Breast Flashcards
Plasma-cell mastitis: Clinical appearance.
May evolve into a hard mass that, together with axillary lymphadenopathy, can mimic carcinoma.
Plasma-cell mastitis: Inflammatory changes (2).
Extensive lymphoplasmacytic infiltrate.
Xanthomatous reaction sometimes.
Plasma-cell mastitis: Epithelial changes (2).
Hyperplasia, necrosis.
Plasma-cell mastitis: Special stains.
Negative: GMS, PAS, AFB.
Subareolar abscess:
A. Surgical association.
B. Clinical appearance.
A. Reduction mammoplasty.
B. Can mimic that of inflammatory carcinoma.
Subareolar abscess: Causes (5).
Staphylococcus.
Streptococcus.
Bacteroides.
Proteus.
Mycobacterium tuberculosis.
Subareolar abscess: Epithelial changes (2).
Squamous metaplasia of ducts.
Keratin plugs in lactiferous ducts.
Plasma-cell mastitis: Typical patient.
Woman who has stopped lactating years ago.
Granulomatous mastitis:
A. Etiology.
B. Clinical appearance.
A. Unknown.
B. Hard mass that may mimic carcinoma.
Granulomatous mastitis: Histology (2).
Granulomatous inflammation of lobules.
Giant cells, plasma cells, and eosinophils accompany the granulomas.
Granulomatous mastitis vs. sarcoidosis.
Sarcoidosis: Noncaseating, naked granulomas that are usually found between the lobules.
Granulomatous mastitis: Behavior.
May recur and require many excisions.
Fat necrosis: Clinical appearance.
May mimic carcinoma clinically and on mammogram.
Fat necrosis: Later histologic changes (3).
Fibroblasts and collagen deposition.
Scar.
Calcification (“eggshell calcifications”) on mammogram.
Diabetic mastopathy: Typical patient.
Premenopausal woman with diabetes of the first type.
Diabetic mastopathy:
A. Clinical appearance (2).
B. Mamographic appearance.
A. Hard, mobile mass; often bilateral.
B. Nonspecific.
Diabetic mastopathy: Histology (3).
Densely fibrotic, keloid-like stroma.
Lymphocytes around small vessels, lobules, ducts.
Calcifications may be visible.
Juvenile hypertrophy:
A. Age of patient.
B. Mammographic appearance.
A. Less than 16 years.
B. Benign.
Juvenile hypertrophy: Histology (2).
Proliferation of ducts and connective tissue but not of lobules.
May resemble gynecomastia.
Juvenile hypertrophy: Genetics.
Most cases are sporadic.
Cases with PTEN mutation are more likely to turn malignant.
Granular-cell tumor:
A. Typical location.
B. Mammographic appearance.
A. Upper inner quadrant.
B. Mimics carcinoma.
Granular-cell tumor: Immunohistochemistry (2,1).
Positive: S100, CEA.
Variable: CD68.
Granular-cell tumor: Electron microscopy (2).
Many lysosomes.
Myelin figures.
Granular-cell tumor: Morphologic differential diagnosis (4).
Apocrine carcinoma.
Metastatic renal-cell carcinoma.
Metastatic melanoma.
Metastatic alveolar soft-part sarcoma.
Granular-cell tumor: Treatment.
Ya gotta cut it all out, or it might come back.
Fibrocystic changes: Histologic components (5).
Cysts.
Stromal fibrosis.
Apocrine metaplasia.
Sclerosing adenosis.
Epithelial hyperplasia without atypia.
Fibrocystic disease: Risk of carcinoma.
Sclerosing adenosis and florid ductal hyperplasia without atypia: Slightly increased risk.
All other changes: No increase in risk.
Columnar-cell lesions: Types (3).
Columnar-cell change.
Columnar-cell hyperplasia.
Flat epithelial atypia.
Columnar-cell lesions: Histologic location.
Terminal ductal-lobular units.
Columnar-cell change: Histology (4).
Dilated acini.
Bland, mitotically inactive cells.
Up to two layers of epithelium.
Apocrine snouts and luminal secretions may be visible.
Columnar-cell hyperplasia: Histology (2).
More than two layers of epithelium.
Papillae.
Flat epithelial atypia: Histology.
Essentially columnar-cell change or columnar-cell hyperplasia with cytologic atypia.
Nuclei are round and no longer oriented perpendicular to the basement membrane.
