity, tongue, oropharynx and hypopharynx are shown in Figure 3.1 for men and women diagnosed in1991-95 and 1996-99. 3 The best outcome was for cancer of the lip with over 90% of patients surviving five years and most of these will be cured. The five year rates for lip cancer improved slightly for both men and women during the 1990s. The lowest survival was for hypopharyngeal tumours. In general, prognosis worsens with increasing inaccessibility of the tumour. For cancers of both the tongue and oral cavity, women had higher survival rates than men. In the case of tongue cancer there was an 11% difference (55 v 44%) for patients diagnosed in 1996-99, for cancers of the oral cavity it was 8% (55 v 48%) for 1996-99 patients.

Figure 3.1: Comparison of age-standardised 5 year relative survival rates for patients diagnosed in 1991-1995 and 1996-1999, England and Wales

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Oral cancer survival by age

As for most cancers, survival is better for younger than older patients as shown in Figure 3.2 for cancers of the oral cavity, oropharynx and tongue.

Figure 3.2: Five-year relative survival by age, cancers of the oral cavity, oropharynx and tongue, 1996-1999 patients England and Wales

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Oral cancer survival by deprivation group

When the five year survival rates for 1986-90 patients were analysed by deprivation category, there were significant differences between the most affluent and most deprived groups for cancers of the tongue, oropharynx and oral cavity ( Table 3.2 ). 4

After the improvement in survival over time was analysed by deprivation group, it became clear that most of the improvement had occurred in the affluent group. Five-year relative oral cancer survival rates increased from 43 to 55% between 1971-75 and 1986-90 for the affluent patients compared with a very small increase over the same time period of 42 to 44% for the most deprived patients. 4

Table 3.2: Comparison of survival in affluent and deprived patients, 1986-90, England and Wales

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Updated: 30/04/2005 0:00

Oral cancer - risk factors

This page presents oral cancer risk factors including tobacco, alcohol, diet and nutrition, ultraviolet light,human papillomavirus and immunosuppression and other factors.

The main causes of oral cancer have long been known and many cases of the disease could be prevented. The most important aetiological factors are tobacco usage and excess consumption of alcohol, and these factors together are thought to account for about three-quarters of oral cancer cases in Europe. 2 

A diet deficient in fruit and vegetables also predisposes towards the development of oral cancers and it has been estimated that this may be responsible for 10-15% of cases in Europe. 2 For lip cancers only, over exposure to UV light is implicated.

Tobacco

In the UK, cigarette, cigar and pipe smoking are the main forms of tobacco use and all are causes of oral cancer. 3 In the earlier parts of the last century, pipe smoking was associated with lip cancer (most lip cancers arise on the lower lip) and its decline in popularity may be linked with some of the decrease in lip cancer. A recent case control study in Spain showed an increased risk of lip cancer when smokers were in the habit of leaving the cigarette on the lip. 4 Since the 1920s smoking cigarettes has been the main form of tobacco use in the UK. According to a meta-analysis, on average current smokers have a three-fold increased risk of oral cancer. 62 The risk of oral cancer associated with smoking is both dose and duration dependent while smoking cessation leads to a fall in risk. 1, 5, 6 However, a recent study showed that it takes 20 years or longer for the risk to reduce to that of never smokers. 73

In 2003, it was estimated that of the 28% of British men who smoked, 4% smoked cigars and 1% pipes. 8 Very few women in the UK smoke pipes or cigars. In one case control study of oral cancer carried out in Cuba, the odds ratio associated with smoking 30 or more cigarettes a day was comparable with that for smoking 4 or more cigars a day. Indian women who practice reverse chutta smoking, with the lighted end of the cigar inside the mouth, have particularly high rates of oral cancer of the palatal mucosa. 9 Smoking bidi(s) which are made of hand-rolled tobacco wrapped in tendu leaf also increases the risk of oral cancer. 10

A recent evaluation by the International Agency for Research on Cancer (IARC) has confirmed that smokeless tobacco is also carcinogenic. 11, 12 Risk varies according to the composition of smokeless tobacco used in different countries. A recent meta-analysis showed a more than doubling in risk of oral cancer with use of smokeless tobacco in the United States and Canada, a five-fold risk increase for India and other Asian countries and a seven-fold risk increase in Sudan. No risk increase for oral cancer was shown with smokeless tobacco use in the Nordic countries. 63 In the UK and Europe (with the notable exception of Sweden) the use of smokeless tobacco is rare except in minority ethnic groups (see next paragraph). 13 In the USA it is a major problem with a reported 6% of the adult male population as regular users 14. In some areas, particularly the southern states, the prevalence is much higher with up to a third of young men using smokeless tobacco. 15

The primary cause of the very high incidence of oral cancer in South Asia is the widespread habit of chewing betel quid (or paan) and related areca nut use (areca nut is the seed of the fruit of the oriental palm, Areca catechu). 16 Chewing betel is thought to date back at least 2000 years and worldwide an estimated 200-400 million people practice the habit. 17 The components of the betel quid vary between different populations but the main ingredients are the leaf of the vine, Piper betel, areca nut, slaked lime (calcium hydroxide) and spices. 18 Tobacco was introduced to South Asia in the seventeenth century. Areca nut is carcinogenic to humans and the risk of oral cancer is increased with chewing paan without tobacco, although the risk is higher for paan containing tobacco. 19-21,64 As with smoking tobacco, risk is dependent on dose and duration of use. 22 Among Asian communities in the UK, Bangladeshis are the most likely to retain the habit of betel quid chewing as Figure 4.1 shows with 9% of men and 16% of women using smokeless tobacco. 23 The most commonly used chewing tobacco product is betel quid with tobacco. 24

