Non-Hispanic white women tend to have the highest incidence of DCIS in the US population, followed by black and Asian women, while Hispanic women have the lowest incidence (Fig. 1.3) [12]. This may be reflective of the screening behaviors of each of these racial and ethnic groups [13]. These national results have been echoed in other studies as well. Innos et al., for example, evaluated the trends in racial and ethnic differences in the incidence on DCIS in California in women ≥ 40 years, from 1988 to 1999. They observed an average annual age-adjusted incidence of DCIS of 45.3 per 100,000 in white women, 35.0 in black women, 30.9 in Asian-Pacific Islander women, and 21.8 in Hispanic women. Interestingly, while they found a steady increase in the incidence of DCIS in all racial/ethnic groups over the study period, Asian-Pacific Islander women were found to have experienced the steepest increase of a 9.1 % estimated annual percentage change, particularly in the age group 50–64 years in whom it was 12 % [14].

While DCIS is primarily considered a disease of women, it can also occur in men. Anderson et al., in a review of in situ breast cancers reported in the SEER database from 1973 to 2001, found in situ carcinomas comprised 9.4 % of all male (280 of 2984) and 11.9 % of all female breast carcinomas (53,928 of 454,405). In situ rates rose 123 % for men and 555 % for women over this time period, perhaps due to screening mammography which would make it more detectable in women. Men also seem to be slightly older than women at diagnosis, with a median age of 62 years versus 58 years for their female counterparts [15].

In addition to race/ethnicity and gender, other sociodemographic factors have also been linked to higher rates of DCIS. For example, there seems to be a higher incidence of DCIS in urban areas compared to rural areas, and the incidence of DCIS seems to be positively correlated, increasing socioeconomic status [16, 17]. It is plausible that these trends may be due to increasing use of mammography.

In the broadest classification scheme, DCIS can be grouped into “comedo” and “noncomedo” types; the latter comprising various other subtypes including cribiform, solid, micropapillary, and papillary [18]. While the value of such classification schemes can be debated, particularly in the current era of genomic and molecular medicine, there have been a number of studies evaluating trends in the aggressiveness of DCIS cases diagnosed over time using these broad definitions. For example, Li et al. evaluated the trends in the incidence of comedo and noncomedo DCIS from 1980 to 2001, using the SEER database. Rates of noncomedo DCIS increased 6.1-fold (95 % CI: 5.7–6.5) over this time frame, while rates of comedo DCIS increased 15.7 times (95 % CI: 13.5–18.4) [19]. Pandya et al. evaluated the clinical and pathological characteristics of 204 DCIS patients treated before (1969–1985) and after (1986–1990) increased use of screening mammography. Between the two time periods, the incidence of comedo DCIS increased from 14 to 36 %, and grade 3 DCIS cases increased from 24 to 33 % [20].

A first-degree family history of breast cancer is associated with an increased risk of DCIS, and this risk increases with the number of affected family members, particularly if there is a family history of breast cancer being diagnosed at a young age. In an analysis of the Million Women Study in the UK, Reeves et al. found no difference in the increased risk that a first-degree family history imparted for DCIS or invasive breast cancer (RR = 1.56 and 1.60, respectively) [21]. Reinier et al. also noted that the effect of family history also did not significantly vary in increasing the risk of premenopausal versus postmenopausal DCIS (RR = 1.9; 95 % CI: 1.2–2.8, and RR = 1.4; 95 % CI: 1.0–2.0 for pre- and postmenopausal women, respectively) [22]. Other studies have reported risk estimates ranging from 1.48 to 2.67 [23–25].

Claus et al. evaluated the BRCA 1 and BRCA 2 mutation status in 369 DCIS patients. They found, three patients (0.8 %) had mutations in BRCA 1 and nine (2.45 %) patients had mutations in BRCA 2, similar to rates found in patients with invasive breast cancer [26]. Similar to invasive cancers, mutation carriers also tend to present with DCIS at an earlier age than nonmutation carriers [27].

In general, the reproductive factors that put women at risk of invasive breast cancer have a similar effect in increasing their risk of in situ disease. Several studies have found that the risk conferred by early menarche, parity, later age at first full-term pregnancy, and later menopause on the development of invasive cancer was the same as that for DCIS [21, 28, 29]. Interestingly, Reinier et al. found that nulliparity was more strongly associated with the development of DCIS than with invasive cancer [22]. While Meeske et al. found that parity reduced the risk of developing DCIS, they found no correlation between age at first full-term pregnancy and risk of DCIS [30]. Kabat et al., in evaluating data in the Women’s Health Initiative, found that only older age at menopause was associated with increased risk of developing DCIS; age at menarche, parity, and months of breast-feeding were not significant predictors [31]. Meeske et al., on the other hand, found that long duration of breast-feeding ( > 24 months) was associated with an increased risk of DCIS (odds ratio (OR) = 2.00; 95 % CI: 1.11–3.60) [30].

Oral contraceptive use has not been shown to increase the risk for developing DCIS [32, 33]. Studies by Longnecker et al. and Reeves et al. have shown an increased risk for DCIS with the use of hormone replacement therapy (OR = 1.60; 95 % CI: 1.00–2.58, and OR = 1.51; 95 % CI: 1.39–1.63, respectively) [21, 28]. Other studies, however, have not found a correlation between hormone replacement therapy and DCIS [29, 34].