Rizki Hanriko

Bagian Anatomi, Patologi Anatomi & Histologi

FK UNILA
2017
 Milkline remnants (p. 1067): These can produce
hormoneresponsive supernumerary nipples or breast
tissue from the axilla to the perineum. These mainly
come to attention secondary to painful pre-menstrual
enlargement.
 Accessory axillary breast tissue: Occasionally,
normal ductal tissue extends into subcutaneous
tissue of the axilla or chest wall. This can present
as a lump in the setting of lactational hyperplasia,
or it can give rise to carcinoma outside the breast
proper.
 Congenital nipple inversion: This is common and
usually spontaneously corrects during pregnancy
or with traction; acquired nipple inversion is
concerning for carcinoma or inflammatory
conditions.
Acute Mastitis
 >> first month of lactation when the breast is
vulnerable to bacterial infections (Staphylococcus
and Streptococcus) through nipple cracks and
fissures.
 Usually resolves with antibiotic treatment and
continued breastfeeding.
Granulomatous Mastitis
 This can be associated with systemic diseases (e.g.,
sarcoidosis, Wegener granulomatosis), foreign
bodies (e.g., piercings), or granulomatous
infections (e.g., mycobacteria or fungi).
 Essentially no malignant potential; “lumpy
bumpy” breasts.
Morphology
 Cysts form by lobular dilation lined by flattened
atrophic epithelium or metaplastic apocrine cells
and frequently exhibit calcifications.
 Fibrosis occurs secondary to cyst rupture and
inflammation.
 Adenosis increased acini per lobule; lined by
columnar epithelium that can exhibit atypia;
calcification is occasionally present.
 Epithelial hyperplasia is defined by more than two cell
layers around ducts and lobules.
 Sclerosing adenosis is reflected by increased numbers of
acini per lobule with central distortion and compression
and peripheral dilation.
 Complex sclerosing lesions have components of sclerosing
adenosis, papillomas and epithelial hyperplasia.
 Papillomas reflect epithelial growth and associated
fibrovascular cores within dilated ducts; more than 80% of
large duct papillomas produce a nipple discharge
 Atypical hyperplasia lacks sufficient features to
diagnose carcinoma;
 These epithelia have many of the same acquired
genetic changes present in carcinoma in situ.
 Atypical ductal hyperplasia shares some morphologic
features with ductal carcinoma in situ (DCIS) but is
limited in extent.
 Atypical lobular hyperplasia shares features with
lobular carcinoma in situ (LCIS), but cells do not
distend more than 50% of acini within a lobule.
 Patients with DCIS have a greatly increased risk for
development of invasive ductal carcinoma.
 DCIS is not detected as density on mammogram.
 Can be associated with calcification (clustered, or linear
and branching), which can be detected on mammogram.
 Risk of breast carcinoma: 8.0–10.0 times the normal
population; the higher the grade of the DCIS, the greater
the risk.
 Microscopic morphology of DCIS: Proliferation of cells
within the duct. The collections of cells produce punched-
out lumens (as opposed to slit-like lumens in hyperplasia),
and cells “obey” each other’s borders (as opposed to
hyperplasia, where they overlap).
 Have a greatly increased risk for development of
invasive breast carcinoma (either lobular or ductal
type). The cancer does not necessarily occur at the
site of the LCIS—it can occur at a different location
or even in the opposite breast.
 Incidental, lack of e-cadherin.
 Varies from close clinical follow-up to the
possibility of bilateral mastectomy; 25–35% of
patients with LCIS progress to invasive carcinoma.
 Microscopic: Monotonous proliferation of small
cells with oval to round nuclei, which expand the
lobule.
 Gross morphology: Erythematous eruption
with scaling crust.
 Microscopic: Neoplastic cells in the epidermis.
 Paget disease of the nipple is always associated
with underlying DCIS, which extends to the
epidermis through the lactiferous ducts.
 Breast carcinoma is the most common non-skin
malignancy in women;
 a female living to age 90 years has a one in eight
chance of developing breast cancer.
 less than 20% of women with invasive breast cancer
die of it.
 Mutations: Del 16q22.1—CAM such as e-cadherin and
β-catenin.
 Metastases to peritoneum, retroperitoneum,
leptomeninges, gastrointestinal system, and ovaries.
 Metabolites of estrogen can cause mutations or
generate DNA-damaging free radicals, or estrogen
itself can drive proliferation of premalignant
lesions and carcinomas.
 Inherited mutations (responsible for 10% of
tumors): BRCA1 (17q21.3) or BRCA2 (13q12-13), both
of which have gene products that play a role in
DNA repair. Inheritance of either mutation results
in 60–80% risk of carcinoma.
 Rare in females younger than 25 years of age; 70%
of breast carcinomas occur in females older than
50 years of age.
 Family history.
 Increased exposure to estrogen:
 early menarche, late menopause,
 nulliparous or first pregnancy late in life, or
 exogenous intake)
 Good prognosis: Size 2.0 cm, ER and PR positivity,
Her-2- Neu negativity, and negative lymph nodes.
 Poor prognosis: Size 2.0 cm or 5.0 cm, ER and PR
negativity, Her-2-Neu positivity, aneuploidy, and high
proliferative rate.
 Her-2-Neu is a proto-oncogene expressed in 30% of
breast cancers; it is an epidermal growth factor
receptor.
 Invasive ductal: Ranges from neoplastic glands to
sheets of
 neoplastic cells.
 Invasive lobular: Neoplastic cells occur in single-
file & targetoid lesion.
 Colloid: Produce abundant mucin.
 Tubular:Well-formed tubules.
 Medullary: Well-circumscribed border; sheets of
anaplastic cells associated with lymphocytic
infiltrate.
 Females younger than 25 years of age.
 Almost always benign; carcinoma rarely occurs
within a fibroadenoma.
 Potential for producing a proliferative lesion and,
therefore, in general, have an increased risk of
later development of cancer.
 Gross: Well-circumscribed, firm, tan nodule;
often multiple and bilateral.
 Microscopic: Proliferation of stroma and glands
with glandular proliferation greater in amount
than stromal proliferation.
 Most commonly after age 60 years,
 Typically presenting as palpable masses.
 The stroma frequently overgrows the epithelial
component, forming clefts and slits and creating
bulbous protrusions; increased cellularity, mitotic
activity, stromal overgrowth, and infiltrative borders
differentiate them from fibroadenomas.
 The frequency of chromosomal changes increases with
grade; high-grade lesions also have epidermal growth
factor (EGF) receptor amplification. Most phyllodes
tumors can be cured by wide local excision; nodal or
distant metastases are rare.