A review on family history of breast cancer: screening and counseling proposals for women with familial (non-hereditary) breast cancer

Patient Education and Counseling 32 (1997) 117–127

A review on family history of breast cancer: screening and counselingproposals for women with familial (non-hereditary) breast cancer

a , b c a*Ivana Unic , Peep F.M. Stalmeier , Petronella G.M. Peer , Willem A.J. van DaalaInstitute Of Radiotherapy, University Of Nijmegen, Nijmegen, The Netherlands

bThe Nijmegen Institute For Cognition And Information, University Of Nijmegen, Nijmegen, The NetherlandscDepartment Of Epidemiology, University Of Nijmegen, Nijmegen, The Netherlands

Received 21 September 1995; received in revised form 12 January 1996; accepted 20 January 1996

Abstract

With the aim to specify screening recommendations for women with familial (non-hereditary) breast cancer(FBC) we analysed 59 studies using quantitative methods of pooling. The pooled relative risk (RR) and cumulativeprobability were used to estimate breast cancer risk. The RRs for women with a family history of breast cancer in afirst-degree relative was 2.03 (95% CI 1.09–2.22). The highest RR is observed for women with a family history andatypical hyperplasia in their breast biopsy specimen (RR 5 10.87, 95% CI 6.05–19.69). A high cumulativeprobability before the age of 50 was only found for women with a combination of two risk factors: a family historyand atypical hyperplasia, namely 19% (95% CI 11–33%). The cumulative probabilities of women aged 50 to 70years who have a family history were between 11% (95% CI 9–13%, a family history in combination with age atfirst birth before 22 years) and 53% (95% CI 35–75%, a family history in combination with atypical hyperplasia).These high risks suggest that women over 50 years of age who have a family history of FBC have to be activelyencouraged to participate in a screening program consisting of a biannual palpation by a specialist, an annualmammogram and a monthly self-control. Yearly screening is recommended for women under 50 years of age whohave a family history and atypical hyperplasia. These recommendations remain valid until the effectiveness of suchscreening programs is assessed. u 1997 Elsevier Science Ireland Ltd.

Keywords: Breast neoplasms; Family history; Genetic counseling; Mass-screening; Risk factors

1. Introduction assessment of risk is important to these women,of whom a majority (47%) overestimate their

A large proportion of women with a family breast cancer risk [1]. The reason for the over-history of breast cancer are very concerned about estimation lies in the fact that most of the citedtheir probability of developing breast cancer. An relative risks (RR) and preventive policies are

related to women with a family history of her-* editary breast cancer (HBC). It has to be consid-Corresponding author. Tel.: 1 31 80 613972/ 1 31 80

614515; fax: 1 31 80 568350. ered that most of the women who develop breast

0738-3991/97/$17.00 u 1997 Elsevier Science Ireland Ltd. All rights reserved.PII S0738-3991( 97 )00062-1

118 I. Unic et al. / Patient Education and Counseling 32 (1997) 117 –127

cancer, have breast cancer that is not of HBC or women with a family history and with othertype but of familial breast cancer type (FBC). risk factors for breast cancer) and epidemiologi-

