Abstract
Increasing evidence suggests that prostatic inflammation plays a key role in the development of prostate cancer. It remains controversial whether non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of prostate cancer. Here, we investigate how a previously reported inverse association between NSAID use and the risk of aggressive prostate cancer is modulated by variants in several inflammatory genes. We found that NSAIDs may have differential effects on prostate cancer development, depending on one’s genetic makeup. Further study of these inflammatory pathways may clarify the mechanisms through which NSAIDs impact prostate cancer risk.
Highlights
Chronic inflammation has been implicated as a causative factor in a wide range of malignancies, including lung, colorectal, pancreatic, bladder, hepatocellular, and prostatic carcinomas [1]
In order to determine whether genetic variation modulated the effect of non-steroidal anti-inflammatory drugs (NSAIDs) on prostate cancer risk, we focused on SNPs in candidate genes potentially involved with innate immunity and inflammation (e.g., cyclooxygenase-2 (COX-2), toll-like receptor 4 (TLR4), transforming growth factor beta-1 (TGF 1), interleukin-12 subunit beta (IL-12 ), and macrophage scavenger receptor 1 (MSR1))
We investigated the independent associations between theses SNPs and prostate cancer risk; 52 SNPs in 22 of the genes were associated with the risk of aggressive disease irrespective of NSAID use (p-values < 0.05) and so were studied here for their potential interaction with NSAIDs
Summary
Chronic inflammation has been implicated as a causative factor in a wide range of malignancies, including lung, colorectal, pancreatic, bladder, hepatocellular, and prostatic carcinomas [1]. Much research in recent years has focused on the potential chemoprotective effects of non-steroidal anti-inflammatory drugs (NSAIDs) [2]. This group of medications, of which ibuprofen and aspirin (ASA) are the most prominent, act as inhibitors of cyclooxygenase (COX), a key enzyme in the pro-inflammatory pathway. NSAIDs are widely used, both acutely and chronically, for their analgesic, anti-pyretic, and anti-inflammatory effects. The potential cardioprotective effect of aspirin has markedly increased the number of chronic NSAID users in recent years [3,4]
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