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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.