It is estimated that about 25–30% of the cal domain (e.g. most epidemiological studieswomen who develop breast cancer have at least deal with the RR of breast cancer withoutone first-degree relative with the disease [2–4]. distinguishing between the RR of women with aThe generally accepted idea is that a woman with family history of FBC and the RR of womena history of breast cancer in a first-degree rela- with a family history of HBC).tive has a risk of developing the same malignancy In view of these issues, we tried to draft someabout two to three times higher as compared to a screening recommendations for women with awoman lacking such a family history [5–8]. Dif- family history of FBC on the basis of the cumula-ferences in risk are present among women with a tive probability of developing the disease. Wefamily history. The highest risk is found in also estimated the cumulative probabilities forwomen with a family history of HBC [5]. The these women if a family history comes togethercharacteristics of HBC according to Lynch et al. with other breast cancer risk factors such as early[9] are: development of breast cancer across age at menarche; late age at first birth; nullipari-several generations (both maternal as well as ty; late age at menopause and personal history ofpaternal lines) consonant with autosomal domi- benign breast disease. Our recommendations fornant inheritance; early onset of breast cancer in women with a family history of FBC are inthe family, often occurring in the thirties; mul- general agreement with proposals for screeningtiple primary cancers occurrence in addition to of high risk women [5].breast cancer; and an increased incidence ofbilateral breast cancer. For women with a familyhistory of HBC, the lifetime probability of de-veloping breast cancer may approach 50% [5] or 2. Methodseven more. Of all women who develop breastcancer, about 5% have HBC [2–4]. FBC is We estimated RRs for single and joint riskdefined as breast cancer associated with a family factors by calculating weighted averages of thehistory lacking clear genetic evidence of HBC. RRs published in the literature. The naturalSome of the explanations for a familial tendency logarithms (ln) of the RRs were weighted withof breast neoplasm in FBC are weak gene the reciprocal of the squared standard error ofexpression and low gene penetrance. The under- each RR estimate. The weighted average is thelying concept of FBC is probably more compli- weighted sum of these ln(RR), divided by thecated and best described with the multistep sum of weights [10].theory where one or more cancer predisposinggenes accumulate in kindreds, acting as initiatorsof the tumorigenic process together with one or 2.1. Review of the literaturemore environmental factors. Genes and environ-mental factors presumably operate through com- By using a computerized literature searchmon mechanic pathways. Therefore, in FBC, a (MEDLINE) for papers published from Januarysingle germline mutation may be a sufficient, but 1980 until August 1993, and by checking refer-not necessary, cause of the disease. About 20– ences of the resulting manuscripts, we identified25% of the women who develop breast cancer available studies on RRs of breast cancer, pub-have FBC [4]. lished in English. No attempt was made to

Even in the current presence of genetic testing identify unpublished studies. When a study hadfor the deleterious genotype, instructing women been reported in more than one paper, only thewith a family history is complicated with many most recent report was included in our analysisdebatable issues in the counseling (e.g. how to (unless the necessary data appeared in an earlieradvise women who have a family history of FBC paper). A study was included in the analysis if:

I. Unic et al. / Patient Education and Counseling 32 (1997) 117 –127 119

menarche. All other risk factors were still poten-(a) it employed a case-control or cohort de- tially present in the control group.sign; We tried to separate studies on a family history(b) a family history of breast cancer as a risk of HBC from studies on a family history of FBCfactor was presented either as a single risk looking for risk factors associated with HBC (i.e.factor or in combination with other risk fac- number of relatives affected with breast cancer,tors; bi /unilaterality status of the disease and early(c) the outcome phenomenon was invasive age at onset of breast cancer in relatives) [3,9,12–breast cancer (any histological type of tumor); 16]. We decided that results from studies where(d) estimates of risk of developing breast authors reported risks for relatives of breastcancer (odds ratios, RR) and a corresponding cancer patients, younger than 50 years of age andmeasure of precision (confidence interval) having bilateral breast cancer, present breastwere presented or could be derived [11]; cancer risk for relatives with HBC. These results(e) white women were the majority of the were not included in the analysis. We also as-studied population. sumed that the reported family histories repre-

sent more often relatives with FBC and not HBCIn the first part of the study, we selected studies [2–4].for the estimation of breast cancer risk accordingto the different categories of a family history. We 2.2. Analysiswere interested in the following types of a familyhistory of breast cancer: The studies were classified as case-control or

(1) breast cancer in a mother; (2) breast cohort studies. The RR estimations were donecancer in sister(s); (3) breast cancer in first- for each study design separately. The effectdegree relatives (mother, daughter, sister); (4) measure in the case-control studies was the oddsbreast cancer in second-degree relatives (grand- ratio and in the cohort studies the RR. We usedmother, aunt). Unfortunately, the selected the term RR throughout to refer to both effectstudies did not present data on the characteristics measures. If available, the RRs adjusted forof relatives with breast cancer or presented multiple risk factors were used for the analysis.different ages of onset of breast cancer in differ- When an article provided proportions of exposedent type of relatives. In the case-control studies, cases and controls instead of the RR, the crudethe reference group consisted of women without RR was calculated. To obtain 95% confidencea family history of breast cancer. intervals (95% CI) on RR, we used Woolf’s

