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Fulltext Helicobacter pylori infection--a boon or a bane: lessons from studies in a low-prevalence population

Lee YY, Mahendra Raj S, Graham DY

Helicobacter, 2013 Oct;18(5):338-46.
PMID: 23607896 DOI: 10.1111/hel.12058

Helicobacter pylori (H. pylori) infection is etiologically associated with gastric cancer and peptic ulcer diseases which are both important public health burdens which could be largely eliminated by H. pylori eradication. However, some investigators urge caution based on the hypothesis that eradication of H. pylori may result in an increase in the incidence of gastroesophageal reflux disease, esophageal adenocarcinoma, and childhood asthma. The ethnic Malays of northeastern Peninsular Malaysia have long had a low prevalence of H. pylori infection and, as expected, the incidence of gastric cancer and its precursor lesions is exceptionally low. The availability of a population with a low H. pylori prevalence and generally poor sanitation allows separation of H. pylori from the hygiene hypothesis and direct testing of whether absence of H. pylori is associated with untoward consequence. Contrary to predictions, in Malays, erosive esophagitis, Barrett's esophagus, distal esophageal cancers, and childhood asthma are all of low incidence. This suggests that H. pylori is not protective rather the presence of H. pylori infection is likely a surrogate for poor hygiene and not an important source of antigens involved in the hygiene hypothesis. Helicobacter pylori in Malays is related to transmission from H. pylori-infected non-Malay immigrants. The factors responsible for low H. pylori acquisition, transmission, and burden of H. pylori infection in Malays remain unclear and likely involves a combination of environmental, host (gene polymorphisms), and strain virulence factors. Based on evidence from this population, absence of H. pylori infection is more likely to be boon than a bane.

Matched MeSH terms: Stomach Neoplasms/etiology*
Pathogenesis and treatment of gastric carcinoma: "an up-date with brief review"

Khan FA, Shukla AN

J Cancer Res Ther, 2007 11 14;2(4):196-9.
PMID: 17998703

Gastric cancer is one of the most common cancers and most frequent causes of cancer-related deaths in the world. The overall survival rate is 15-20%. Although the incidence is declining, its prognosis remains poor. The etiological factors and pathogenesis of gastric cancer are not yet fully understood. The integrated research in molecular pathology clarified the details of genetic and epigenetic abnormalities of cancer-related genes in the course of development and progression of gastric cancer. Although epidemiological evidences indicate that environmental factors play a major role in the carcinogenesis, the role of immunological, genetic and immunogenetic factors are thought to contribute to etiopathogenesis of gastric carcinoma. In addition to better understanding of pathogenesis of gastric cancer, the incidence, diagnostic studies and the therapeutic options have also undergone important changes in the last decade. There is ongoing debate regarding the role of adjuvant treatment. In advanced disease, palliation of symptoms, rather than cure, is the primary goal of patient management. Several combination therapies have been developed and have been examined in phase III trials; however, in most cases, they have failed to demonstrate a survival advantage over the reference arm. This review summarizes the newer concepts of molecular biology on gastric carcinogenesis and the new important recommendations for the management of patient with gastric carcinoma.

Matched MeSH terms: Stomach Neoplasms/etiology*
Tobacco chewing and risk of gastric cancer: a case-control study in Yemen

Al-Qadasi FA, Shah SA, Ghazi HF

East Mediterr Health J, 2017 Jan 23;22(10):719-726.
PMID: 28134423

This study aimed to assess the risk factors for gastric cancer in Yemen. A hospital-based case-control study of 70 cases and 140 controls was carried out in Sana'a city between May and October 2014. A structured questionnaire was used to collect information through direct interview. Living in rural areas, tobacco chewing and drinking untreated water were significant risk factors for gastric cancer. Frequent consumption of chicken, cheese, milk, starchy vegetables, cucumber, carrots, leeks, sweet pepper, fruit drinks, legumes and olive oil were associated significantly with decreased risk of gastric cancer. Multiple logistic regression analysis showed that chewing tobacco and frequent consumption of white bread were associated with increased risk of gastric cancer, whereas frequent consumption of chicken, cooked potatoes and fruit drinks had an inverse association. Risk of gastric cancer can be prevented by health education and increasing community awareness.