Columnar-cell lesions: Immunohistochemistry (4,3).
Positive: ER, PR, bcl-2, LMW-CK.
Negative: p53, Her-2, HMW-CK.
Columnar-cell change: Genetics.
Loss of 16q.
Adenosis: Potentially misleading histologic features (4).
Florid adenosis: Focal necrosis, infarction.
Sclerosing adenosis: Growth around nerves.
Microglandular adenosis: Absence of myoepithelial cells (even by IHC), loss of lobular pattern.
Microglandular adenosis: Additional histologic features (3).
Extension around normal epithelial structures and sometimes into the fat.
Bland cells; rare mitotic figures.
PAS-positive eosinophilic secretions.
Atypical microglandular adenosis.
Consists of typical adenosis + areas of more complex structure and cytologic atypia.
Microglandular adenosis: Immunohistochemistry (4,2).
Positive: Cytokeratin, S100, cathepsin D, collagen IV.
Negative: EMA, ER.
Microglandular adenosis vs. infiltrating tubular carcinoma (4).
Tubular carcinoma:
− Angular ducts.
− Stroma is rich in fibroblasts instead of hypocellular.
− No eosinophilic secretions.
− Usually expresses EMA and ER.
Adenosis: Risk of carcinoma.
Slightly increased.
Radial sclerosing lesion: Types.
Radial scar: Less than 1 cm in diameter.
Complex sclerosing lesion: At least 1 cm in diameter.
Radial sclerosing lesion: Radiography.
Center: Dense radiolucency.
Periphery: Radiating linear densities.
Radial sclerosing lesion: Histology.
Center: Collagenous scar with fibrosis and elastosis.
Periphery: Entrapped ducts with epithelial layer, myoepithelial layer, and basement membrane.
Radial sclerosing lesion: Infiltration (2).
Can infiltrate around nerves.
Should not infiltrate into the adjacent fat.
Radial sclerosing lesion: Relation to carcinoma (3).
May be confused mammographically and pathologically with carcinoma.
Carcinoma may arise in it.
May be associated with a increased risk of carcinoma.
Solitary intraductal papilloma:
A. Location.
B. Presentation.
A. Subareolar mass.
B. Serous or bloody discharge from the nipple.
Multiple papilloma: Location.
Peripheral breast tissue.
Intraductal papilloma: Myoepithelial layer.
Present but may be focally absent.
Intraductal papilloma: Possible types of metaplasia (5).
Apocrine.
Squamous.
Mucinous.
Clear-cell.
Sebaceous.
Intraductal papilloma: Confounding histologic features (2).
Sclerosis of cores with entrapment of ductal epithelium.
Infarction due to torsion of the papillae.
Atypical intraductal papilloma.
Intraductal papilloma containing ADH or DCIS.
Intraductal papilloma: Myoepithelial markers (6).
S100.
Calponin.
p63.
SMA.
Smooth-muscle-myosin heavy chain.
CD10.
Intraductal papilloma vs. atypical intraductal papilloma: Immunohistochemistry (2).
ER
− Papilloma without atypia: Expressed by only a minority of cells.
− Atypical papilloma: Expressed diffusely in areas of ADH and DCIS.
High-molecular-weight cytokeratins
− Papilloma without atypia: Expressed.
− Atypical papilloma: Not expressed in areas of ADH and DCIS.
Intraductal papilloma vs. encapsulated papillary carcinoma.
Papillary carcinoma: No myoepithelial cells.
Intraductal papilloma: Risk of carcinoma.
Increased with all types, solitary and multiple, with or without atypia.
Intraductal papilloma: Mutation.
Loss of heterozygosity at 16p13 in papillomas with florid hyperplasia.
Intraductal papilloma: Favorable histologic feature.
Apocrine metaplasia.
Florid papillomatosis of the nipple:
A. Presentation.
B. Clinical appearance.
A. Serous or bloody discharge.
B. Ulceration, erythema, and scaling of the nipple.
Florid papillomatosis of the nipple: Basic histology.
Florid ductal hyperplasia.
Florid papillomatosis of the nipple: Patterns of growth (4).
Sclerosing papillomatosis.
Papilloma.
Adenosis.
Mixed proliferative.
Florid papillomatosis of the nipple: Myoepithelial cells.
May be inconspicuous or absent in sclerosing lesions.
