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Cancer at the Gastro-oesophageal Junction (Epidemiology)
Gill M. Lawrence
Aims
To identify change patterns of gastro- oesophageal cancer.
Introduction
Cancers of the stomach and the oesophagus are amongst the ten most common cancers in the world. In 1985 there were estimated to be 755 000 new stomach cancers and 304 000 new oesophageal cancers diagnosed worldwide [1].
At that time, as now, there were marked differ- ences in the incidence of stomach cancer between countries with this cancer being the most common cancer in developing countries and the fourth most common cancer in devel- oped countries. In 1985 the lowest incidence of stomach cancer was recorded in India (age- standardised incidence rate 2.1 per 100 000 population) and the highest in Japan (age- standardised incidence rate 93.3 per 100 000 population) where stomach cancer accounted for one-third of all male cancers and almost one-quarter of female cancers. Because of these high incidence rates, the Japanese have intro- duced a screening programme for stomach cancer which has led to the diagnosis of 30–40%
of tumours at an early stage. Coupled with aggressive treatment, this has resulted in much improved survival rates [2].
Stomach cancer incidence and mortality have been linked with dietary risk factors such as high intake of salt, fat, starches and carbohy- drates (from grains and starchy foods), and dietary nitrate (from water or via the pickling and smoking of food) [3]. A high intake of pre- served foods is believed to increase the risk of stomach cancer due to the presence of nitrites which form carcinogenic N-nitroso compounds when mixed with gastric juices. Chronically high levels of infection with Helicobacter pylori have also been positively correlated with a high incidence of stomach cancer [4], with carriers of the bacteria having 3–6 times the risk. This link with H. pylori infection has been suggested as an explanation for the higher levels of stomach cancer in the more deprived sections of the UK population [5]. Other risk factors for stomach cancer include occupational exposure to dust (pottery industry), medical conditions such as atrophic gastritis, intestinal metaplasia and per- nicious anaemia. Stomach cancer rates are also higher in people with blood group A and with hereditary non-polyposis colon cancer.
In 1985 the lowest rates of oesophageal cancer were recorded in Israeli Jews (age-standardised incidence rate 1.4 per 100 000 population) and the highest in Calvados in France (age- standardised incidence rate 26.5 per 100 000 population) [1]. There is also a high risk
“Asian oesophageal cancer belt” extending from
the Caspian Sea in northern Iran, through the
former southern Republics of the USSR to
western and northern China [6]. Almost half of
the world’s oesophageal cancers occur in China [1]. In China and Iran, poor nutrition (in par- ticular zinc deficiency) and ingestion of opium pyrolysates and preserved food high in nitrosamines and mycotoxins is thought to be responsible for the high incidence rates. Human papilloma virus (subtypes 16 and 18) has also been implicated in areas of particularly high prevalence in China. Squamous cell carcinoma is the most common histology in the upper two thirds of the oesophagus and adenocarcinoma in the lower third.
Alcohol and tobacco consumption are major risk factors associated with squamous cell car- cinoma of the oesophagus in Europe and the Americas and the two compounds act synergis- tically. Thus, in a French control study, the relative risks for heavy drinkers and heavy smokers were 5.1 and 18 respectively, while the relative risk for those who smoked and drank heavily was 44.4 [7]. Furthermore, in Calvados where the incidence of oesophageal cancer in men is particularly high, the trend in risk amongst successive birth cohorts has a pattern characteristic of other alcohol-related cancers such as those of the tongue, mouth, pharynx and larynx. Gastro-oesophageal reflux and body mass index have been identified as factors strongly associated with increased risk of ade- nocarcinoma of the oesophagus [8].