Figure 4.1: Percentage of South Asians in the UK that use any form of chewing tobacco, 2004

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Alcohol

Alcohol is a major risk factor for oral cancer. A meta-analysis reported risk ratios for alcohol intake of 25 grams/day, 50 grams/day and 100 grams/day after adjustment for smoking of 1.8, 2.9 and 6.1, respectively. 65 One study showed a doubling in risk for people drinking 14 grams of alcohol/day. 66 People who both drink and smoke have a much higher risk of oral cancer than those using only alcohol or tobacco as Figure 4.2 demonstrates using US data. 28

Figure 4.2: Relative risk of oral/pharyngeal cancer in males by alcohol/tobacco consumption using US measures

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Heavy drinkers and smokers have 38 times the risk of abstainers from both products. 67 The effect of alcohol consumption in non-smokers differs by subsite, with a recent pooled analysis showing no increase in risk of oral cavity cancer in this group, although there was an increase in risk of cancers of the oropharynx/hypopharynx, two other subtypes of oral cancer. 75 Results from the Million Women Study in the UK also supported this finding. 76 Risk of alcohol consumption also interacts with risk of smokeless tobacco, with a combined risk of regular alcohol consumption and tobacco chewing of 24 shown in one study. 74

It has been suggested that it is the total amount of ethanol ingested rather than the type of product (beer, wine, spirits) which is important. 68 . The rising trends in oral cancer mortality in Europe have been related to increasing levels of alcohol consumption. For example, in Denmark the alarming increase in oral cancers has been attributed predominantly to greater alcohol consumption. 30 An exception to this rise in alcohol consumption is seen in France, where a decrease in alcohol consumption has been linked to the fall in oral cancer mortality rates in the 1980s. 31

In the UK, consumption of alcohol has more than doubled since the middle of the last century, from 3.9 to 8.6 litres of pure alcohol per head per year- see Figure 4.3. 32, 33

Figure 4.3: Alcohol consumption in the UK, 1900-2000, per capita consumption of 100 per cent alcohol

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The percentage of the population who exceed the recommended weekly guideline of 21 units for men and 14 for women rose from around 10% of women and 26% of men in 1988 to 18% and 30%, respectively, in 2002. 34 The heaviest drinkers are aged 16-24 years and this age group is also the most likely to binge drink. 33

At present the UK level of drinking (8.6 litres per year) is lower than in most European countries, for example, France (10.7 litres), Portugal (11.0 litres), Spain (9.9 litres) and Germany (10.6 litres). However, whereas consumption is either falling or stabilising in most of these countries, in the UK it is rising quickly. It is estimated that if current trends continue, the UK could rise to near the top of the consumption table within the next ten years. 33 Co-ordinated and funded action is needed to tackle the UK’s complex drinking problems. 35

Concern has also been expressed about the use of mouthwashes, particularly those with high alcoholic content. 36 However, the majority of studies show no increase in risk with use of alcoholic mouthwash. 59-61,69-71

Diet and nutrition

A meta-analysis showed a significant risk reduction of about 50% for each additional daily serving of fruit or vegetables. 37 A large prospective study, published since this meta-analysis, showed a smaller significant risk reduction for oral cavity cancer of 26% for each additional serving of vegetables, but no association for fruit intake. 38 Results may vary by smoking status, with a large case-control study showing risk reductions with the highest intake of fruit and vegetables among smokers and alcohol consumers but not among people who had never smoked or drunk alcohol. 39

Risk of oral cancer appears to fall with increasing body mass index (BMI). A recent case-control study in Spain reported a significant reduction in risk of oral cancer with higher BMI at diagnosis and two years prior to diagnosis, after adjustments for smoking, drinking, fruit and vegetable intake, although the association was not significant among people who had never smoked. 43 Since then, a case-control study showed a lower risk with higher BMI two years prior to the study among never and ever smokers. 72

Sun-exposure

Solar irradiation is a risk factor for cancer of the lip. 77 Lip cancer is three times more common in men than women which may be an effect of occupation, smoking and sun-exposure. 4 The use of sunscreens and protective clothing would significantly reduce exposure.

Human papillomavirus and immunosuppression

There is evidence that infection with high-risk human papillomaviruses (HPV) increases risk of oral cancer, particularly HPV-16. 44-47 The association is strongest for cancers of the oropharynx. 71 Studies show an increased risk of oral cancer in women with previous HPV-associated anogenital cancer, providing more evidence of a link with HPV infection. 48-49 An increased risk of oral cancer has been shown in individuals with HIV/AIDS or people who have undergone organ transplants, supporting a role of immunosuppression. 50

Oral lesions and conditions

Several oral lesions and conditions precede oral carcinoma and the most common of these are leukoplakia and erythroplakia. Other rare precancerous conditions include lichen planus, oral submucous fibrosis, syphilitic glossitis and sideropenic dysphagia. Leukoplakia has many clinical variants but is much less likely to progress to malignancy than erythroplakia. The precise prevalence of these conditions in the UK is unknown. Estimates of leukoplakia prevalence outside the UK range from 0.2 to 11.7% of the population and the prevalence of erythroplakia is considerably less. 51 It has recently been estimated that the annual transformation rate of oral leukoplakia to oral squamous cell carcinoma may not exceed 1%. 52 Erythroplakia is rare and mainly occurs in people aged over 60. 53

Risk in young and middle-aged adults

The rising incidence and mortality rates in young and middle-aged adults is incontrovertible, but there has been debate over the causes of this increase and whether their disease is inherently more aggressive than that occurring in older patients. 48, 54-56 A series of studies in southern England looking at risk factors for patients under 45 years concluded that most young patients are exposed to the traditional risk factors of tobacco smoking and alcohol while consumption of fresh fruit and vegetables is protective. 48, 57, 58 However, the relatively short duration of exposure to these known risk factors suggests that other factors may also be involved and there was a small sub-group of patients who had little, if any, exposure to the major risk factors.

