NSAIDs and breast cancer recurrence in a prospective cohort study

Kwan, Marilyn L.; Habel, Laurel A.; Slattery, Martha L.; Caan, Bette J.

doi:10.1007/s10552-007-9003-y

Cited by 97 publications

(106 citation statements)

References 20 publications

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“…32 Our results are consistent with two other studies reported in 2007. Kwan et al 33 reported on NSAID use and recurrence among 2,292 women with early-stage breast cancer. They found a reduced risk of recurrence for current regular (Ն 3 days per week) use of ibuprofen (RR ϭ 0.56; 95% CI, 0.32 to 0.98) but not aspirin (RR ϭ 1.09; 95% CI, 0.74 to 1.61); short follow-up (5 years) may have precluded detecting an association.…”

Section: Discussionmentioning

confidence: 99%

Aspirin Intake and Survival After Breast Cancer

Holmes

Chen

et al. 2010

JCO

332

261

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A B S T R A C T PurposeAnimal and in vitro studies suggest that aspirin may inhibit breast cancer metastasis. We studied whether aspirin use among women with breast cancer decreased their risk of death from breast cancer. MethodsThis was a prospective observational study based on responses from 4,164 female registered nurses in the Nurses' Health Study who were diagnosed with stages I, II, or III breast cancer between 1976 and 2002 and were observed until death or June 2006, whichever came first. The main outcome was breast cancer mortality risk according to number of days per week of aspirin use (0, 1, 2 to 5, or 6 to 7 days) first assessed at least 12 months after diagnosis and updated. ResultsThere were 341 breast cancer deaths. Aspirin use was associated with a decreased risk of breast cancer death. The adjusted relative risks (RRs) for 1, 2 to 5, and 6 to 7 days of aspirin use per week compared with no use were 1.07 (95% CI, 0.70 to 1.63), 0.29 (95% CI, 0.16 to 0.52), and 0.36 (95% CI, 0.24 to 0.54), respectively (test for linear trend, P Ͻ .001). This association did not differ appreciably by stage, menopausal status, body mass index, or estrogen receptor status. Results were similar for distant recurrence. The adjusted RRs were 0.91 (95% CI, 0.62 to 1.33), 0.40 (95% CI, 0.24 to 0.65), and 0.57 (95% CI, 0.39 to 0.82; test for trend, P ϭ .03) for 1, 2 to 5, and 6 to 7 days of aspirin use, respectively. ConclusionAmong women living at least 1 year after a breast cancer diagnosis, aspirin use was associated with a decreased risk of distant recurrence and breast cancer death.

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Section: Discussionmentioning

confidence: 99%

Aspirin Intake and Survival After Breast Cancer

Holmes

Chen

et al. 2010

JCO

332

261

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“…Ibuprofen and aspirin are attractive intervention agents as both are affordable non-specific COX-2 inhibitors that can be used for decades with minimal side effects. In fact, COX-2 is considered a viable target for prevention and treatment in a variety of cancers (Thun et al, 1991;Elder & Paraskeva, 1998;Kwan et al, 2007;Holmes et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Non-steroidal anti-inflammatory drugs target the pro-tumorigenic extracellular matrix of the postpartum mammary gland

O’Brien¹,

Hansen²,

Barkan³

et al. 2011

Int. J. Dev. Biol.

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Breast cancer patients diagnosed postpartum have poor prognosis. The postpartum mammary gland undergoes tissue regression to return to the pre-pregnant state. This involution is characterized by wound healing programs known to be tumor promotional in other contexts. Previous studies have shown that mammary extracellular matrix (ECM) from nulliparous rats has tumor suppressive attributes, while mammary ECM from involuting mammary glands is promotional. In models of pregnancy-associated breast cancer, non-steroidal anti-inflammatory drug (NSAID) treatment targeted to postpartum involution inhibits tumor progression, in part by suppressing COX-2 dependent collagen deposition. Because mammary ECM proteins are coordinately regulated, NSAID treatment is anticipated to result in additional protective changes in the mammary extracellular matrix. Here, systemic NSAID treatment was utilized during postpartum involution to reduce mammary COX-2 activity. ECM was isolated from actively involuting glands of rats treated with NSAIDs and compared to ECM isolated from control-involution and nulliparous rats in 3D cell culture and xenograft assays. Compositional changes in ECM between groups were identified by proteomics. In four distinct 3D culture assays, normal and transformed mammary epithelial cells plated in NSAID-involution ECM, phenocopied cells plated in ECM from nulliparous rats rather than ECM from control-involution rats. Tumor cells mixed with NSAID-involution ECM and injected orthotopically in mice formed smaller tumors than cells mixed with control-involution ECM. Proteomic analyses identified and 3D culture assays implicated the ECM protein tenascin-C as a potential mediator of tumor progression during involution that is decreased by NSAID treatment. In summary, NSAID treatment decreases tumor-promotional attributes of postpartum involution mammary ECM.

