REPORTS |
Effect of Hormone Replacement Therapy on Breast Cancer Risk: Estrogen Versus Estrogen Plus Progestin
Ronald K. Ross,
Annlia Paganini-Hill,
Peggy C. Wan,
Malcolm C. Pike
Affiliation of authors: University of Southern California/Norris Comprehensive
Cancer Center, Los Angeles.
Correspondence to: Ronald K. Ross, M.D., University of Southern
California/Norris
Comprehensive Cancer Center, 1441 Eastlake Ave., Rm. 8302B, Los Angeles, CA 90089-9181
(e-mail: ross_r{at}ccnt.hsc.usc.edu).
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ABSTRACT
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BACKGROUND: Hormone replacement therapy (HRT) given as unopposed estrogen
replacement
therapy (ERT) gained widespread popularity in the United States in the 1960s and 1970s. Recent
prescribing practices have favored combination HRT (CHRT), i.e., adding a progestin to estrogen
for
the entire monthly cycle (continuous combined replacement therapy [CCRT]) or a
part of
the cycle (sequential estrogen plus progestin therapy [SEPRT]). Few data exist on the
association between CHRT and breast cancer risk. We determined the effects of CHRT on a
woman's risk of developing breast cancer in a population-based, case-control study.
METHODS: Case subjects included those with incident breast cancers diagnosed over 4
years in Los Angeles County, CA, in the late 1980s and 1990s. Control subjects were
neighborhood
residents who were individually matched to case subjects on age and race. Case subjects and
control
subjects were interviewed in person to collect information on known breast cancer risk factors as
well
as on HRT use. Information on 1897 postmenopausal case subjects and on 1637 postmenopausal
control subjects aged 55-72 years who had not undergone a simple hysterectomy was analyzed.
Breast
cancer risks associated with the various types of HRT were estimated as odds ratios (ORs) after
adjusting simultaneously for the different forms of HRT and for known risk factors of breast
cancer. All P values are two-sided. RESULTS: HRT was associated with a 10%
higher
breast cancer risk for each 5 years of use (OR5 = 1.10; 95% confidence
interval [CI] = 1.02-1.18). Risk was substantially higher for CHRT use (OR5 = 1.24; 95% CI = 1.07-1.45) than for ERT use (OR5
= 1.06; 95% CI = 0.97-1.15). Risk estimates were higher for SEPRT (OR5 = 1.38; 95% CI = 1.13-1.68) than for CCRT (OR5
=
1.09; 95% CI = 0.88-1.35), but this difference was not statistically significant. Conclusions: This study provides strong evidence that the addition of a progestin to HRT
enhances
markedly the risk of breast cancer relative to estrogen use alone. These findings have important
implications for the risk-benefit equation for HRT in women using CHRT.
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INTRODUCTION
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Hormone replacement therapy (HRT) in the form
of unopposed (without progestins) estrogen replacement therapy (ERT)
gained widespread popularity in the United States in the 1960s and
early 1970s. In the peak year of 1974, 28 million prescriptions were
filled for noncontraceptive use of estrogens (1). The first
definitive studies (2,3) demonstrating a causal relationship
between endometrial cancer and ERT were published in 1975. The
increased incidence of endometrial cancer among women using ERT led
initially to a marked decline in the number of prescriptions of this
category of drugs, followed by increases when new strategies for
delivering HRT were defined to protect the endometrium from the
carcinogenic effects of unopposed estrogen. Accordingly, combination
hormone replacement therapy (CHRT), in which a progestin is given with
an estrogen either sequentially or continuously during a monthly cycle,
has grown rapidly in popularity (4).
