II. MAMMARY DUCT ECTASIA
Duct ectasia is a nonspecific dilatation of the major
subareolar ducts with occasional involvement of the
smaller ducts, unrelated to fibrocystic change.
Microscopically, the dilated ducts contain foamy
macrophages mixed with lipid material, cholesterol clefts
and eosinophilic debris (Slide
28). The material within the ducts often calcifies.
Infiltration of lymphocytes, plasma cells, and
histiocytes occurs in the periductal tissue. With time,
fibrosis increases in amount (Slide
29). Thus terms, such as plasma cell mastitis,
obliterative mastitis and comedomastitis, were used. The
etiology of the condition is unknown. The theory of an
initial inflammatory process leading to destruction of
the elastic network and secondary ductal ectasia and
periductal fibrosis is favored.
III. BENIGN PAPILLARY
NEOPLASM AND CHANGES
A. Intraductal papilloma
Intraductal papilloma usually occurs within a
major duct in the subareolar region. When a similar
papilloma occurs in the nipple, the term nipple
adenoma or papillomatosis is used (see later
section).
The clinical presentation is bloody, or serous
nipple discharge. The excised lesion is usually
small, less than 1-2 cm in size (Slide 30). However, some
papillomas are larger than 4 cm, especially those
associated with hemorrhage and cystic change.
Sometimes the papillomas are multiple involving a
group of ducts. Multiple peripheral papillomas are
associated with an increased risk for local
recurrence and subsequent development of breast
carcinoma.
Microscopically, the papillomas form papillary
fronds supported by fibrous cores and covered with
hyperplastic epithelium (Slides
31 and 32). In
addition, solid areas are common, either focal or
predominant (Slide 33).
The proliferative epithelium is made up of epithelial
and myoepithelial cells.
Secondary changes occur often in the form of
hemorrhage, infarct, fibrosis and hyalinization, most
likely resulting from torsion of the fibrous stalks
and ischemic injury. The damaged epithelium and
hyalinized stroma may also deposit calcium. In core
biopsies, potential diagnostic problems include
entrapped ducts in the hyaline stroma interpreted as
invasive carcinoma (Slide
34). Nuclear atypia in papillary lesions needs
careful evaluation to rule out atypical hyperplasia
and ductal carcinoma in situ.
Juvenile papillomatosis refers to a marked ductal
hyperplasia in adolescents and young women. The
involved ducts are cystically dilated with a Swiss
cheese pattern. Atypical ductal hyperplasia and
carcinoma may occur (Rosen et al, 1980 and 1985).
B. Radial Scar
Radial scar is a benign lesion known by a variety
of names in the literature, including infiltrating
epitheliosis, nonencapsulated sclerosing lesion,
indurative mastopathy, scleroelastic lesion,
sclerosing papillary proliferation, benign sclerosing
ductal hyperplasia, and radial sclerosing lesion.
Most radial scars are spiculated masses or areas
of architectural distortion, often with multiple long
spicules and central areas of lucency.
Radial scar occurs in the background of benign
ductal hyperplasia, intraductal papilloma and/or
sclerosing adenosis, in which fibrous stromal
undergoes fibrosis and elastosis (Slides 35 and 36). As a result, the
ducts and ductules become distorted and arranged in a
radiating pattern (Slide
35). The ducts entrapped in the scar
superficially resemble invasive carcinoma (Slide 36). These benign
ducts retain the usual epithelial and myoepithelial
cells without significant nuclear atpyia.
III. FIBROEPITHELIAL TUMORS
A.
Fibroadenoma
Fibroadenoma is the most common benign breast
tumors seen in women under the age of 35 years. The
peak age of incidence is in the third decade.
Most fibroadenomas are 2-3 cm in size, but may
reach to 6-7 cm, the so called giant fibroadenomas.
They are well-circumscribed, but not encapsulated.
Cut surfaces have a lobulated, grey-white myxoid,
semitransparent to dense fibrous appearance.
Cleft-like spaces corresponding to branching ducts
may be evident (Slide 37).
About 10-20% of fibroadenomas are multiple and
bilateral (Slide 38)
and may increase in size during pregnancy and undergo
infarct following childbirth.
