Effect of aspirin and NSAIDs on risk and survival from colorectal cancer

Din, Farhat V N; Τheodoratou, Evropi; Farrington, Susan M.; Tenesa, Albert; Barnetson, Rebecca A.; Cetnarskyj, Roseanne; Stark, Lesley A.; Porteous, Mary; Campbell, Harry; Dunlop, Malcolm G.

doi:10.1136/gut.2009.203000

Cited by 252 publications

(203 citation statements)

References 82 publications

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“…These data support a rational DPT approach for treating OC that embodies a therapy that targets specifically nonproliferating cancer cells in combination with a drug regimen that is operational on cells in the proliferative stage of the disease. Although many studies have looked at the role of NSAIDs in cancer therapy, the majority of these have focused on COX inhibition as a mechanism of action for these drugs (21)(22)(23). Decreased sensitivity to chemotherapy and poor prognostic outcome has been associated with ovarian carcinomas expressing COX-2 (24).…”

Section: Discussionmentioning

confidence: 99%

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NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

et al. 2012

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Ovarian cancer (OC) is one of the most lethal gynaecological cancers, which usually has a poor prognosis due to late diagnosis. A large percentage of the OC cell population is in a nonproliferating and quiescent stage, which poses a barrier to success when using most chemotherapeutic agents. Recent studies have shown that several nonsteroidal anti‐inflammatory drugs (NSAIDs) are effective in the treatment of OC. Furthermore, we have previously described the molecular mechanisms of NSAIDs' induction of cancer apoptosis. In this report, we evaluated various structurally distinct NSAIDs for their efficacies in inducing apoptosis in nonproliferating OC cells. Although several NSAIDs‐induced apoptosis, Flufenamic Acid, Flurbiprofen, Finasteride, Celocoxib, and Ibuprofen were the most potent NSAIDs inducing apoptosis. A combination of these agents resulted in an enhanced effect. Furthermore, we demonstrate that the combination of Flurbiprofen, which targets nonproliferative cells, and Sulindac Sulfide, that affects proliferative cells, strongly reduced tumor growth when compared with a single agent treatment. Our data strongly support the hypothesis that drug treatment regimens that target nonproliferating and proliferating cells may have significant efficacy against OC. These results also provide a rationale for employing compounds or even chemically modified NSAIDs, which selectively and efficiently induce apoptosis in cells during different stages of the cell cycle, to design more potent anticancer drugs. © 2012 IUBMB IUBMB Life, 64(7): 636–643, 2012

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Section: Discussionmentioning

confidence: 99%

“…NSAIDs have been evaluated as therapies in different types of cancer (23,34,35) and have been shown to have a synergistic effect with known chemotherapeutic agents (31)(32)(33)(36)(37)(38). However, none of these studies have looked specifically at NSAIDs effects on nonproliferating cells.…”

Section: Discussionmentioning

confidence: 99%

NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

et al. 2012

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“…In this context, it has been demonstrated that an inhibition of COX enzymes by non-steroid antiinflammatory drugs or aspirin can reduce the risk of Wnt/ -catenin dependent colorectal cancers significantly [460]. Furthermore, it was shown that Rp-8-Br-cAMP (Table 1), a small molecule inhibitor of PKA, reduces the translocation of -catenin to the nucleus and reduces the expression of Wnt/ -catenin target genes [461].…”

Section: Cross-talk With Other Pathways: Interconnections Between Infmentioning

confidence: 99%

Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

Voronkov¹,

Krauß²

2012

CPD

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Wnt/ -catenin signaling is a branch of a functional network that dates back to the first metazoans and it is involved in a broad range of biological systems including stem cells, embryonic development and adult organs. Deregulation of components involved in Wnt/ -catenin signaling has been implicated in a wide spectrum of diseases including a number of cancers and degenerative diseases. The key mediator of Wnt signaling, -catenin, serves several cellular functions. It functions in a dynamic mode at multiple cellular locations, including the plasma membrane, where -catenin contributes to the stabilization of intercellular adhesive complexes, the cytoplasm where -catenin levels are regulated and the nucleus where -catenin is involved in transcriptional regulation and chromatin interactions. Central effectors of -catenin levels are a family of cysteine-rich secreted glycoproteins, known as Wnt morphogens. Through the LRP5/6-Frizzled receptor complex, Wnts regulate the location and activity of the destruction complex and consequently intracellularcatenin levels. However, -catenin levels and their effects on transcriptional programs are also influenced by multiple other factors including hypoxia, inflammation, hepatocyte growth factor-mediated signaling, and the cell adhesion molecule E-cadherin. The broad implications of Wnt/ -catenin signaling in development, in the adult body and in disease render the pathway a prime target for pharmacological research and development. The intricate regulation of -catenin at its various locations provides alternative points for therapeutic interventions.

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“…It has been indicated to reduce the risk of cancers, including bladder cancer (1), breast cancer (2), glioma (3), and particularly colorectal cancer (4,5). Although the considerable evidence demonstrating that aspirin prevents cancer progression is compelling, the underlying molecular mechanism remains enigmatic.…”

Section: Introductionmentioning

confidence: 99%

Aspirin may inhibit angiogenesis and induce autophagy by inhibiting mTOR signaling pathway in murine hepatocarcinoma and sarcoma models

Zhao¹,

Zhao-peng

et al. 2016

Oncology Letters

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Effect of aspirin and NSAIDs on risk and survival from colorectal cancer

Abstract: This is the first study to demonstrate a protective effect against CRC associated with the lowest dose of aspirin (75 mg per day) after only 5 years use in the general population. NSAID use prior to CRC diagnosis does not influence survival from the disease.

Cited by 252 publications

References 82 publications

NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

NSAIDs induce apoptosis in nonproliferating ovarian cancer cells and inhibit tumor growth in vivo

Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

Aspirin may inhibit angiogenesis and induce autophagy by inhibiting mTOR signaling pathway in murine hepatocarcinoma and sarcoma models

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