Previous cancer diagnosis

People with a previous oral and pharyngeal cancer have a more than 30-fold increased risk of second oral and pharyngeal cancer, and risk remains 20-fold higher 10 or more years after the first diagnosis. 25 An almost seven-fold increase in risk of oral and pharyngeal cancer has been shown after a diagnosis of squamous cell carcinoma of the oesophagus, with risk remaining higher five or more years after the first diagnosis. 26

Updated: 04/09/2009 0:00

Oral cancer - symptoms and treatment

This page contains information on the symptoms, treatment and prognosis for oral cancer. 

Most oral cancers are asymptomatic in their early stages but as the malignancy progresses the symptoms may include those shown in Table 5.1.

Table 5.1: Possible symptoms of oral cancer

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Symptoms will vary according to the site of the tumour, for example, pain is often the first symptom of cancer of the tongue, either in the tongue or referred to the ear, whereas discomfort and difficulty in swallowing may indicate a tumour in the pharynx. White or red patches on the oral mucosa may indicate a cancerous or precancerous condition, and biopsy is essential for the diagnosis of any oral cancer. a Leukoplakia is more common than erythroplakia, but the latter is much more likely (75-90% of cases) to be premalignant or malignant and should be excised and checked histologically. 1 Up to 10% of leukoplakias become malignant over a ten year period and some may regress spontaneously making their management difficult. 2 A recent Cochrane review concluded that there is no effective treatment for preventing malignant transformation of leukoplakia: treatment with beta carotene and vitamin A retinoids was associated with significant rates of clinical resolution of the lesion but there was a high rate of relapse. 3

Although the majority of squamous cell carcinomas are slow growing (though a few may be very aggressive), most oral cancer patients are diagnosed at a late stage in their disease. The overall prognosis would be considerably improved if patients could be diagnosed at an earlier stage. Small and early oral cancers are highly curable but many patients, particularly when their cancer is diagnosed at an advanced stage, have to cope with the sometimes debilitating consequences of their treatment. These may include difficulties with speaking, chewing and swallowing and facial disfigurement. Prognosis is best for patients with cancer of the lip, the most accessible site for treatment.

Recent guidelines for improving services for head and neck patients have been published by the National Institute for Clinical Excellence (NICE). 4-6 Previous treatment guidelines have also been published. 7-9 One of the key recommendations of the NICE guidance is that services for head and neck patients should be centralised b so that patients with these relatively rare cancers receive specialist care. The need to provide a complete service from pre-treatment assessment through treatment to rehabilitation is highlighted and patients should be treated within multi-disciplinary teams including clinical oncologists, specialist surgeons, radiologists, clinical nurse specialists, speech therapists, dieticians and prosthetics experts. Participation in multicentre clinical trials should also be encouraged and supported.

The main forms of curative treatment are surgery and radiotherapy. 10 For small tumours the choice of treatment depends on several factors including the site, the risk of hidden disease, the need to preserve function, other side-effects, medical resources and patients’ wishes. If there is a risk of hidden disease, radiotherapy may be used but if the tumour is small and well defined, surgery may be better. For larger tumours, combined therapy will be applied. Chemotherapy was previously reserved for palliation but may now be used curatively in patients with advanced disease to enhance the effects of radiation (chemoradiation). 11 There is still some debate over the treatment of oral cancers and meanwhile some patients are almost certainly receiving less than optimal treatment. Trials are ongoing to evaluate the best form of radiotherapy and other treatments. 12

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aOral lesions are also associated with HIV infection but this is outside the scope of this report.

bin cancer centres serving populations of over a million patients.

Updated: 21/04/2005 0:00

Oral Cancer molecular biology and genetics

Many gene alterations have been implicated in the development and progression of oral squamous cell carcinomas and the stages of carcinogenesis have been clearly defined. 1, 2 Expression of genes involved in DNA repair and the stability of the genome is frequently altered.

Genetic changes commonly observed in oral cancers, include loss of heterozygosity at the site of known or suspected tumour suppressor genes, in particular 3p (FHIT), 9p (CDKN2A) and 17p (TP53). The TP53 gene is mutated in the majority of oral cancers and other genes in the p53 pathway are frequently disrupted, including deletion of CDKN2A. 3, 4

Gene amplification and overexpression of particular oncogenes is also seen, including the CCND1 locus at 11q13 and the PIK3CA locus at 3q26.3. 2 Mutations in Ras genes are commonly observed, although there is considerable variation between different populations. This may be due to exposure to different carcinogens, for example mutations in H-Ras are more frequently observed in patients from India whose cancer is linked to tobacco chewing. 5 Telomerase activation, which promotes the survival of cells carrying genetic abnormalities, has also been observed. Overexpression of cyclooxygenase-2 (COX2) and phospho-epidermal growth factor receptor (pEGFR) is also important in carcinogenesis and may provide useful molecular targets for treatment. 6

Polymorphisms in genes involved in the metabolism of carcinogens contained in tobacco and alcohol have been linked to individual susceptibilty. The gluthione S-transferase enzymes (GSTM1 and GSTT1) are expressed in oral tissue and play a role in detoxifying certain carcinogens in tobacco. Some studies have suggested that people with a null genotype for either GSTM1 or GSTT1 have a slightly increased risk of oral cancer. 3, 7 Other enzymes that metabolise carcinogens have also been implicated in oral cancer susceptibility, including cytochrome p450, the N-acetyltranferases and alcohol dehydrogenase, but their role has not been clearly determined.

