The oesophagus is the food pipe that connects from the lower throat to the stomach. The stomach is part of the digestive system, located between the oesophagus and the small intestine. The stomach secretes enzymes and acid, breaking down food using these secretions and through churning via muscular contractions.
Gastric cancer
Gastric (stomach) cancer is one of the most common cancers in the world with a high risk of mortality, particularly for men. It is the fifth leading cause of cancer death on a global scale.1 Incidence rates are highest in Eastern and Central Asia.2 In Australia the incidence of this cancer is relatively low compared to these regions. There were 2,584 cases diagnosed and 1,146 deaths in Australia from gastric cancer in 2024.3,4 People in Australia diagnosed with gastric cancer have a 39% chance of surviving for at least five years, based on data from the period 2016–2020.5 The age-standardised incidence rate of gastric cancers has approximately halved in Australia since 1982.3
The mortality rate from gastric cancers in Australia has fallen in the past 50 years. In 1971 the mortality rate was over 20 per 100,000 people, compared to 4.2 per 100,000 in 2024.4 Australian men have had a higher mortality rate from gastric cancer than women over these years 4
There are many risk factors for stomach cancer, including smoking, alcohol consumption, obesity, infection with Helicobacter pylori, family history of stomach cancer and eating salt-preserved foods (e.g. ham) or some fermented foods.6,7
There are numerous different classification systems for gastric cancers.8 Pertinent to the research discussed here is the cardia versus non-cardia classification system, based on the region of origin in the stomach. Cancers occurring at the gastric cardia, which is near the junction of the oesophagus and stomach, are referred to as gastric cardia cancers. Cancers of the gastric fundus (dome shaped region near and above the cardia), corpus (the main, large part) and the antrum (final region before the lower outlet), are termed non-cardia cancers.
Oesophageal cancer
Cancer registry records indicate that 1,785 people were diagnosed with cancer in their oesophagus in 2024 in Australia.3 Mortality from oesophageal cancer is relatively high, with only 25.1% of people surviving for five years after diagnosis (2016–2020 data).5 An estimated 1,439 people died from oesophageal cancer in Australia in 2024.4
Risk factors for oesophageal cancer include smoking, obesity, alcohol and consumption of some types of fermented foods.6,9
Oesophageal cancer has two main histological types: adenocarcinoma (which has further sub-types) and squamous cell carcinoma.
The lived experience of stomach and oesophageal cancer is one of difficulty. People with these cancers experience pain, considerable side effects from treatment and difficulty eating, with some left unable to eat solid food.6
3.5.3.1 Risk associated with smoking
Gastric cancer
Smoking causes gastric cancer.10,11
A meta-analysis of 46 case–control studies found an estimated 50% increased odds of gastric cancer for people who have smoked.12 For people who currently smoke, the odds of gastric cancer were about 70% higher (1.7-fold increased) compared to never smokers. A meta-analysis of 21 case–control and three cohort studies found that smoking increased the risk of gastric cardia adenocarcinoma by 76%.13 A 2020 meta-analysis of 232 studies (with over 33 million people) found that current smoking increased the odds of gastric cancers by 61% (1.61-fold).14
People who use tobacco in other forms than cigarettes may have an increased risk of stomach cancer (see Section 3.27). People who smoke bidis have an increased rate of gastric cancer15 and men who smoke waterpipes have an increased risk of dying from gastric cancer.16 The use of smokeless tobacco has been found to be associated with an increased risk of stomach cancer (see Section 18A.3).17
Smoking causes the deaths of about 10% of people who die from stomach cancer and almost half the deaths of people who die from oesophageal cancer in Australia. This was about 770 out of 2700 deaths from these types of cancers in Australia in 2015.18
Oesophageal cancer
Smoking causes both main forms of oesophageal cancer (adenocarcinoma and squamous cell carcinoma of the oesophagus).11
Numerous studies have shown that smoking strongly increases the risk of squamous cell carcinoma and moderately increases the risk of adenocarcinoma of the oesophagus.19-21 A pooled analysis of data from 10 case–control studies of adenocarcinoma also found that smoking doubled the risk.22 A similar analysis of 13 case–control and two cohort studies found an 85% increase in the risk of oesophageal adenocarcinoma associated with smoking.13 For Australians aged 45 and over who smoke, the risk of oesophageal cancer was estimated to be 3.8-fold higher than for non-smokers.23 A meta-analysis of African studies showed that the odds of developing oesophageal cancer were over 3-fold higher for people who smoke or chew tobacco compared to unexposed people.24
3.5.3.2 How tobacco smoke causes stomach and oesophageal cancers
Cancer-causing chemicals from tobacco smoke can reach the oesophagus and stomach through the bloodstream. For people who use smokeless tobacco that is chewed or sucked, chemicals from this tobacco can directly enter these organs in saliva that is swallowed. These chemicals can damage DNA and disrupt cellular processes, as described briefly above in Section 3.5.1.2 and in more detail in Section 3.3.
