Atypical Lobular Hyperplasia and Lobular Carcinoma In Situ

Atypical lobular hyperplasia (ALH) and lobular carcinoma in situ (LCIS) are noninvasive neoplastic proliferative lesions comprised of generally small, dyscohesive cells originating in the terminal duct lobular units (TDLUs), with or without pagetoid extension to terminal ducts [1, 2]. The loss of cell-to-cell cohesion is secondary to absence or dysfunction of E-cadherin. ALH and LCIS are distinguished from one another by the degree of involvement of the TDLUs, with ALH showing less involvement (Figs. 14.1 and 14.2). Both lesions are often grouped under the term lobular neoplasia (LN), which was first introduced by Haagensen et al. in 1978 [3]. Lesions consistent with LN were noted as early as 1850 in a book by John Birkett, who pictorialized “cecal terminations of glandular tissue” [4]. A few other LN references subsequently followed, most notably in 1919 by James Ewing, who in his book Neoplastic Diseases showed two photographs which resembled LCIS and pagetoid involvement of duct that were described as “atypical proliferation of acinar cells” and “atypical proliferation of a segment of a duct” [5]. However, it was not until 1941 that Foote and Stewart first coined the term LCIS in their seminal paper [6]. Most of their detailed descriptions on the clinical and pathological features of LCIS have remained remarkably current more than 80 years later.