Nonaspirin NSAIDs and contralateral breast cancer risk

Bens, Annet; Cronin‐Fenton, Deirdre; Dehlendorff, Christian; Jensen, Maj-Britt; Ejlertsen, Bent; Kroman, Niels; Friis, Søren; Mellemkjær, Lene

doi:10.1002/ijc.31949

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…With the advent of aspirin in the 1990s, the application of NSAIDs has been extended to the treatment of pain, fever, and other inflammatory processes. Multiple studies have addressed the preventative effect of NSAIDs on cancer, leading to reduced incidence of colorectal [277], breast [278], and esophageal cancer [279]. In a randomized clinical trial, daily administration of aspirin effectively prevented adenoma growth in patients with familial adenomatous polyposis [280,281].…”

Section: Non-steroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

Targeting inflammation as cancer therapy

Wang,

Chen,

et al. 2024

J Hematol Oncol

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Inflammation has accompanied human beings since the emergence of wounds and infections. In the past decades, numerous efforts have been undertaken to explore the potential role of inflammation in cancer, from tumor development, invasion, and metastasis to the resistance of tumors to treatment. Inflammation-targeted agents not only demonstrate the potential to suppress cancer development, but also to improve the efficacy of other therapeutic modalities. In this review, we describe the highly dynamic and complex inflammatory tumor microenvironment, with discussion on key inflammation mediators in cancer including inflammatory cells, inflammatory cytokines, and their downstream intracellular pathways. In addition, we especially address the role of inflammation in cancer development and highlight the action mechanisms of inflammation-targeted therapies in antitumor response. Finally, we summarize the results from both preclinical and clinical studies up to date to illustrate the translation potential of inflammation-targeted therapies.

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Section: Non-steroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

Targeting inflammation as cancer therapy

Wang,

Chen,

et al. 2024

J Hematol Oncol

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“…The effect of aspirin and other NSAID use on CBC risk has been studied in two Danish cohort studies (Table 3 and Figure 1). Among 52,723 breast cancer patients, HRs for CBC of 0.91 (95% CI: 0.76-1.09) and 0.98 (95% CI: 0.87-1.11) were observed for low-dose aspirin (75-150 mg) and non-aspirin NSAID use, respectively [65,66]. The ongoing Add-Aspirin trial (NCT02804815), assessing the efficacy of adjuvant aspirin (100 mg or 300 mg versus placebo) in breast cancer patients, may provide further understanding of the potential of aspirin in prevention of CBC among breast cancer survivors.…”

Section: Non-steroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

Preventive drug therapy and contralateral breast cancer: summary of the evidence of clinical trials and observational studies

et al. 2019

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Background: Breast cancer patients have a lifelong 2-4-fold increased risk of developing a second primary tumor in the contralateral breast compared with the risk for a first primary breast cancer in the general female population. Prevention of contralateral breast cancer (CBC) has received increased attention during recent decades. Here, we summarize and discuss the available literature on drug preventive therapy and CBC. Results: The endocrine-targetting drugs, tamoxifen and aromatase inhibitors are used as standard adjuvant treatment for estrogen receptor (ER)-positive breast cancer. Both are associated with relative risk reductions of CBC of up to 50%, but incur serious side effects. Several prescription drugs originally developed for other purposes, including bisphosphonates, statins, non-steroidal anti-inflammatory drugs, metformin, anti-hypertensives and retinoids, have shown anti-cancer activity in preclinical models. However, results of observational studies on CBC are sparse and inconsistent, with only statins demonstrating promise as preventive agents and a potential treatment option for ER-negative breast cancer patients. Conclusion: Future studies are needed to assess the effect of statins in risk reduction and to identify other drugs with chemopreventive potential against CBC. Eventually, efforts must be directed towards identifying those breast cancer patients likely to benefit most from specific preventive therapies.

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“…It has been reported that people who regularly take aspirin or other non-steroidal anti-inflammatory drugs have a lower risk of colon cancer, gastric cancer, esophageal cancer, lung cancer and breast malignancy [4][5][6][7]. Non-steroidal anti-inflammatory medications suppress the synthesis of prostaglandin and block prostaglandin-induced immunosuppression to enhance immune responses and induce cell apoptosis [8]. The purpose of this study was to explore the influences of aspirin on the proliferation and apoptosis of gastric cancer cells through the interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3) signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Aspirin inhibits proliferation of gastric cancer cells via IL 6/STAT3 signaling pathway

Tang¹,

Liu²,

Liu³

et al. 2022

Trop. J. Pharm Res

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Purpose: To study the effect of aspirin on the proliferation and apoptosis of gastric cancer cells, and its key molecular mechanism of action. Methods: Gastric cancer SGC7901 cells were treated with aspirin at concentrations of 0, 1, 2 and 4 mmol/L. Cell proliferation was measured using cell counting kit (CCK)-8 assay, while messenger ribonucleic acid (mRNA) expressions of interleukin (IL)-6, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were assessed by reverse transcription-polymerase chain reaction (RT-PCR). Cell apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Furthermore, the protein expression levels of the signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 (p-STAT3), Bcl-2 and Bax were evaluated by Western blotting. Results: Compared with control group, 1, 2 and 4 mmol/L aspirin groups showed lower cell proliferation, and decreased mRNA expressions of Bcl-2 and Bax and IL-6 release at 24, 48 and 72 h (p < 0.05). Cell apoptosis in the aspirin groups was higher than in the control group. Also, compared with the control group, 1 mmol/L aspirin group did not exhibit significant changes in the expressions of STAT3 and p-STAT3 at 72 h. On the other hand, the 2 mmol/L aspirin group at 72 h and the 4 mmol/L aspirin group exhibited significant increases in the expressions of STAT3 and p-STAT3 (p < 0.05). Furthermore, the levels of Bcl-2 and Bax declined in the aspirin groups when compared with the control group (p < 0.05). Conclusion: Aspirin inhibits the proliferation of gastric cancer SGC7901 cells, and induces their apoptosis in vitro in IL-6/STAT3 signaling pathway. The results of the current study may provide new insight into the treatment of gastric cancer.

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Nonaspirin NSAIDs and contralateral breast cancer risk

Cited by 8 publications

References 24 publications

Targeting inflammation as cancer therapy

Targeting inflammation as cancer therapy

Preventive drug therapy and contralateral breast cancer: summary of the evidence of clinical trials and observational studies

Aspirin inhibits proliferation of gastric cancer cells via IL 6/STAT3 signaling pathway

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