Florid papillomatosis of the nipple: Variation.
Areas of ADH, DCIS, or invasive carcinoma within the papillomatosis.
Florid papillomatosis of the nipple: Immunohistochemistry of the epithelial cells.
Positive: Cytokeratin 34βE12.
Florid papillomatosis of the nipple: Association with carcinoma.
Carcinoma is present or occurs later in 10% of cases.
Florid papillomatosis of the nipple: Treatment.
Complete excision, usually including the nipple.
Pseudoangiomatous stromal hyperplasia: Patients (2).
Woman of childbearing age.
Man with gynecomastia.
Pseudoangiomatous stromal hyperplasia: Gross pathology.
Well circumscribed and typically encapsulated.
Pseudoangiomatous stromal hyperplasia: Histology.
Myofibroblasts line slitlike spaces.
Densely collagenous stroma.
Pseudoangiomatous stromal hyperplasia: Differential diagnosis.
Low-grade angiosarcoma.
Pseudoangiomatous stromal hyperplasia: Treatment.
Wide local excision with clear margins.
Adenoma: Types (3).
Tubular.
Lactating.
Apocrine.
Tubular adenoma: Histology.
Densely packed ductal structures composed of a single layer of bland epithelial cells surrounded by myoepithelial cells.
Lactating adenoma: Histologic changes related to pregnancy (2).
Less secretion (than in adenomas resected postpartum).
Tendency toward infarction.
Adenoma: Association with carcinoma.
No increased risk of subsequent carcinoma.
Carcinoma can arise in an adenoma.
Fibroadenoma: Pharmacologic association.
Cyclosporine.
Giant fibroadenoma.
A fibroadenoma that is larger than 5 cm or that weighs more than 500 g.
Fibroadenoma vs. phyllodes tumor (3).
Phyllodes tumor:
− Leaflike architecture.
− May show cytologic atypia.
− May show increased mitotic activity.
Juvenile fibroadenoma.
Occurs in young girls.
More stromal cellularity than in typical fibroadenoma.
Fibroadenoma: Association with breast cancer.
No association if
− Fibroadenoma is not complex.
− There is no family history of breast cancer.
Fibroadenoma: Malignancies that can arise in it (3).
Lobular carcinoma in situ (#1).
Invasive lobular carcinoma.
Invasive ductal carcinoma.
Fibroadenoma: Treatment.
Rarely recurs if incompletely excised.
Phyllodes tumor: Age group.
Fifth and sixth decades.
Phyllodes tumor: Behavior.
Aggressive; frequently recurs.
Phyllodes tumor: Epithelial component (2).
Ductal epithelium similar to that of fibroadenoma.
Squamous metaplasia may occur.
Phyllodes tumor: Mesenchymal component.
Cellularity tends to be greatest around the ducts.
Phyllodes tumor: Metaplasia of the mesenchymal component.
Osseous, cartilaginous, fatty, or muscular.
Benign phyllodes tumor: Histology (5).
Fewer than 5 mitotic figures per 10 hpf.
Minimal pleomorphism.
No necrosis.
Discrete margins.
Cellularity may vary.
Malignant phyllodes tumor: Stromal overgrowth.
At least 10 microscopic fields without epithelium.
Malignant phyllodes tumor: Other histologic features (4).
More than 5 mitotic figures per 10 hpf.
Nuclear pleomorphism.
Necrosis.
Infiltrative margins.
Phyllodes tumor vs. carcinosarcoma.
Carcinosarcoma: Malignant epithelial and stromal components are separate from each other.
Phyllodes tumor: Metastasis (2).
Hematogenous dissemination to lungs, pleura, bones.
Usually only the sarcomatous component is represented.
Phyllodes tumor: Genetics (3).
+1q.
Overexpression of p53.
Complex karyotypic abnormalities.
Atypical ductal hyperplasia: Definition.
No more than 3 mm in diameter
− or −
No more than two duct spaces involved.
Atypical ductal hyperplasia vs. DCIS (4).
ADH:
− Smaller.
− More nuclear overlap.
− Less distinct cell membranes.
− Irregular (not “punched-out” secondary lumens).
Ductal carcinoma in situ: Variants (4).
Comedocarcinoma.
Cribriform.
Solid.
Micropapillary.
