4 research outputs found
Menopausal hormone use and ovarian cancer risk : individual participant meta-analysis of 52 epidemiological studies
Background Half the epidemiological studies with information about menopausal hormone therapy and ovarian cancer risk remain unpublished, and some retrospective studies could have been biased by selective participation or recall. We aimed to assess with minimal bias the effects of hormone therapy on ovarian cancer risk. Methods Individual participant datasets from 52 epidemiological studies were analysed centrally. The principal analyses involved the prospective studies (with last hormone therapy use extrapolated forwards for up to 4 years). Sensitivity analyses included the retrospective studies. Adjusted Poisson regressions yielded relative risks (RRs) versus never-use. Findings During prospective follow-up, 12 110 postmenopausal women, 55% (6601) of whom had used hormone therapy, developed ovarian cancer. Among women last recorded as current users, risk was increased even with Interpretation The increased risk may well be largely or wholly causal; if it is, women who use hormone therapy for 5 years from around age 50 years have about one extra ovarian cancer per 1000 users and, if its prognosis is typical, about one extra ovarian cancer death per 1700 users
Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23 257 women with ovarian cancer and 87 303 controls
Background Oral contraceptives were introduced almost 50 years ago, and
over 100 million women currently use them. Oral contraceptives can
reduce the risk of ovarian cancer, but the eventual public-health
effects of this reduction will depend on how long the protection lasts
after use ceases. We aimed to assess these effects.
Methods Individual data for 23 257 women with ovarian cancer (cases) and
87 303 without ovarian cancer (controls) from 45 epidemiological studies
in 21 countries were checked and analysed centrally. The relative risk
of ovarian cancer in relation to oral contraceptive use was estimated,
stratifying by study, age, parity, and hysterectomy.
Findings Overall 7308 (31%) cases and 32 717 (37%) controls had ever
used oral contraceptives, for average durations among users of 4 . 4 and
5 . 0 years, respectively. The median year of cancer diagnosis was 1993,
when cases were aged an average of 56 years. The longer that women had
used oral contraceptives, the greater the reduction in ovarian cancer
risk (p<0. 0001). This reduction in risk persisted for more than 30
years after oral contraceptive use had ceased but became somewhat
attenuated over time the proportional risk reductions per 5 years of use
were 29% (95% CI 23-34%) for use that had ceased less than 10 years
previously, 19% (14-24%) for use that had ceased 10-19 years
previously, and 15% (9-21%) for use that had ceased 20-29 years
previously. Use during the 1960s, 1970s, and 1980s was associated with
similar proportional risk reductions, although typical oestrogen doses
in the 1960s were more than double those in the 1980s. The incidence of
mucinous tumours (12% of the total) seemed little affected by oral
contraceptives, but otherwise the proportional risk reduction did not
vary much between different histological types. In high-income
countries, 10 years use of oral contraceptives was estimated to reduce
ovarian cancer incidence before age 75 from 1 . 2 to 0 . 8 per 100 users
and mortality from 0 . 7 to 0 . 5 per 100; for every 5000 woman-years of
use, about two ovarian cancers and one death from the disease before age
75 are prevented.
Interpretation Use of oral contraceptives confers long-term protection
against ovarian cancer. These findings suggest that oral contraceptives
have already prevented some 200000 ovarian cancers and 100000 deaths
from the disease, and that over the next few decades the number of
cancers prevented will rise to at least 30 000 per year
Menopausal hormone use and ovarian cancer risk: individual participant meta-analysis of 52 epidemiological studies
Background Half the epidemiological studies with information about
menopausal hormone therapy and ovarian cancer risk remain unpublished,
and some retrospective studies could have been biased by selective
participation or recall. We aimed to assess with minimal bias the
effects of hormone therapy on ovarian cancer risk.
Methods Individual participant datasets from 52 epidemiological studies
were analysed centrally. The principal analyses involved the prospective
studies (with last hormone therapy use extrapolated forwards for up to 4
years). Sensitivity analyses included the retrospective studies.
Adjusted Poisson regressions yielded relative risks (RRs) versus
never-use.
Findings During prospective follow-up, 12 110 postmenopausal women, 55%
(6601) of whom had used hormone therapy, developed ovarian cancer. Among
women last recorded as current users, risk was increased even with <5
years of use (RR 1.43, 95% CI 1.31-1.56; p<0.0001). Combining
current-or-recent use (any duration, but stopped <5 years before
diagnosis) resulted in an RR of 1.37 (95% CI 1.29-1.46; p<0.0001); this
risk was similar in European and American prospective studies and for
oestrogen-only and oestrogen-progestagen preparations, but differed
across the four main tumour types (heterogeneity p<0.0001), being
definitely increased only for the two most common types, serous (RR
1.53, 95% CI 1.40-1.66; p<0.0001) and endometrioid (1.42, 1.20-1.67;
p<0.0001). Risk declined the longer ago use had ceased, although about
10 years after stopping long-duration hormone therapy use there was
still an excess of serous or endometrioid tumours (RR 1.25, 95% CI
1.07-1.46, p=0.005).
Interpretation The increased risk may well be largely or wholly causal;
if it is, women who use hormone therapy for 5 years from around age 50
years have about one extra ovarian cancer per 1000 users and, if its
prognosis is typical, about one extra ovarian cancer death per 1700
users
Ovarian cancer and smoking: individual participant meta-analysis including 28 114 women with ovarian cancer from 51 epidemiological studies
Background Smoking has been linked to mucinous ovarian cancer, but its
effects on other ovarian cancer subtypes and on overall ovarian cancer
risk are unclear, and the findings from most studies with relevant data
are unpublished. To assess these associations, we review the published
and unpublished evidence.
Methods Eligible epidemiological studies were identified by electronic
searches, review articles, and discussions with colleagues. Individual
participant data for 28 114 women with and 94 942 without ovarian cancer
from 51 epidemiological studies were analysed centrally, yielding
adjusted relative risks (RRs) of ovarian cancer in smokers compared with
never smokers.
Findings After exclusion of studies with hospital controls, in which
smoking could have affected recruitment, overall ovarian cancer
incidence was only slightly increased in current smokers compared with
women who had never smoked (RR 1.06, 95% CI 1.01-1.11, p=0.01). Of 17
641 epithelial cancers with specified histology, 2314 (13%) were
mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086
(52%) serous. Smoking-related risks varied substantially across these
subtypes (p(heterogeneity)<0.0001). For mucinous cancers, incidence was
increased in current versus never smokers (1.79, 95% CI 1.60-2.00,
p<0.0001), but the increase was mainly in borderline malignant rather
than in fully malignant tumours (2.25, 95% CI 1.91-2.65 vs 1.49,
1.28-1.73; p(heterogeneity)=0.01; almost half the mucinous tumours were
only borderline malignant). Both endometrioid (0.81, 95% CI 0.72-0.92,
p=0.001) and clear-cell ovarian cancer risks (0.80, 95% CI 0.65-0.97,
p=0.03) were reduced in current smokers, and there was no significant
association for serous ovarian cancers (0.99, 95% CI 0.93-1.06, p=0.8).
These associations did not vary significantly by 13 sociodemographic and
personal characteristics of women including their body-mass index,
parity, and use of alcohol, oral contraceptives, and menopausal hormone
therapy.
Interpretation The excess of mucinous ovarian cancers in smokers, which
is mainly of tumours of borderline malignancy, is roughly
counterbalanced by the deficit of endometrioid and clear-cell ovarian
cancers. The substantial variation in smoking-related risks by tumour
subtype is important for understanding ovarian carcinogenesis