An increased risk of oral cancer is associated with a number of inherited cancer syndromes, including Li-Fraumeni, Fanconi’s anaemia and xeroderma pigmentosum. 8 Some studies have suggested that there is an inherited component to sporadic oral cancer. First-degree relatives of people with oral cancer have been reported to be at greater risk of developing the disease. 8 There are difficulties in separating the effects of shared genes from a common environment in family studies, but there is increasing evidence for an inherited genetic component to oral cancer, possibly associated with a greater susceptibility to genetic damage by environmental mutagens. Those with an inherited susceptibility may be more likely to develop multiple primary tumours. 9

Genome-wide expression profiling using microarrays is being used to monitor changes during different stages of oral carcinogenesis. 2, 10Targeting early events in carcinogenesis may help in early detection and treatment of the disease and the use of inhibitors of both COX2 and EGFR is already being investigated for use in both chemoprevention and treatment. 6

Updated: 21/04/2005 0:00

Oral Cancer prevention

Primary prevention

At least three-quarters of oral cancers could be prevented by the elimination of tobacco smoking and a reduction in alcohol consumption. The removal of these two risk factors also reduces the risk of second tumours in people with oral cancer. Smoking cessation is associated with a rapid reduction in the risk of oral cancers, with a 50% reduction in risk within 3 to 5 years. 1 Ten years after smoking cessation, the risk for ex-smokers approaches that for life-long non-smokers. Protection against solar irradiation would further reduce the incidence of lip cancers.

In India and Sri Lanka efforts are being made to reduce the prevalence of the traditional habit of betel quid chewing. 2 The greatest cost-benefit is gained by educating children not to take up the chewing habit. 3 A recent study has shown that tobacco chewing in Indian men is the strongest risk factor for oral cancer while tobacco smoking is the main risk factor for developing pharyngeal and oesophageal tumours. 4 In developing countries especially, dietary supplementation may help to reduce the risk of oral cancer. In the UK, knowledge about the risks of betel chewing and the symptoms of oral cancer seems to be lacking in the high-risk south Asian populations. 5, 6 More research is needed into effective interventions for populations who use betel quid with or without tobacco. 7

Patient delay has been cited as the main reason for late presentation and it seems probable that in both high-risk groups and the general population, neither the symptoms of oral cancer nor the main risk factors are well understood. 8-10 With rising incidence rates, in younger age groups whose expectation of cancer is low, public education is urgently needed. 11 One award-winning example is the West of Scotland Mouth Cancer Awareness Project 12. Cancer Research UK has also run a mouth cancer awareness initiative with funding from the Department of Health for three years ending in 2008 21.

Secondary prevention: screening

Treatment of early stage oral cancers achieves higher survival rates with less attendant morbidity but at present far too many patients present with late stage disease. Therefore screening for premalignant or early stage oral cancers is worthy of consideration. However, in 1993 the UK Working Group on Screening for Oral Cancer and Precancer concluded that there was insufficient evidence to support population screening. 13 Problems include the relative rarity of the disease, a lack of knowledge of the natural history of the disease, disagreement over disease management and the lack of evidence on the efficacy of different screening methods. 14-16 An alternative strategy would be to encourage opportunistic screening of high-risk groups attending primary care services. 17 The educational needs of primary carers including dentists must be addressed and there is still the difficulty of reaching high risk groups. 18, 19

Future

Despite the overall fall in incidence and mortality rates for oral cancer in the last century, there is no place for complacency especially as recent trends report some significant increases among young and middle-aged men. Studies have reported an alarming lack of awareness about oral cancer, its symptoms and causes and this needs to be addressed by further public education, possibly targeted at high risk groups.

Survival rates have risen slightly over the last twenty years but could be further improved by earlier detection and more effective treatments. Advances in surgical techniques have helped to reduce disfigurement and functional impairment. Over the next few years as the new government service guidelines come into practice, patients should benefit. A nationwide audit is ongoing with the aim of improving the data for head and neck patients so that the impact of new services can be measured and areas of concern can be addressed. 20

The debate on screening is ongoing but better still would be the primary prevention of at least three quarters of cases through the elimination of tobacco consumption and the moderation of alcohol-intake.

More research is needed into the natural history of the disease, particularly which precancerous lesions will progress over time and how the risk factors interplay in the development of premalignant conditions and their carcinogenic transformation. At the molecular level there is a need to develop tumour markers so that treatment can be tailored to the individual patient.

Updated: 21/04/2005 0:00

References

Oral cancer - UK incidence statistics

  1.  Office for National Statistics. Cancer Statistics registrations: Registrations of cancer diagnosed in 2006, England. Series MB1 no.37. 2009
  2.  ISD Online. 2009, Information and Statistics Division, NHS Scotland.
  3.  Northern Ireland Cancer Registry, Cancer Incidence and Mortality. 2009
  4.  Welsh Cancer Intelligence and Surveillance Unit 2009. Cancer Incidence in Wales.
  5.  Daley, T. and M. Darling, Nonsquamous cell malignant tumours of the oral cavity: an overview. J Can Dent Assoc, 2003. 69(9): p. 577-82
  6.  Statistical Information Team, CR-UK. 2004
  7.  Warnakulasuriya, K.A., et al., Cancer of mouth, pharynx and nasopharynx in Asian and Chinese immigrants resident in Thames regions. Oral Oncol, 1999. 35(5): p. 471-5.
  8.  IARC. GLOBOCAN 2002. Cancer Incidence, Mortality and Prevalence Worldwide (2002 estimates). 2004
  9.  Macfarlane, G.J., P. Boyle, and C. Scully, Rising mortality from cancer of the tongue in young Scottish males. Lancet, 1987. 2(8564): p. 912.
  10.  Macfarlane, G.J., P. Boyle, and C. Scully, Oral cancer in Scotland: changing incidence and mortality. Bmj, 1992. 305(6862): p. 1121-3
  11.  Macfarlane, G.J., et al., Rising trends of oral cancer mortality among males worldwide: the return of an old public health problem. Cancer Causes Control, 1994. 5(3): p. 259-65
  12.  Moller, H., Changing incidence of cancer of the tongue, oral cavity, and pharynx in Denmark. J Oral Pathol Med, 1989. 18(4): p. 224-9.
  13.  Annertz, K., et al., Incidence and survival of squamous cell carcinoma of the tongue in Scandinavia, with special reference to young adults Int J Cancer, 2002. 101(1): p. 95-9
  14.  Schantz, S.P. and G.P. Yu, Head and neck cancer incidence trends in young Americans, 1973-1997, with a special analysis for tongue cancer. Arch Otolaryngol Head Neck Surg, 2002. 128(3): p. 268-74
  15.  Llewellyn, C.D., N.W. Johnson, and K.A. Warnakulasuriya, Risk factors for squamous cell carcinoma of the oral cavity in young people--a comprehensive literature review. Oral Oncol, 2001. 37(5): p. 401-18