Ductal carcinoma in situ: V
E
Comedocarcinoma:
A. Nuclei.
B. Associated histologic feature.
A. High-grade (grade III).
B. Retrograde cancerization of lobules.
Cribriform DCIS: Nuclei (4).
Monotonous.
May show mild or moderate atypia.
Few mitotic figures.
Areas of necrosis may be seen.
Solid DCIS: Nuclei (2).
Intermediate grade.
Otherwise similar to those of cribriform DCIS.
Micropapillary DCIS: Histology (3).
False papillae are regularly distributed within the duct.
Minimal cytologic atypia.
Extensive involvement of the breast.
Ductal carcinoma in situ: Immunohistochemistry (4).
Her-2/neu: More often positive in high-grade tumors.
Ki-67: Positive in more than 20% of cells of high-grade tumors.
ER and PR: More often positive in low-grade tumors.
Laminin and type IV collagen: Positive.
Ductal carcinoma in situ: Low-grade.
Minimal nuclear pleomorphism.
No necrosis.
Ductal carcinoma in situ: Intermediate-grade.
Minimal nuclear pleomorphism + necrosis
− or −
Moderate nuclear pleomorphism without necrosis.
Ductal carcinoma in situ: High-grade.
Marked cytologic atypia + necrosis.
High mitotic rate.
Ductal carcinoma in situ involving lobules vs. lobular carcinoma in situ (3).
DCIS:
− Cells are larger and more pleomorphic.
− Cell borders are more distinct.
− No intracytoplasmic mucin.
Atypical ductal carcinoma: Association with carcinoma.
Fourfold to fivefold risk.
Mammographic appearance of ___.
A. Atypical lobular hyperplasia.
B. Lobular carcinoma in situ.
Nonspecific calcifications.
Atypical lobular hyperplasia and lobular carcinoma in situ: Laterality.
Much more often bilateral and multifocal than DCIS.
Atypical lobular hyperplasia: Histology (3).
Bland cells fill lobules but do not distend them.
Only one lobular unit is involved and usually less than half of the acini.
Usually no intracytoplasmic mucin droplets (signet-ring cells).
Lobular carcinoma in situ: Histology (3).
Bland cells expand the lobules.
May exhibit pagetoid spread into the adjacent ducts.
Signet-ring cells are often visible.
Pleomorphic LCIS: Cytology.
Nucleoli are more conspicuous, and nuclei are considered grade III.
Conventional LCIS: Immunohistochemistry (2,3).
Variable: ER, PR.
Negative: Her-2, p53, E-cadherin.
Pleomorphic LCIS: Immunohistochemistry (3,2).
Positive: Her-2, GCDFP-15, p53.
Negative: ER, PR.
Lobular neoplasia in situ.
Term that includes both atypical lobular hyperplasia and lobular carcinoma in situ.
Atypical lobular hyperplasia and lobular carcinoma in situ: Treatment (2).
Diagnosed on needle biopsy: Excision.
Diagnosed on excision: Close follow-up and hormonal therapy.
Atypical lobular hyperplasia and lobular carcinoma in situ: Most important mutated gene.
CDH1 (E-cadherin).
Atypical lobular hyperplasia and lobular carcinoma in situ: Association with carcinoma (3).
Subsequent carcinoma may develop in either breast.
Any type of invasive carcinoma can occur.
LCIS: Up to tenfold risk.
Infiltrating ductal carcinoma: Risk factors (5).
Family history.
Early menarche.
Late menopause.
Nulliparity or first parturition after age 30.
Obesity.
Infiltrating ductal carcinoma: Genes associated with increased risk (5).
BRCA1 (chromosome 17), BRCA2 (chromosome 13): Up to 85% lifetime risk.
p53: Li-Fraumeni syndrome.
ATM, even in carriers.
PTEN.
Infiltrating ductal carcinoma: Most important predictor of prognosis.
The status of the lymph nodes.
Infiltrating ductal carcinoma: Grade I (3).
Ducts make up 75% of the tumor.
Relatively bland cells.
Rare mitotic figures.
Infiltrating ductal carcinoma: Grade II (4).
Tubules are present but make up less than 75% of the tumor.
Twofold to threefold variation in size of cells.
Moderate nuclear pleomorphism.
Moderate mitotic activity.
Infiltrating ductal carcinoma: Grade III (4).
No tubules.
Greater than threefold variation in size of cells.
Marked nuclear pleomorphism.
