The Prevention of Breast Cancer: An Overview

Abstract

The role of lifestyle modifications, antioestrogens, cyclo-oxygenase-2 inhibitors and prophylactic mastectomy in reducing breast cancer is reviewed. It is concluded that avoiding postmenopausal obesity and regular physical activity are simple measures that seem to reduce breast cancer risk. There is no conclusive evidence that dietary modification and vitamin supplementation significantly reduce the risk of breast cancer. The evidence suggests that tamoxifen significantly reduces the risk of breast cancer in women at increased risk, but whether it reduces breast cancer mortality remains unknown. Ongoing clinical trials may prove that raloxifene is superior to tamoxifen in breast cancer prevention due to its anti-oestrogenic effects on the endometrium. Bilateral prophylactic mastectomy reduces the risk of breast cancer by 90% in high risk women.

Population attributable risks for modifiable lifestyle factors and breast cancer in New Zealand women

“…Reports of an association between diet and breast cancer are inconsistent. Prospective studies, including some intervention studies, have not found consistent evidence of any association between dietary factors and breast cancer . This meant that diet was not considered further as a modifiable risk factor for breast cancer.…”

“…[32][33][34] Use for 5 years or more increases the risk of breast cancer by about 35%, with the risk returning to normal 5 years after stopping HRT. 16,25,32 There is a 66% increased risk of breast cancer for current use of HRT compared with the not used category; RR 1.7 (1.6-1.8). 35…”

Prostanoid receptor EP1 expression in breast cancer

“…Nonsteroidal anti-inflammatory drugs (NSAIDs), which act through inhibition of cyclooxygenase enzyme (COX), are one such class of drugs that have been studied for their possible role in breast cancer prevention. Epidemiological studies investigating the relationship between NSAID use and breast cancer have reported conflicting results; some studies [3][4][5] show 30-40% reduction in breast cancer incidence with NSAID use, whereas others failed to confirm this relationship. 6,7 NSAIDs work by inhibiting both constitutive and inducible cyclooxygenase enzymes (COX-1 and COX-2, respectively), both of which have been postulated to play a role in carcinogenesis.…”

“…11 The cyclooxygenase enzymes are involved in prostaglandin synthesis; prostaglandin E2 (PGE2) is an important mediator of tumorigenesis. 12,13 PGE2 acts by binding to one of four separate receptors, EP 1 through EP 4 , which are members of the rhodopsintype receptors coupled to hetero-trimeric GTPbinding proteins. 14 Activation of EP 1 and EP 3 receptors leads to increased intracellular calcium and decreased cyclic AMP levels.…”

The Covalent Advantage: A New Paradigm for Cell Signaling Mediated by Thiol Reactive Lipid Oxidation Products

“…For example, several lines of evidence suggest that there is a connection between COX-2, obesity, and cancer (Leris and Mokbel, 2001;Na and Surh, 2003;Raju and Bird, 2003). Products of COX-2 have been shown to promote cellular proliferation and angiogenesis.…”