The use of CHRT has necessitated a re-examination of the risk-benefit equation associated
with
HRT (5). We recently provided (6) the most
definitive
results to date that CHRT, whether given as continuous combined therapy (CCRT, estrogen and
progestin prescribed together during each day of the monthly cycle in which HRT is taken) or
sequential
estrogen and estrogen plus progestin therapy (SEPRT), with the progestin given for 10 or more
days
per month, are associated with little or no increased risk of endometrial cancer. Although CHRT
is
more widely prescribed to women with an intact uterus, it is sometimes prescribed to women who
have
had hysterectomy, possibly because of the belief that progestins will also negate any carcinogenic
effects of estrogens on the breast (7). Studies (8)
of
mitotic activity in the breast during the normal menstrual cycle cast doubt on this premise,
however,
since mitotic activity peaks at the time of maximum serum progesterone. Direct evidence that
progestins
may actually be harmful in terms of breast cancer risk was first presented in the mid-1980s, when
results from a cohort study of Swedish women were published suggesting that women who
received
CHRT for more than 6 years had a 4.4-fold increased risk of breast cancer (9). No increased risk was observed with shorter term use, however, and the 4.4-fold
increased risk was
based on only 10 patients and did not achieve statistical significance. A subsequent report on this
cohort with more precise risk estimates showed a more modest 1.6-fold increase in risk with more
than
6 years of CHRT use (10). There have been additional papers describing
results on CHRT use and breast cancer risk but none with substantial statistical power or great
detail on
CHRT usage patterns (11).
We have conducted a population-based, case-control study designed primarily to determine
the
effects of CHRT use on breast cancer risk. We report here the results based on interviews of 2653
breast cancer patients and 2429 control subjects. This study provides the most definitive and
detailed
data yet available on the relationship between CHRT use and breast cancer risk.
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SUBJECTS AND METHODS
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For this study, breast cancer patients were identified by the Cancer Surveillance Program
(CSP),
the population-based cancer registry of Los Angeles County, CA. Registration is estimated to be
more
than 98% complete (12). Since June 1987, the CSP has been part
of
the statewide California Cancer Registry, whose methodology for ascertainment and quality
control has
been previously described (13). In 1992, the CSP became part of the
National
Surveillance, Epidemiology, and End Results (SEER)1
Program of the U.S. National
Cancer Institute, Bethesda, MD.
Qualifying case subjects included female patients with a diagnosis of breast cancer of
epithelial
origin registered by the CSP who were English-speaking residents of Los Angeles County. Cases
were
ascertained in three diagnostic periods. Group I case subjects were first diagnosed during the
period
from March 1, 1987, through December 31, 1989; these case subjects were white (including
Hispanic); were born in the United States, Canada, or Western Europe; and were aged 55-64
years at
first diagnosis. Group II case subjects were first diagnosed during the period from January 1,
1992,
through December 31, 1992; these case subjects were also white (including Hispanic) or
African-American, were born in the United States, and were aged 55-69 years at first diagnosis.
Group
III case subjects were first diagnosed during the period from September 1, 1995, through April
30,
1996; these case subjects were white (including Hispanic) or African-American, were born in the
United States, and were aged 55-72 years at first diagnosis. This sequence of data collection was
adopted to make maximal use of personnel and other resources. Since CHRT first became popular
in
the late 1970s and early 1980s, changing the targeted age range over time also maximized the
likelihood of long-term use of CHRT. Interviews were completed with 2653 of the 3976
qualifying
patients. We sought physician approval before initiating patient contact, but 144 physicians
(4%)
refused, as did 794 patients (20%) themselves. An additional 385 patients (10%) had
died or were too ill to participate at the time we contacted them (Table 1
).
All
patients were generally interviewed within 1 year of diagnosis.
Control women were individually matched to case subjects by age (±3 years),
race-ethnicity, and neighborhood of residence (hence, roughly by social class). These
neighborhood
control subjects were identified by "control walkers" who followed a
predetermined
algorithm beginning with a residence bearing a specific relationship to the residence of the patient
at her
time of diagnosis. The walkers proceeded though a sequence of houses, canvassing each until a
matched control subject was identified. Matched control subjects were interviewed for 2429
patients
(Table 1
); no matched control subject was found for 224 patients. The
first qualifying control subject
refused to participate in 536 instances and an additional matched control subject was sought. The
median number of households canvassed before a qualifying control subject was identified was 33.