Gastric cancer
DNA adducts (DNA bonded to a cancer-causing chemical) have been identified in tissue samples from the stomach of people who smoke.25 Laboratory studies indicate that a cancer-causing chemical specific to tobacco called NNK (4-(methylnitrosamino)-1(3-pyridyl)-1-butanone) may play a role in the formation of gastric cancer.26,27 Nicotine itself also affects gastric physiology, although it is currently unclear whether this affects carcinogenesis.28
Oesophageal cancer
Studies in rats have shown that DNA adducts containing the tobacco-specific chemical N′-nitrosonornicotine (NNN) have been found in the oesophaguses of these animals after exposure to tobacco smoke.29 NNN is the most prevalent and potent oesophageal carcinogen detected in cigarette smoke.25 Other types of nitrosamines are also expected to play a role in the development of oesophageal cancer.25 Laboratory experiments and clinical studies indicate that a disruption in DNA repair processes (cellular processes that identify and correct damage to DNA) by smoking is one way that it leads to oesophageal cancer.30,31 Mutations in genes such as k-Ras and PT53 are seen in oesophagus cancer cells from smokers, consistent with mutations caused by smoke exposure in laboratory experiments, indicating a likely role for these mutations in oesophagus cancer caused by smoking.32
3.5.3.3 Factors affecting risk
Intensity and duration of smoking
The 2004 International Agency for Research on Cancer (IARC) report10 concluded that gastric cancer risk increases with duration of smoking and number of cigarettes smoked. A recent meta-analysis found that the risk of gastric cancer increased sharply with a low number of cigarettes (5–10) up to 20 cigarettes per day and increased in a dose-dependent manner with smoking duration.33
An Australian study found that the duration of smoking was closely and linearly related to the risk of oesophageal cancer and a stronger risk factor than intensity of smoking.34 A meta-analysis of studies from Africa showed that the risk of oesophageal cancer was 4.7-fold higher for pipe smokers and 3.8-fold higher for those who smoked hand-rolled cigarettes and 2.5-fold higher for factory-made cigarette smokers compared to non-smokers. The risk of oesophageal cancer was also higher in people who smoked more packs per year than for those who smoked lesser amounts, with the highest risk for people in the category who smoked more than 183 packs per year.35
Alcohol consumption
Consumption of alcohol is a major risk factor for oesophageal cancer. Some studies have found that people who smoke as well as drink alcohol have a very high risk of oesophageal cancer. In a study of over 160,000 Japanese men, those who smoked had a 3-fold increased risk, drinkers a 2.7- fold increased risk and men who smoked and drank had a 9-fold increased risk of oesophageal cancer compared to people who abstained.36 A similar synergistic effect of alcohol and smoking was found in a study that examined risk factors for the squamous cell carcinoma type of oesophageal cancer.37
Although people with a history of alcohol consumption have a higher risk of gastric cancer, whether alcohol is an independent risk factor for gastric cancer is disputed by some studies.38 Whether a combination of alcohol consumption and smoking leads to a significant increase in the risk of gastric cancer is currently unknown.
