The Decrease in Breast-Cancer Incidence in 2003 in the United States
Peter M. Ravdin, Ph.D., M.D., Kathleen A. Cronin, Ph.D., Nadia Howlader, M.S., Christine D. Berg, M.D., Rowan T. Chlebowski, M.D., Ph.D., Eric J. Feuer, Ph.D., Brenda K. Edwards, Ph.D., and Donald A. Berry, Ph.D.
An initial analysis of data from the National Cancer Institute'sSurveillance, Epidemiology, and End Results (SEER) registriesshows that the age-adjusted incidence rate of breast cancerin women in the United States fell sharply (by 6.7%) in 2003,as compared with the rate in 2002. Data from 2004 showed a levelingoff relative to the 2003 rate, with little additional decrease.Regression analysis showed that the decrease began in mid-2002and had begun to level off by mid-2003. A comparison of incidencerates in 2001 with those in 2004 (omitting the years in whichthe incidence was changing) showed that the decrease in annualage-adjusted incidence was 8.6% (95% confidence interval [CI],6.8 to 10.4). The decrease was evident only in women who were50 years of age or older and was more evident in cancers thatwere estrogen-receptor–positive than in those that wereestrogen-receptor–negative. The decrease in breast-cancerincidence seems to be temporally related to the first reportof the Women's Health Initiative and the ensuing drop in theuse of hormone-replacement therapy among postmenopausal womenin the United States. The contributions of other causes to thechange in incidence seem less likely to have played a majorrole but have not been excluded.
Major changes in cancer incidence and death rates, as detectedin cancer-registry data, provide unique opportunities to examinequestions related to the cause, prevention, detection, and treatmentof cancer. In a preliminary report, we suggested that such amajor change in breast-cancer incidence occurred in 2003 inthe United States.1 In contrast, the 1990s saw an increase inthe annual age-adjusted incidence of breast cancer by an averageof about 0.5% per year, a rise that was particularly evidentamong women who were 50 years of age or older2 (Figure 1). Changesin reproductive factors, in the use of menopausal hormone-replacementtherapy, in mammographic screening, in environmental exposures,and in diet have all been proposed to explain the trend. Ofthese factors, only the use of hormone-replacement therapy changedsubstantially between 2002 and 2003.
Figure 1. Annual Incidence of Female Breast Cancer (1975–2004).
Data are from nine of the NCI's SEER registries. SEER sites include San Francisco, Connecticut, Detroit (metropolitan area), Hawaii, Iowa, New Mexico, Seattle–Puget Sound, Utah, and Atlanta (metropolitan area).
In this report, we provide additional data from 2004 that showlittle change in breast-cancer incidence between 2003 and 2004.A comparison of incidence rates in 2001 with those in 2004 (omittingthe years in which the incidence was in the process of changing)showed that the decrease in annual age-adjusted incidence was8.6% (95% CI, 6.8 to 10.4).
The decrease in breast-cancer incidence began in mid-2002 andoccurred shortly after the highly publicized series of reportsfrom the randomized trial of the Women's Health Initiative,which reported a significant increase in the risks of coronaryheart disease and breast cancer associated with the use of estrogen–progestincombination therapy.3 By the end of 2002, the use of hormone-replacementtherapy had decreased by 38% in the United States, with approximately20 million fewer prescriptions written in 2003 than in 2002.4,5
The analyses we report here used information from the SEER Programof the National Cancer Institute (NCI) collected from nine cancerregistries reporting on 9% of the U.S. population. Trends inthe incidence of female breast cancer were age-adjusted to thestandard population in the year 2000 and were adjusted for reportingdelays. Joinpoint (version 3.0) statistical software (http://srab.cancer.gov/joinpoint/)was used for fitting trends over time and to evaluate when changesin trends occurred. The number of patients with unknown estrogen-receptorstatus changed from 15% in 2001 to 8% in 2004; to adjust forthis change, multiple imputation was used to generate estrogen-receptorvalues for missing data.
Comparison of incidence rates in 2001 with rates in 2004 (omittingthe years in which the incidence was rapidly changing) showedthat the decrease in annual age-adjusted incidence was evidentonly in women who were 50 years of age or more. During thatperiod, there was an increase of 1.3% (95% CI, –3.1 to5.8) in incidence for women below the age of 50 years, a decreaseof 11.8% (95% CI, 9.2 to 14.5) for women between the ages of50 and 69 years, and a decrease of 11.1% (95% CI, 7.9 to 14.2)for women 70 years of age or older.