Oral cancer - UK mortality statistics

  1.  Office for National Statistics, 2009 Mortality Statistics: Cause, 2007
  2.  ISD Online, 2009 Cancer Incidence and Mortality data, 2007
  3.  Northern Ireland Statistics and Research Agency 2009 Northern Ireland Mortality data, 2007.

Oral cancer - survival statistics for England and Wales

  1.  Diamond, J., "C". Because cowards get cancer too. 1998, London: Vermillion.
  2.  South West Cancer Intelligence Service. 2005
  3.  Office for National Statistics. One- and five-year survival of patients diagnosed in 1991-95 and 1996-99: less common cancers, sex and age, England and Wales. 2005.
  4.  Coleman, M., P. Babb, and P. Damiecki, Cancer Survival Trends in England and Wales, 1971-1995: Deprivation and NHS Region. 1999: TSO.

Oral cancer - risk factors

  1.  Rodriguez, T., et al., Risk factors for oral and pharyngeal cancer in young adults. Oral Oncol, 2004. 40(2): p. 207-13.
  2.  La Vecchia, C., et al., Epidemiology and prevention of oral cancer. Oral Oncol, 1997. 33(5): p. 302-12.
  3.  Warnakulasuriya, S., G. Sutherland, and C. Scully,. Tobacco, oral cancer, and treatment of dependence. Oral Oncol, 2005. 41(3): p. 244-260
  4.  Perea-Milla Lopez, E., et al., Lifestyles, environmental and phenotypic factors associated with lip cancer: a case-control study in southern Spain. Br J Cancer, 2003. 88(11): p. 1702-7.
  5.  Castellsague, X., et al., . The role of type of tobacco and type of alcoholic beverage in oral carcinogenesis. Int J Cancer, 2004. 108(5): p. 741-749
  6.  Blot, W.J., et al., Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res, 1988. 48(11): p. 3282-7.
  7.  International Agency for Research on Cancer, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Tobacco smoke and involuntary smoking.Volume83 ed. Vol. 83. 2004, Lyon: IARC Press.
  8.  Office for National Statistics. General Household Survey 2003/4. 2008
  9.  Gupta, P.C., F.S. Mehta, and J.J. Pindborg, Mortality among reverse chutta smokers in south India. Br Med J (Clin Res Ed), 1984. 289(6449): p. 865-6.
  10.  Rahman, M., J. Sakamoto, and T. Fukui, Bidi smoking and oral cancer: a meta-analysis. Int J Cancer, 2003. 106(4): p. 600-4.
  11.  IARC, Monograph on the evaluation of carcinogenic risk to humans. Vol 89: smokeless tobacco and some tobacco-specific nitrosamines. 2004, Lyon: IARC Press.
  12.  Cogliano, V., et al., Smokeless tobacco and tobacco-related nitrosamines. Lancet Oncol, 2004. 5(12): p. 708.
  13.  Levy, D.T., et al., The relative risks of a low-nitrosamine smokeless tobacco product compared with smoking cigarettes: estimates of a panel of experts. Cancer Epidemiol Biomarkers Prev, 2004. 13(12): p. 2035-42.
  14.  US Department of Health and Human Services, Smoking and Tobacco Control Monograph No.2.  
  15.  Rouse, B., Epidemiology of smokeless tobacco use: A national study. National Cancer Institute Monographs 8:29-33. 1989. Link
  16.  Bedi, R., Betel quid and tobacco chewing among the United Kingdom's Bangladeshi community in The Proceedings of the CRC/DoH Symposium on Cancer and Minority Ethnic Groups. BJC, 1996. 74 Supplement.
  17.  Gupta, P.C. and S. Warnakulasuriya, Global epidemiology of areca nut usage. Addict Biol, 2002. 7(1): p. 77-83.
  18.  Warnakulasuriya, S., C. Trivedy, and T.J. Peters, Areca nut use: an independent risk factor for oral cancer. Bmj, 2002. 324(7341): p. 799-800.
  19.  IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Betel-quid and areca-nut chewing and some areca-nut related nitrosamines. 2004, IARC.
  20.  Warnakulasuriya, K.A., Analytical studies of the evaluation of the role of betel quid in oral carcinogenesis. In Bedi R (ed) Betel quid and tobacco chewing among the Bangladeshi community in the United Kingdom. 1995, London: Centre for Transcultural oral health. Link
  21.  van Wyk, C.W., et al., The areca nut chewing habit and oral squamous cell carcinoma in South African Indians. A retrospective study. S Afr Med J, 1993. 83(6): p. 425-9.
  22.  Balaram, P., et al., Oral cancer in southern India: the influence of smoking, drinking, paan-chewing and oral hygiene. Int J Cancer, 2002. 98(3): p. 440-5.
  23.  Health Survey for England 2004: The Health of Minority Ethnic Groups - headline tables. 2005, NHS Health and Social Care Information Centre, Public Health Statistics.
  24.  The Health Survey for England - The Health of Ethnic Minority Groups. 1999, Department of Health.
  25.  Levi, F., et al., Second primary oral and pharyngeal cancers in subjects diagnosed with oral and pharyngeal cancer. Int J Cancer, 2006. 119(11): p. 2702-4.
  26.  Chuang, S.C, et al., Risk of second primary cancer among esophageal cancer patients: a pooled analysis of 13 cancer registries. Cancer Epidemiol Biomarkers Prev, 2008. 17(6): p. 1543-9.
  27.  Doll, R., S. Darby, and E. Whitley, Trends in mortality from smoking related diseases in Charlton J and Murphy M (eds). The Health of Adult Britain. Vol. 1. 1997: TSO. Link
  28.  Blot, W., Alcohol and cancer. Cancer Research, 1992. (suppl) 52: p. 2119-2123.
  29.  Boyle, P., et al., European Code Against Cancer and scientific justification: third version (2003). Ann Oncol, 2003. 14(7): p. 973-1005.
  30.  Moller, H., Changing incidence of cancer of the tongue, oral cavity, and pharynx in Denmark. J Oral Pathol Med, 1989. 18(4): p. 224-9.
  31.  Blot, W., Oral and Pharyngeal cancers in Doll R (ed). Trends in Cancer Incidence and Mortality. Vol. 19/20, 23-42.1994: Cancer Surveys.
  32.  British Beer and Pub Association, Statistical Handbook: A compilation of drinks industry statistics. 2002, London.  
  33.  Prime Minister's Strategy Unit, Alcohol Harm Reduction Project: Interim Analytical Report. 2004: London.
  34.  ONS, Living in Britain: Results from the 2002 General Household Survey. 2004, TSO: London.
  35.  Editorial, Time for coordinated action on alcohol. Lancet, 2004. 363(9414): p. 1001.
  36.  P Boyle, GJ Macfarlane, and T.Z.e. al, Recent advances in epidemiology of head and neck cancer. Curr Opin Oncol, 1992(4): p. 471-477.
  37.  Pavia, M., et al., Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies. Am J Clin Nutr, 2006. 83(5): p. 1126-34.