Temporal Trends in
Stomach Cancer Incidence and Mortality
The incidence of stomach cancer is decreasing by 2–4% worldwide each year, mainly because of a decrease in the “intestinal” type of adeno- carcinoma. These changes have been correlated with the introduction of refrigeration as a means of food preservation, which has reduced the need for salting, pickling and smoking. The increased consumption of fresh fruits, raw veg- etables and salads is also believed to have played an important role in the reduction of stomach cancer worldwide [9]. This is thought to be due to the presence in these foods of antioxidants such as vitamins C and E which inhibit nitrosa- tion. This interpretation is further supported by migrant studies which consistently demonstrate that immigrants and their offspring assume the stomach cancer lifetime risk of their host country.
Overall stomach cancer incidence and mor- tality rates are approximately 2.5 times as high in men, but there is some variation in these ratios with age (see Figure 13.1). In people aged 45 to 74 incidence rates are around three times higher in men than in women but the incidence
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Age of diagnosis3.5 3.0 2.5 2.0 1.5 1.0 0.5 0.0
0– 5– 10– 15– 20– 25– 30– 35– 40– 45– 50– 55– 60– 65– 70– 75– 80– 85+
Age specific rate ratio men : women
Mortality Incidence
Figure 13.1. Age-specific rate incidence and mortality rate ratios for men and women in the West Midlands diagnosed with or dying
from stomach cancer in the period 1996 to 2000.
rate ratio is lower in younger and older people.
Mortality rates are also approximately three times higher in men aged 55 to 75 but the mor- tality rate ratio declines with age in men and women aged less than 55 and over 75.
Figure 13.2 shows the decreases in stomach cancer incidence and mortality that occurred in men and women in England and Wales between 1971 and 1999. Age-standardised incidence rates fell in men by 41% (from 31.8 to 18.9 per 100 000) and in women by 51% (from 15.1 to 7.3 per 100 000). At the same time, age-standard- ised mortality rates decreased in men by 60%
(from 31.7 to 12.6 per 100 000) and in women by 66% (from 14.9 to 5.0 per 100 000). Stomach cancer mortality fell at a faster rate than inci- dence in both sexes, although this effect is slightly greater in men.
Temporal Trends in Oesophageal Cancer Incidence and Mortality
Improvements in oesophageal cancer incidence and mortality in some countries have been cor- related with increases in the consumption of fresh fruit and vegetables. However, in many European countries the benefits of these nutri- tional improvements have been largely offset by
increasing alcohol and tobacco consumption with the result that oesophageal cancer inci- dence and mortality rates are rising. Figure 13.3 shows the increases in oesophageal cancer inci- dence and mortality that occurred in men and women in England and Wales between 1971 and 1999. Age-standardised incidence rates rose in men by 67% (from 7.6 to 12.8 per 100 000) and in women by 34% (from 4.2 to 5.7 per 100 000).
At the same time, age-standardised mortality rates increased in men by 66% (from 7.6 to 12.7 per 100 000) and in women by 28% (from 4.0 to 5.2 per 100 000).
Figure 13.4 shows how age-specific incidence rate ratios for oesophageal cancers diagnosed in men and women in the West Midlands changed between 1980 and 2000. Incidence rates increased by 50% in men and women aged 60 and over during this time period. However, in men there was also a marked increase in the 45–59 age band which was not apparent in women.
Variation in Stomach and Oesophageal Cancer
Incidence with Deprivation
Similar decreases in stomach cancer incidence to those seen in England and Wales have 111
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35 30 25 20 15 10 05 0
Age standardised rate per 100,000 population
Mortality – men Incidence – men
Mortality – women Incidence – women
1971 1973 1975 1977 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999
Figure 13.2. Temporal changes in stomach cancer incidence and mortality in England and Wales during the period 1971 to 1999.
occurred in the West Midlands. However, in this region the rate of change has varied markedly with deprivation status [10], consistent with the suggestion that early infection with Helicobacter pylori prior to the widespread introduction of refrigeration is a major risk factor for stomach cancer. Figure 13.5a shows how stomach cancer incidence in men and women varied in the most affluent and most deprived sections of the West Midlands population between 1984 and 1998.