For women between the ages of 50 and 69 years, the decreasewas more evident in those with estrogen-receptor–positivetumors (14.7%; 95% CI, 11.6 to 17.4) than in those with estrogen-receptor–negativetumors (1.7%; 95% CI, –4.6 to 8.0). The decreases weresimilar for localized disease (11.3%; 95% CI, 8.0 to 14.6) andmore advanced disease (13.6%; 95% CI, 9.2 to 17.9) and wereevident in primary breast cancers (13.7%; 95% CI, 11.0 to 16.4)but not in contralateral second primary or later breast cancers,for which there was a nonsignificant increase (9.4%; 95% CI,–1.6 to 20.5).
Figure 2A shows the quarterly, age-adjusted incidence ratesof breast cancer in women between the ages of 50 and 69 years,categorized according to estrogen-receptor status. The datafor change in trend were examined with the use of Joinpointstatistical software. Changes in trend in mid-2002 and mid-2003were evident for all patients and for patients with estrogen-receptor–positivetumors but not for those with estrogen-receptor–negativetumors. However, the low incidence of estrogen-receptor–negativetumors limited the statistical ability to detect a change intrend. For all patients, the quarterly changes in rate werean increase of 0.08% (95% CI, –0.60 to 0.77) in the firsttime interval, a decrease of 4.43% (95% CI, –12.66 to4.75) in the next time interval defined by Joinpoint analysis,and a decrease of 0.04% (95% CI, –1.56 to 1.50) in thelast time interval.
Figure 2. Quarterly Incidence of Breast Cancer in Women between the Ages of 50 and 69 Years, According to Estrogen-Receptor (ER) Status, and the Number of Prescriptions for Hormone-Replacement Therapy (2000–2004).
In Panel A, data are from nine of the NCI's SEER registries, with trends modeled with regression-analysis statistical software (Joinpoint). Trends were age-adjusted to the standard population in the year 2000 and were adjusted for reporting delays. Panel B shows the number of prescriptions reported in the United States for the combined estrogen–progestin preparation Prempro and the conjugated equine estrogen Premarin, according to year.
What might have been responsible for the sharp decline in breast-cancerincidence, followed by a relative stabilization at a lower incidencerate? One possibility is a SEER reporting flaw, which seemsunlikely. The trend for a decrease in incidence in 2003 wasevident in all nine SEER registries, there was no statisticallysignificant change in the incidence of cancer other than breastcancer in women during this period, and the lower rates continuedin 2004. Could the change have been related to a major decreasein the rate of screening mammography? Although a decrease of3.2% in this rate was reported for women between the ages of50 and 65 years for 2003, as compared with that for 2000,6 sucha change would seem insufficient to explain the observation.A change in screening patterns specific to women who formerlyreceived hormone-replacement therapy is also a possibility.For example, if women who discontinued hormone-replacement therapyalso stopped receiving mammograms, an apparent decrease in incidencecould result. Although visits to physicians would probably decreaseamong women who discontinued hormone-replacement therapy, nopublished data are available showing a substantial decreasein mammographic screening in such women. Another possible explanationis that a decrease in incidence is expected in a heavily screenedpopulation, similar to that reported for prostate cancer. Nosudden decrease has yet been reported for breast-cancer incidencein heavily screened populations.
One of the arguments against changes in mammographic screeningas a primary reason for the decline is that the effect was mainlyon estrogen-receptor–positive tumors. Breast cancers thatare detected on mammography are more likely to be estrogen-receptor–positivethan are tumors not detected on mammography (80% vs. 70%),7but the difference in the percentages according to estrogen-receptorstatus is minor. Thus, a drop in screening would result in anapproximately equal decrease in estrogen-receptor–positiveand estrogen-receptor–negative tumors, an expectationthat differed from our findings.