  38.  Freedman, N.D, et al., Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study. Int J Cancer, 2008. 122(10): p. 2330-6.
  39.  Kreimer, A.R., et al., Diet and body mass, and oral and oropharyngeal squamous cell carcinomas: Analysis from the IARC multinational case-control study. Int J Cancer, 2006. 118(9): p. 2293-7.
  40.  Macfarlane, G.J., et al., Alcohol, tobacco, diet and the risk of oral cancer: a pooled analysis of three case-control studies. Eur J Cancer B Oral Oncol, 1995. 31B(3): p. 181-7.
  41.  Sankaranarayanan, R., B. Mathew, and P.N.e. al, Chemoprevention of cancers of the oral cavity and head and neck. In Hakama M, Beral V, Buiatti E et al (eds). Chemoprevention in cancer control. 1996: IARC. Link
  42.  Hunter, K.D., E.K. Parkinson, and P.R. Harrison, Opinion: Profiling early head and neck cancer. Nat Rev Cancer, 2005. 5(2): p. 127-35.
  43.  Nieto, A., et al., Lifetime body mass index and risk of oral cavity and oropharyngeal cancer by smoking and drinking habits. Br J Cancer, 2003. 89(9): p. 1667-71.
  44.  Gillison, M.L., Human papillomavirus-associated head and neck cancer is a distinct epidemiologic, clinical, and molecular entity. Semin Oncol, 2004. 31(6): p. 744-54.
  45.  Kreimer, A.R., et al., Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systematic review. Cancer Epidemiol Biomarkers Prev, 2005. 14(2): p. 467-75.
  46.  Smith, E.M., et al., Human papillomavirus in oral exfoliated cells and risk of head and neck cancer. J Natl Cancer Inst, 2004. 96(6): p. 449-55.
  47.  Herrero, R., et al., Human papillomavirus and oral cancer: the International Agency for Research on Cancer multicenter study. J Natl Cancer Inst, 2003. 95(23): p. 1772-83.
  48.  Frisch, M. and Biggar, R.J., Aetiological parallel between tonsillar and anogenital squamous-cell carcinomas. Lancet, 1999. 354(9188): p. 1442-3.
  49.  Spitz, M.R., et al., Association between malignancies of the upper aerodigestive tract and uterine cervix. Head Neck, 1992. 14(5): p. 347-51.
  50.  Grulich, A. E., et al., Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet, 2007. 370(9581): p. 59-67.
  51.  Rodrigues, V.C., S.M. Moss, and H. Tuomainen, Oral cancer in the UK: to screen or not to screen. Oral Oncol, 1998. 34(6): p. 454-65.
  52.  Scheifele, C. and P.A. Reichart, Is there a natural limit of the transformation rate of oral leukoplakia? Oral Oncol, 2003. 39(5): p. 470-5.
  53.  Scully, C. and S. Porter, ABC of oral health. Swellings and red, white, and pigmented lesions. Bmj, 2000. 321(7255): p. 225-8.
  54.  Oliver, R.J., J. Dearing, and I. Hindle, Oral cancer in young adults: report of three cases and review of the literature. Br Dent J, 2000. 188(7): p. 362-5.
  55.  Hyam, D.M., et al., Tongue cancer: do patients younger than 40 do worse? Aust Dent J, 2003. 48(1): p. 50-4.
  56.  Annertz, K., et al., Incidence and survival of squamous cell carcinoma of the tongue in Scandinavia, with special reference to young adults. Int J Cancer, 2002. 101(1): p. 95-9.
  57.  Llewellyn, C.D., et al., Squamous cell carcinoma of the oral cavity in patients aged 45 years and under: a descriptive analysis of 116 cases diagnosed in the South East of England from 1990 to 1997. Oral Oncol, 2003. 39(2): p. 106-14.
  58.  Llewellyn, C.D., et al., An analysis of risk factors for oral cancer in young people: a case-control study. Oral Oncol, 2004. 40(3): p. 304-13.
  59.  Guha, N., et al., Oral health and risk of squamous cell carcinoma of the head and neck and esophagus: results of two multicentric case-control studies Am J Epidemiol, 2007. 166(10): p. 1159-73.
  60.  Winn, D.M., et al., Mouthwash in the etiology of oral cancer in Puerto Rico Cancer Causes Control, 2001. 12(5): p. 419-29.
  61.  Winn, D.M., et al., Mouthwash use and oral conditions in the risk of oral and pharyngeal cancer Cancer Res, 1991. 51(11): p. 3044-7.
  62.  Gandini., et al., Tobacco smoking and cancer: a meta-analysis Int J Cancer, 2008. 122(1): p.155-64.
  63.  Boffetta, P., et al., Smokeless tobacco and cancer Lancet Oncol, 2008. 9(7): p. 667-75.
  64.  Thomas, S.J., et al., Betel quid not containing tobacco and oral cancer: A report on a case-control study in Papua New Guinea and a meta-analysis of current evidence Int J Cancer, 2007. 120(6): p. 1318-23.
  65.  Bagnardi, V., et al., A meta-analysis of alcohol drinking and cancer risk Br J Cancer, 2001. 85(11): p. 1700-5.
  66.  Castellsague, X., et al., The role of type of tobacco and type of alcoholic beverage in oral carcinogenesis Int J Cancer, 2004. 108(5): p. 741-749.
  67.  Blot, W.J., et al., Smoking and drinking in relation to oral and pharyngeal cancer Cancer Res, 1988. 48(11): p. 3282-7.
  68.  Altieri, A., et al., Wine, beer and spirits and risk of oral and pharyngeal cancer: a case-control study from Italy and Switzerland Oral Oncol, 2004. 40(9): p. 904-9.
  69.  Garrote, L.F., et al., Risk factors for cancer of the oral cavity and oro-pharynx in Cuba Br J Cancer, 2001. 85(1): p. 46-54.
  70.  Talamini, R., et al., Oral hygiene, dentition, sexual habits and risk of oral cancer Br J Cancer, 2000. 83(9): p. 1238-42.
  71.  D'Souza, G., et al., Case-control study of human papillomavirus and oropharyngeal cancer New Engl J Med, 2007. 356(19): p. 1944-56.
  72.  Kreimer, A.R., et al., Diet and body mass, and oral and oropharyngeal squamous cell carcinomas: Analysis from the IARC multinational case-control study Int J Cancer, 2005. 118(9): p. 2293-7.
  73.  Bosetti, C., et al., Tobacco Smoking, Smoking Cessation, and Cumulative Risk of Upper Aerodigestive Tract Cancers Am J Epidemiol, 2008. 167(4): p. 468-73.
  74.  Znaor, A., et al., Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men Int J Cancer, 2003. 105(5): p. 681-6.
  75.  Hashibe, M., et al., Alcohol drinking in never users of tobacco, cigarette smoking in never drinkers, and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium J Natl Cancer Institute, 2007. 99(10): p. 777-89.
  76.  Allen, N.E, et al., Moderate alcohol intake and cancer incidence in women J Natl Cancer Institute, 2009. 101(5): p. 296-305.
  77.  van Leeuwen, M.T, et al., Immunosuppression and other risk factors for lip cancer after kidney transplantation Cancer Epidemiol Biomarkers Prev, 2009. 18(2): p. 561-9.