These data clearly demonstrate that the overall decrease in male stomach cancer that was
apparent in the West Midlands during this time was mainly due to a 31% decrease in incidence in the most deprived men (from 40.4 per 100 000 in 1984–86 to 27.9 per 100 000 in 1996–98). The majority of this change took place in the period from 1985–87 to 1992–94 when a 34% fall in incidence was seen. The situation was very dif- ferent in the most affluent men. In this group stomach cancer incidence remained reasonably stable at around 19 per 100 000 between 1984–86 and 1994–96 and then increased by 15% to reach 21.9 per 100 000 in 1996–98. Similar effects were
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Age of diagnosis1.8 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 0.0
0– 5– 10– 15– 20– 25– 30– 35– 40– 45– 50– 55– 60– 65– 70– 75– 80– 85+
Age specific rate ratio 1996–00 : 1980–84
Women Men
Figure 13.4. Changes in age-specific oesophageal cancer incidence rate ratios for men and women in the West Midlands diagnosed in 1980–84 and 1996–2000.
14 12 10 8 6 4 2 0
Age standardised rate per 100,000 population Mortality – men
Incidence – men
Mortality – women Incidence – women
1971 1973 1975 1977 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999
Figure 13.3. Temporal changes in oesophageal cancer incidence and mortality in England and Wales during the period 1971 to 1999.
seen in women where stomach cancer incidence in the most deprived group fell by 47% from 18.5 per 100 000 in 1984–86 to 9.9 per 100 000 in 1996–98 while that in the most affluent women remained fairly constant at around 8 per 100 000 until 1994–96 when it decreased by 21% to reach 6.3 per 100 000 in 1996–98.
Table 13.1 shows that these temporal changes in stomach cancer incidence in men and women caused the rates in the most affluent and most deprived categories to converge. In 1984–86 the incidence rates in the most affluent men and women were less than half the rates in the most deprived men and women (rate ratios 0.49 and 0.48 for men and women respectively). By 1996–98, the differences in the stomach cancer incidence in the two groups of men and women were much smaller, with the rates in the most affluent men and women being only 22% and
36% lower than those experienced by their most deprived counterparts (rate ratios 0.78 and 0.64 in men and women respectively).
The overall increase in male oesophageal cancer seen in England and Wales over the last 28 years is also apparent in the West Midlands.
Figure 13.5b shows that this increase occurred in the most affluent and the most deprived men, but that the effect was much greater in the former (127% compared with 57%). In both groups, incidence increased most rapidly between 1984–86 and 1988–90 (from 5.7 per 100 000 to 11.2 per 100 000 in the most affluent men and from 11.4 per 100 000 to 14.2 per 100 000 in the most deprived men). After this time there was a steady and sustained increase in both groups, with incidence rising an addi- tional 14% in the most affluent men and by an additional 25% in the most deprived men.
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50
40
30
20
10
0
3 Yr Rolling directly standardised rate (per 100,000)
Most deprived men Most affluent men Most affluent women Most deprived women
1984–861985–871986–881987–891988–901989–911990–921991–931992–941993–951994–961995–971996–98 a
Year
25
20
15
10
5
0
3 Yr Rolling directly standardised rate (per 100,000)
Most deprived men Most affluent men Most affluent women Most deprived women
1984–861985–871986–881987–891988–901989–911990–921991–931992–941993–951994–961995–971996–98 b
Year
Figure 13.5. Variation in stomach and oesophageal cancer incidence rates with deprivation in men and women diagnosed in the
15-year period 1984–98; 95% confidence intervals are indicated by dotted lines. a Three-year rolling directly age-standardised
stomach cancer incidence rates in men and women from Townsend bands 1 (most affluent) and 5 (most deprived). b Three-year
rolling directly age-standardised oesophageal cancer incidence rates in men and women from Townsend bands 1 (most affluent)
and 5 (most deprived).