In the second part, we selected studies to method [11]. To be sure that the variation in theexplore the joint effects on risk of developing RRs derived from the reviewed studies couldbreast cancer for women with a first-degree only be due to statistical sampling variation, wefamily history in combination with other risk performed a homogeneity test. The RRs werefactors, namely early age at menarche (� 12 not pooled if the homogeneity assumption didyears); late age at first birth (� 30 years); nulli- not hold [10].parity; late age at menopause (� 45 years); and The last part of the estimation was convertingpersonal history of atypical hyperplasia or lobu- the different RRs into the cumulative probabilitylar carcinoma in situ. For the case-control of developing breast cancer till the age of 50 andstudies, the control group consisted of women 70, respectively. This analysis was done using thewithout a family history and without the joint pooled RRs on the joint effects from the cohortrisk factor under investigation. For instance, if studies only because results from cohort studieswe want to know the RR of breast cancer for the were expected to be subject to fewer biases thanjoint effect of a family history and early age at results from case-control studies. For the calcula-menarche then the control group consisted of tion of the cumulative probability, we assumedwomen without a family history and late age at that the RR of developing breast cancer is


constant over time [7,16–18]. We used data on (� 12 years) (Pooled RR 5 1.65, 95% CI 1.23–the baseline cumulative probability of developing 2.12) or late age at menarche (� 14 years)breast cancer in the general population (where (Pooled RR 5 1.53, 95% CI 1.21–1.95).all risk factors were potentially present) from Pooling of the RRs for women with a familybirth till the age of 50 and 70, respectively, from history and late age at first birth (� 30 years)the study of Feuer et al. [19]. These cumulative was not allowed (RRs were in the range from 0.9baseline probabilities of developing breast cancer to 2.01; p� 0.05) [40,50,52]. The estimated RR offor women from the general population were breast cancer for women with a family historyused to calculate two annual probabilities (till and the first birth under the age of 24 years wasthe age of 50 and 70, respectively) of living 2.41 (95% CI 2.03–2.85). For nulliparous womenwithout breast cancer. The product (B) of the with a family history the estimated RR was 2.51estimated RR and the annual probability of (95% CI 1.88–3.35).living without breast cancer was used to compute The RR of breast cancer for women who werethe cumulative probability of living without still premenopausal was 2.22 (95% CI 1.97–2.51).breast cancer (S) for women with one or more Pooling of the data for postmenopausal women

agerisk factors: S(age) 5 (1 2 B) . Finally, the (� 45 years) with a family history was notcumulative probability of developing breast can- allowed (RRs were in the range from 1.36 tocer (F ) for women with one or more risk factors 4.19; P� 0.05) [22,24,45,48,49,52,56,61]. The RRswas computed by F(age) 5 1 2 S(age). This meth- for women with a family history and early age atod is described by Stalpers et al. [20]. menopause were only reported in three studies.

These studies all suggest that women with earlyage at menopause (� 45 years) and a family

3. Results history have no increased risk (Pooled RR 51.12; 95% CI 0.74–1.68) compared to the popula-

A total number of 46 case-control and 13 tion without a family history.cohort studies was included in the analysis. Table Limited data were available on women with a1 lists the case-control studies [18,21–65]. Table 2 family history and personal history of benignpresents the cohort studies [16,66–77]. breast disease-lobular carcinoma in situ or atypi-

cal hyperplasia. The estimated RR for the combi-3.1. The RRs for a family history as a single nation of a family history of breast cancer andrisk factor lobular carcinoma in situ was 2.97 (95% CI 1.93–