Matched MeSH terms: Stomach Neoplasms/etiology*
Fulltext Inflammatory potential of the diet and risk of gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

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/etiology*
Fulltext General and abdominal obesity and risk of esophageal and gastric adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition

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/etiology*
Fulltext Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE)

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/etiology
Leptin enhances N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced tumour growth in gastric mucosa of male Sprague-Dawley rats

Isyraqiah F, Kutty MK, Durairajanayagam D, Singh HJ

Mol Biol Rep, 2019 Dec;46(6):5967-5975.
PMID: 31444698 DOI: 10.1007/s11033-019-05030-z

Individuals who are obese are at a greater risk of developing gastric cancer. They are however also hyperleptinaemic. Chronic leptin treatment has been shown to upregulate numerous cancer-causing genes in the stomach of male Sprague-Dawley rats. It is however unclear if leptin enhances the effect of gastric carcinogens in vivo. This study was therefore done to investigate the effect of leptin on gastric carcinogenesis in rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Twenty-four, 6-week old male Sprague-Dawley rats were divided equally into three groups: G1 served as age-matched controls; G2 was treated with MNNG in drinking water ad libitum (200 mg L-1); G3 was given leptin and MNNG. Rats were euthanized after 40 weeks of treatment and their stomachs were removed for histopathology, microarray, and RT-qPCR analysis. Fisher's exact test and one-way ANOVA were used to analyse the data. Fifty percent of the MNNG-treated rats developed gastric hyperplasia (p stomachs of Sprague-Dawley rats and its role in gastric cancer requires further scrutiny.

Matched MeSH terms: Stomach Neoplasms/etiology*
Fulltext The NOD-like receptor signalling pathway in Helicobacter pylori infection and related gastric cancer: a case-control study and gene expression analyses

Castaño-Rodríguez N, Kaakoush NO, Goh KL, Fock KM, Mitchell HM

PLoS One, 2014;9(6):e98899.
PMID: 24901306 DOI: 10.1371/journal.pone.0098899

Currently, it is well established that cancer arises in chronically inflamed tissue. A number of NOD-like receptors (NLRs) form inflammasomes, intracellular multiprotein complexes critical for generating mature pro-inflammatory cytokines (IL-1β and IL-18). As chronic inflammation of the gastric mucosa is a consequence of Helicobacter pylori infection, we investigated the role of genetic polymorphisms and expression of genes involved in the NLR signalling pathway in H. pylori infection and related gastric cancer (GC).

Matched MeSH terms: Stomach Neoplasms/etiology*
Chronic atrophic antral gastritis and risk of metaplasia and dysplasia in an area with low prevalence of Helicobacter pylori

Yeh LY, Raj M, Hassan S, Aziz SA, Othman NH, Mutum SS, et al.

Indian J Gastroenterol, 2009 08 21;28(2):49-52.
PMID: 19696988 DOI: 10.1007/s12664-009-0017-0

INTRODUCTION: The Northeastern region of Peninsular Malaysia is an area with exceptionally low prevalence for Helicobacter pylori infection. The risk of intestinal metaplasia and dysplasia in patients with chronic atrophic gastritis (CAG) and its association with Helicobacter pylori is unknown in this region.
METHODS: This was a cross-sectional study on gastric biopsies from 234 consecutive patients (mean age 53.5 [14.8] years) who underwent upper gastrointestinal endoscopy between January 2006 and December 2006.
RESULTS: There were 137 (59%) men and 185 (79%) Malay patients. Among 234 biopsies, CAG was found in 99 and non-atrophic gastritis in 135. Intestinal metaplasia and dysplasia were detected in 8 and 6 atrophic gastritis biopsies, respectively, and in 10 and 3 of non-atrophic gastritis biopsies, respectively. H. pylori were detected in 16 (9 Malays, 7 non- Malays) biopsies (p=0.024); intestinal metaplasia was detected in 4 biopsies (p=0.3) and dysplasia in 5 biopsies (p=0.3). Of the 218 biopsies negative for H. pylori, intestinal metaplasia was found in 14 and dysplasia in 4. The risk of intestinal metaplasia as well as dysplasia was associated with presence of H. pylori infection (p=0.029 and p<0.001 respectively).
CONCLUSION: Even in a setting of low prevalence of H. pylori, intestinal metaplasia and dysplasia were significantly associated with H. pylori infection. The frequency of intestinal metaplasia and dysplasia was similar different between biopsies with atrophic gastritis and non-atrophic gastritis.

Matched MeSH terms: Stomach Neoplasms/etiology*