UK Stomach Cancer incidence statistics
UK Stomach Cancer incidence statistics
This page presents stomach cancer incidence statistics for the UK by sex, by age, histology, trends over time, geographic variation and deprivation. There is also a section looking at incidence of adenocarcinomas of the gastric cardia. The ICD code for stomach cancer is ICD9 151, and ICD 10 C16.
Stomach cancer incidence by sex
Stomach cancer is the seventh most common cancer in males in the UK and fourteenth in females. There were 7,713 new cases of stomach cancer diagnosed in 2006 ( Table 1.1) 1-4. The male:female ratio is around 1.8:1
Stomach cancer incidence by age
Figure 1.1 shows the age-specific cases and rates for stomach cancer in the UK. 1-4 Stomach cancer occurs mainly in older people. Less than 8% of cases are diagnosed before the age of 55 years and the rates increase steeply from age 60 onward reaching a rate of around 140 per 100,000 population in men aged 85 and over.
Stomach cancer histology
Most stomach cancers (around 95%) are adenocarcinomas which may be further classified into 'intestinal' and 'diffuse' type.
'Intestinal' adenocarcinomas are associated with a history of atrophic gastritis, have better survival and are associated with older patients, whereas the 'diffuse' adenocarcinomas are more common, with poorer survival and occur more frequently in women and people with blood group 'A'. 5
Other stomach malignant histologies include lymphomas and leiomyosarcomas.
Trends in stomach cancer incidence
In Britain the age-standardised incidence rates for males have more than halved from 31.0 per 100,000 in 1975 to 13.3 in 2006. The trend is similar for females. ( Figure 1.2) 1-3.
The stomach cancer incidence trend for the UK is shown in Figure 1.31-4.
Geographic variation in stomach cancer incidence
In 2006 there were around 86,000 new cases of stomach cancer diagnosed in the European Union (EU). Within the EU there is a more than fourfold difference in incidence across countries. The highest incidence rates were in Lithuania for both males and females. The lowest stomach cancer incidence rates in the EU were in Denmark. Rates for the UK were below the EU average ( Figure 1.4) 6.
International incidence rates of stomach cancer vary widely. The highest rates of stomach cancer in the world occur in Eastern Asia (China, Japan, Republic of Korea, Democratic Republic of Korea and Mongolia) where the rate is 46 per 100,000 males and 21 per 100,000 females ( Figure 1.5). High rates also occur in Eastern Europe, Polynesia and South America - these are all above the world average of 22 and 10 per 100,000 males and females respectively. The lowest international incidence rates occur in Western and Northern Africa. 7
Deprivation
Incidence and mortality from stomach cancer are strongly related to social class and measures of deprivation, with higher rates in socially and economically deprived groups. 8
Using Carstairs deprivation scores (a score of material deprivation derived from four census variables - car ownership, household overcrowding, head of household in social class IV or V and male unemployment), the incidence and mortality rates in England and Wales are about twice as high in the most deprived groups compared to the least deprived. 9
A strong association with social deprivation is also reported for Scotland (Figure 1.6).
Gastric cardia
Despite an overall decline in incidence rates of stomach cancer, several countries, including England, Wales and Scotland, 10-11 have seen an increase in the incidence of adenocarcinomas of the gastric cardia, which is the region of the stomach that joins the lower oesophagus, sometimes referred to as proximal gastric cancer.
The rising rates of cancer in the gastric cardia in contrast to the falling rates elsewhere in the stomach are illustrated in Figure 1.7 using England data.
As the incidence of adenocarcinoma of the lower oesophagus is also increasing it has been suggested that tumours in the region of the gastro-oesophageal junction (GOJ) may share similar risk factors and should be treated as a separate entity. 12-13 Tumours of the lower oesophagus are particularly associated with a condition called Barrett’s oesophagus that may develop as a result of gastric reflux (see Oesophageal cancer.).
UK Stomach Cancer mortality statistics
This page contains information on the mortality from stomach cancer for the UK, by age and sex and trends over time.
Stomach cancer mortality in the UK
In 2007 there were 5,236 deaths from stomach cancer in the UK, making it the seventh most common cause of cancer death and responsible for over 3% of all cancer deaths.
The annual number of deaths in the UK and its constituent countries together with the rates for the year 2007 are shown in Table 2.11-3.