Data Collection
Each participant was interviewed in person in her home. Each case-control pair was generally
interviewed by the same interviewer. The interview took about three quarters of an hour to
complete,
was highly structured, and obtained information on demographics, physical characteristics,
menstrual
and reproductive experiences, physical exercise activity, benign breast disease history, family
history of
breast cancer, use of mammographic screening, history of smoking, alcohol and caffeine
consumption,
and a detailed history of use of HRT and oral contraceptives. Exposure histories were ascertained
up to
1 year before the diagnosis date (reference date) of the breast cancer patient, both for the patient
herself and for her matched control subject. An album of color photographs of exogenous
hormones
marketed in the United States was available as an aid to facilitate recall of specific hormone
preparations used by the respondent. The respondents were asked to sign an informed consent
form
outlining the study's purpose, procedures, benefits, and risks that was reviewed and
approved
on an annual basis by the federally designated University of Southern California School of
Medicine
Institutional Review Board.
Statistical Analyses
Women undergoing a hysterectomy without oophorectomy (simple hysterectomy) before
menopause were excluded from all analyses related to HRT, since we have demonstrated that
alternative methods for assigning an age at menopause to such women will lead to substantially
biased
estimates of HRT effects on breast cancer risk (14). Premenopausal
women
were also excluded.
Age at last menstrual period cannot be used to uniformly estimate age at menopause, since
women
who use SEPRT usually continue to have monthly menstrual periods, irrespective of their ovarian
function, and women on ERT and CCRT can rarely distinguish breakthrough bleeding from
ovarian
function-determined menses. For a woman taking HRT before her reported age at last menstrual
period, we set her age of menopause as the year in which she began HRT use (6), with the rationale that HRT use was started because of menopausal symptoms. For
women taking oral contraceptives, age at menopause was taken as the end of the period of oral
contraceptive use, if no natural menstruation occurred thereafter. Natural menstruation was taken
to
mean menstruating and not using oral contraceptives or HRT at the time. This is the same schema
to
approximate age at menopause as we used in our earlier study of HRT and endometrial cancer (6).
Statistical analyses were conducted using standard conditional multivariate logistic regression
techniques (15) by use of the EPILOG statistical package program
(Epicenter
Software, Pasadena, CA). Although the study was designed as a matched case-control study,
because
of the large number of exclusions, we report results using a stratified analytic approach by use of
strata
formed from 2-year "age at reference date" by 2-year "year of birth"
by
four "socioeconomic status" divisions (based on the average educational and
income
levels in the geographic area of residence) and three ethnicity groupings. Because of this strategy,
control subjects under the age of 55 years and over the age of 72 years were also excluded.
Matched
analyses of the case-control pairs in which both were eligible for inclusion produced similar risk
estimates to the stratified risk estimates reported here. All of the reported risk estimates were
adjusted
for the major risk factors of breast cancer: type of menopause (natural versus bilateral
oophorectomy),
age at natural menopause (continuous variable), age at bilateral oophorectomy (continuous
variable),
age at menarche (continuous variable), family history of breast cancer in mother or daughter
(yes/no),
personal history of benign breast disease (yes/no), nulliparity (yes/no), age at first full-term
pregnancy
(continuous variable), duration of oral contraceptive use (continuous variable), weight
(continuous
variable), and drinks of alcohol per week (continuous variable). All P values determining
statistical significance are two-sided.
Tumor stage was determined by a review of all original pathology reports and cancer registry
abstracts, both of which are routinely collected by the CSP.
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RESULTS
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HRT was used by 54% of the 1897 breast cancer patients included in
the analysis and by 52% of the 1637 control subjects. The 1897
patients averaged 46.3 months of HRT use compared with 42.9 months for
control subjects. The majority of HRT use was unopposed ERT, with
conjugated equine estrogen in relatively low doses (
0.625 mg/day)
being the most popular formulation and dose. Combination therapy was
more commonly prescribed sequentially, usually in combination with
0.625 mg of conjugated equine estrogen. Sequential use was roughly 50%
more common among control women in this population than continuous
combined therapy. Medroxyprogesterone acetate comprised the great
majority of all progestin use.
The association between breast cancer risk and months of use of any form of HRT is shown in
Table 2.
Breast cancer risk increased 10% per 5 years of use of
HRT
(odds ratio [OR]5 = 1.10; 95% confidence interval
[CI] = 1.02-1.18; P = .015). Although the observed risk did
not
increase monotonically with increasing months of use, the data are compatible with a steady
increase in
risk with increasing duration of HRT use. After 15 years of use, the observed breast cancer risk
was
increased 36%.
