Displaying publications 1 - 20 of 28 in total

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  1. Lim KG
    Med J Malaysia, 2009 Mar;64(1):91-2.
    PMID: 19852334 MyJurnal
    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.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  2. Goh KL
    J Dig Dis, 2007 Nov;8(4):179-85.
    PMID: 17970873
    The new millennium has seen distinct changes in the pattern of gastrointestinal disease in the Asia-Pacific region. These changes are important as more than half of the world's population come from the region and therefore impact significantly on the global disease burden. The highest incidence of gastric cancer (GCA) has been reported from Asia and GCA remains a very important cancer. However time-trend studies have shown a decrease in GCA incidence in several countries in Asia. A rise in cardio-esophageal cancers as seen in the West has not been reported. On the other hand, colorectal cancer has been steadily increasing in Asia with age-standardized incidence rates of some countries approaching that of the West. The pattern of acid-related diseases has also changed. Gastroesophageal reflux disease is a fast emerging disease with an increasing prevalence of reflux esophagitis and reflux symptoms. The prevalence of peptic ulcer disease has at the same time declined in step with a decrease in H. pylori infection. Many of the changes taking place mirror the Western experience of several decades ago. Astute observation of the epidemiology of emerging diseases combined with good scientific work will allow a clearer understanding of the key processes underlying these changes. With rapid modernization, lifestyle changes have been blamed for an increase in several diseases including gastroesophageal reflux disease, nonalcoholic fatty liver disease and colorectal cancer. A worrying trend has been the increase in obesity among Asians, which has been associated with an increase in metabolic diseases and various gastrointestinal cancers. Conversely, an improvement in living conditions has been closely linked to the decrease in GCA and H. pylori prevalence.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  3. Kandasami P, Tan WJ, Norain K
    Med J Malaysia, 2003 Dec;58(5):758-62.
    PMID: 15190664 MyJurnal
    Gastric cancer is an important cause of death among patients with malignancies in Malaysia. Survival of patients with gastric cancer is dependent on the stage at which diagnosis is made. We report our experience in dealing with gastric cancer in a major Ministry of Health Hospitals in Malaysia. A retrospective review of two hundred and fifty consecutive histologically proven gastric adenocarcinoma at Hospital Ipoh for the period January 1988 to 1998 was performed. The study confirms that gastric cancer is a disease of the elderly and has a male preponderance. It is also identifies the Chinese and Indians to be at increased risk of gastric cancer when compared to the Malays. The most striking finding in this study was the very late stage of disease at time of presentation. Eighty-two percent of the patients presented with stage IV disease and curative surgery was offered only to a 16% of them. In a substantial number of patients not even a palliative procedure was offered. Early detection is the key to improving survival in gastric cancer patients. There is an urgent need for clinicians to change their approach to the management of the disease. Patients with dyspeptic symptoms should be investigated early rather then wait for classical symptoms of gastric cancer.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  4. Quek KF, Goh KL
    Am J Gastroenterol, 2008 Jun;103(6):1575.
    PMID: 18510600 DOI: 10.1111/j.1572-0241.2008.01850.x
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  5. Katz AR
    Am J Gastroenterol, 2007 Sep;102(9):2114-5.
    PMID: 17727450
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  6. Goh KL
    Med J Malaysia, 2009 Sep;64(3):187-92.
    PMID: 20527265
    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.
    Matched MeSH terms: Stomach Neoplasms/epidemiology
  7. Goh KL, Wong HT, Lim CH, Rosaida MS
    Aliment Pharmacol Ther, 2009 Apr 1;29(7):774-80.
    PMID: 19183160 DOI: 10.1111/j.1365-2036.2009.03930.x
    Dramatic changes in the prevalence and pattern of gastrointestinal disease has taken place in Asia in recent years.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  8. Tan HJ, Goh KL
    J Dig Dis, 2008 Nov;9(4):186-9.
    PMID: 18959588 DOI: 10.1111/j.1751-2980.2008.00344.x
    As in developed societies, the prevalence of Helicobacter pylori has declined rapidly in Asia. This has been shown in both seroprevalence-based and endoscopy-based studies. While the decline in the incidence of gastric cancer has now been observed, a decrease in peptic ulcer disease has not been so clearly evident. This apparent paradox can be explained by an increase in non-H. pylori associated ulcers - such as those related to non-steroidal anti-inflammatory drugs or idiopathic ulcers. The increase of gastroesophageal reflux disease in Asia has been widely observed and commented on and its relationship to the decline in H. pylori speculated upon. However there have been few conclusive studies from Asia on this subject. While the improved diagnosis and elimination of H. pylori has contributed to its decline, a more basic change involving large segments of the Asian population must be responsible. An improvement in hygiene and living conditions that results from more affluent Asian societies is thought to be a possible cause.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  9. Gurjeet K, Subathra S, Bhupinder S
    Med J Malaysia, 2004 Oct;59(4):560-1.
    PMID: 15779598 MyJurnal
    A retrospective study on demographics of gastric carcinoma was conducted in Hospital Pulau Pinang (HPP) with the aim of comparing it to a previous study done in Hospital Universiti Sains Malaysia (HUSM), Kelantan. The incidence of gastric carcinoma was much higher in Penang compared to Kelantan. It was commonest in males and Chinese. The incidence and site of gastric carcinoma closely parallels Helicobacter pylori infection rates. This was evidenced by the higher incidence and non-cardia location of gastric carcinomas in an area with higher H. pylori infection rates (HPP) compared to a much lower incidence and preponderance of cardia tumours in HUSM where the H. pylori infection rate is exceptionally low.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  10. Kang JY
