“Recently published secondary analyses of cardiovascular trials provide the first randomized evidence that daily aspirin use may also reduce the incidence of all cancers combined, even at low doses (75-100 mg daily)”

“10% reduction in overall cancer incidence beginning during the first 10 years of treatment could tip the balance of benefits and risks favourably in average-risk populations.”

"This Review considers the general mechanism of action that defines aspirin and other non-steroidal anti inflammtory drugs (NSAIDs) as a class, the specific advantages of aspirin over other NSAIDs for prophylactic use, the current evidence concerning the main health outcomes affected by aspirin use, and the hypothesis that inhibition of platelet activiation may mediate both the cardioprotective and cancer preventive effects of low-dose aspirin."

"Our baseline results are in line with earlier studies, which have shown an association between glycemic control and urinary 11-DHTXB₂ excretion. In addition, improving glycemic control has been shown to lead to a decreased 11-DHTXB₂ excretion."

"In the present study, the difference in urinary 11-DHTXB₂ excretion was also influenced by C-reactive protein levels, which were different between the study groups and may reflect the influence of the inflammatory state found in diabetes on thromboxane formation."

"There is increasing appreciation of the role of platelets in tumor growth and metastatic dissemination (Gay and Felding-Habermann, 2011). Platelet activiation can lead to the release of growth and angiogenesis factors present in a-granules into the tumor microenvironment. (Italiano et al., 2008).  Moreover, platelets and the factors they release can up-regulate cyclooxygenase (COX)-2 which is considered an early event of cell transformation (Patrono et al., 2001). In colorectal cancer, COX-2 expression is induced early in stromal cells and subsequently at high levels in epithelial cells (Prescott, 2000), where it correlates with advanced tumor invasion and poor clinical outcomes (Sheehan et al., 1999)."

"Intestinal tumorigenesis was associated with enhanced urinary TX-M levels, but unaffected by celecoxib, suggesting the involvement of a COX-1-dependent pathway, presumably from platelets."

"Inflammation is a major cause of cancer and may condition its progression.  The deregulation of the cyclooxygenase (COX) pathway is implicated in several pathophysiological processes, including inflammation and cancer.  Although, its targeting with nonsteroidal antiinflammatory drugs (NSAIDs) and COX-2 selective inhibitors has been investigated for years with promising results at both preventive and and therapeutic levels, undesirable side effects and the limited understanding of the regulation and functionalities of the COX pathway compromise a more extensive application of these drugs.  Epigenetics is bringing additional levels of complexity to the understanding of basic biological and pathological processes.  The deregulation of signaling and biosynthetic pathways by epigenetic mechanisms may account for new molecular targets in cancer therapeutics.  Genes of the COX pathway are seldom mutated in neoplastic cells, but a large proportion of them show aberrant expression in different types of cancer.  A growing body of evidence indicates that epignetic alterations play a critical role in the deregulation of the genes of the COX pathway.  This review summarizes the current knowledge on the contribution of epignetic processes to the deregulation of the COX pathway in cancer, getting insights into how these alterations may be relevant for the clinical management of patients."

"Residual TX production, as revealed by different methods, may derive from COX-1 or COX-2.”

"Extra-platelet sources may contribute to aspirin-insensitive TX generation: monocytes/macrophages and vascular endothelial cells express COX-2 in response to inflammatory stimuli, and the up regulation of COX-2 activity may account for a TX biosynthesis not sensitive to once daily low-dose aspirin."

"Cardiovascular disease (CVD) risk can be underestimated in HIV-infected patients receiving antiretroviral therapy (ART). Novel CVD risk markers in this population are needed.  We hypothesized that eicosanoid metabolite production is increased with metabolic complications of ART.  Our objective was to determine relationships between urine eicosanoids and traditional CVD risk factors in a cohort of HIV-infected persons receiving ART."

"In this pilot study of predominantly virologically suppressed HIV-infected individuals on ART, there were sex-specific differences in urinary eicosanoids, with females having more risk-associated parameters despite low Framingham score.  Eicosanoids might be useful CVD biomarkers in ART-treated, HIV-infected patients."

“Studies consistently report that groups of individuals with major depressive disorder (MDD) demonstrate increased levels of a variety of peripheral inflammatory biomarkers when compared with groups of nondepressed individuals."

 “Two randomized, placebo-controlled studies have reported that the addition of an inhibitor of the cyclooxygenase enzyme to a standard antidepressant enhances symptomatic improvement in medically healthy individuals with depression.  Similarly, preclinical and clinical data suggest that acetylsalicylic acid (aspirin) may hold promise as an augmenting strategy in patients who fail to respond to monotherapy with a serotonin reuptake inhibitor."

“Increased cyclooxygenase (COX)-2 expression has been described in a variety of human cancers, which has focused attention on TXA₂ as a downstream metabolite of the COX-2-derived PGH2.”

“It is a great importance to further determine whether and how prostanoids, such as TXA_2, mediate the effects of COX-2 in cancer, potentially leading to a more targeted approach for cancer prevention and treatment."

Cigarette smoking is a major cause of mortality and morbidity worldwide.  Cyclooxygenase (COX and its derived prostanoids, mainly including prostaglandin E2 (PGE2), thromboxane A₂ (TXA₂) and prostacyclin (PGI2), have well-known roles in cardiovascular disease and cancer, both of which are associated with cigarette smoking.  This article is focused on the role of the COX-2 pathway in smoke-related pathologies and cancer."

"Cigarette smoke exposure can induce COX-2 expression and activity, increase PGE2 and TxA₂ release, and lead to an imbalance in PGI2 and TxA₂ production in favor of the latter."

"Thromboxane synthase (TXS) metabolizes prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS over-expression has been reported in a range of cancers, and associated with a poor prognosis. TXS inhibition induces cell death in-vitro, providing a rationale for therapeutic intervention.  We aimed to determine the expression profile of TXS in NSCLC and if it is prognostic and/or a survival factor in the disease."

“Measurement of TXB₂ levels in human plasma would be indicative of circulating levels in the blood. Thromboxane B₂ levels were found to be significantly (p<0.01) higher in plasma samples taken from patients with NSCLC, relative to age-matched controls (3307 ± 189 pg/mL versus 2201 ± 317 pg/mL); n= 49 NSCLC patients, 19 cancer-free controls."