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Table 2. Odds ratios (ORs) and 95% confidence intervals
(CIs) for breast cancer in relation to duration of use of any HRT and to duration of use of ERT
and CHRT*
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ERT use was not associated with breast cancer risk except in long-term users (OR for
15
years of use = 1.24; Table 2
). The data are, however, compatible
with a steady increase in risk
of 6% per 5 years of ERT use (OR5 = 1.06; 95% CI =
0.97-1.15; P = .18), although this result is not statistically significant. Relative
risks
were higher in thin women than in heavy women (data not shown).
Breast cancer risk was increased much more substantially, however, with the use of CHRT
(Table
2
). Risk increased consistently with increasing duration of CHRT use,
with an OR of 1.51 associated
with use for 10 or more years. The estimated risk per 5 years of use was 1.24 (95% CI
= 1.07-1.45; P = .005).
Risk appeared to be higher with SEPRT than with CCRT, but the difference was not
statistically
significant (Table 3
). For SEPRT, the observed risk associated with 10 or
more years of use was 1.79; the comparable risk for CCRT was 1.23. The OR per 5 years of
SEPRT
use was 1.38 (95% CI = 1.13-1.68; P = .0015) compared with 1.09
(95% CI = 0.88-1.35; P = .44) for CCRT, but this difference was
not
statistically significant.
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Table 3. Odds ratios (ORs) and 95% confidence intervals
(CIs) for breast cancer in relation to duration of use of SEPRT and CCRT*
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Among the 1897 breast cancer patients, 186 presented with in situ disease, 1116 had
their cancer confined to the breast at the time of diagnosis, 566 had regional lymph node
involvement or
metastatic disease, and 29 had unknown stage. Risks per 5 years of use of various HRT categories
by
pathologic stage are shown in Table 4.
For ERT, excess risk was confined
almost entirely to in situ disease (OR5 = 1.41; 95% CI
=
1.18-1.69). On the other hand, for CHRT, risks were comparable across all stages at presentation.
We
also included mammographic screening (never, within 1 year, and >1 year ago) as a covariate
in our
risk estimate models as an alternative method of determining whether observed risk differences
might
be due to different screening behaviors in HRT users and nonusers. The OR for CHRT (per 5
years of
use) actually increased slightly (from 1.24 to 1.27).
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Table 4. Odds ratios (ORs) and 95% confidence intervals
(CIs) for breast cancer per 5 years of use of different types of HRT in relation to pathologic stage
at
diagnosis*
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We explored whether the effect of CHRT on breast cancer risk might be restricted to current
users, as has been suggested by others concerning ERT use (16). CHRT is
a
relatively recent phenomenon so that most users were either current users or had ceased usage
only in
the recent past. Nonetheless, there was no clear difference in risk level between current users and
those
who had stopped use at least 2 years previously (data not shown).
There were substantial missing data on progestin dose, but data on conjugated equine
estrogen
dose were quite complete. Risks were generally modestly higher with increasing estrogen dose
(data
not shown).
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DISCUSSION
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The results of this study on the relationship between ERT and breast
cancer are compatible with the conclusions of a recent
meta-analysis (11) and other summary assessments
(17,18) of the extensive literature on this subject. We
designed this study to have high statistical power, to conduct careful
adjustment for potential confounders, including especially age at
menopause, to make careful and systematic collection of detailed
exposure histories, and to make use of healthy and closely age-related
population control subjects (19). In particular, possible
differences in HRT use by socioeconomic status, age, calendar year, or
ethnicity were controlled in analysis by stratification.
This study provides detailed data on the effects of an added progestin on breast cancer risk.
These
data strongly refute the notion that progestins will be protective against breast cancer
development (20), a belief that has persisted despite the absence of any
strong biologic
rationale for an antiestrogenic, anticancer effect of progestins on the breast. In fact, this study
provides
the strongest evidence to date that progestins not only do not protect the breast from the
carcinogenic
effects of estrogen but also increase substantially the small ERT-related increase in breast cancer
risk.
The biologic effects of progestins on the breast, while not extensively studied, support the
observations
in this study that progestins may enhance breast cancer risk. As noted above, maximum mitotic
activity
in breast tissue occurs in the mid-to-late luteal phase of the menstrual cycle, at the time of
maximum
progesterone levels (8). This situation is clearly different from that in the
endometrium where the influence of progesterone during the luteal phase of the cycle is to inhibit
any
further mitotic activity.