Similar but smaller increases in oesophageal cancer incidence were recorded in the most affluent women, with a 46% rise between 1984–86 and 1988–90 (from 3.8 per 100 000 to 5.5 per 100 000) and a further 16% increase from 1988–90 onwards. The picture in the most deprived women is, however, more complex. In this group, there was no significant change in oesophageal cancer incidence between 1984–86 and 1996–98, but this overall picture masks a 29% increase in incidence to 8.8 per 100 000 in 1991–93 followed by a similar decrease over the following 7 years.
As with stomach cancer, these temporal changes in oesophageal cancer incidence with time in women caused the rates in the most affluent and most deprived categories to con- verge (Table 13.1). Thus, in 1984–86 the inci- dence rate in the most affluent women was only half the rate in the most deprived women (rate ratio 0.55) but, by 1996–98, the incidence rates in the two groups of women are almost the same (rate ratio 1.01). A similar but less marked reduction in the difference in inci- dence between the most affluent and the most deprived groups was seen in men. Here, whereas in 1984–86 oesophageal cancer incidence in the most affluent men was only half the rate of that
in the most deprived men, by 1996–98 the rate in the most affluent men was only 28% lower (rate ratios 0.50 and 0.72 for 1984–86 and 1996–98 respectively).
Survival from Stomach and Oesophageal Cancer
Survival from stomach and oesophageal cancer is generally poor. Survival varies markedly with stage at diagnosis, with 5-year survival rates for stage I, II, III, IVA and IVB tumours diagnosed in the West Midlands region in 1972–91 being 76.9%, 33.5%, 10.7%, 2.1% and 0.2% respectively [11]. Overall survival rates in England and Scotland are lower than the European average, with only 11–12% of stomach cancer patients and 7–9% of oesophageal cancer patients diagnosed in 1985–89 alive after 5 years; the European weighted averages being 21% and 10%
respectively [12]. It is likely that varia- tion in stage at diagnosis is the main factor accounting for the differences in survival between England and other European countries.
However, after subsite and stage are taken into consideration, the low proportion of stomach
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Midlands in men and women in the most affluent (Townsend band 1) and most deprived (Townsend band 5) categories with cancers diagnosed in the 15-year period 1984–98 (95% confidence intervals are shown in brackets)
Men Women
Diagnosis Most affluent Most deprived Most affluent: Most affluent Most deprived Most affluent:
years incidence rate incidence rate Most deprived incidence rate incidence rate Most deprived
Incidence rate Incidence rate
ratio ratio
Stomach cancer
1984–86 19.86 40.43 0.49 8.80 18.45 0.48
(17.65–22.07) (37.04–43.82) (7.50–10.09) (16.47–20.42)
1990–92 18.05 30.90 0.58 7.70 13.79 0.56
(15.89–20.21) (27.93–33.88) (6.50–8.89) (12.08–15.51)
1996–98 21.91 27.92 0.78 6.34 9.85 0.64
(19.51–24.30) (25.03–30.81) (5.26–7.42) (8.41–11.29)
Oesophageal cancer
1984–86 5.65 11.36 0.50 3.75 6.84 0.55
(4.47–6.82) (9.53–13.19) (2.91–4.60) (5.54–8.14)
1990–92 10.46 15.02 0.70 5.40 8.53 0.63
(8.84–12.07) (12.91–17.14) (4.37–6.43) (7.13–9.92)
1996–98 12.81 17.84 0.72 6.37 6.29 1.01
(10.99–14.63) (15.48–20.20) (5.25–7.50) (5.12–7.47)
cancer patients undergoing surgery has also been identified as a factor contributing to the relatively poor survival recorded in England.
Five-year survival rates for these cancers diag- nosed in whites in the USA in 1983–88 at 18%
and 9% are similar to the European average [13].
Much higher 5-year survival rates (47% and 15%
respectively for stomach and oesophageal can- cers diagnosed in 1975–89) have been reported in Japan. Although more widespread use of endoscopy in Japan and the introduction of a mass screening programme are probably res- ponsible in part for these variations, the use of different criteria for the histological diagnosis of early gastric carcinoma in Japan and Western countries may also be a contributory factor [14].