    Aust N Z J Med, 1988 Aug;18(5):661-4.
    PMID: 3072950
    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.
    Matched MeSH terms: Stomach Neoplasms/epidemiology
  11. King M, Kutty MK
    Br J Surg, 1971 Feb;58(2):123-6.
    PMID: 5548502
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  12. Misra V, Pandey R, Misra SP, Dwivedi M
    World J Gastroenterol, 2014 Feb 14;20(6):1503-9.
    PMID: 24587625 DOI: 10.3748/wjg.v20.i6.1503
    Helicobacter pylori (H. pylori) is a gram negative microaerophilic bacterium which resides in the mucous linings of the stomach. It has been implicated in the causation of various gastric disorders including gastric cancer. The geographical distribution and etiology of gastric cancer differ widely in different geographical regions and H. pylori, despite being labeled as a grade I carcinogen, has not been found to be associated with gastric cancer in many areas. Studies in Asian countries such as Thailand, India, Bangladesh, Pakistan, Iran, Saudi Arabian countries, Israel and Malaysia, have reported a high frequency of H. pylori infection co-existing with a low incidence of gastric cancer. In India, a difference in the prevalence of H. pylori infection and gastric cancer has been noted even in different regions of the country leading to a puzzle when attempting to find the causes of these variations. This puzzle of H. pylori distribution and gastric cancer epidemiology is known as the Indian enigma. In this review we have attempted to explain the Indian enigma using evidence from various Indian studies and from around the globe. This review covers aspects of epidemiology, the various biological strains present in different parts of the country and within individuals, the status of different H. pylori-related diseases and the molecular pathogenesis of the bacterium.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  13. Goh KL
    J Gastroenterol Hepatol, 2018 Jun;33(6):1177-1184.
    PMID: 29498759 DOI: 10.1111/jgh.14131
    The study of Helicobacter pylori in Malaysia has given several important insights into the epidemiology of the infection and pathogenesis of disease. Malaysia has a multiracial Asian population with three major Asian races living together-Malay, Chinese, and Indian. Races remain fairly distinct because of a paucity of interracial marriages. The "Racial Cohort Hypothesis" proposes that the infection occurs within racial groups rather than between. As such, the high prevalence among Indians (> 50%) and Chinese (40-50%) reflects the high prevalence in their countries of origin even though migration had taken place more than two generations before. The Malays have a comparatively low prevalence of about 10-20%. Despite the high prevalence of H. pylori, the Indians have a low gastric cancer incidence of less than 10 per 100 000 per year. This is in contrast to the Chinese who has an incidence in excess of 20 per 100 000 per year. We have called this the "Indian Enigma." The reason for this enigma is unclear and is the result of interaction between bacterial virulence factors, host susceptibility, and environmental factors. Phylogenetically, Chinese bacterial strains are distinct from Indians and Malays and are predominantly hpEastAsia/hsp EAsia. CagA EPIYA motifs among Chinese belong predominantly to the more virulent ABD motif. There is no clear distinguishing profile among host genetic factors. Environmental factors particularly diet may play an important role. Indians consume chilies and curries, which may be gastro protective, whereas Chinese consume more preserved and salted foods, which are thought to be carcinogenic.
    Matched MeSH terms: Stomach Neoplasms/epidemiology
  14. Lim KG, Palayan K
    Asian Pac J Cancer Prev, 2019 Jan 25;20(1):5-11.
    PMID: 30677863
    Incidence rates of gastric cancer in Malaysia has declined by 48% among males and 31% among females in the latest reporting period of 13 years. Malays used to have age-standardized-rates only a fifth of those in Chinese and Indians, but the incidence among them is slightly rising even as the rates drop in the other races. Besides ethnicity, a low level of education, high intake of salted fish and vegetables, H pylori infection and smoking are risk factors. Consumption of fresh fruit and vegetable is protective. Variation in the strains of H pylori infection affect gastric cancer risk, with hspEAsia isolates among Chinese appearing linked to a high incidence than with hpAsia2 or hpEurope strains among Indians and Malays. It was reported in the 1980s that only about 3% of patients presented with early gastric cancer, but more encouraging rates reaching 27% with Stage 1 and 2 disease have been reported in the twenty-first century from leading centres. More tumours occur in the distal stomach except in Kelantan, where the incidence is low and main site is the cardia. Prompt endoscopy is advocated and open access, with direct referrals, to such services using a weighted scoring system should be more utilized. In view of the high rate of late disease laparoscopic staging unnecessary laparotomy needs to be avoided. Late presentation of gastric cancer however, is still predominant and the mortality to incidence ratio is relatively high. Besides seeking to reduce risk factors and achieve early detection, implementation of improved care for patients with late disease must be promoted in Malaysia.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  15. Agudo A, Cayssials V, Bonet C, Tjønneland A, Overvad K, Boutron-Ruault MC, et al.
    Am J Clin Nutr, 2018 Apr 01;107(4):607-616.
    PMID: 29635497 DOI: 10.1093/ajcn/nqy002
    BACKGROUND: Chronic inflammation plays a critical role in the pathogenesis of the 2 major types of gastric cancer. Several foods, nutrients, and nonnutrient food components seem to be involved in the regulation of chronic inflammation.

