The Malaysian National Cancer Registry (NCR) report for the period 2003-2005 shows an incidence of stomach cancer of 2.2 for Malay, 11.3 for Chinese and 11.9 for Indian males per 100,000 population. Malay (1.3), Chinese (7.2) and Indian (7.2) women have rates lower than men. Malays in Peninsular Malaysia have five times less stomach cancer than Chinese and Indians. This racial difference is more marked than that noted in the Singapore cancer registry. Regional data from Kelantan has an even lower rate for Malays there (1.5 for males and 0.9 for females per 100,000 population). The incidence of Helicobacter pylori infection, a known risk factor for stomach cancer, is low among Malays.
Observations of racial differences in the prevalence of Helicobacter pylori in Malaysia have been intriguing. The Indians and Chinese consistently have a higher prevalence compared to the Malays. The racial cohort theory has been proposed to explain these differences where transmission and perpetuation of infection takes place within a racial group rather than between races, races being separate owing to the low rate of interracial marriages. Studies have demonstrated distinctive bacterial strains between races. Phylogenetic studies have shown that H. pylori isolates amongst Chinese and Indians are distinctive while Malays have Indian and other strains suggesting a more recent acquisition of the bacterium from Indians. H. pylori is recognized as the major causative factor in peptic ulcer disease and gastric cancer. Despite the high prevalence of H. pylori, Indians have a relatively low prevalence of peptic ulcer disease and a low incidence of gastric cancer. This paradox with regards to gastric cancer has been termed the "Indian enigma". Bacterial strain differences between races may be putative but this observation may also indicate gastroprotective environmental factors or a lower genetic susceptibility to develop cancer in the Indians.
The incidence of surgery for gastric cancer in Singapore increased during the period 1951 to 1980 (males from 3.5 to 8.7 per 100,000 per year: females from 0.5 to 4.2 per 100,000 per year). This increase occurred mainly during the first decade of the study and was confined to persons aged 55 and above. Chinese had the highest incidence, followed by Indians and then Malays. These racial differences remained unchanged over the period of study.
The multiracial population in Malaysia has lived together for almost a century, however, the risk of gastric cancer among them varies. This study aimed to determine the distribution of different gastric adenocarcinoma subtypes and Helicobacter pylori infection status among gastric adenocarcinoma patients. Patients with gastric adenocarcinoma were enrolled from November 2013 to June 2015. Blood samples were collected for detection of H. pylori using ELISA method. Gastric adenocarcinoma cases were more prevalent in the Chinese (52.8%), followed by the Malays (41.7%) and least prevalent in the Indians (5.6%). Gastric adenocarcinoma located in the cardia was significantly more prevalent in the Malays (66.7%) compared to the Chinese (26.3%), whereas non-cardia cancer was diagnosed more in the Chinese (73.7%) compared to the Malays (33.3%) [P = 0.019; OR = 5.6, 95 CI: 1.27 to 24.64]. The Malays also had significantly higher prevalence of gastric tumour located at the cardia or fundus than other gastric sites compared to the Chinese (P = 0.002; OR: 11.2, 95% CI: 2.2 to 56.9). Among the cardia gastric cancer patients, 55.6% of the Malays showed intestinal histological subtype, whereas all the Chinese had the diffuse subtype. More than half of the patients (55.3%) with gastric adenocarcinoma were positive for H. pylori infection and among them, 66.7% were Chinese patients. The risk of gastric adenocarcinoma in our population is different among ethnicities. Further studies on host factors are needed as it might play an important role in gastric cancer susceptibility in our population.
The great variability in gastric cancer rates across Asia, with very high incidences in Japan and Korea, and exceedingly low incidences in ethnic Malays, whether in Malaysia or Indonesia, appears largely due to variation in Helicobacter pylori infection rates. While between 2% and 10.6% of gastric cancers in a recent Japanese survey were considered to be negative for bacterial infection on the basis of seropositivity and H. pylori-dependent mucosal atrophy, it is notoriously difficult to preclude past infection. The situation is greatly complicated by reported differences in the etiology of gastric cardia and non-cardia cancers. In the Western world there do appear to be tumours arising close to the esophageal-gastric junction which are not related to H. pylori and associated inflammation, but in most Asian populations these appear to be very rare. Therefore preventive efforts, and particularly screening, should be focused on markers of bacterial infection, with avoidance of unnecessary exposure to X-ray radiation.