4.57). The pooled RR observed for the combina-The results are presented in Table 3. The tion of atypical hyperplasia and a family history

estimated RRs from the case-control studies for was 3.7 (95% CI 1.21–11.36). For all studies on athe history of breast cancer in a mother, sister(s), family history and atypical hyperplasia, the con-and in second-degree-relatives were 1.93 (95% trol group consisted both of women withoutCI 1.75–2.14); 2.03 (95% CI 1.84–2.25) and 1.52 breast cancer as well as women without benign(95% CI 1.42–1.63), respectively. The estimated breast diseases.RR obtained from the analysis of the cohortstudies, was 2.05 (95% CI 1.9–2.22). 3.3. The RRs for joint risk factors from the

cohort studies3.2. The RRs for joint risk factors from thecase-control studies The results are presented in Table 5. All joint

risks are only for women with a first-degreeThe results are presented in Table 4. The joint family history. The estimated RR for the combi-

RRs were only available for women with a first- nation of a family history and menstrual ordegree family history. Similar RRs were ob- reproductive risk factors were all very similarserved for a first-degree family history and early (RRs about 1.7). In contrast, the RR of the


Table 1Characteristics of the case-control studies

First Year Age Number Number Source ofauthor of range of of controls

diagnoses cases controlsof cases

Adami [35] 1977–1978 25–100 i. 1330 1330 PBrignone [26] 1974–1983 All ages i. 853 853 SBruning [65] 1986–1987 38–75 i. 225 450 PBurns [37] 1971–1975 30–79 p. 1232 602 SByrne [52–55] 1973–1980 All ages i. 2980 3180 SChaudary [48] 1979–1980 All ages i. 204 792 PCusimano [42] 1983–1985 30–94 i. 143 286 HDubin [46] 1968–1979 � 34 i. 1292 2173 SDuffy [44] 1974–1978 40–59 i. 236 2962 SFolsom [47] 1986–1987 55–69 i. 229 183 PHelmrich [43] 1976–1980 � 69 i. 1185 3227 HHislop [24] 1980–1982 � 70 p. 512 540 PHolowaty [41] 1980–1988 40–59 i. 289 5780 SJoensuu [60] 1987–1990 40–74 i. 204 612 SLa Vecchia [39,40] 1982–1983 26–74 p. 1108 1281 HLipnick [49,50] 1971–1976 30–55 p. 844 8440 PLivolsi [21] 1977–1979 45–74 i. 332 1354 HLubin [27,33] 1976–1977 30–80 p. 577 826 PMettlin [18] 1982–1987 25–98 i. 779 1558 HMorabia [61] 1973–1975 25–74 i. 427 560 HNajem [36] 1973–1980 Not presented p. 60 15 SNomura [34] 1975–1980 45–74 i. 344 1288 H/PPaffenbarger [22] 1970–1977 All ages p. / i. 1868 3391 HPalli [63] 1975–1987 All ages i. 62 315 SRoseman [23] 1968–1986 � 29 p. 5684 3316 SRosero-Bixby [62] 1982–1984 25–58 i. 171 826 PRuder [64] 1971–1975 21–60 i. 291 461 HSattin [56–58,28–32] 1980–1982 20–54 i. 4735 4688 PSchapira [25] 1987–1988 25–83 i. 216 432 PSegala [45] 1983–1987 26–66 i. 450 576 HToti [38] 1980–1983 All ages i. 1556 1505 HWHO Study [59] 1976–1986 20–62 i. 2116 12077 H

i. 5 incident cases; p. 5 prevalent cases; S 5 screening controls; P 5 population controls; H 5 hospital controls.

combination of a family history and atypicalhyperplasia was 10.87 (95% CI 6.05–19.69). It is

Table 2 by far the highest RR reported in this study.Characteristics of the cohort studies

First author Study Age Study size 3.4. The cumulative probabilities for single andinterval range

joint risk factors from the cohort studiesBodian [68,77] 1930–1982 All ages 1799Carter [72] 1973–1986 35–74 16692 Table 6 shows the cumulative probabilities ofCarter [69] 1971–1984 25–74 7426

breast cancer developing till the age of 50 or 70,Colditz [70] 1976–1988 30–55 121700respectively, in women with relatives with breastPage [66,74–76] 1959–1976 � 19 10366

Sellers [16] 1986–1989 55–69 37105 cancer. A sharp increase of the cumulative prob-Tavassoli [73] 1965–1975 � 14 199 abilities of developing breast cancer is observedWrensch [71,67] 1973–1991 30–79 2701 between the age 50 and 70.