Although survival from stomach and oesophageal cancer is poor, relative survival rates have improved in both men and women in England and Wales over the last 25 years (Figure 13.6). Thus, for stomach cancer 5-year relative survival rates increased in men from 3.9% to 9.7% and in women from 4.9% to 11.6% for cancers diagnosed in 1992–94 compared with 1971–75. For oesophageal cancer 5-year relative survival rates increased in men from 2.9% to 5.7% and in women from 5.1% to 8.8% for cancers diagnosed in the two time periods.
Stomach cancer survival varies with age at diagnosis in both men and women, with between 15 and 20% of men and women aged 15–49 diagnosed in England and Wales in
1992–94 surviving for 5 years compared with only 5–10% of those aged 70 or older (Figure 13.7a). Five-year relative survival rates from oesophageal cancers diagnosed in the same time period were generally lower than for stomach cancer in men, ranging from 0.9% in men aged 80–99 to 8.8% in men aged 40–49. Five-year rel- ative survival was significantly higher in women in all but the oldest age group studied, varying between 2.5% in women aged 80–99 and 29.1%
in woman aged 15–39 (Figure 13.7b). The reason for these large variations in survival between men and women is not clear but it may be related to the relatively higher incidence of ade- nocarcinoma in men compared with women.
Cancer at the Gastro- oesophageal Junction
It is generally accepted that intestinal metaplasia both in the oesophagus (Barrett’s oesophagus) and at the gastro-oesophageal junction has pre- malignant potential and that these metaplastic changes can progress through dysplasia to adenocarcinoma [15]. The mucosal changes characteristic of Barrett’s oesophagus are be- lieved to occur as a consequence of extended gastro-oesophageal reflux during which con- tents of the stomach or duodenum pass into the oesophagus. Gastro-oesophageal reflux occurs 111
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12
10
8
6
4
2
0
5 year relative survival (%)
Oesophagus – men Stomoach – men
Oesophagus – women Stomach – women
1971–75 1976–80 1981–85 1986–90 1992–94
Figure 13.6. Temporal changes in 5-year relative survival from stomach and oesophageal cancers diagnosed in men and women in
England and Wales between 1971 and 1994.
more frequently in overweight individuals, par- ticularly those with excess abdominal fat. This may be in part due to a reduction of pressure in the lower oesophageal sphincter related to high fat consumption. It has also been suggested that drugs such as proton pump inhibitors and H
2- receptor blockers might potentiate adenocarci- noma of the gastro-oesophageal junction by reducing the acidity of the gastric juice and decreasing its bile-neutralising capability. More recently, dietary nitrate has been implicated in the development of cancers at the gastro- oesophageal junction through conversion in the gastric juice in the presence of vitamin C into the highly reactive and potentially toxic NO free radical.
Annual increases in the incidence of adeno- carcinoma of the oesophagus in men of between 9% and 20% have been reported in the UK and other parts of Europe, the USA and Australia [16]. Figure 13.8 illustrates the increase in age- standardised incidence of adenocarcinoma in the oesophagus that occurred in men and
women in England and Wales between 1971 and 1998. Over this time period there was a 3.68-fold increase in the incidence of adenocarcinoma in men and a 2.65-fold increase in women while the incidence of cancers with other or non-specific morphology remained relatively constant in both sexes. This suggests that the increases in adenocarcinoma did not arise because of improvements in the coding and classification of oesophageal tumours.
Further evidence to support this interpreta- tion comes from an examination of the relation- ship between oesophageal cancer subsite and morphology. Figure 13.9 shows the subsite dis- tribution in the oesophagus of adenocarcinomas and cancers with other morphology (including squamous cell carcinomas and cancers with non-specific morphology) in men and women in England and Wales diagnosed in 1971 and 1998. Over this time period in men there was a 8.17-fold increase in the number of aden- carcinomas diagnosed in the lower third of the oesophagus and a 3.36-fold increase in the
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3025
20
15
10
5
0
Relative survival (%)
15–39 40–49 50–59 60–69 Age at diagnosis
70–79 89–89 a
Women Men
30
25
20
15
10
5
0
Relative survival (%)
15–39 40–49 50–59 60–69 Age at diagnosis
70–79 89–89 b
Women Men
Figure 13.7. Five-year relative survival rates for (a) stomach cancer and (b) oesophageal cancer diagnosed in men and women in
England and Wales in the period 1992 to 1994.
number of adenocarcinomas diagnosed in unspecified subsites within the oesophagus.
