Patrick Maisonneuve, Albert B Lowenfels
Journal: International journal of epidemiology 2015;44(1):186-98
PMID: 25502106
Pancreatic cancer (PC) is one of the four or five most common causes of cancer mortality in developed countries. The aim of this review was to summarize results from pooled analyses and meta-analyses to estimate the fraction of PCs attributable to many different risk factors. A comprehensive review of the literature was carried out by searching for meta-analytical studies on the association between specific risk factors and PC risk or multiple cancer sites. Results indicate that PC has a multifactorial aetiology. All identified factors can be combined into a specific aetiological (the philosophy or study of causation) pathway for PC. The main pathways include insulin resistance (central adiposity, diabetes, metabolic syndrome), inflammation (tobacco, alcohol, pancreatitis), DNA damage (tobacco, red meat) and haemostasis (blood group, history of thrombosis). Authors conclude that about two-thirds of the major risk factors associated with PC are potentially modifiable, affording a unique opportunity for preventing one of our deadliest cancers.
BACKGROUND
The aetiology of pancreatic cancer (PC) has been extensively studied and is the subject of numerous meta-analyses and pooled analyses. We have summarized results from these pooled and meta-analytical studies to estimate the fraction of PCs attributable to each of the identified risk factors.
METHODS
Using a comprehensive strategy, we retrieved 117 meta-analytical or pooled reports dealing with the association between specific risk factors and PC risk. We combined estimates of relative risk and estimates of exposure to calculate the fraction of PCs caused or prevented by a particular exposure.
RESULTS
Tobacco smoking ('strong' evidence) and Helicobacter pylori infection ('moderate' evidence) are the major risk factors associated with PC, with respective estimated population attributable fractions of 11-32% and 4-25%. The major protective factors are history of allergy ('strong' evidence) and increasing fruit or folate intake ('moderate' evidence), with respective population preventable fractions of 3-7% and 0-12%.
CONCLUSIONS
We summarized results of 117 meta-analytical or pooled data reports dealing with 37 aetiological exposures, to obtain robust information about the suspected causes of PC. By combining these estimates with their prevalences in the population, we calculated population attributable or population preventable fractions. About two-thirds of the major risk factors associated with PC are potentially modifiable, affording a unique opportunity for preventing one of our deadliest cancers.
© The Author 2014; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
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