Oral cancer - symptoms and treatment

  1.  Scully, C. and S. Porter, ABC of oral health. Swellings and red, white, and pigmented lesions.Bmj, 2000. 321(7255): p. 225-8
  2.  Scheifele, C. and P.A. Reichart, Is there a natural limit of the transformation rate of oral leukoplakia? Oral Oncol, 2003. 39(5): p. 470-5
  3.  Lodi G, S.A., Bez C, Demarosi F, Carrassi A, Interventions for treating oral leukoplakia. 2004, The Cochrane Database of Systematic Reviews, Issue 3.
  4.  National Centre for Clinical Excellence, Improving Outcomes in Head and Neck Cancers. The Manual. 2004.
  5.  National Centre for Clinical Excellence, Improving Outcomes for Head and Neck Cancer: The Research Evidence, 2004
  6.  University of York Centre for Reviews and Dissemination, Effective Health Care: Management of head and neck cancers. 2004
  7.  Yorkshire Cancer Network, Head and Neck Cancer Treatment Guidelines. 2003
  8.  Royal College of Surgeons of England, Clinical Guidelines. The Oral Management of Oncology Patients requiring Radiotherapy: Chemotherapy: Bone Marrow Transplantation. 1999
  9.  . British Association of Otorhinolaryngologists Head and Neck Surgeons, Effective Head and Neck Cancer Management: Third Consensus Document. 2003, Royal College of Surgeons: London
  10.  Scully, C. and S. Porter, ABC of oral health. Oral cancer. Bmj, 2000. 321(7253): p. 97-100.
  11.  Sanderson, R.J. and J.A. Ironside, Squamous cell carcinomas of the head and neck. Bmj, 2002. 325(7368): p. 822-78
  12.  CancerHelp UK. Clinical trials database. March 2004