Smaller increases were also apparent in women, with an 85% increase in adenocarcinomas in the lower third of the oesophagus and a 75%
increase in unspecified subsites. These changes were, however, not accompanied by equivalent
decreases in the incidence of oesophageal can- cers with unspecified subsite and morphology.
Therefore data indicate that increases in adeno- carcinomas of the oesophagus are not spurious and that they have not arisen because of improvements in the collection of information relating to subsite and morphology.
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10
8
6
4
2
0
Age standardised rate per 100,000 population
Other morphologies – men Adenocarcinoma – men
Other morphologies – women Adenocarcinoma – women
1971 1973 1975 1977 1979 1981 1983 1985 1987 1989 1991 1993 1995 1997
FFigure 13.8. Age-standardised incidence rates of adenocarcinoma and other morphologies (including non-specific morphologies) in the oesophagus in men and women in England and Wales from 1971 to 1998.
1200
1000
800
600
400
200
0
Oesophagus lower third – adenoca
Oesophagus other subsite –
adenoca
Oesophagus unspecified subsite – adenoca
Oesophagus lower third –
other
Oesophagus other subsite –
adenoca
Oesophagus unspecified
other
Number of cancers registered
1998 – men 1998 – women 1998 – women 1971 – men
Figure 13.9. Temporal changes in subsite and morphology recorded in oesophageal cancers diagnosed in men and women in
England and Wales in 1971 and 1998.
On the other hand, comparable data for stomach cancer shown in Figure 13.10 cannot be used to refute the suggestion that overall increases in the incidence of adenocarcinoma between 1971 and 1998 are due mainly to improvements in the quality of the data relating to subsite and morphology. Thus, although the number of adenocarcinomas registered in the stomach during this time period increased by 77% in men and 35% in women, these changes were accompanied in both sexes by 3-fold decreases in the numbers of cancers with other or unspecified morphology. It is, however, pos- sible that the 4.31-fold increase in adenocarci- noma of the gastric cardia is real because the male to female incidence rate ratio at this site (3.6–4.0) is much higher than for other sites (2.0–2.4). If the increase in adenocarcinoma in the cardia was due to improved subsite record- ing, the male to female rate ratio for gastric cancer with an unspecified subsite should have decreased as the sex rate ratio in the cardia increased. In fact, the male to female incidence rate ratios increased at both sites between 1971 and 1998 (from 3.6 to 4.4 in the cardia and from 2.0 to 2.2 in the unspecified subsites).
Adenocarcinoma is the most common type of cancer in the stomach. Increases in the inci- dence of adenocarcinoma in the lower oesopha- gus could therefore occur if more tumours at or
near the gastro-oesophageal junction were iden- tified as being of oesophageal rather than gastric origin. It has been suggested that only centres with a special interest in oesophageal and gastric surgery can accurately classify whether a tumour of the gastro-oesophageal junction is in the distal oesophagus, the true gastric cardia or the gastro-oesophageal junction. It may thus be reasonable from an epidemiological standpoint, to consider adenocarcinoma of the oesophagus and the gastric cardia to be the same disease and to combine the incidences of adenocarcinomas at the two locations [17]. Such an approach is consistent with the two cancers having a similar phenotype and a similar prevalence of the p53 gene mutation.
