Abstract
Increased mammographic density (MD) has been shown beyond doubt to be a marker for increased breast cancer risk, though the underpinning pathobiology is yet to be fully elucidated. Estrogenic activity exerts a strong influence over MD, which consequently has been observed to change predictably in response to tamoxifen anti-estrogen therapy, although results for other selective estrogen receptor modulators and aromatase inhibitors are less consistent. In both primary and secondary prevention settings, tamoxifen-associated MD changes correlate with successful modulation of risk or outcome, particularly among pre-menopausal women; an observation that supports the potential use of MD change as a surrogate marker where short-term MD changes reflect longer-term anti-estrogen efficacy. Here we summarize endocrine therapy-induced MD changes and attendant outcomes and discuss both the need for outcome surrogates in such therapy, as well as make a case for MD as such a monitoring marker. We then discuss the process and steps required to validate and introduce MD into practice as a predictor or surrogate for endocrine therapy efficacy in preventive and adjuvant breast cancer treatment settings.
Highlights
Breast cancer (BC) is the most common cancer in women and the second leading cause of cancer-related death among females in the US according to 2016 statistics [1]
We have reviewed the mammographic density (MD) changes in relation to the spectrum of endocrine therapy (ET) employed in different BC scenarios to explore whether evidence to date supports this hypothesis and, if this proves to be the case, to ascertain what further research is required to bring this into routine practice
MD reduction is relatively frequent for patients on tamoxifen, with reasonable evidence in both primary and secondary preventative settings that this correlates with risk reduction
Summary
Breast cancer (BC) is the most common cancer in women and the second leading cause of cancer-related death among females in the US according to 2016 statistics [1]. Latest global cancer statistics show that 1.7 million BC diagnoses and 522,000 BC-related deaths were recorded in 2012, with a 20% increase in the BC incidence rate and 14% increase in the BC-related mortality rate, in comparison with 2008 estimates [2]. Such striking statistics highlight the importance of optimizing the prevention and treatment of this disease. Factors that modulate estrogen exposure throughout life, including endogenous elements such as age of www.impactjournals.com/oncotarget menarche and menopause, breast feeding and postmenopausal obesity, and exogenous elements such as oral contraceptives and hormone replacement therapy (HRT), all influence BC risk in a direction predictable by their impact on estrogen levels [5]
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