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Blogger's Note: see blog postings (2013) for more research on this issue specific to HRT use/post-WHI; not all scientists/researcher agree that cancer rates declined in direct relation to HRT use; in addition, the decline in the use of HRT was short lived post 2002; cause-effect remains an outstanding issue; what is not included in this article is the potential/cause/effect of prophylactic surgeries as prevention either mastectomies and/or salpingoo-oopherectomies; it is important to note that many of these studies preclude pre-menopausal women who never took HRT/ERT yet were diagnosed
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Purpose After a report
from the Women’s Health Initiative (WHI) in 2002, a precipitous decline
in menopausal hormonal therapy (MHT)
use in the United States was linked to a decline
in breast cancer incidence rates. Given that MHT use is also associated
with
increased ovarian cancer risk, we tested whether
ovarian cancer incidence rates changed after 2002.
Methods Using the
North American Association of Central Cancer Registries database (1995
to 2008; N = 171,142 incident ovarian cancers),
we applied standard analytic approaches and
age-period-cohort (APC) models to estimate ovarian cancer incidence rate
changes
before (1995 to 2002) and after (2003 to 2008)
the WHI report.
Results Among women
age ≥ 50 years, age-standardized ovarian cancer incidence declined by
0.8% per year (95% CI, −1.8% to −0.5% per
year) before the WHI announcement; after the WHI
report, the rate declined by 2.4% per year (95% CI, −2.5% to −2.2% per
year).
APC models confirmed an accelerated decline in
ovarian cancer incidence after the WHI report, adjusted for age and
birth cohort
effects. This sudden change was notable among
women most likely to have used MHT (ie, women age 50 to 69 years, white
women,
and residents of regions with highest MHT
prescription frequency). The largest changes were found for the
endometrioid histologic
subtype.
Conclusion After a
marked reduction in MHT use around 2002, ovarian cancer incidence rates
demonstrated an accelerated decline, with
the largest changes for endometrioid carcinomas.
This strong temporal association, although not proving a causal role of
hormones
in ovarian carcinogenesis, suggests that future
analytic research supporting cancer control efforts should clarify the
role
of hormonal exposures on the development and
behavior of subtypes of ovarian cancer.
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