Figure 13.11 shows the increases in age-stan- dardised incidence rates that occurred between 1980 and 1998 in cancers diagnosed in the oesophagus and gastric cardia in men and women in the West Midlands. During this time the incidence rate of adenocarcinoma in men increased 1.8-fold (from 6.8 per 100 000 to 12.1 per 100 000) and that in women more than doubled (from 1.3 per 100 000 to 2.8 per 100 000). During the same time period the inci- dence of squamous cell carcinoma remained constant at around 3.7 per 100 000 in both sexes and the incidence of cancers with other non- specific morphologies decreased slightly.
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40003500 3000 2500 2000 1500 1000 500 0
Stomach cardia – adenoca
Stomach non-cardia –
adenoca
Stomach unspecified
subsite – adenoca
Stomach cardia – other
Stomach non-cardia –
other
Stomach unspecified subsite – other
Number of cancers registered
1998 – men 1998 – women 1998 – women 1971 – men
Figure 13.10. Temporal changes in subsite and morphology recorded in stomach cancers diagnosed in men and women in England
and Wales in 1971 and 1998.
Details of the subsite specific changes in inci- dence rate that took place in cancers of the oesophagus and gastric cardia in men and women in the West Midlands between 1980 and 1998 are provided in Figure 13.12. This shows that in both sexes, the increases in the incidence of adenocarcinoma could not be accounted for by decreases in squamous cell carcinomas or cancers with other non-specific morphology. It is therefore likely that these cancers arose because of new factors affecting the aetiology of the disease.
Conclusions
While stomach cancer incidence and mortality are generally declining, increases in oesophageal cancer incidence and mortality have occurred in many countries over the last 20–30 years. In the West Midlands, decreases in stomach cancer incidence are much greater in the most deprived men and women. Improvements in food preser- vation with the introduction of refrigeration resulting in reduced levels of infection with Helicobacter pylori are probably the most likely 111
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14 12 10 8 6 4 2 0
Adenocarcinoma Squamous cell carcinoma Other morphologies
Age standardised incidence rate per 100,000
1998 – men 1980 – women 1998 – women 1980 – men
Figure 13.11. Variation in age-standardised incidence rates with morphology for cancers in the oesophagus and gastric cardia diagnosed in men and women in the West Midlands in 1980 and 1998.
6 5 4 3 2 1 0 –1 2
Adenocarcinoma Squamous cell carcinoma Other morphologies Difference in age standardised incidence rate 1998 : 1980
Women Men
Figure 13.12. Differences between the age-standardised incidence rates for adenocarcinomas, squamous cell carcinomas and cancers
with other and non-specific morphologies for cancers in the oesophagus and gastric cardia diagnosed in men and women in the
West Midlands in 1980 and 1998.
explanation for this finding. Although, as with stomach cancer, the incidence of oesophageal cancer is generally higher in the most deprived men and women, the rate of increase of oesophageal cancer incidence in the West Midlands is considerably greater in the most affluent men and women. Oesophageal cancer incidence and mortality are approximately twice as high in men and in recent years there has been a marked increase in incidence in the 45–59 age band which is not apparent in women.
Epidemiological studies combining data for the gastric cardia and the oesophagus have shown that adenocarcinomas account for the majority of this rise in incidence. Increased gastro- oesophageal reflux linked to high fat consump- tion and the expanding use of proton pump inhibitors and H
2-receptor blockers may be responsible for these changes.
Acknowledgements
I am grateful to Dr Mike Quinn, Director of the National Cancer Intelligence Centre at the Office for National Statistics, for providing the inci- dence and mortality data for England and Wales that have been included in this chapter. I would also like to thank the staff in the West Midlands Cancer Intelligence Unit who diligently abstract, code and quality assure the cancer registration data collected for the West Midlands region and Dr Cheryl Livings and Miss Sarah Baggott for their assistance with data analysis. Finally, my thanks go to the NHS Trusts and Private Hospitals which provide cancer registration data and without whose continued cooperation valuable epidemiological studies such as those I have described would not be possible.
Questions
1. Where is cancer of the stomach common?
2. Where is cancer of the oesophagus common?
3. What has happened to the incidence of these two cancers?
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