The aim of this study was to analyze the association between aspirin intake and its effect for chemoprevention of pancreatic cancer incidence by using a meta-analysis method.
The databases of MEDLINE, EMBASE, and Wangfang (Chinese database) were retrieved to identify eligible studies. Odds ratio (OR) and 95% confidence interval (CI) were calculated using a random-effects model.
A total of 10 studies (4 case-control studies, 5 prospective cohort studies, and 1 randomized controlled trial) with 7,252 cases of pancreatic cancer and more than 120,0000 healthy control subjects were enrolled in the studies. Pooled analyses showed that high-dose aspirin intake was marginally associated with decreased risk for pancreatic cancer for overall analysis (OR, 0.88; 95% CI, 0.76-1.01) as well as for both cohort and case-control studies (OR, 0.70; 95% CI, 0.54-1.16, for the cohort studies; OR, 0.82; 95% CI, 0.62-1.02, for the case-control studies), without between-study heterogeneity. Stratified analysis for Americans showed a similar result (OR, 0.82; 95% CI, 0.65-1.02). In contrast, our study inferred that low-dose aspirin intake was not associated with risk for pancreatic cancer for the total and subgroup analyses.
In summary, our study indicated that high-dose aspirin, rather than low-dose aspirin, might be associated with decreased risk for pancreatic cancer, especially for Americans.
[Show abstract][Hide abstract] ABSTRACT: Pancreatic cancer is one of the most lethal cancers worldwide. No effective screening methods exist, and available treatment modalities do not effectively treat the disease. Inflammatory conditions such as pancreatitis represent a well-known risk factor for pancreatic cancer development. Yet only in the past 2 decades has pancreatic cancer been recognized as an inflammation-driven cancer, and the precise mechanisms underlying the pathogenic role of inflammation are beginning to be explored in detail. A substantial amount of preclinical and clinical evidence suggests that bacteria are likely to influence this process by activating immune receptors and perpetuating cancer-associated inflammation. The recent explosion of investigations of the human microbiome have highlighted how perturbations of commensal bacterial populations can promote inflammation and promote disease processes, including carcinogenesis. The elucidation of the interplay between inflammation and microbiome in the context of pancreatic carcinogenesis will provide novel targets for intervention to prevent and treat pancreatic cancer more efficiently. Further studies toward this direction are urgently needed.
The Cancer Journal 05/2014; 20(3):195-202. DOI:10.1097/PPO.0000000000000045 · 4.24 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The pancreas plays a central role in metabolism, allowing ingested food to be converted and used as fuel by the cells throughout the body. On the other hand, the pancreas may be affected by devastating diseases, such as pancreatitis, pancreatic adenocarcinoma (PAC), and diabetes mellitus (DM), which generally results in a wide metabolic imbalance. The causes for the development and progression of these diseases are still controversial; therefore it is essential to better understand the underlying mechanisms which compromise the pancreatic homeostasis. The interest in the study of the commensal microbiome increased extensively in recent years, when many discoveries have illustrated its central role in both human physiology and maintenance of homeostasis. Further understanding of the involvement of the microbiome during the development of pathological conditions is critical for the improvement of new diagnostic and therapeutic approaches. In the present review, we discuss recent findings on the behavior and functions played by the microbiota in major pancreatic diseases and provide further insights into its potential roles in the maintenance of pancreatic steady-state activities.
Journal of Diabetes Research 08/2015; 2015(1). DOI:10.1155/2015/284680 · 2.16 Impact Factor
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