    OBJECTIVE: We assessed the association between the inflammatory potential of the diet and the risk of gastric carcinoma, overall and for the 2 major subsites: cardia cancers and noncardia cancers.

    DESIGN: A total of 476,160 subjects (30% men, 70% women) from the European Investigation into Cancer and Nutrition (EPIC) study were followed for 14 y, during which 913 incident cases of gastric carcinoma were identified, including 236 located in the cardia, 341 in the distal part of the stomach (noncardia), and 336 with overlapping or unknown tumor site. The dietary inflammatory potential was assessed by means of an inflammatory score of the diet (ISD), calculated with the use of 28 dietary components and their corresponding inflammatory scores. The association between the ISD and gastric cancer risk was estimated by HRs and 95% CIs calculated by multivariate Cox regression models adjusted for confounders.

    RESULTS: The inflammatory potential of the diet was associated with an increased risk of gastric cancer. The HR (95% CI) for each increase in 1 SD of the ISD were 1.25 (1.12, 1.39) for all gastric cancers, 1.30 (1.06, 1.59) for cardia cancers, and 1.07 (0.89, 1.28) for noncardia cancers. The corresponding values for the highest compared with the lowest quartiles of the ISD were 1.66 (1.26, 2.20), 1.94 (1.14, 3.30), and 1.07 (0.70, 1.70), respectively.

    CONCLUSIONS: Our results suggest that low-grade chronic inflammation induced by the diet may be associated with gastric cancer risk. This pattern seems to be more consistent for gastric carcinomas located in the cardia than for those located in the distal stomach. This study is listed on the ISRCTN registry as ISRCTN12136108.