High mitotic activity; atypical mitotic figures.
Infiltrating ductal carcinoma: Expression of ER and PR.
Grades I and II: Usually both are expressed.
Grade III: Usually neither is expressed.
ER is expressed and PR is lost in about 10-15% of tumors.
Infiltrating ductal carcinoma: Expression of Her-2.
More common in tumors of higher grade.
Infiltrating ductal carcinoma: Other immunohistochemistry (5).
Positive: CK8/18, CK19, CK7, EMA, E-cadherin.
Infiltrating ductal carcinoma: Mutated genes (2).
RAS, Her-2.
Infiltrating ductal carcinoma: Importance of concurrent DCIS.
Tumors in which more than 25% is DCIS have a worse prognosis.
Infiltrating ductal carcinoma: Mutations that affect prognosis (2).
Expression of Her-2 and mutation of p53 bring a worse prognosis.
Infiltrating ductal carcinoma: Cytogenetic effect on prognosis.
Increased S-phase fraction.
Infiltrating lobular carcinoma: Classic pattern of growth.
Single cells or single files of cells in a sclerotic background, often growing concentrically around ducts.
Infiltrating lobular carcinoma: Other patterns of growth (5).
Solid.
Tubulolobular.
Alveolar.
Apocrine.
Pleomorphic.
Infiltrating lobular carcinoma: Immunohistochemistry.
Variable: ER, PR, Her-2.
Infiltrating lobular carcinoma: Cytogenetics (2).
Classic: Loss of 16q, gain of 1p.
Pleomorphic: Overexpression of Her-2 and p53, loss of ER and PR.
Infiltrating lobular carcinoma: Metastasis (4).
More likely than invasive ductal carcinoma to metastasize to bone marrow, ovary, serosal surfaces, CSF.
Triple-negative carcinoma:
A. Frequency.
B. Epidemiology.
A. Accounts for 10-17% of all breast carcinomas.
B. More common in premenopausal women.
Triple-negative carcinoma: Histology (4).
Most tumors are high-grade ductal carcinomas of no specific type.
Geographic necrosis.
Squamous metaplasia.
May undergo focal sarcomatoid change.
Triple-negative carcinoma: Immunohistochemistry (6).
Most triple-negative carcinomas exhibit the basal-like phenotype, thus expressing
− CK 5/6, CK14, CK17.
− EGFR.
− SMA, p63.
Triple-negative carcinoma: Related types of breast cancer (2).
Basal-like breast cancers.
BRCA1-related breast cancers.
Triple-negative carcinoma: Metastasis.
Hematogenous, mainly to lungs and brain, less often to lymph nodes and bones.
Medullary carcinoma: Gross pathology.
Firm and may be well circumscribed, sometimes even with a distinct capsule.
Medullary carcinoma: Histology (5).
Syncytial growth.
High-grade nuclei.
Many mitotic figures.
Brisk lymphoplasmacytic response.
Well-defined, pushing borders.
Medullary carcinoma: Incompatible histologic features (2).
Invasion of surround fat.
Glandular or ductal structures.
Medullary carcinoma: Immunohistochemistry (3,1,3).
Positive: CK5/6, p53, Ki-67.
Often positive: EGFR.
Negative: ER, PR, Her-2.
Medullary carcinoma: Genetics.
Often associated with mutation in BRCA1.
Medullary carcinoma: Flow cytometry.
Tumor cells are often aneuploid or polyploid.
Medullary carcinoma: Behavior.
Better prognosis.
Less likely to metastasize to axillary lymph nodes.
Mucinous carcinoma:
A. Synonym.
B. Mammographic appearance.
A. Colloid carcinoma.
B. Well-circumscribed mass (also on gross examination).
Mucinous carcinoma: Histology (2).
Lakes of mucin surround groups of infiltrating tumor cells.
Cells form sheets or clusters but usually form no glands.
Mucinous carcinoma: Histologic subtypes.
Type A: Paucicellular, no neuroendocrine differentiation.
Type B: Hypercellular, neuroendocrine differentiation.
Mucinous carcinoma: Immunohistochemistry (2,2,1).
Positive: CK7, neuroendocrine markers (in Type B).
Usually positive: ER, PR.
Negative: Her-2.
Mucinous carcinoma: Flow cytometry.
Cells of pure mucinous carcinoma are usually diploid.
