Rosen's Breast Pathology, 4e

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Chapter 11

displaced from the duct into the stroma at such sites. This might be the mechanism responsible for the presence of cal- cifications in the stroma associated with DCIS when no in- vasion is evident. Accentuation and duplication of basement membrane components in the form of a thick eosinophilic band may also be evident in such foci (Fig. 11.30). It is important to distinguish between comedonecrosis and the accumulation of secretion accompanied by an inflam- matory reaction that occurs in duct stasis. Both conditions are prone to the formation of irregular microcalcifications. Cellular necrosis is rarely seen in duct stasis, and when pres- ent the degenerated cells are usually histiocytes. The duct contents in comedocarcinoma consist of necrotic carcinoma cells represented by ghost cells and karyorrhectic nuclear debris, typically with little or no intraductal inflammation. There is a sharp demarcation between viable carcinoma cells at the periphery and the necrotic core (Figs. 11.28 and 11.30). A space may be formed between the surviving cells and the cellular debris, presumably because of shrinkage of the latter during tissue processing. Dying cells at the inner edge of the viable zone have pyknotic nuclei and frayed cy- toplasmic borders. The outlines of necrotic carcinoma cells (ghost cells) may be visible in the center of the duct. Dystrophic calcification develops in the necrotic core. The calcification tends to be finely granular and mixed with cel- lular debris in some instances, whereas in others, it forms more solid irregular fragments (Fig. 11.27). Calcifications in comedocarcinoma almost always consist of calcium salts, mainly calcium phosphate, rather than crystalline calcium oxalate, which is typically found in benign apocrine lesions. Calcium oxalate calcifications have also been described in apocrine DCIS. 121,122 In routine hematoxylin and eo- sin (H&E)-stained sections, calcifications are magenta to purple whether in the comedo or other varieties of DCIS. Large calcifications may be fractured in the course of his- tologic processing, and fragments can be physically pushed by the microtome blade from the duct into the surround- ing stroma. Neoplastic epithelium may be coincidentally displaced as well. This artifact is usually readily recognized, because the path of the displaced calcification through the tissue is indicated by one or more linear scratches. Crystalloids are eosinophilic, noncalcific protein deposits that usually occur in various types of DCIS (Figs. 11.19 and 11.31). They appear to be formed by crystallization of pro- teins in necrotic debris formed in some DCIS. Rarely, crys- talloids are formed in benign breast ducts. 123 Morphometric analysis has demonstrated a correla- tion between duct diameter and the presence of necrosis in solid DCIS. 124 In one study, the mean diameter of ducts with necrosis was 470 μm, compared with a mean diameter of 192 μm for solid nonnecrotic duct carcinoma. 124 A diameter of 180 μm proved to be important for distinguishing between ducts with and without necrosis. Necrosis occurred in 94% of ducts greater than 180 μm in diameter and in 34% of smaller ducts. The viable rim of carcinomatous epithelium surround- ing the necrotic core averaged 105 μm and exceeded 180 μm in less than 10% of cases. These observations suggest that cen- tral necrosis occurs because cells at the center of ducts with

FIG. 11.26.  DCIS, solid. A,B : Central necrosis is present in these ducts with intermediate nuclear grade. Minute inter- cellular spaces convey the appearance of microlumina (A) .

FIG. 11.27.  DCIS, “comedo.” Central necrosis, calcifica- tion, and high-grade nuclei are evident.