Breast cancer incidence and estrogen receptor ? in normal mammary tissue?An epidemiologic study among Japanese women in Japan and Hawaii

Abstract Background Westernization and etiologic heterogeneity may play a role in the rising breast cancer incidence in Asian American (AA) women. We report breast cancer incidence in Asian-origin populations. Methods Using a specialized Surveillance, Epidemiology, and End Results-9 Plus API Database (1990–2014), we analyzed breast cancer incidence overall, by estrogen receptor (ER) status, and age group among non-Hispanic white (NHW) and AA women. We used age-period-cohort models to assess time trends and quantify heterogeneity by ER status, race and ethnicity, and age. Results Overall, breast cancer incidence increased for most AA ethnicities (Filipina: estimated annual percentage change [EAPC] = 0.96%/year, 95% confidence interval [CI] = 0.61% to 1.32%; South Asian: EAPC = 1.68%/year, 95% CI = 0.24% to 3.13%; Chinese: EAPC = 0.65%/year, 95% CI = 0.03% to 1.27%; Korean: EAPC = 2.55%/year, 95% CI = 0.13% to 5.02%; and Vietnamese women: EAPC = 0.88%/year, 95% CI = 0.37% to 1.38%); rates did not change for NHW (EAPC = -0.2%/year, 95% CI = -0.73% to 0.33%) or Japanese women (EAPC = 0.22%/year, 95% CI = -1.26% to 1.72%). For most AA ethnicities, ER-positive rates statistically significantly increased, whereas ER-negative rates statistically significantly decreased. Among older women, ER-positive rates were stable for NHW and Japanese women. ER-negative rates decreased fastest in NHW and Japanese women among both age groups. Conclusions Increasing ER-positive incidence is driving an increase overall for most AA women despite declining ER-negative incidence. The similar trends in NHW and Japanese women (vs other AA ethnic groups) highlight the need to better understand the influences of westernization and other etiologic factors on breast cancer incidence patterns in AA women. Heterogeneous trends among AA ethnicities underscore the importance of disaggregating AA data and studying how breast cancer differentially affects the growing populations of diverse AA ethnic groups.

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Neuronatin is a modifier of estrogen receptor-positive breast cancer incidence and outcome

Breast Cancer Research and Treatment ◽

10.1007/s10549-019-05307-8 ◽

2019 ◽

Vol 177 (1) ◽

pp. 77-91

Author(s):

Cody Plasterer ◽

Shirng-Wern Tsaih ◽

Amy R. Peck ◽

Inna Chervoneva ◽

Caitlin O’Meara ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cancer Incidence ◽

Breast Cancer Incidence ◽

Estrogen Receptor Positive ◽

Positive Breast Cancer

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Phthalate Exposure and Breast Cancer Incidence: A Danish Nationwide Cohort Study

Journal of Clinical Oncology ◽

10.1200/jco.18.02202 ◽

2019 ◽

Vol 37 (21) ◽

pp. 1800-1809 ◽

Cited By ~ 13

Author(s):

Thomas P. Ahern ◽

Anne Broe ◽

Timothy L. Lash ◽

Deirdre P. Cronin-Fenton ◽

Sinna Pilgaard Ulrichsen ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cancer Incidence ◽

Dibutyl Phthalate ◽

Cox Regression ◽

Breast Cancer Incidence ◽

Drug Products ◽

Phthalate Exposure ◽

Long Term Treatment ◽

High Level

PURPOSE Phthalate exposure is ubiquitous and especially high among users of drug products formulated with phthalates. Some phthalates mimic estradiol and may promote breast cancer. Existing epidemiologic studies on this topic are small, mostly not prospective, and have given inconsistent results. We estimated associations between longitudinal phthalate exposures and breast cancer risk in a Danish nationwide cohort, using redeemed prescriptions for phthalate-containing drug products to measure exposure. METHODS We ascertained the phthalate content of drugs marketed in Denmark using an internal Danish Medicines Agency ingredient database. We enrolled a Danish nationwide cohort of 1.12 million women at risk for a first cancer diagnosis on January 1, 2005. By combining drug ingredient data with the Danish National Prescription registry, we characterized annual, cumulative phthalate exposure through redeemed prescriptions. We then fit multivariable Cox regression models to estimate associations between phthalate exposures and incident invasive breast carcinoma according to tumor estrogen receptor status. RESULTS Over 9.99 million woman-years of follow-up, most phthalate exposures were not associated with breast cancer incidence. High-level dibutyl phthalate exposure (≥ 10,000 cumulative mg) was associated with an approximately two-fold increase in the rate of estrogen receptor–positive breast cancer (hazard ratio, 1.9; 95% CI, 1.1 to 3.5), consistent with in vitro evidence for an estrogenic effect of this compound. Lower levels of dibutyl phthalate exposure were not associated with breast cancer incidence. CONCLUSION Our results suggest that women should avoid high-level exposure to dibutyl phthalate, such as through long-term treatment with pharmaceuticals formulated with dibutyl phthalate.

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