Two papers published in 1941 established LCIS as a distinct morphologic entity. The description by Muir¹ appeared in an overview of the earliest stages of mammary carcinoma. Lesions were subdivided according to whether carcinoma appeared to originate in ducts or lobules (“acini”). Muir found that it may be difficult to prove origin from the lobular epithelium in some cases:

Among Muir’s illustrations of “intra-acinous” carcinoma are some with histologic patterns that might be regarded today as ductal in type, thus constituting a condition now recognized as extension of duct carcinoma into lobules. One picture showed the typical features of LCIS.

Foote and Stewart² introduced the term “lobular carcinoma in situ” to describe “a disease of small lobular ducts and lobules.” They described and commented on almost all of the important clinical and pathologic features of the disease:

Because LCIS is a microscopic lesion that does not form a palpable tumor, the incidence of the disease is unknown among asymptomatic women. When it occurs alone in biopsied patients, LCIS constitutes 1% to 6% of mammary carcinomas and 30% to 50% of noninvasive carcinomas.^3,4

In retrospective reviews, each involving several thousand “benign” breast specimens, the frequency of LCIS was 1.5%,⁵ 1.4%,⁶ 0.6%,⁷ and 0.5%.⁸ A review of nearly 10,000 breast biopsies without other neoplastic lesions performed from 1960 through 1979 revealed that the annual frequency of LCIS or lobular neoplasia (LN) ranged from 1.2% to 4.3%, averaging 2.7%.⁹

An autopsy study of breasts from 83 elderly hospitalized women revealed LCIS in 3, or 3.6%.¹⁰ This relatively small series, which included six women previously known to have breast carcinoma, cannot be regarded as generally representative. Nielsen et al.¹¹ examined breasts from young women, many of whom died unexpectedly, including only one with previously diagnosed breast carcinoma, and they found LCIS in 4 (3.6%) of 110 cases. Three other autopsy studies including more than 300 women failed to detect any examples of LCIS.^12,13,14

Analysis of population-based data from 1978 to 1998 in the United States revealed an increase in the incidence of LCIS from 0.90/100,000 person-years to 3.19/100,000 person-years.¹⁵ Incidence increased continuously throughout the study period among postmenopausal women, with the highest rate among women 50 to 59 years of age in 1996 to 1998 (11.47/100,000 person-years). Analysis of data from the Surveillance Epidemiology and End Results (SEER) program for 1999 to 2004 revealed that the age-related incidence of LCIS, not otherwise specified, rose from 0.9 per 100,000 women in the 30- to 39-year age group to a peak of 10.2 per 100,000 in the 50- to 59-year age group and then declined to 2.4 per 100,000 among women 80 or more years of age.¹⁶ By contrast, the age-related incidence of DCIS peaked among women 70 to 79 years of age. The incidence of LCIS among White women (3.6 per 100,000) was nearly twice that of Black women (1.9 per 100,000), whereas the incidence of DCIS among White women (23.3 per 100,000) was only slightly greater than the incidence of DCIS among Black women (20.2 per 100,000). The annual incidence of LCIS remained relatively stable between 1999 and 2004, with a low rate of 3.2 per 100,000 women in 1999 and a high rate of 3.6 per 100,000 in 2002. The annual incidence of DCIS exhibited greater variation, rising from 22.1 per 100,000 in 1999 to 23.8 per 100,000 in 2001 and 2004.

The increasing use of mammography leading to more frequent biopsies is probably the most important factor responsible for the increased incidence of LCIS. In particular, columnar cell hyperplasia (CCH), a condition predisposed to develop calcifications, so often coexists with LCIS that this association is probably not coincidental. CCH is a frequent benign abnormality responsible for mammographically detected calcifications in the absence of a palpable lesion (see Chapter 9).