    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  16. Sanikini H, Muller DC, Sophiea M, Rinaldi S, Agudo A, Duell EJ, et al.
    Int J Cancer, 2020 Feb 15;146(4):929-942.
    PMID: 31050823 DOI: 10.1002/ijc.32386
    Obesity has been associated with upper gastrointestinal cancers; however, there are limited prospective data on associations by subtype/subsite. Obesity can impact hormonal factors, which have been hypothesized to play a role in these cancers. We investigated anthropometric and reproductive factors in relation to esophageal and gastric cancer by subtype and subsite for 476,160 participants from the European Prospective Investigation into Cancer and Nutrition cohort. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models. During a mean follow-up of 14 years, 220 esophageal adenocarcinomas (EA), 195 esophageal squamous cell carcinomas, 243 gastric cardia (GC) and 373 gastric noncardia (GNC) cancers were diagnosed. Body mass index (BMI) was associated with EA in men (BMI ≥30 vs. 18.5-25 kg/m2 : HR = 1.94, 95% CI: 1.25-3.03) and women (HR = 2.66, 95% CI: 1.15-6.19); however, adjustment for waist-to-hip ratio (WHR) attenuated these associations. After mutual adjustment for BMI and HC, respectively, WHR and waist circumference (WC) were associated with EA in men (HR = 3.47, 95% CI: 1.99-6.06 for WHR >0.96 vs. <0.91; HR = 2.67, 95% CI: 1.52-4.72 for WC >98 vs. <90 cm) and women (HR = 4.40, 95% CI: 1.35-14.33 for WHR >0.82 vs. <0.76; HR = 5.67, 95% CI: 1.76-18.26 for WC >84 vs. <74 cm). WHR was also positively associated with GC in women, and WC was positively associated with GC in men. Inverse associations were observed between parity and EA (HR = 0.38, 95% CI: 0.14-0.99; >2 vs. 0) and age at first pregnancy and GNC (HR = 0.54, 95% CI: 0.32-0.91; >26 vs. <22 years); whereas bilateral ovariectomy was positively associated with GNC (HR = 1.87, 95% CI: 1.04-3.36). These findings support a role for hormonal pathways in upper gastrointestinal cancers.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  17. Steffen A, Huerta JM, Weiderpass E, Bueno-de-Mesquita HB, May AM, Siersema PD, et al.
    Int J Cancer, 2015 Aug 01;137(3):646-57.
    PMID: 25598323 DOI: 10.1002/ijc.29432
    General obesity, as reflected by BMI, is an established risk factor for esophageal adenocarcinoma (EAC), a suspected risk factor for gastric cardia adenocarcinoma (GCC) and appears unrelated to gastric non-cardia adenocarcinoma (GNCC). How abdominal obesity, as commonly measured by waist circumference (WC), relates to these cancers remains largely unexplored. Using measured anthropometric data from 391,456 individuals from the European Prospective Investigation into Cancer and Nutrition (EPIC) study and 11 years of follow-up, we comprehensively assessed the association of anthropometric measures with risk of EAC, GCC and GNCC using multivariable proportional hazards regression. One hundred twenty-four incident EAC, 193 GCC and 224 GNCC were accrued. After mutual adjustment, BMI was unrelated to EAC, while WC showed a strong positive association (highest vs. lowest quintile HR = 1.19; 95% CI, 0.63-2.22 and HR = 3.76; 1.72-8.22, respectively). Hip circumference (HC) was inversely related to EAC after controlling for WC, while WC remained positively associated (HR = 0.35; 0.18-0.68, and HR=4.10; 1.94-8.63, respectively). BMI was not associated with GCC or GNCC. WC was related to higher risks of GCC after adjustment for BMI and more strongly after adjustment for HC (highest vs. lowest quintile HR = 1.91; 1.09-3.37, and HR = 2.23; 1.28-3.90, respectively). Our study demonstrates that abdominal, rather than general, obesity is an indisputable risk factor for EAC and also provides evidence for a protective effect of gluteofemoral (subcutaneous) adipose tissue in EAC. Our study further shows that general obesity is not a risk factor for GCC and GNCC, while the role of abdominal obesity in GCC needs further investigation.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  18. Schmidt HM, Ha DM, Taylor EF, Kovach Z, Goh KL, Fock KM, et al.
    J Gastroenterol Hepatol, 2011 Dec;26(12):1725-32.
    PMID: 21649724 DOI: 10.1111/j.1440-1746.2011.06799.x
    BACKGROUND AND AIM: The contribution of human genetic polymorphisms to Helicobacter pylori infection and gastric cancer (GC) development remains unclear due to geographic variation in the association between specific host genetic polymorphisms and GC. In the current study we investigated the association between polymorphisms related to immune and cancer-related pathways and H. pylori infection among the major ethnicities, Chinese, Malay and Indian, resident in Singapore and Malaysia as well as the association between these polymorphisms and GC development in ethnic Chinese patients.

