Atypical lobular hyperplasia (ALH) is always an incidental finding in breast specimens removed for other reasons. It has no grossly identifiable features and usually lacks microcalcifications. ALH is loosely defined as a hyperplasia that has only some features of lobular carcinoma in situ (LCIS); however, this definition is still controversial. Molecularly, ALH can be confirmed with the absence of E-cadherin expression in tumor cells. Most pathologists use both qualitative and quantitative criteria when making an ALH diagnosis. According to Page et al., less than one half of the spaces in a lobule should be filled with, and distended by, lobular cells in order to make the diagnosis of ALH (Fig. 35.2). Anything more than that should be diagnosed as LCIS [2]. The subsequent risk of developing invasive breast carcinoma once diagnosed with ALH is considered to be four to five times higher than the general population [2]. Previously, lobular neoplasia was considered a risk factor for developing invasive breast cancer in both breasts, which warranted a conservative approach [13]. However, recent studies have shown that invasive carcinoma is more likely to arise in the breast diagnosed with ALH, suggesting that ALH acts more like a premalignant lesion [14]. However, the risk of developing invasive cancer approaches the level of LCIS, with ductal involvement by cells of atypical lobular hyperplasia (DIALH) [15].

The guidelines for the treatment of patients diagnosed with ALH are not clear due to conflicting results in the literature. For instance, the risk of progression to ductal carcinoma in situ and invasive cancer after a core biopsy showing ALH ranges anywhere from 3.1 % to 25 % [16, 17]. The discrepancies in the frequency of worsening diagnoses in different studies may be due to selection criteria in these studies, such as the consideration of various other risk factors within the patient population [17]. The clinical management of ALH is similar to that with ADH, with the current recommendations to completely remove the area with a lumpectomy in most, if not all, cases.

Flat epithelial atypia (FEA) is characterized by enlarged terminal duct lobular units (TDLU), in which luminal cells are replaced by up to several layers of monomorphic low-grade epithelial cells (Fig. 35.3) [18]. These lesions are flat and do not have the same architectural patterns of ADH or DCIS. Cytologically, the epithelial cells are monomorphic, round, and perpendicular to the basement membrane similar to low-grade DCIS [19, 20]. Additionally, columnar cell lesions have been associated with tubular carcinoma and LCIS [21, 22].

Due to its apparent clinical benign nature, FEA was ignored by pathologists for a long time. However, it has gained renewed interest based upon recent observations suggesting that some cases of FEA may progress to invasive breast cancer [23, 24]. For example, one study has shown that there is an approximately twofold increase in breast cancer risk for patients diagnosed with FEA compared to the general population [25]. However, the risk of progression to breast cancer is lower than that of ADH and ALH. Given the limited nature of the data, it is unclear whether the current recommendation for surgical excision following a biopsy diagnosis of FEA is warranted. As a result, radiological-pathological correlation is still recommended in each case [18]. However, many surgeons still recommend complete removal of such areas of FEA, discussing the risks and benefits with each patient.

The WHO classification of the tumors of the breast provides the entire list of breast tumors, including rare types [18]. However, it is beyond the scope of this chapter to cover exceptionally rare types and variants of breast cancer. Instead, we will discuss the most common breast tumors in this chapter. Readers are, therefore, encouraged to refer to classical pathology textbooks for more detailed information about the types of tumors not discussed herein.