Serum pepsinogen level, atrophic gastritis and the risk of incident pancreatic cancer—A prospective cohort study

Laiyemo, Adeyinka O.; Kamangar, Farin; Taylor, Philip R.; Virtamo, Jarmo; Albanês, Demetrius

doi:10.1016/j.canep.2009.09.001

Cited by 8 publications

(13 citation statements)

References 25 publications

(19 reference statements)

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“…In a Finnish study on male smokers, the authors found that neither low pepsinogen level nor histologically confirmed atrophic gastritis was associated with subsequent pancreatic cancer risk. 37 However, in our study, we found a significant positive association between chronic corpus atrophic gastritis and pancreatic cancer in the stratum seronegative for both H. pylori and CagA, but not in the stratum seropositive for H. pylori or CagA. Given the very small number of study subjects in the seronegative stratum (only three controls with chronic corpus atrophic gastritis), caution is needed in interpreting this finding.…”

Section: Discussioncontrasting

confidence: 69%

“…Few studies have directly examined the association between chronic corpus atrophic gastritis and pancreatic cancer risk. In a Finnish study on male smokers, the authors found that neither low pepsinogen level nor histologically confirmed atrophic gastritis was associated with subsequent pancreatic cancer risk . However, in our study, we found a significant positive association between chronic corpus atrophic gastritis and pancreatic cancer in the stratum seronegative for both H. pylori and CagA, but not in the stratum seropositive for H. pylori or CagA.…”

Section: Discussionmentioning

confidence: 99%

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Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case‐control study

Huang

Zagai

Hallmans

et al. 2017

Intl Journal of Cancer

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The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR=0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR=1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR=0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR=1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR=5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.

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Section: Discussioncontrasting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case‐control study

Huang

Zagai

Hallmans

et al. 2017

Intl Journal of Cancer

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“…Two cohort studies and 1 nested case–control study investigated the associations of AG status with pancreatic cancer risk, and 31,364 observations were analyzed (Tables 2 , 3 ). [ 27 , 28 , 30 ] As a whole, the AG status was not associated with pancreatic cancer risk (OR = 1.18, 95% CI 0.80–1.72, P = .40) (Fig. 4 A).…”

Section: Resultsmentioning

confidence: 91%

“…Therefore, it was hypothesized that the causative factors of AG might lead to pancreatic cancer development, or biomarkers of AG might also predict pancreatic cancer risk. [ 30 ] Nevertheless, to date, the epidemiologic evidence is still sparse to clarify the linkage of pancreatic cancer to AG and its biomarkers. Particularly, 2 population-based cohort studies did not support the hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori infection, atrophic gastritis, and pancreatic cancer risk

Liu¹,

Chen

Wang³

et al. 2017

Medicine

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Background:To investigate the associations of Helicobacter pylori (Hp) infection and atrophic gastritis (AG) with pancreatic cancer risk.Methods:A literature search in PubMed was performed up to July 2017. Only prospective cohort and nested case–control studies enrolling cancer-free participants were eligible. Incident pancreatic cancer cases were ascertained during the follow-up. The risks of pancreatic cancer were compared between persons infected and noninfected with Hp, or between those with and without AG status at baseline. Odds ratios (ORs) or hazard ratios were combined. Subgroup and sensitivity analyses were performed, and publication bias was estimated.Results:Three cohort studies and 6 nested case–control studies, including 65,155 observations, were analyzed. The meta-analyses did not confirm the association between pancreatic cancer risk and Hp infection (OR = 1.09, 95% confidence interval [CI] = 0.81–1.47) or AG status (OR = 1.18, 95% CI = 0.80–1.72). However, particular subpopulations potentially had increased risks of pancreatic cancer. Cytotoxin-associated gene A (CagA)-negative strains of Hp might be a causative factor of pancreatic cancer (OR = 1.30, 95% CI = 1.05–1.62), but a sensitivity analysis by leave-one-out method did not fully warrant it (OR = 1.20, 95% CI = 0.93–1.56). In 1 nested case–control study, AG at stomach corpus in Hp-negative subpopulation might have increased risk of pancreatic cancer, but with a poor test power = 0.56. Publication biases were nonsignificant in the present meta-analysis.Conclusion:Based on current prospective epidemiologic studies, the linkage of pancreatic cancer to Hp infection or AG status was not warranted on the whole. Nevertheless, prospective studies only focusing on those specific subpopulations are further required to obtain better power.

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“…Serum pepsinogen I (PGI) is a serologic marker of gastric atrophy. PGI was measured using a radioimmunoassay, as previously described (24), and subjects with PGI < 25μg/l were defined as having gastric atrophy (24, 25). PGI measurements were available for only 218 cases, 310 controls, and 206 matched sets.…”

Section: Methodsmentioning

confidence: 99%

Iron in Relation to Gastric Cancer in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study

Cook

Kamangar

Weinstein

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background Iron is an essential micronutrient that can have carcinogenic effects when at high or low concentrations. Previous studies of iron in relation to gastric cancer have not assessed subtype-specific relationships. We used the prospective ATBC Cancer Prevention Study to assess whether iron metrics were associated with gastric cardia cancer (GCC) and gastric noncardia cancer (GNCC). Methods We selected 341 incident gastric cancer cases (86 cardia, 172 noncardia, and 83 non-specified), accrued during 22 years of follow-up, and 341 individually matched controls. We measured prediagnostic serum iron, ferritin, unsaturated iron binding capacity (UIBC), and C-reactive protein. Total iron binding capacity (TIBC) and transferrin saturation were estimated from these metrics. Dietary iron exposures were estimated from a food frequency questionnaire. Multivariable logistic regression was used for analysis. Results Serum iron metrics were not associated with GCC, except for a potential ‘n’-shaped relationship with TIBC (global p=0.038). GNCC was inversely associated with serum ferritin (global p=0.024), serum iron (global p=0.060) and, possibly, transferrin saturation. TIBC appeared to share a ‘u’shaped relationship with GNCC (global p=0.033). Dietary iron exposures were not associated with either subsite. Adjustment for Helicobacter pylori and gastric atrophy had little effect on observed associations. Conclusions We found little evidence for the involvement of iron exposure in the pathogenesis of GCC. GNCC was associated with an iron profile similar to that of iron deficiency.

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Serum pepsinogen level, atrophic gastritis and the risk of incident pancreatic cancer—A prospective cohort study

Cited by 8 publications

References 25 publications

Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case‐control study

Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case‐control study

Helicobacter pylori infection, atrophic gastritis, and pancreatic cancer risk

Iron in Relation to Gastric Cancer in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study

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