Microglandular Adenosis and Associated Invasive Carcinoma

Context.— Microglandular adenosis is a rare borderline neoplastic lesion of the breast composed of haphazardly located small, round tubules with a single cell layer interspersed within breast stroma and/or adipose tissue. Microglandular adenosis is devoid of a myoepithelial cell layer, and has a characteristic immunophenotype, being positive for S100 and negative for estrogen receptor, progesterone receptor, and HER2/neu. When associated with cancer, microglandular adenosis and associated invasive carcinoma share the same molecular alterations, including TP53 mutation; therefore, microglandular adenosis is considered a nonobligate precursor of triple (HER2/neu, estrogen and progesterone receptors)–negative breast carcinoma. Microglandular adenosis is an important diagnostic pitfall as it can be easily mistaken for a low-grade invasive carcinoma. Objective.— To provide a review of the clinicopathologic features of microglandular adenosis and associated invasive carcinoma, with emphasis on key features separating entities in the differential diagnosis. Data Sources.— Review of current literature on microglandular adenosis and associated invasive carcinoma and personal experience of authors. Conclusions.— Microglandular adenosis can mimic breast carcinoma; attention to key features, including morphologic-immunophenotypic correlation, is essential in establishing the diagnosis.

Microglandular Adenosis: A Possible Non-Obligate Precursor to Breast Carcinoma With Potential to Either Luminal-Type or Basal-Type Differentiation

Microglandular adenosis (MGA) of the breast is exceedingly rare, with only a few case reports and series published to date. Previous studies have elegantly demonstrated the progression of benign MGA to atypical MGA to MGA-in situ carcinoma to invasive carcinoma and therefore suggest MGA as a possible non-obligate precursor lesion to a subset of breast carcinomas. Immunohistochemically, MGA is negative for estrogen receptor (ER), progesterone receptor (PR), and HER2-neu oncoprotein expression, and carcinomas arising in the setting of MGA are often reported to be triple negative. In this article, we present a unique case of an ER+/PR+/HER2− invasive carcinoma associated with MGA and atypical MGA. Our case highlights the diagnostic pitfall of MGA and suggests that MGA is a heterogeneous group of lesions with potential for either luminal-type or basal-type differentiation during progression to breast carcinoma.