    METHODS: Thirty-four polymorphisms in 26 genes were typed by mass spectrometry in 422 patients undergoing endoscopy (162 Chinese, 113 Indian and 87 Malay controls and 60 Chinese GC cases). Patients were assessed for evidence of H. pylori infection. Odds ratios (OR) and confidence intervals (CI) were obtained using logistic regression models.

    RESULT: The prevalence of 16 polymorphisms varied significantly among the ethnicities. In the Chinese subgroup, nominally significant associations were shown between (i) EBBR2+1963G (rs1801200) and H. pylori infection (per-allele OR: 0.48, 95% CI 0.23, 0.98, P = 0.04), (ii) PTGS2-1195G (rs689466) and an increased risk of GC on adjusting for H. pylori status (OR: 1.53, 95% CI 0.99, 2.37, P = 0.05), and (iii) IL1B-1473C (rs1143623) and a decreased risk of GC (OR: 0.64, 95% CI 0.41, 0.99, P = 0.05). Borderline significant associations were seen between IL2-330G (rs2069762) (OR 1.45, 95% CI 0.95, 2.15, P = 0.06) and IL13-1111T (rs1800925) (OR 0.65, 95% CI 0.42, 1.01, P = 0.06) and H. pylori infection.

    CONCLUSION: These findings contribute to the understanding of the genetic variation between ethnicities, which may influence H. pylori susceptibility and the outcome of infection.

    Matched MeSH terms: Stomach Neoplasms/epidemiology
  19. Nagel G, Stafoggia M, Pedersen M, Andersen ZJ, Galassi C, Munkenast J, et al.
    Int J Cancer, 2018 10 01;143(7):1632-1643.
    PMID: 29696642 DOI: 10.1002/ijc.31564
    Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancers of the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient air pollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-use regression models for particulate matter (PM) below 10 µm (PM10 ), below 2.5 µm (PM2.5 ), between 2.5 and 10 µm (PMcoarse ), PM2.5 absorbance and nitrogen oxides (NO2 and NOX ) as well as approximated by traffic indicators. Cox regression models with adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined with random effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastric cancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5 µg/m3 of PM2.5 was 1.38 (95% CI 0.99; 1.92) for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures considered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influence markedly the effect estimate for PM2.5 and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5 was found in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study shows an association between long-term exposure to PM2.5 and gastric cancer, but not UADT cancers, suggesting that air pollution may contribute to gastric cancer risk.
    Matched MeSH terms: Stomach Neoplasms/epidemiology*
  20. Rajadurai P, Fatt HK, Ching FY
    J Gastrointest Cancer, 2018 Jun;49(2):150-157.
    PMID: 28124769 DOI: 10.1007/s12029-017-9921-1
    PURPOSE: Human epidermal growth factor receptor 2 (Erbb2/HER2) overexpression, which was previously detected in invasive breast cancer, has now been implicated in advanced gastric cancer (GC) and gastroesophageal junction cancer (GEC). A study was conducted to determine the rate of HER2 positivity in patients with locally advanced or metastatic GC and GEC in Malaysia and to assess the impact of various demographic and clinical parameters on HER2 positivity.

    METHODS: A total of 228 adult patients with GC or GEC were enrolled from Subang Jaya Medical Centre, Malaysia, for retrospective (210) and prospective study. All patients were subjected to the HER2 immunohistochemistry test using an FDA-approved, standardized test kit. Carcinomas scoring 2+ on immunohistochemistry were further tested with HER2 in situ hybridization (ISH) using an FDA-approved test kit.

    RESULTS: The overall rate of HER2 positivity in the population studied was 24.6% (n = 56). The rate was significantly higher in men than in women (29.6 vs. 16.3%; p = 0.024). HER2 overexpression was significantly more common in diffuse type than in intestinal type of tumors (39.8 vs. 14.9%; p 

    Matched MeSH terms: Stomach Neoplasms/epidemiology
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