Mucinous carcinoma vs. mucocele-like tumor.
Mucocele-like tumor: Mucous lakes are lined by benign epithelium and contain no floating clusters of cells.
Mucinous carcinoma: Prognosis.
Better than that of infiltrating ductal carcinoma of no special type.
Tubular carcinoma:
A. Most common age at presentation.
B. Mammographic appearance.
C. Gross appearance.
A. Fourth decade.
B. May be undetectable.
C. Firm, stellate, sclerotic.
Tubular carcinoma: Cytology.
Bland; rare mitotic figures.
Tubular carcinoma: Histology
Small, angulated tubules in a dense stroma.
May infiltrate into adjacent fat.
Tubular carcinoma: Histologic requirement.
Pure tubular carcinoma: Essentially 100% of the tumor has tubular architecture.
Tubular carcinoma: Immunohistochemistry (1,2).
Usually positive: ER.
Negative: Her-2, EGFR.
Papillary carcinoma: Cytology.
Degree of atypia is typically not helpful in distinguishing between papillary carcinoma and benign papillary lesions.
Mucinous carcinoma: Histologic requirement.
Extracellular mucin must make at least half of the tumor.
Papillary carcinoma: Histology
Distended duct containing many complex papillary fronds.
Papillary carcinoma: Incompatible features (2).
Complete layer of myoepithelial cells.
Apocrine metaplasia.
Infiltrating papillary carcinoma: Histologic requirement.
There must be unequivocal infiltration of extracapsular stroma.
Papillary carcinoma: Immunohistochemistry (2,2).
Positive: ER, PR.
Negative: Her-2, HMWCK.
Papillary carcinoma vs. benign papillary lesions: Immunohistochemistry.
CEA: Most papillary carcinomas express it; benign papillary lesions do not.
Invasive papillary carcinoma: Behavior.
Rarely spreads to lymph nodes.
Metaplastic carcinoma: Types.
Biphasic: Carcinomatous and sarcomatous component.
Monophasic: Sarcomatous only.
Metaplastic carcinoma: Histology of the carcinomatous component (2).
Most often poorly differentiated ductal carcinoma.
Squamous-cell carcinoma.
Metaplastic carcinoma: Histology of the sarcomatous component (2).
Most often bone or cartilage.
Fibromatosis-like metaplastic carcinoma may be a low-grade variant.
Metaplastic carcinoma: Histology of metastatic deposits.
Adenocarcinoma, metaplastic components,or both.
Metaplastic carcinoma: Immunohistochemistry of the carcinomatous component (3).
Positive: Cytokeratin, EMA, vimentin.
Metaplastic carcinoma: Immunohistochemistry of the sarcomatous component (3).
Positive: p63, vimentin, cytokeratin (focal).
Metaplastic carcinoma: Prognostic markers.
Usually triple-negative.
Metaplastic carcinoma: Effect of type of metaplasia on prognosis.
Chondroid or osseous: Worse prognosis.
Squamous: No effect on prognosis.
Papillary carcinoma: Mutations (2).
Loss of heterozygosity of 16q23.
Loss of heterozygosity at locus of TP53.
Secretory carcinoma: Mean age at presentation.
25 years.
Secretory carcinoma: Histology (3).
Bland cells form back-to-back ducts.
Abundant eosinophilic cytoplasm.
Intracellular and extracellular PASD-positive secretions.
Secretory carcinoma: Immunohistochemistry (4).
Positive: CEA, EMA, S-100, α-lactalbumin.
Secretory carcinoma: Prognostic markers.
ER and PR are often not expressed.
Secretory carcinoma: Electron microscopy.
Many membrane-bound secretory granules lined by microvilli.
Secretory carcinoma: Mutation.
t(12;15)(p13;q35) :: ETV6−NTRK3.
Secretory carcinoma vs. lactating adenoma (2).
Lactating adenoma:
− Sharply circumscribed.
− Retains myoepithelial cells.
Secretory carcinoma: Prognosis.
Better than that of ductal carcinoma of no special type.
Apocrine carcinoma: Mammographic appearance.
Similar to that of typical infiltrating ductal carcinoma.
Apocrine carcinoma: Histology (3).
Apocrine cells forming nests, sheets, glands.
More pleomorphic nuclei and large nucleoli than in benign apocrine cells.
Architecture of intraductal apocrine carcinoma is similar to that of typical IDC.