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“…Kwan et al [102] examined the association between NSAID use and breast cancer recurrence among 2292 women diagnosed with breast cancer in the Life After Cancer Epidemiology Study. They observed that regular ibuprofen users experienced 44% less recurrence than non-users after five years of follow-up.…”

Section: Therapeutic Studies Of Nsaids In Human Breast Cancermentioning

confidence: 99%

Cyclooxygenase-2 and the inflammogenesis of breast cancer

Harris

Casto

Harris

2014

WJCO

154

125

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Cohesive scientific evidence from molecular, animal, and human investigations supports the hypothesis that constitutive overexpression of cyclooxygenase-2 (COX-2) is a ubiquitous driver of mammary carcinogenesis, and reciprocally, that COX-2 blockade has strong potential for breast cancer prevention and therapy. Key findings include the following: (1) COX-2 is constitutively expressed throughout breast cancer development and expression intensifies with stage at detection, cancer progression and metastasis; (2) essential features of mammary carcinogenesis (mutagenesis, mitogenesis, angiogenesis, reduced apoptosis, metastasis and immunosuppression) are linked to COX-2-driven prostaglandin E2 (PGE-2) biosynthesis; (3) upregulation of COX-2 and PGE-2 expression induces transcription of CYP-19 and aromatase-catalyzed estrogen biosynthesis which stimulates unbridled mitogenesis; (4) extrahepatic CYP-1B1 in mammary adipose tissue converts paracrine estrogen to carcinogenic quinones with mutagenic impact; and (5) agents that inhibit COX-2 reduce the risk of breast cancer in women without disease and reduce recurrence risk and mortality in women with breast cancer. Recent sharp increases in global breast cancer incidence and mortality are likely driven by chronic inflammation of mammary adipose and upregulation of COX-2 associated with the obesity pandemic. The totality of evidence clearly supports the supposition that mammary carcinogenesis often evolves as a progressive series of highly specific cellular and molecular changes in response to induction of constitutive overexpression of COX-2 and the prostaglandin cascade in the "inflammogenesis of breast cancer". Key words: Breast Cancer; Cyclooxygenase-2; Nonsteroidal anti-inflammatory drugs; Inflammogenesis; Estrogen; Aromatase Core tip: Mammary carcinogenesis often evolves as a series of highly specific cellular and molecular changes in response to induction of constitutive over-expression of cyclooxygenase-2 (COX-2) and the prostaglandin cascade; reciprocally, agents that block COX-2 have significant value in the chemoprevention and therapy of breast cancer.Harris RE, Casto BC, Harris ZM. Cyclooxygenase-2 and the inflammogenesis of breast cancer. World J Clin Oncol 2014; 5(4): 677-692 Available from: URL: http://www.wjgnet.com/2218-4333/full/v5/ i4/677.htm DOI: http://dx.doi.org/10.5306/wjco.v5.i4.677 INTRODUCTIONMore than a century ago, Virchow et al [1,2] chronic inflammation leads to cancer development by increasing cellular proliferation [3] . Various models of carcinogenesis have been proposed involving inflammatory stimuli and mediators of wound healing [4][5][6] . The recent discovery of the inducible cyclooxygenase-2 (COX-2) gene has rekindled interest in the causal link between inflammation and cancer, and various models of carcinogenesis have been proposed involving inflammatory stimuli and COX-2 expression [7][8][9][10] . The current review synthesizes and interprets the accumulating body of evidence supporting COX-2 driven inflammogenesis as a ge...

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NSAIDs and breast cancer recurrence in a prospective cohort study

Abstract: Our findings provide support for an inverse association between current, regular ibuprofen use and breast cancer recurrence.

Cited by 97 publications

References 20 publications

Aspirin Intake and Survival After Breast Cancer

Aspirin Intake and Survival After Breast Cancer

Non-steroidal anti-inflammatory drugs target the pro-tumorigenic extracellular matrix of the postpartum mammary gland

Cyclooxygenase-2 and the inflammogenesis of breast cancer

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