Abstract
Morphological criteria for the diagnosis of intraductal proliferative lesions of the breast have been an object of research and much controversy, and its terminology is rather confusing. Knowledge of the molecular aspects of this disease probably necessitates further research to clarify if these entities can be identified as breast cancer precursors or as a malignant preinvasive disease. These issues are of great interest not only for their biological implications, but also to the clinician who must understand the disease and direct therapies. Molecular studies have shown that epitheliosis (usual ductal hyperplasia) is not monoclonal, while malignant lesions (atypical ductal hyperplasia, flat epithelial atypia, low-grade and high-grade intraductal carcinoma) constantly show these characteristics. These malignant lesions, classified with a DIN grading system (ductal intraepithelial neoplasia), are not obligate precursors of invasive ductal carcinoma and do not represent different evolving grades in a linear model of cancerogenesis. Breast cancerogenesis probably has different pathways with different morphologic precursors.
Highlights
Intraductal proliferative lesions (IPLs) of the breast are confined to the duct-lobular system, originating from the terminal duct-lobular unit (TDLU) with different cytological and architectural patterns of proliferation
It diminishes the dualism cancer/no cancer, retains separation of all different subcategories but places Low-grade ductal carcinoma in situ (LG-DCIS) in the same group of atypical ductal hyperplasia (ADH), because it considers the differences between these lesions quantitative, not qualitative
Wiechmann and Kuerer [44] characterize the differences between LG-DCIS and high-grade DCIS (HG-DCIS) and their risk of progression in invasive ductal carcinoma (IDC) by means of the expression of steroid receptor (LG-DCIS is frequently Estrogen Receptor (ER)/Progesteron Receptor (PgR) positive), growth characteristics (Ki67 is lower in LG-DCIS than in HGDCIS), expression of c-erbB2, bcl2 and p53, expression of psoriasin (S-100A7) and metalloproteinases (MMPs), and allelic imbalance (LG-DCIS has frequently gain of 1q and loss of 16q, whereas HG-DCIS shows frequently 17q12 and 11q13 amplification)
Summary
Intraductal proliferative lesions (IPLs) of the breast are confined to the duct-lobular system, originating from the terminal duct-lobular unit (TDLU) with different cytological and architectural patterns of proliferation They are characterized by an increase in the number of cells perpendicular to the basement membrane resulting in total alteration and distension of the normal unit structure of the breast without increasing in number [1]. Diagnostic variability is due to interpretation of different patterns, and to the difficulty in recognizing atypical cells isolated or in small clusters in TDLU In this regard, there are several open questions in the literature, including the minimum threshold for grading, the risk of progression for different type of lesions, and the relationships between normal epithelium, IPLs, and invasive ductal carcinoma (IDC). Understanding the biology of these lesions is paramount, and will contribute to a better delineation of appropriate guidelines for surgical treatment, as well as adjuvant and diagnostic recommendations
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