Stomach cancer mortality by age and sex
The distribution of deaths by age for males and females separately are shown in Figure 2.11-3.
Stomach cancer mortality trends over time
The age-standardised mortality rates between 1971 and 2007 for the UK are shown in Figure 2.21-3.
Mortality rates in the UK have fallen by around 70% in males and females over the last 30 years as shown in Figure 2.2.
In 1978 the age-standardised rate per 100,000 population (males and females) was 19.1; by 2007 this figure has fallen to 5.7 per 100,000. 1-3
Throughout the world mortality from stomach cancer has been falling but at different times and rates for different countries. The global decrease has occurred without any significant improvements in diagnosis or treatment: possible reasons are discussed in the Risk factors section.
Mortality in England and Wales between 1953 and 1992 is compared to that of Japan, Chile, Portugal, Poland, Australia and the USA White population in Figure 2.3. 4
Earlier data shows that mortality rates for England and Wales and USA Whites began to fall in the 1930s whilst Japanese rates continued to rise until the 1950s and then began their decrease. In Poland and other eastern European countries the peak in rates was reached later in the 1960s and into the 1970s for Portugal.
The decline of stomach cancer within the EU as a whole between 1955 - 1998 is shown in Figure 2.4 where it is contrasted with the equally striking upward trend for lung cancer which has overtaken stomach cancer to become the leading cause of cancer death. 5
Stomach Cancer survival statistics
This page presents stomach cancer survival statistics including one year survival, five year survival, ten year survival trends and survival by age.
One, five and ten year survival rates for stomach cancer
Over the last 25 years 5-year relative survival rates for stomach cancer have tripled in Britain, but are still very low at around 15%. 1, 2
The 1-, 5- and 10-year age-standardised relative survival rates for patients diagnosed in England & Wales between 1971 and 2001 are shown in Figure 3.1, Figure 3.2 and Figure 3.3. 2
Survival rates have risen consistently despite increasing numbers of gastric cardia cases which are more difficult to treat. The 1-year relative survival rate was only 14% in the early 1970s but is now 35% - which parallels a decline in peri-operative mortality. 3 There appears to be only a small fall in survival between 5- and 10-year rates.
Five year survival rates by age for stomach cancer
Relative survival is considerably higher for younger patients as Figure 3.4 shows. 4 For people under 50, 5-year relative survival rates are 19-22% compared to 7-14% for people over 70. At most ages, women have a slight survival advantage over men.
Five year survival rates by stage at diagnosis for stomach cancer
In the UK most patients are diagnosed with widespread disease (stage four) and their 5-year survival rates are less than 5%. However, very good results can be obtained when patients have small tumours (less than 5cm), no serosal invasion or lymph node metastases.
For the latter, 5-year survival rates in excess of 80% can be achieved. The challenge is to increase the number of patients diagnosed at an early stage.
In Japan, where the disease is very common and population screening has been introduced, 5-year survival rates of 90% have been reported for early screen-detected disease. 5
Stomach Cancer risk factors
This section contains information on risk factors for stomach cancer including Helicobacter pylori, smoking and alcohol, diet, medical conditions and medications, family history, radiation and occupation.
Wide international variations in incidence and the dramatic falls seen across the developed world suggest that environmental factors are very important in gastric carcinogenesis.
Evidence suggests a large number of risk factors for stomach cancer and it is very likely that its aetiology is multifactorial with the importance of different risk factors varying across populations and between individuals. The universal demographic factors are old age, male gender and low socio-economic status (The rising rates of adenocarcinoma of the gastric cardia have been principally associated with higher socio-economic status).
Helicobacter pylori and severe chronic atrophic gastritis and Stomach cancer risk
Infection with Helicobacter pylori (H. pylori) is the most important known risk factor for stomach cancer.
H. pylori is a common bacterial infection, with particularly high prevalence in the developing world. Crowded living conditions, poor hygiene, large families and low socio-economic status are all associated with high rates of H. pylori infection.