Apocrine carcinoma: Histologic requirement.
All or nearly all of the tumor cells are apocrine.
Apocrine carcinoma: Immunohistochemistry (1,1,1).
Positive: CEA.
Often positive: Androgen receptor.
Negative: S100.
Apocrine carcinoma: Prognostic markers.
ER and PR are variable expressed.
Apocrine carcinoma: Special stain.
PAS-positive, diastase-resistant.
Apocrine carcinoma: Behavior.
Similar to that of invasive ductal carcinoma of no special type.
Adenoid-cystic carcinoma: Location.
Periareolar or subareolar.
Adenoid-cystic carcinoma: Histology (3).
No perineural invasion.
May show squamous differentiation or sebaceous features.
Otherwise similar to AdCC of the salivary gland.
Adenoid-cystic carcinoma: Grading.
Grade I: None of the tumor is solid.
Grade II: No more than 30% of the tumor is solid.
Grade III: More than 30% of the tumor is solid.
Adenoid-cystic carcinoma: Immunohistochemistry (2).
Positive: Myoepithelial markers, CK7.
Adenoid-cystic carcinoma: Prognostic markers.
ER and PR are usually not expressed.
Adenoid-cystic carcinoma vs. invasive cribriform carcinoma (3).
Invasive cribriform carcinoma:
− No dual-cell population.
− No basement-membrane-like matter.
− Negative: S-100, SMA.
Adenoid-cystic carcinoma: Behavior.
Much less aggressive than other mammary carcinomas.
Much less aggressive than AdCC of the salivary gland.
Adenoid-cystic carcinoma: Mutation.
Alterations of chromosome 6q.
Inflammatory carcinoma: Histology (2).
Usually an infiltrating ductal carcinoma, high-grade or poorly differentiated.
Tumor within dilated dermal lymphatics.
Inflammatory carcinoma: Immunohistochemistry (2).
Positive: p53, E-cadherin.
Inflammatory carcinoma: Prognostic markers.
Positive: Her-2.
Negative: ER, PR.
Inflammatory carcinoma: Histologic requirements (2).
Invasive mammary carcinoma.
Tumor in the dermal lymphatics.
Inflammatory carcinoma: Treatment.
Chemotherapy.
Mastectomy.
Radiation.
Inflammatory carcinoma: Prognosis.
60% are dead within 5 years.
Inflammatory carcinoma: Mutated genes (3).
Her-2.
RhoC.
LIBC/WISP3.
Paget’s disease of the nipple: Association with carcinoma (2).
Usually accompanies concurrent carcinoma in the same breast, but rarely occurs without it.
Carcinoma is usually intraductal, often with an infiltrating component.
Paget’s disease of the nipple: Cytology.
Nucleus: Large, with large nucleus.
Cytoplasm: Abundant, pale, vacuolated, may contain intracytoplasmic lumens.
Paget’s disease of the nipple: Architecture.
Cells may occur individually are form clusters or glandlike structures.
Paget’s disease of the nipple: Special stains.
Positive (50-60% of cases): Mucicarmine, PAS.
Paget’s disease of the nipple: Immunohistochemistry (5,2).
Positive: CK7, EMA, CEA, AR, p53.
Negative: HMWCK, S100.
Paget’s disease of the nipple: Prognostic markers (2).
Positive: Her-2, ER.
Paget’s disease of the nipple: Treatment (2).
Mastectomy, whether or not a breast mass has been identified.
Tamoxifen may be used in premenopausal women with positive lymph nodes.
Hemangioma: Typical location.
Perilobular breast tissue.
Hemangioma: Most frequent type.
Cavernous.
Hemangioma vs. low-grade angiosarcoma: Possibly helpful immunohistochemical stain.
Ki-67.
Infantile hemangioma.
Associated with
− Decreased expression of Hox-A5.
− Immunopositivity for GLUT1.
Angiosarcoma: Mean age at presentation.
Fourth decade.
Angiosarcoma: Associations (2).
Irradiation.
Pregnancy.
Angiosarcoma, low-grade: Histology (4).
Recognizable vascular channels with little or no endothelial tufts or papillary fronds.
Hyperchromatic nuclei without significant pleomorphism.
Few or no mitotic figures.
Angiosarcoma, intermediate-grade: Histology (3).
Endothelial tufts and papillary fronds create focal hypercellular areas.