Table 3 Table 5The estimated relative risks for breast cancer development by The estimated relative risks for breast cancer developmenttype of a family history of breast cancer among women with a first-degree family history of breast

cancer by the selected risk factors (the cohort studies)Family history Number of Pooled 95% confidence

reference RR interval Risk factor Number of Pooled 95%reference RR confidenceaMother [22,27,35,38], 1.93 1.75–2.14

interval[39,44,46,49],[52,56,60,64] Age at menarche [16,70]

� 12 years 1.65 1.39–1.95aSister(s) [22,27,35,38] 2.03 1.84–2.25[39,44,46,49], Nulliparity [16,70,75] 1.84 1.32–2.56[52,56,64]

Age at first birth [16,70,75]aSecond-degree [23,35,38,44], 1.52 1.42–1.63 � 22 years 1.61 1.08–2.36

relatives [46,52,56,64]Atypical hyperplasia [73,74,76] 10.87 6.05–19.69

bFirst-degree [16,69–72,74], 2.05 1.90–2.22relatives [77]a Case-control studies. pared to the cumulative probabilities of womenb Cohort studies. with a first-degree family history only were

similar to each other but as a group higher thanTable 4 the cumulative probabilities of women without aThe estimated relative risks for breast cancer development

family history. The highest cumulative probabili-among women with a first-degree family history of breastty is observed for women with a family history ofcancer in combination with other risk factors (the case-

control studies) breast cancer and the personal history of atypicalhyperplasia. Women with atypical hyperplasiaRisk factor Number of Pooled 95%

reference RR confidence and a family history, both before the age of 50interval and between 50 and 70 years had very high

cumulative probabilities of developing breastAge at menarche [40,50,54],� 12 years 1.65 1.23–2.12 cancer (19% and 53%, respectively).� 14 years 1.53 1.21–1.95

Age at first birth [40,50,52]� 24 years 2.41 2.03–2.85 4. Conclusions

Premenopausal status [22,24,36],[45,48,49], 2.22 1.97–2.51 This summary of the published data on breast[52,56,61] cancer risk associated with a family history

Nulliparity [50,52,54] 2.51 1.88–3.35 suggests a two-fold increase in breast cancer riskfor relatives of breast cancer patients as com-Age at [40,52,61]pared to women without a family history. Ourmenopause

� 45 years 1.12 0.74–1.68 results may suggest that the menstrual and re-productive risk factors have a limited effect onLCIS [21,58] 2.97 1.93–4.57the manifestation of breast cancer in individuals

Atypical hyperplasia [51,53], 3.70 1.21–11.36with a first-degree family history, probably of[57]FBC type. For these risk factors, the RR of

LCIS 5 lobular carcinoma in situ.breast cancer was always smaller than 2.51 or1.84, namely for the combination of nulliparity

All joint risks are only for women with a and a family history in the case-control andfirst-degree family history. The cumulative prob- cohort studies, respectively. Shapiro et al. foundabilities of developing breast cancer for women a modest association between a family historywith the combination of a family history and and gravidity [78]. Negri et al. [79] also state thatsome menstrual and reproductive factors com- reproductive factors may be of limited impor-


Table 6The cumulative probabilities (CP) of developing invasive breast cancer for women with a first-degree family history of the diseaseby age and the selected risk factors (the cohort studies)

aRisk factor CLP (95% CI)

Till the age of 50 Till the age of 70

No family history 2% 7%

First–degree family history 4% (3.7–4.3%) 13% (12.5–14.3%)Age at menarche� 12 years 3.3% (2.8–3.8%) 11% (9–13%)Age at first birth� 22 years 3% (2.14–5%) 11% (7.3–15%)Nulliparity 4% (3–5%) 12% (9–16%)Atypical hyperplasia 19% (11–33%) 53% (35–75%)

a Cumulative probability of developing breast cancer.