Discontinuation of hormone-replacement therapy could have causeda decreased incidence of breast cancer by direct hormonal effectson the growth of occult breast cancers, a change that wouldhave been expected to affect predominantly estrogen-receptor–positivetumors. If the decrease in breast-cancer incidence had beenassociated with discontinuation of hormone-replacement therapy,the rapidity of change suggested that clinically occult breastcancers stopped progressing or even regressed soon after discontinuationof the therapy. The hypothesis that hormone withdrawal can rapidlyinfluence the growth of breast cancer is supported by anecdotalreports of regression of breast cancer after discontinuationof hormone-replacement therapy.8 A cessation of such therapywas associated with a reduction in the proliferative index ofbreast-cancer cells within 1 month in women with estrogen-receptor–positivetumors but not in those with estrogen-receptor–negativetumors in the same setting,9 and responses within weeks afterestrogen deprivation have been seen in clinical trials of neoadjuvanthormones. An early effect of tamoxifen was seen in the BreastCancer Prevention Trial, in which the cumulative rates of invasivebreast cancer in the tamoxifen group and the placebo group appearedto diverge within the first few months and differed statisticallyat the end of the first year.10 An analysis of 51 epidemiologicstudies showed that an elevated risk of breast cancer afterthe use of hormone-replacement therapy had largely if not whollydisappeared within 5 years after discontinuation of therapy,although a more detailed analysis of the time course of changesin risk within this period was not presented.11
Notably, the change in the use of hormone-replacement therapyalso followed a time course that was similar to the declinein breast-cancer incidence, with a sharp decline followed bya relative stabilization at a new, lower level. The total numberof prescriptions for the two most commonly prescribed formsof hormone-replacement therapy in the United States —Premarin and Prempro — had their steepest declines startingin 2002 and particularly in 2003 (62 million prescriptions in2000, 61 million in 2001, 47 million in 2002, 27 million in2003, 21 million in 2004, and 18 million in 2005)12 (Figure 2B).
Other medications can influence the incidence of breast cancer.These drugs include tamoxifen and raloxifene, and there is someevidence for beneficial effects of nonsteroidal antiinflammatorydrugs, statins, and calcium and vitamin D supplements. However,none of these agents were used by a substantial portion of postmenopausalwomen or showed substantial change in use during the periodfrom 2000 to 2004.12,13 Therefore, the drugs are unlikely candidatesfor causing the decrease in incidence.
When the results of the Women's Health Initiative hormone trialwere announced, women were asked to discontinue their studymedications (placebo or hormone) but were encouraged to continueundergoing annual mammography. These women continue to be followedfor clinical outcome, and a report of follow-up of the combinedestrogen-plus-progestin trial is anticipated later this year.This report will provide the highest level of evidence concerningthe influence of cessation of hormone-replacement therapy onthe incidence of breast cancer. Other observers have noted adecline in breast-cancer incidence after 2002. A report froma subgroup of California registries also showed a sharp decreasein breast-cancer incidence in 2003 and suggested that it extendedinto 2004.14 A recent analysis of national cancer data by Jemalet al.15 showed a decline in the incidence of breast cancerin 2003 but did not comment on its clinical relevance. The joinpointin that study was done with annual (rather than quarterly) data.Annual rates obscure within-year trends, in this case withinyears 2002 and 2003. In addition, the statistical method usedby Jemal et al. cannot select the final year in a range (inthis case, 2003) as demonstrating a discontinuity.
It is possible that the ultimate understanding of the effectof cessation of hormone-replacement therapy will be complex;it will probably depend on more than one mechanism and willbe affected in different ways by various forms of postmenopausalhormone-replacement therapy. The time course of the decreasein breast-cancer incidence is of both practical and theoreticalinterest. Our data suggest that much of the decrease in breast-cancerincidence that is attributable to changes in the use of hormone-replacementtherapy has already occurred, but important questions remain.Can we expect only a delay in the appearance of clinically detectabletumors, with no reduction in long-term incidence, or will therebe a long-term reduction? A change in the hormonal milieu mayhave slowed the growth of tumors slightly or temporarily. Ifthis is the case, as the use of hormone-replacement therapystabilizes, breast-cancer incidence should rise again. Alternatively,the change in hormonal milieu may have a more profound effect,similar to that of hormonal adjuvant therapy.16
We believe that the data are most consistent with a direct effectof hormone-replacement therapy on preclinical disease, but thisconclusion does not rule out some contribution from changesin screening mammography. In any case, attempts to understandthe rapid reduction in incidence using theoretical models ofbreast-cancer evolution and the effects of screening and treatment— such as those of the NCI's Cancer Intervention and SurveillanceModeling Network17 — may lead to new insights into thedevelopment and prevention of breast cancer.
No potential conflict of interest relevant to this article wasreported.
Source Information
From the Department of Biostatistics, M.D. Anderson Cancer Center, Houston (P.M.R., D.A.B.); the Division of Cancer Control and Population Sciences (K.A.C., N.H., E.J.F., B.K.E.) and the Division of Cancer Prevention (C.D.B.), National Cancer Institute, Bethesda, MD; and the Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, Torrance, CA (R.T.C.).
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A Decline in Breast-Cancer Incidence
Bluming A. Z., Elfenbein G. J., Kliewer E. V., Demers A. A., Nugent Z. J., Zahl P.-H., Mæhlen J., Cady B., Chung M. A., Michaelson J. S., Robbins A. S., Clarke C. A., Signorello L. B., Tarone R. E., Ravdin P. M., Cronin K. A., Chlebowski R. T.
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