Association of Frequency and Duration of Aspirin Use and Hormone Receptor Status With Breast Cancer Risk

Terry, Mary Beth; Gammon, Marilie D.; Zhang, Fang Fang; Tawfik, Heba; Teitelbaum, Susan L.; Britton, Julie A.; Subbaramaiah, Kotha; Dannenberg, Andrew J.; Neugut, Alfred I.

doi:10.1097/01.ogx.0000137848.03898.07

Cited by 52 publications

(82 citation statements)

References 21 publications

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“…Aspirin use for a year or longer protects against breast cancer development; no risk reduction seen with other NSAIDs Terry et al (2004) Epidemiological (case -control) NSAID use (as well as frequency of use) is inversely related to risk of breast cancer…”

Section: Resultsmentioning

confidence: 99%

“…This differs with ibuprofen use where frequency and duration of use was not associated with decreasing risk. Acetaminophen was unrelated to the incidence of breast cancer (Terry et al, 2004). The authors examined the relationship between the observed risk reduction of breast cancer in patients taking NSAIDs and hormone receptor status.…”

Section: Epidemiology Of Cox Inhibitor Use and Breast Cancer Incidencementioning

confidence: 99%

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COX inhibitors and breast cancer

2006

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There is considerable evidence to suggest that prostaglandins play an important role in the development and growth of cancer. The enzyme cyclo-oxygenase (COX) catalyses the conversion of arachidonic acid to prostaglandins. In recent years, there has been interest in a possible role for COX inhibitors in the prevention and treatment of malignancy. Cyclo-oxygenase-2 (COX-2) is overexpressed in several epithelial tumours, including breast cancer. Preclinical evidence favours an antitumour role for COX inhibitors in breast cancer. However, the epidemiological evidence for an association is conflicting. Trials are being conducted to study the use of COX inhibitors alone and in combination with other agents in the chemoprevention of breast cancer, and in the neoadjuvant, adjuvant, and metastatic treatment settings. In evaluating the potential use of these agents particularly in cancer chemoprophylaxis, the safety profile is as important as their efficacy. Concern over the cardiovascular safety of both selective and nonselective COX-inhibitors has recently been highlighted. Breast cancer is the most common malignancy in women in industrialised nations and the second leading cause of female cancer-related mortality. Approximately 40 000 women develop breast cancer in the UK each year. The incidence of breast cancer has increased by two-thirds over the last 15 years. Mortality rates though have fallen by one-third, and this is likely to be due to earlier detection of breast cancer because of screening, and the increased use of adjuvant therapies. In recent times, the prospect of further improvements in mortality rates has grown with hope provided by new chemotherapy agents and monoclonal antibody therapy directed at cell surface molecules. But can we do even better for women with breast cancer using cheap and simple treatments that are in current use?Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of widely available, inexpensive medicines. The analgesic, antiinflammatory, antipyretic and antithrombotic effects of salicylate in willow bark and other plant extracts were recognised in ancient Egypt and Greece. These properties have been extensively exploited in numerous fields of clinical medicine since the 19th century, and in cancer patients primarily for analgesia.

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Section: Resultsmentioning

confidence: 99%

Section: Epidemiology Of Cox Inhibitor Use and Breast Cancer Incidencementioning

confidence: 99%

COX inhibitors and breast cancer

2006

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“…2,36,37 The long-term ingestion of various NSAIDs is associated with a reduced incidence of colorectal, 37 esophageal, 38 gastric, 39 prostate, lung and breast cancer. 2,40 To date, however, the mechanisms underlying the effects of these drugs on cancer cells are not fully defined. 2 Although inhibition of COX with subsequent decrease in prostaglandin production may confer antitumor activity, these drugs also exert antiinflammatory and antitumor activity in COX-independent manners; 7,41 for example, NSAIDs inhibit several transcription and signaling cascades including nuclear factor kappa B [42][43][44] p42/44 MAPK, 45 and b-catenin/TCF.…”

Section: Discussionmentioning

confidence: 99%

Novel etodolac analog SDX-308 (CEP-18082) induces cytotoxicity in multiple myeloma cells associated with inhibition of β-catenin/TCF pathway

et al. 2007

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We have reported previously that R-enantiomer of etodolac (R-etodolac), which is under investigation in phase 2 clinical trials in chronic lymphocytic leukemia, induces potent cytotoxicity at clinically relevant concentrations in multiple myeloma (MM) cells. In this study, we demonstrated that SDX-308 (CEP-18082), a novel analog of etodolac, has more potent cytotoxicity than R-etodolac against both MM cell lines and patient MM cells, including tumor cells resistant to conventional (dexamethasone, doxorubicine, melphalan) and novel (bortezomib) therapies. SDX-308-induced cytotoxicity is triggered by caspase-8/9/3 activation and poly (ADP-ribose) polymerase cleavage, followed by apoptosis. SDX-308 significantly inhibits b-catenin/T-cell factor pathway by inhibiting nuclear translocation of b-catenin, thereby downregulating transcription and expression of downstream target proteins including myc and survivin. Neither interleukin-6 nor insulinlike growth factor-1 protect against growth inhibition triggered by SDX-308. Importantly, growth of MM cells adherent to bone marrow (BM) stromal cells is also significantly inhibited by SDX-308. Our data therefore indicate that the novel etodolac analog SDX-308 can target MM cells in the BM milieu.

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“…In the USA, CVD intervention strategies should be applied once the AtheroSclerotic CardioVascular Disease (ASCVD) risk calculator derived 10-year risk exceeds 7.5% while the UK NICE guidelines recommend intervention at a 10% threshold derived from Q-Research Risk Calculator (QRISK). These two superficially different cut-points are in fact almost equivalent and differences derive from different cohorts sampled (5). UK epidemiology surveys such as The Health Improvement Network (THIN) cohort suggest such a reduction in the risk threshold from 20% to 10% will increase the percentage of CVD events potentially detectable to 67% from 30%, but at the cost of having to screen 30% rather than 10% of the population (6).…”

Section: Disclosuresmentioning

confidence: 99%

“…I'm very worried. ' This media frenzy is reminiscent of when results from epidemiological studies regarding aspirin use and the risk of breast cancer became available (4,5). News outlets such as the BBC declared that '.…”

mentioning

confidence: 99%

Rosacea and dementia: relative vs. absolute effect sizes

Citrome

2016

Int J Clin Pract

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Association of Frequency and Duration of Aspirin Use and Hormone Receptor Status With Breast Cancer Risk

Cited by 52 publications

References 21 publications

COX inhibitors and breast cancer

COX inhibitors and breast cancer

Novel etodolac analog SDX-308 (CEP-18082) induces cytotoxicity in multiple myeloma cells associated with inhibition of β-catenin/TCF pathway

Rosacea and dementia: relative vs. absolute effect sizes

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