tance in women with a family history. Our results ally accepted theory of the progression of breastalso agree with the results of Anderson et al. [80] diseases, in which atypical hyperplasia precedeswho found comparable risk factors for women and favors carcinoma in situ. Only the case-with unilateral disease in the family, probably control studies reported RRs on lobular car-FBC. On the contrary, Anderson et al. [80] also cinoma in situ and a family history. We did notreport increased joint RRs of breast cancer for find a significant difference (P� 0.05) betweenmenstrual and reproductive factors in women the RRs for a family history and lobular car-with bilateral breast cancer in the family, pre- cinoma in situ (RR 5 2.97, 95% CI 1.93–4.57)sumably the women with HBC. This suggests and a family history and atypical hyperplasiathat menstrual and reproductive risk factors may (RR 5 3.7, 95% CI 1.21–11.36) though the rela-independently operate in women with a family tive magnitude of the RRs was not in thehistory of probably HBC type. expected direction. We think that the authors

We found that women with a combination of used broad definition of lobular carcinoma in situearly menopause (� 45 years) and a first-degree that may explain the relatively low estimated RRfamily history have the same RR of developing (RR 5 2.97) for women with a family history andbreast cancer as women without a family history lobular carcinoma in situ versus a family history(RR 5 1.12; 95% CI 0.74–1.68). This is in agree- and atypical hyperplasia. We conclude that ourment with earlier results [81,82]. Therefore, early results do indeed indicate that atypical hyper-age at menopause has a protective effect in the plasia is the predictor of breast cancer develop-general population but also in women with ment in women with a family history [83].relatives with breast cancer. We found good agreement between the study

In contrast to the above rather low RRs, we results from the case-control and cohort studies.found a very high RR of 10.87 for the joint effect This may be explained by the fact that weof a family history with atypical hyperplasia from included, if possible, only the population basedthe cohort studies. The presence of atypical case-control studies, thus making the controlhyperplasia in conjunction with a first-degree population more comparable to the populationfamily history of breast cancer placed these from the cohort studies [84]. Furthermore, therewomen at substantial risk of breast cancer. We were few publications on the combined effects ofexpected a higher RR for women with a first- the considered risk factors and a family history.degree family history and personal history of Finally, we tried to separate the risk factorslobular carcinoma in situ compared to the RR of pertaining to FBC and HBC forms. Unfortuna-women with a family history and atypical hy- tely, the selected studies did not enable us toperplasia. This expectation is based on the gener- make a clear distinction between FBC and HBC


cases due to the lack of data on the characteris- Clinicians have to be aware that the wrong risktics of relatives with breast cancer (age at onset perception may interfere and even decreaseof breast cancer, number of affected relatives, women’s ability to perform breast-self examina-laterality status of the disease). In general, we tion or mammography. We think that the follow-assumed that the reported family histories repre- ing counseling proposals may be given to helpsent more often relatives with FBC and not HBC these women to get a more realistic risk percep-[2–4]. We conclude that population based studies tion and to stimulate compliance to the screen-do not yield sufficient data to estimate the RR ing: 1. Clinicians need to be aware of the signifi-for women with HBC. For individual risk assess- cance of specific family patterns of breast cancer,ment in these women, pedigree studies could be surveillance guidelines, and psychological con-used. cerns of these women; 2. Women have to be

educated about breast cancer risk and risk fac-tors associated with this disease; 3. Breast cancer

5. Recommendations for counseling and risk needs to be individually assessed and dis-screening cussed with the woman; 4. Screening recom-

mendations have to be tailored according toIn spite of the recent wide spreading of in- these individual risk levels.