The relationship between mammographic density patterns and breast cancer risk is well
established
(21). Mammographic densities were measured as part of the
Postmenopausal
Estrogen/Progestin Interventions Trial (22). In this trial, 875
postmenopausal
women were assigned to either placebo or 0.625-mg conjugated equine estrogen alone or in
combination with medroxyprogesterone acetate either as SEPRT or as CCRT. There was a much
greater increase in mammographic densities in women treated with SEPRT or CCRT than in
those
treated with ERT. There was little difference between women on sequential versus continuous
combined therapy, however. To the extent that mammographic densities are a reliable predictor of
breast cancer, these data strongly support an added impact of progestin on the breast cancer risk
associated with ERT.
Risks associated with CCRT in this study tended to be substantially less than those associated
with
SEPRT. However, these differences are compatible with chance, and the results of the
Postmenopausal
Estrogen/Progestin Intervention Trial described above found no differences between SEPRT and
CCRT on mammographic densities. However, because the differences in the observed ORs in the
current study are sufficiently large, it would seem prudent to consider the possibility that these
differences are real and have an underlying biologic basis. One explanation might be that standard
regimens for CCRT call for lower daily doses of progestins (typically, 2.5 mg of
medroxyprogesterone
acetate) than sequential therapy (typically, 5-10 mg). Alternatively, these data suggest that the
effect of
added progestin on breast cancer risk might be greater after "priming" of tissue by
unopposed estrogen. Estrogen stimulation in vitro results in increased cellular
progesterone
receptor content, whereas constant progesterone stimulation, even with estrogen present (as in
CCRT),
reduces progesterone receptor synthesis and/or increases progesterone receptor degradation (23).
Even with a slight increased risk of breast cancer and a more substantial increased risk of
endometrial cancer, the overall risk-benefit equation for ERT balances strongly on the side of
benefit (24), primarily because of the marked reduction in risk from
cardiovascular
disease. We have calculated that, for each incident case of breast cancer in women due to
long-term
ERT use, more than six deaths from heart disease are prevented; moreover, mortality overall is
substantially reduced in women using ERT (25). Unfortunately, the sparse
available epidemiologic data, in particular with regard to heart disease risk, limit similar
calculations for
CHRT, but it is clear from the data presented here that the overall risk-benefit equation will be
considerably less favorable than for ERT. If the main purpose for prescribing CHRT is to protect
the
endometrium from the carcinogenic effects of estrogen, then this study would argue that the
adverse
effect on the breast may outweigh the beneficial effect on the endometrium, at least in terms of
cancer
morbidity and mortality. Women who are candidates for HRT should be provided with this
information
as well as that on other established risks and benefits associated with various types of HRT and
should
also be told where uncertainty still exists in the risk-benefit equation.
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NOTES
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1 Editor's note: SEER is a set of
geographically defined,
population-based, central cancer registries in the United States, operated by local nonprofit
organizations under contract to the National Cancer Institute (NCI). Registry data are submitted
electronically without personal identifiers to the NCI on a biannual basis, and the NCI makes the
data
available to the public for scientific research. 
Supported by Public Health Service grants CA17054 and CA14089
(National Cancer Institute), by contract PC67010 (National Cancer
Institute), and by grant ES07048 (National Institute of Environmental
Health Sciences) from the National Institutes of Health, Department of
Health and Human Services; and by subcontract 050-E8709 from the
California Public Health Institute, which is supported by the
California Department of Health Services as part of its statewide
cancer-reporting program mandated by Health and Safety Code Section 210
and 211.3. A. Paganini-Hill has received grant support and has
consulted for Wyeth-Ayerst Laboratories, Philadelphia, PA.
R. K. Ross contributed to the design, overall direction, analysis, and writing; A. Paganini-Hill
contributed to the design and conduct of the study; P. C. Wan contributed to the computer
programming and analysis; and M. C. Pike contributed to the analysis and writing.
 |
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Manuscript received June 7, 1999;
revised December 6, 1999;
accepted December 16, 1999.
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