Oral Cancer molecular biology and genetics

  1. Mao, L., W.K. Hong, and V.A. Papadimitrakopoulou, Focus on head and neck cancer. Cancer Cell, 2004. 5(4): p. 311-6.
  2. Hunter, K.D., E.K. Parkinson, and P.R. Harrison, Opinion: Profiling early head and neck cancer. Nat Rev Cancer, 2005. 5(2): p. 127-35.
  3. Jefferies, S. and W.D. Foulkes, Genetic mechanisms in squamous cell carcinoma of the head and neck. Oral Oncol, 2001. 37(2): p. 115-26.
  4. Scully, C., J.K. Field, and H. Tanzawa, Genetic aberrations in oral or head and neck squamous cell carcinoma 2: chromosomal aberrations. Oral Oncol, 2000. 36(4): p. 311-27.
  5. Saranath, D., et al., High frequency mutation in codons 12 and 61 of H-ras oncogene in chewing tobacco-related human oral carcinoma in India. Br J Cancer, 1991. 63(4): p. 573-8.
  6. Lippman, S.M., J. Sudbo, and W.K. Hong, Oral cancer prevention and the evolution of molecular-targeted drug development. J Clin Oncol, 2005. 23(2): p. 346-56.
  7. Cheng, L., et al., Glutathione-S-transferase polymorphisms and risk of squamous-cell carcinoma of the head and neck.Int J Cancer, 1999. 84(3): p. 220-4.
  8. Prime, S.S., et al., A review of inherited cancer syndromes and their relevance to oral squamous cell carcinoma.Oral Oncol, 2001. 37(1): p. 1-16.
  9. Bongers, V., et al., The relation between cancer incidence among relatives and the occurrence of multiple primary carcinomas following head and neck cancer. Cancer Epidemiol Biomarkers Prev, 1996. 5(8): p. 595-8.
  10. Arora, S., et al., Identification of differentially expressed genes in oral squamous cell carcinoma. Mol Carcinog, 2005. 42(2): p. 97-108.

Oral Cancer prevention

  1.  Samet, J.M., The health benefits of smoking cessation. Med Clin North Am, 1992. 76(2): p. 399-414.
  2.  Pindborg, J.J., D.K. Daftary, and P. Gupta, Public Health Aspects of Oral cancer: Implications for cancer prevention in the Community. Oral cancer: Detection of patients and lesions at risk, ed. Johnson N W. 1991: Cambridge University Press.
  3.  Stjernsward, J., Cost-benefit in Sri Lanka, (pers. comm)
  4.  Znaor, A., et al., Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men. Int J Cancer, 2003. 105(5): p. 681-6.
  5.  Ahmed, S., A. Rahman, and S. Hull, Use of betel quid and cigarettes among Bangladeshi patients in an inner-city practice: prevalence and knowledge of health effects. Br J Gen Pract, 1997. 47(420): p. 431-4.
  6.  Shetty, K.V. and N.W. Johnson, Knowledge, attitudes and beliefs of adult South Asians living in London regarding risk factors and signs for oral cancer. Community Dent Health, 1999. 16(4): p. 227-31.
  7.  West, R., A. McNeill, and M. Raw, Smokeless tobacco cessation guidelines for health professionals in England. Br Dent J, 2004. 196(10): p. 611-8.
  8.  Scully, C., et al., Sources and patterns of referrals of oral cancer: role of general practitioners. Br Med J (Clin Res Ed), 1986. 293(6547): p. 599-601.
  9.  Warnakulasuriya, K.A., C.K. Harris, and D.M. Scarrot, An Alarming lack of public awareness towards oral cancer. Br Dent J, 1999(187): p. 319-322.
  10.  Sanderson, R.J. and J.A. Ironside, Squamous cell carcinomas of the head and neck. Bmj, 2002. 325(7368): p. 822-7.
  11.  Llewellyn, C.D., N.W. Johnson, and S. Warnakulasuriya, Factors associated with delay in presentation among younger patients with oral cancer. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2004. 97(6): p. 707-13.
  12.  NHS Scotland. West of Scotland Mouth Cancer Awareness Project. Accessed 2005;
  13.  Speight, P.M., M.C. Downer, and J. Zakrzewska, Screening for oral cancer and precancer. A report of the UK Working Group on Screening for Oral cancer and precancer. Community Dent Health (suppl), 1993(10): p. 1-89.
  14.  Cox, G., A. Alcock, and R. Corbridge, Biopsy under local anaesthetic is inadequate (letter). BMJ, 1999(319): p. 706-707.
  15.  Rodrigues, V.C., S.M. Moss, and H. Tuomainen, Oral cancer in the UK: to screen or not to screen.Oral Oncol, 1998. 34(6): p. 454-65.
  16.  Kujan, O., et al., Evaluation of screening strategies for improving oral cancer mortality: a cochrane systematic review. J Dent Educ, 2005. 69(2): p. 255-65.
  17.  Zakrzewska, J., I. Hindle, and P.M. Speight, Practical considerations for the establishment of an oral screening programme. Community Dent Health, 1993(10): p. 79-85.
  18.  British Dental Association, BDA Occasional paper No. 6 Opportunistic Oral Cancer Screening. April 2000.
  19.  Warnakulasuriya, K.A. and N.W. Johnson, Dentists and oral cancer prevention in the UK: opinions, attitudes and practices to screening for mucosal lesions and to counselling patients on tobacco and alcohol use: baseline data from 1991. Oral Dis, 1999. 5(1): p. 10-4.
  20.  British Association of Head and Neck Oncologists. DAHNO.
  21.   Open up to Mouth Cancer Campaign, Cancer Research UK.