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The multistep model for breast carcinogenesis suggests that invasive carcinomas arise from preinvasive "hyperplastic" and neoplastic proliferations. These early proliferative lesions have taken on greater significance as a result of the mammographic screening and detection programs. Pathologists are encountering these proliferative lesions with increasing frequency, and this has highlighted deficiencies in classification systems as well as a lack of data on natural history, making clinical management a challenge.

Invasive carcinomas are divided into ductal carcinoma no-special-type (IDC-NST) and the "special types," of which lobular carcinoma (ILC) is the major component. While there has been little debate or controversy about the precursor nature of ductal carcinoma in situ (DCIS), there is considerable argument regarding the role of lobular carcinoma in situ (LCIS) in progression to invasive disease. The picture is further complicated by the identification of lesions that are qualitatively the same but less developed (atypical lobular hyperplasia, ALH) and those showing intermediate features between hyperplasia and in situ carcinoma (atypical ductal hyperplasia, ADH).

The evidence for progression and the risks associated with these lesions is derived from morphology, clinical follow-up, and molecular relationships. The path from normal to invasive carcinoma is certainly not a linear one, and there is evidence that breast cancer and the evolutionary pathways are heterogeneous.1 The overall paucity of data to stratify individual patients into meaningful risk categories and the often long time-frame to progression has created challenges in surgical management of these preinvasive lesions. This is further confounded by the diagnostic difficulties from small tissue samples in core biopsies used as part of the workup in screening programs. In this chapter, we discuss the pathology, biology, and management of lobular neoplasia and atypical ductal hyperplasia.

Historical Perspective

Foote and Stewart gave the first clear clinical-pathologic description of LCIS in 19412 describing the morphologic similarities between these in situ lesions and ILC. This, together with the frequent concurrent diagnosis of LCIS and ILC, suggested a progressive relationship prompting management, ultimately removal of LCIS by mastectomy. This management strategy was subsequently supported by independent clinical follow-up that demonstrated a cumulative (and bilateral) risk of carcinoma in LCIS patients.3 Over the next 30 years, the combination of bilateral risk, the long time-frame to progression, and the identification of IDC in association with LCIS raised questions about the precursor nature of LCIS. The lesion was considered only a "risk indicator," and hence management recommendations became varied, ranging from mastectomy to surveillance only.4-10

ALH was introduced more recently to describe lesions that are less well-developed but morphologically similar to LCIS. In 1978 the term "lobular neoplasia" (LN) was introduced to encompass both ALH and LCIS4; however, the term has not gained universal acceptance.


Lack of specific clinical abnormalities has made estimation of the true incidence of LN very difficult. LN is neither palpable nor usually associated with ...

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