Fibroadenomas consist of epithelial and fibrous
components. Branching and budding ducts are
surrounded by fibrous tissue. The pericanalicular
fibroadenoma maintains round and oval dilated ductal
spaces (Slide 39).
Whereas in the intracanalicular type, the ductal
lumens are compressed by polypoid fibrous stroma
creating slit-like irregular spaces. The ducts are
lined by two layers of cells: epithelial and
myoepithelial cells. Under the influence of hormones,
the ducts become hyperplastic with papillary
formation and more than two layers of cells.
The fibrous stroma varies from myxoid and
hypocellular to fibrous and moderately cellular. Rare
mitotic figures may occur, but nuclear atypia is
absent or minimal, allowing separation from phyllodes
tumor.
Involution is common with increasing age of the
lesion. The stroma becomes less cellular, more
fibrotic and hyalinized (Slide
40). Coarse calcifications. In old fibroadenomas,
the ductal epithelium becomes so atrophic as to
disappear completely. Rarely, fibroadenomas enlarge
in postmenopausal women, with or without hormone
replacement therapy.
Several variants of fibroadenomas have been
described. The giant fibroadenoma is simply a
fibroadenoma that has reached a large size.
Microscopically these are the same as other
fibroadenoma, the cellularity can be high.
Tubular adenomas contain predominantly tubular
elements and minimal amount of fibrous stroma and
sometimes are found during pregnancy. Lactational
change may produce a localized mass having enlarged
lobules and ducts with vacuolated cytoplasm and
secretory product in the lumens.
Very rarely ductal or lobular carcinoma in situ
occurs within fibroadenomas (Slides 41 and 42) (Pick and
Iossifides). Invasive carcinoma has also been report
to arise in a fibroadenoma. When in situ or invasive
carcinoma involves the fibroadenoma, about 50% of
women also have disease outside of fibroadenoma
(Rosen et al, 1993). Thus, it is important to
evaluate the surrounding tissue of fibroadenoma to
determine the extent of disease for optimal
treatment.
B. Phyllodes Tumor
(Cystosarcoma Phyllodes)
The malignant counterpart of fibroadenoma is
cystosarcoma phyllodes or the newer term of phyllodes
tumor, in which the epithelial elements are benign,
but the stromal tissue is malignant. It results from
malignant degeneration of fibroadenoma, estimated to
occur in 1% of patients, who have fibroadenoma for
many years.
At presentation, most women are between 40 and 50
years with a typical presentation of a rapidly
growing mass.
The phyllodes tumor has a lobulated, leaf-like
appearance and varies in size from 1 cm to greater
than 15 cm (Slide 43).
Microscopically, the branching, hyperplastic ducts
are surrounded by a stroma, which is mostly fibrous
and much more cellular than fibroadenoma (Slide 44). In addition,
nuclear atypia and increased mitotic activity occur (Slides 45 and 46).
The stromal components may contain liposarcoma,
leiomyosarcoma, rhabdomyosarcoma, malignant fibrous
histiocytoma, angiosarcoma, chondrosarcoma and
osteosarcoma. For this reason, it is important to
adequately sample the neoplasm to determine whether
ductal elements are present. In the absence of
epithelial cells, the neoplasm is classified as
primary stromal sarcoma of the breast, which is
generally more aggressive than phyllodes tumor.
The clinical behavior of phyllodes tumor is
unpredictable. The majority of phyllodes tumors are
local problems and do not metastasize. Less than 20%
of phyllodes tumors metastasize by vascular spread,
most commonly to the lung, pleura, and bone. (Hart,
1978; Pietrusz, 1978). Thus, lymph node dissection is
not indicated. Local recurrence is likely, if
incompletely excised. Therefore, a wide local
excision is required.
Some recent studies have attempted to separate
cystosarcoma phyllodes into benign and malignant
groups. The benign group is characterized by smooth,
non-infiltrative borders and the fibrous elements
have minimal nuclear atypia and low mitotic activity.
This is in contrast to infiltrative borders (Slide 47), presence of
nuclear atypia and increased mitotic activity usually
greater than five mitotic figures per 10 high power
fields in the malignant group (Hart et al; Pietrusz
and Barnes). It should be mentioned that not all
metastatic phyllodes tumors meet the above criteria.
Thus, it is more appropriate to classify the
phyllodes tumors into low and high grades and to
treat these tumors with wide clear margins.
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