Moderate nuclear pleomorphism.
Few mitotic figures.
Angiosarcoma, high-grade: Histology (5).
More endothelial tufts and papillae.
Marked nuclear pleomorphism.
Many mitotic figures, often atypical.
Necrosis.
Blood lakes.
Angiosarcoma: Expression of cytokeratins.
Present in up to 35% of epithelioid angiosarcomas.
Angiosarcoma, high-grade:
A. Epidemiology.
B. Prognosis.
A. Younger patients.
B. Poor.
Angiosarcoma: Treatment.
Total mastectomy.
Axillary dissection is not indicated.
Postmastectomy angiosarcoma: Association.
Status post mastectomy with or without irradiation.
Postmastectomy angiosarcoma:
A. Frequency.
B. Timing.
A. Occurs in less than 0.45% of patients after mastectomy.
B. Occurs around 10 years after mastectomy.
Postmastectomy angiosarcoma: Histology (5).
High-grade angiosarcoma in a densely collagenous background.
Changes of chronic lymphedema: − Epidermal hyperplasia. − Subcutaneous edema. − Fibrosis. − Proliferation of small vessels.
Postmastectomy angiosarcoma vs. postirradiation angiosarcoma (2).
Postirradiation angiosarcoma:
− Occurs within the irradiated area.
− Occurs within 5 years after irradiation.
Postmastectomy angiosarcoma: Treatment.
Amputation and chemotherapy.
Postmastectomy angiosarcoma: Prognosis.
Most patients are dead within 2 years.
Gynecomastia: Associated non-neoplastic diseases (4).
Cirrhosis.
Renal failure.
Chronic pulmonary disease.
Klinefelter’s syndrome.
Gynecomastia: Associated neoplasms (4).
Germ-cell tumors.
Large-cell carcinoma of the lung.
Some gastric cancers.
Some renal cancers.
Gynecomastia: Associated drugs (5).
Cimetidine.
Spironolactone.
Protease inhibitors.
Ethanol.
Anabolic steroids.
Others.
Gynecomastia: Architecture.
Cribriform or micropapillary pattern is typical.
Gynecomastia: Stromal changes (2).
Fibrosis.
Pseudoangiomatous stromal hyperplasia sometimes.
Gynecomastia: Association with carcinoma.
None.
Gynecomastia: Treatment (3).
Treatment of the causative disease.
Tamoxifen in early stage.
Surgery.
Carcinoma of the male breast: Genetic risk factors (2).
Genes of high penetrance such as BRCA2.
Klinefelter’s syndrome.
Carcinoma of the male breast: Other risk factors (5).
Hyperthyroidism.
Obesity.
Damage to liver.
Damage to testicles.
Damage to chest wall.
Carcinoma of the male breast: Peak age at diagnosis.
71 years.
Carcinoma of the male breast: Presentation.
Painless mass.
Carcinoma of the male breast: Typical histology.
Infiltrating ductal carcinoma.
DCIS is rare.
Carcinoma of the male breast: Immunohistochemistry (4).
Variable: ER, PR, AR, Her-2.
Carcinoma of the male breast: Main differential diagnosis.
Metastatic carcinoma of the prostate gland.
Carcinoma of the male breast:
A. Frequency of metastasis to axillary lymph nodes.
B. Sites of distant metastasis (3).
A. About 50% at presentation.
B. Lungs, bones, CNS.
Metastasis to the ___ breast: Leading primary sites.
A. Female.
B. Male.
A. The other breast.
B. The prostate.
Primary vs. metastatic tumor in the breast: Stromal change.
Elastosis is more common in primary breast cancer.
Primary vs. metastatic tumor in the breast: Epithelial change.
Calcification is more common in primary breast cancer.
Primary breast carcinoma vs. metastatic melanoma: Immunohistochemical pitfalls (2).
Melanoma can express cytokeratin and EMA.
Breast carcinoma can express S100.
Primary breast carcinoma vs. metastatic ovarian carcinoma: Immunohistochemistry (3,1).
Ovarian carcinoma
− Positive: WT-1, CA125, mesothelin.
− Negative: GCDFP-15.
Primary breast carcinoma vs. metastatic gastric carcinoma: Immunohistochemistry (2).
Gastric carcinoma tends to express CDX2 and CD20.
Metastasis to the breast: Prognosis.
Death usually within 2 years.