Helicobacter pylori infection
Infection with the bacteria Helicobacter pylori is a major risk factor and cause of non-cardia gastric cancer. A prospective study of 1,071 Japanese men who were followed up for 14 years found that smoking and H. pylori infection had a synergistic effect on the risk of gastric cancer.39 The risk of gastric cancer for men who smoked was almost 2-fold higher than non-smokers, and the risk of gastric cancer from H. pylori infection in non-smokers was 6.9-fold higher than those uninfected. But for people who both smoked and were infected, the risk of gastric cancer was 11.4-fold higher than those with neither risk factor. The effects of both risk factors together were therefore greater than the sum of their individual effects. In this population, 7.3% of gastric cancer was estimated as due to smoking alone, 30.1% was due to H. pylori infection alone and 49.6% was due to cigarette smoking with simultaneous H. pylori infection. The mechanism for this synergistic effect of smoking and H. pylori infection is not yet known, but smoking does not appear to increase the risk of H. pylori infection.40
H. pylori infection does not appear to be associated with the risk of oesophageal cancer.41
Cancer type
The pathogenesis of gastric cancer is thought to differ between cardia and non-cardia types. H. pylori, a strong risk factor for gastric cancer in general, increases the risk of non-cardia cancers.42
Studies that distinguish between cardia and non-cardia gastric cancers show that smoking is significantly associated with both types.10 A 2009 meta-analysis concluded that12 smoking significantly increased the risk of both types of cancer; the risk of cardia cancer was increased by 47% and the risk of non-cardia cancer by 32%.
Whilst concluding that smoking is a cause of gastric cancer in general, the 2004 US Surgeon General’s report stated that: ‘The evidence is suggestive but not sufficient to infer a causal relationship between smoking and non-cardia gastric cancers’.11 This issue has been difficult to resolve because many studies of the risk of gastric cancer associated with smoking have not distinguished between cancer subtypes and have not accounted for infection with H. pylori.
An Australian case–control study that included more than 1,000 people found the risks of both squamous cell carcinoma and the rare gastro-oesophageal junction adenocarcinoma were about four-fold higher in people who smoke compared with never smokers. The risk of oesophageal adenocarcinoma was about two-and-a-half-fold higher in people who smoke.34
Gender differences
A meta-analysis from 2019 that included over three million people examined risk factors for gastric cancer. This study showed that the risk for males who smoke was 1.3-fold higher than for females who smoke, indicating a potential sex difference in the risk of gastric cancers.43
Smoking cessation
Smoking cessation reduces the risk of stomach cancer.44 Numerous studies and meta-analyses have demonstrated that the risk of gastric cancer is lower in people who have quit compared to people who currently smoke and decreases with increasing duration of quitting.10,44
Smoking cessation reduces the risk of oesophageal cancer;44 however, even after a long period of abstinence, the risks for oesophageal cancer do not return to that of never smokers.45 A meta-analysis of 52 studies found that the risk for squamous cell carcinoma of the oesophagus was lower among former smokers (2-fold higher than for non-smokers) than people who currently smoke (over 4-fold higher than for non-smokers).46 A large meta-analysis of 52 studies also showed that smoking cessation decreased the risk of oesophageal squamous cell carcinoma, while it had limited influence on the risk of oesophageal adenocarcinoma.21
3.5.3.4 Impact on prognosis
People diagnosed with stomach or oesophageal cancer have higher risks of poor outcomes and of dying from these cancers.47-49
A large international study found that people who currently smoke had a 1.7-fold increased risk of dying from stomach cancer.49 Those who were former smokers had a risk of 1.3-fold higher than non-smokers. Smoking cessation for 10 years or more significantly reduced these risks.49
A meta-analysis involving 4,286 patients showed that current and former smokers with oesophageal squamous-cell carcinoma had a poorer prognosis and lower survival rates than never smokers. This was also the case for oesophageal adenocarcinoma.47 A study from China examined the risk of dying within 5 years of diagnosis with oesophageal cancer. People who smoked at the time of diagnosis had a 3-fold increased risk of dying, and former-smokers had a 1.6-fold increased risk of dying compared to people with no history of smoking.48
Related reading
Test your knowledge
References
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