formation about breast cancer risks, only a small Our results show that women with a first-proportion of women with a family history of the degree family history of FBC before the age ofdisease correctly estimate risks for themselves or 50 have a cumulative probability of breast cancerfor the general population. We were concerned development of 4% (95% CI 3.7–4.3%). Such aabout women with a family history who overesti- cumulative probability is comparable to themate their breast cancer risk. In our opinion, cumulative probability of women without a fami-there are at least three reasons for the overesti- ly history. For the latter group, the regularmations. The main reason may lie in the fact that screening program between the age 50 and 70most of the cited relative risks are related to (the screening policy in the Netherlands) iswomen with HBC. It seems to many women with deemed as a sufficient preventive measure anda positive family history that they are appro- no special preventive actions are taken beforepriately concerned. However, some of these the age of 50. Similarly, for women with a familywomen are convinced that they will be the next history of FBC screening before the age of 50one who will develop the disease, not realising appears to be unnecessary because they have athat only a minority (about 5%) of women with a comparable cumulative probability.family history of breast cancer have a very high For women with a family history of FBC, arisk of breast cancer. The second reason may be, sharp increase in cumulative probability occurrsthat for some women, the maximum Mendelian between the age 50 and 70. In this period, allrisk of 50% is below their perceived cancer risk. women are recommended to participate in theThese women will not assess their own risk regular screening programs. We expect that ourcorrectly. The third reason, we believe, is that screening proposal may be helpful althoughthere are other less known social factors that having a family history of breast cancer is not aaffect the risk perception and produce differ- modifiable risk factor. This report provides sup-ences between the objective and the subjective port that screening of women with a familyrisk perception. history of FBC has to be considered as a method

Targeting women with a family history of of secondary prevention. We think that evenbreast cancer with breast cancer counseling and yearly screening consisting of a biannual palpa-screening is an important issue. Both knowledge tion by a specialist, an annual mammogram and aof objective risk and perceptions of personal monthly self-control would be an optimal screen-sensibility to breast cancer are important ing option for women with a family history ofmotivators of breast cancer screening behavior. FBC. The reason for this recommendation lies in


[7] Anderson DE, Badzioch MS. Risk of familial breastthe following facts: screening is already widelycancer. Cancer 1985;56:383–7.use; it is non-invasive; the available data on

[8] Kelsey JL, Hildreth NG. Breast and gynecologic cancerbenefits of early breast cancer screening show epidemiology. Boca Raton: CRC Press, 1983.high rates of cure after an appropriate medical [9] Lynch HT, Kullander S. Cancer genetics in women.

Boca Raton: CRC Press, 1987.management of early detected breast cancer and[10] Greenland S. Quantitative methods in the review of thegives clear evidence that screening can reduce

epidemiologic literature. Epidemiol Rev 1987;9:1–30.breast cancer mortality in women over 50 years. [11] Kahn HA. An introduction to epidemiologic methods.For women with a family history of FBC, even New York: Oxford University Press, 1983.

[12] Ottman R, Pike MC, King M et al. Familial breastlarger beneficial effects of screening are ex-cancer in a population-based series. Am J Epidemiolpected.1986;123:15–21.Our data show that yearly screening of the

[13] Adami HO, Hansen J, Jung B et al. Characteristics ofsubgroup of women with a family history and familial breast cancer in Sweden. Cancer 1981;48:1688–atypical hyperplasia before the age of 50 is 95.

[14] Anderson DE. A genetic study of human breast cancer.mandatory (cumulative probability 5 19%, 95%J Natl Cancer Inst 1972;48:1029–34.CI 11–33%). The reason for this recommenda-

[15] Anderson DE. Genetic study of breast cancer: identifica-tion lies in the fact that the cumulative probabili- tion of a high risk group. Cancer 1974;34:1090–7.ty for this combination of risk factors is compar- [16] Sellers TA, Kushi LH, Potter JD et al. Effect of familyable to the cumulative probabilities of women history, body-fat distribution, and reproductive factors

on the risk of postmenopausal breast cancer. N Engl Jwith a family history of HBC and that for theMed 1992;326:1323–9.latter group yearly screening before the age of 50

[17] Claus EB, Risch NJ, Thompson WD. Age at onset as anis recommended. indicator of familial risk of breast cancer. Am J Epi-

demiol 1990;131:961–72.[18] Mettlin I, Croghan I, Natarajan N et al. The association

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A review on family history of breast cancer: screening and counseling proposals for women with familial (non-hereditary) breast cancer