Prevalence of H. pylori infection has been declining in the UK, which may explain the falling incidence of distal stomach cancer. 1
H. pylori infection doubles the risk of stomach cancer and the risk is almost three-fold among those infected with cagA-positive H. pylori strains. 2
Findings from the European Prospective Investigation into Cancer (EPIC) suggest that the increase in risk may be as much as seven-fold in those with evidence of long-term H. pylori infection. 1
H. pylori can induce the pre-cancerous lesion severe chronic atrophic gastritis (SCAG), the first step in the chain of events leading from normal intestinal mucosa to adenocarcinoma. Eradication of H. pylori through treatment can cause regression of precursor lesions. SCAG increases the risk for cancers of the gastric cardia by around 11-fold and gastric non-cardia by three-fold. 1
Risk increases with the severity of gastric atrophy; people with severe multifocal atrophic gastritis have over 90 times increased risk of stomach cancer. 3
There is evidence that H. pylori eradication may help prevent gastric cancer. 4,5,60-62
Find out more on Helicobacter pylori.
Smoking and alcohol and stomach cancer risk
Current smokers have around double the risk of stomach cancer compared to non-smokers and risk remains higher for 10-20 years after giving up. 6,7
The combined effect of smoking and H. pylori infection may be more than additive, with a 16-17-fold increased risk of gastric non-cardia cancer. 8 It has been estimated that almost one in five stomach cancers in Europe are caused by smoking, with a higher proportion in men (22%) than women (14%). 7 Nitrosamines are present in tobacco smoke, which may explain the increased risk. 9
While alcohol has been extensively studied as a cause of stomach cancer there is no conclusive evidence that it increases risk. However, results from at least three studies suggest that heavy alcohol consumption may increase the risk of stomach cancer in heavy smokers. 10,11,12
Diet and Stomach cancer risk
High fruit and vegetable intake is associated with a reduced risk of gastric cancer in both cohort and case-control studies. 13,59
High salt intake has been linked to risk of stomach cancer in a number of studies. 59 Intake of salt is difficult to measure, but one of the most recent prospective studies to examine the relationship between salt intake and stomach cancer in Japan showed that risk is three times higher among individuals with a salt intake of 16g/day or more, compared to intakes of less than 10g/day. The risk increase with high salt intake was limited to subjects with H.pylori infection and atrophic gastritis. 15
It is not clear whether salt intake at current normal levels in European countries is linked to stomach cancer risk. A recent Danish study found no clear associations between salt intake and stomach cancer risk, although there were suggestive associations particularly for people with stomach disorders. 17 A Norwegian study found no association. 63
Heavily salted foods are often high in N-nitroso compounds. There is limited evidence that individuals with high intakes of N-nitrosodimethylamine (NDMA) or nitrite have an increased risk of stomach cancer. 19,20,21
Processed meat was linked to stomach cancer risk in a recent meta-analysis. 23 However, the World Cancer Research Fund deemed evidence on processed meat and stomach cancer limited. 59 Results from the EPIC study suggest an association with processed meat consumption in subjects that are infected with H. pylori. 26
Medical conditions and medications and stomach cancer risk
People diagnosed with gastro-oesophageal reflux disease (GORD) have a doubling in their risk of gastric cardia adenocarcinoma. 30 People who have undergone surgery to correct acid reflux have five times the risk of gastric cardia cancer. 31 People diagnosed with Barrett's oesophagus have an 18-fold risk increase. 33
High BMI (Body Mass Index) is linked to a two-fold increased risk of gastric cardia adenocarcinoma. 21,34 Most studies show an association between high BMI and gastric reflux symptoms, and this might provide an explanation for the association of this type of stomach cancer with BMI. 33 Around 13% of gastric cardia adenocarcinomas in the USA have been linked to people having a BMI of 27 or higher. 21
H. pylori infection is linked with both gastric and duodenal ulcers but only gastric ulcer is associated with increased risk of stomach cancer, while the presence of duodenal ulcer appears to reduce risk. 35, 36 Patients who have undergone surgery for gastric ulcer have a lower risk than patients who have not received surgery. 36 Both conditions respond well to the elimination of H. pylori and are becoming less common in populations where the prevalence of H. pylori is declining. 37 Vagotomy - a surgical procedure to reduce acid secretion in the stomach - is associated with an increased risk of stomach cancer in the following 10 years. 36 People who have part of their stomach surgically removed (partial gastrectomy) for a benign stomach condition, such as an ulcer, have an increased risk of stomach cancer, which is highest 15 or more years after the operation. 65
Patients with pernicious anaemia - where there is severe gastric atrophy caused by an autoimmune condition - have two to three times increased risk of stomach cancer. 38,39
The risk of being diagnosed with stomach cancer is increased in people with a previous diagnosis of oesophageal cancer, non-melanoma skin cancer, bowel cancer and non-Hodgkin’s lymphoma. In addition, men with a previous prostate, bladder or testis cancer and women with a previous ovarian, cervical or breast cancer have an increased risk of stomach cancer. 40,41,64 Some of the risk increase may be related to treatment for the first cancer.
Regular use of aspirin and other non-steroidal anti-inflammatories (NSAIDS) is associated with a 30-40% reduction in risk of non-cardia stomach cancer. 42,67 One study has shown a reduced risk of stomach cancer in women who have taken hormone replacement therapy (HRT). 43
There is evidence that people with HIV/AIDS or who have undergone an organ transplant have a doubling in risk of stomach cancer. 66
Family history and stomach cancer risk
Having a parent or sibling diagnosed with a stomach cancer increases risk 1.5-fold and three-fold respectively. 41
Some of this increased risk may be environmental, as studies have shown elevated risk in spouses of stomach cancer patients, 44 and that relatives of gastric cancer patients are twice as likely to be infected with H. pylori. 45
Radiation and stomach cancer risk
Studies of atomic bomb survivors show that risk of stomach cancer is directly related to dose of radiation, with almost double the risk in people most heavily exposed to radiation from the atomic bombs in Japan. 46 An increased risk has also been shown in people treated with radiotherapy for ankylosing spondylitis. 47
Occupation and stomach cancer risk
Occupational exposure to metal dusts, 48-54 and other types of dusts - such as from mining or quarrying or stone cutting 52,55,56 - has been associated with an increased risk of gastric cancer in several studies.
Stomach Cancer molecular biology and genetics
This page contains information on the molecular biology and genetics relating to stomach cancer
Chronic infection with Helicobacter pylori (H.pylori) leads to chronic gastric inflammation, which in turn increases the risk of developing stomach cancer. However this risk is dependent upon variable factors in both the individual and the bacterial strain(s) with which they are infected. 1,2
For example, variation in the strength of immune and inflammatory responses to H. pylori infection is important. Genetic variations (polymorphisms), which enhance the inflammatory response, such as those in genes producing inflammatory cytokines ,(e.g. IL-1B, IL1RN, TNF-A and IL-10), have been associated with increased gastric cancer risk. 1,2
H. pylori infection induces inflammation through activation of NF-kB and its pro-inflammatory transcriptional targets in the gastric cells. 2 Pro-inflammatory Cox-2 is also induced, and in turn facilitates tumour growth via inhibition of apoptosis, increased cellular proliferation and stimulation of angiogenesis2.
Differences in the expression of various bacterial genes can also affect the risk of stomach cancer.
Strains which express the genes CagA, BabA and SabA, increase the risk of developing stomach cancer, as do certain genetic variants of the VacA gene. 1,2
As well as the induction of inflammation, this increased risk is also due to direct effects on the proliferation and apoptosis of gastric epithelium cells. 1,2 For example, the presence of the bacterium also induces cell cycle arrest, both through the reduced expression of the cell cycle regulatory protein p27 3,4 and through direct damage to host cell DNA, 5,6 for example by the production of reactive oxygen and nitrogen species. 2
The presence of the bacterium is also thought to interfere with gastric antioxidant defence mechanisms. 7
The host response to H. pylori infection has also been shown to promote cellular proliferation by inducing the production of gastrin, 8 although the exact role of this hormone in the development of gastric cancer remains unknown. 9
As well as variations in inflammatory response genes, several other genetic changes have been identified in gastric cancers.
These include the activation or amplification of the oncogenes c-met, K-sam and c-erbB2 and inactivation of the tumour suppressor genes p53, APC, bcl-2 and RUNX3. In addition, genes of the E-cadherin family, involved in cell adhesion, are often lost. 2
Approximately 10% of gastric cancers cluster in families. Hereditary diffuse gastric cancer is a rare form of the disease with autosomal dominant inheritance. The E-cadherin gene, CDH1, is mutated in around 25% of inherited cases. 10
Symptoms and Treatment of Stomach Cancer
This page contains information on the symptoms and treatment of stomach cancer through surgery, chemotherapy and radiotherapy. There is also information on the management of the symptoms of stomach cancer.
Stomach cancer symptoms
Early stage stomach cancer may be symptom-less or have vague and non-specific symptoms such as indigestion, tiredness or loss of appetite. Consequently it is difficult to differentiate between benign conditions and early cancer by symptoms alone.
Fewer than 2% of patients presenting to their GP with dyspepsia for the first time are estimated to have gastric cancer. 1 Government guidelines have been published on identifying patients who should be referred urgently to a specialist or for endoscopy within a 2-week period. 2
These are patients over 55 with dyspepsia or for those of any age who have the classic ‘alarm’ symptoms of dysphagia, vomiting, loss of appetite, weight loss or symptoms associated with gastrointestinal bleeding. 3
Unfortunately the majority of patients present with advanced disease: their symptoms may include nausea, vomiting, pain, weight loss, and, in the case of GOJ disease, dysphagia.
Surgical treatment of stomach cancer
Surgery is the primary form of treatment and may be useful for palliation. Around half of patients have some form of surgery but due to the late diagnosis of the disease in the UK only around 20% of patients have curative resections. 4
Whenever possible, partial gastrectomy rather than total gastrectomy should be carried out as the less extensive procedure has fewer complications and no survival disadvantage has yet been shown. 5 One survey of 23 NHS hospitals has shown that 37% of stomach cancer patients have a resection. 3
Postoperative mortality is higher in western countries than in Japan and a recent study has shown perioperative mortality rates of 14% in south-west England 3 although some surgeons achieve rates of 5% or below. 6
The lowest rates were associated with surgeons who carried out the highest volume of work and government recommendations are that patients should be treated in centralised specialist oesophago-gastric oncology units.
Debate continues about the optimum extent of lymph node resection for curative surgery. D1 dissection (local nodes) remains the standard, but D2 dissection (locoregional nodes) is gaining acceptance in the UK, particularly for more advanced operable cancers. 7,8 Modified D2 resection does not involve removal of the pancreas or spleen. One recent Welsh study cited cumulative 5-year survival after resection for stage 3 cancer of 8% following D1 resection compared to 33% after modified D2 resection. 9
Current consensus is that removal of adjacent organs during gastrectomy should only be carried out if necessary for complete resection of tumour. 5,7
Chemotherapy, radiotherapy and symptom control
Benefit has been clearly demonstrated for the use of pre-operative chemotherapy. In a recent trial perioperative chemotherapy with the ECF regimen improved overall 5-year survival from 23% to 36% when compared to surgery alone. 10
Further research is investigating the use of targeted biological therapies, such as bevacizumab (Avastin), in combination with ECF chemotherapy. 11
Different forms of adjuvant chemotherapy and radiotherapy have also been investigated. A large systematic review has shown adjuvant chemotherapy to provide a small survival advantage , 12 although this is not regarded as standard therapy. 7
Radiotherapy combined with chemotherapy given post-operatively has also shown positive results 13 and this treatment strategy is regarded as the standard practice in North America. The benefits of various chemo-radiotherapy schedules used both pre-operatively and post-operatively are being tested in ongoing trials.
More than two-thirds of gastric cancer patients will have unresectable disease. For this group, a review has shown that palliative chemotherapy is superior to supportive care alone. 14 However, even the most intensive regimes are unlikely to extend median survival above a year. 14
ECF or ECX chemotherapy is the standard regimen used within the UK. 14 Docetaxel based regimens are commonly used in North America. Trials are ongoing to evaluate different chemotherapy combinations and biological agents.
There are various treatment options which are aimed at providing symptom control alone, these include; radiotherapy to control gastric bleeding or pain from bone metastases, stent insertion or laser therapy for dysphagia, and surgery for the palliation of intestinal obstruction.
References
UK Stomach Cancer incidence statistics
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UK Stomach Cancer mortality statistics
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Stomach Cancer survival statistics
- Gatta G,Ciccolallo L, Kunkler I et al.; EUROCARE Working Group., Survival from rare cancer in adults: a population-based study. Lancet Oncol, 2006. 7(2): p. 132-40
- ISD Scotland Online. 2007 Information and Statitistics Division, NHS Scotland.
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- Bowles, M.J. and I.S. Benjamin, ABC of the upper gastrointestinal tract: Cancer of the stomach and pancreas. Bmj, 2001. 323(7326): p. 1413-6.
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