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ETIOLOGY
Risk Factors
Increasing Age
Uncommon before age of 25
Steady increase in risk to time of menopause
Followed by slower rate of increase
Increased risk for women having first child after 30 years old
Estrogen replacement therapy
Obesity
Possibly due to ectopic production of estrogen in adipocytes
Genetic Predisposition
BRCA1 and BRCA2 mutation
Account for majority of hereditary breast cancers
MORPHOLOGY
Routes of Spread
Local Involvement
Invasion into skin, skeletal muscles and ribs
- Rare due to early detection of disease with screening
Lymph Node Metastasis
Axillary lymph node most important prognostic factor
Distant Metastasis
Bone most common site of spread
- Usually osteolytic metastasis
Liver and lungs
Gross Appearance
Usually felt as a rubbery or hard lump
Malignant features:
Tethered to the skin
BREAST PATHOLOGY
Fixation to chest wall
Retraction of nipple
HISTOPATHOLOGY
2 major variants:
Ductal carcinoma
Lobular carcinoma
Ductal Carcinoma
Most common form of breast cancer
Typical Histology of Adenocarcinoma
Atypical, pleomorphic and hyperchromatic cells
Formation of tubules
Most exhibit marked increase of dense fibrous tissue stroma
Morphology
- Similar to ductal carcinoma without invasion through basement membrane
- With areas of calcifications and central necrosis
- Historically classified into:
Lobular Carcinoma
5 to 10% of breast carcinomas
Tends to be bilateral and multicentric
Appearance Differs from Ductal Carcinoma
Monomorphic cells with round or oval nuclei
- Signet ring cells commonly seen
Cells lack cohesion
- Strands of infiltrating cells in the form of a single file
Indian Files
- Loosely dispersed in fibrous matrix
BREAST PATHOLOGY
Lobular Carcinoma In Situ
See Ductal Carcinoma In Situ
Monomorphic and loosely cohesive population of lobular carcinoma cells
Confined within the basement membrane of the involved lobule
CLINICAL SIGNIFICANCE
Clinical Presentation
Most patients present with a breast lump or
Mammographic abnormality detected during routine screening
Inflammatory Carcinoma
- Infiltration of majority of dermal lymphatics in the affected breast
- Causing redness and tenderness
Mammographic Appearance
Density
Most tumors grow as solid masses
- Radiologically denser than surrounding connective and adipose tissues
Commonly presents as a spiculated lesion with irregular infiltration
Architectural Distortion
Diffusely infiltrating masses may distort architecture without producing discrete density
Calcifications
Due to calcified secretory material or necrotic debris
Prognosis
Vastly improved due to better surgical techniques and neo-adjuvant therapy
Prognostic Factors
Axillary Lymph Node Metastases
- Most important prognostic factor
Tumor Grade
- Nuclear abnormality, tubule formation and mitotic rate
- Determines degree of differentiation of tumor
Her2/Neu Amplification
- Found in up to 20% of breast cancers
BREAST PATHOLOGY
PATHOGENESIS
Response to hormones in an exaggerated manner by the lobules and stroma in the breast
MORPHOLOGY
3 principal changes
Cyst formation
Solitary or multiple cysts lined by polygonal cells
Resembling apocrine epithelium of sweat glands
- Apocrine metaplasia
Blue-dome Cyst
Gross appearance of large solitary cyst containing brownish blue fluid
Fibrosis
Chronic inflammation and fibrosis
Due to rupture of cysts
BREAST PATHOLOGY
Adenosis
Increase in number of acinar units per lobule
Gland lumens are often enlarged
CLINICAL SIGNIFICANCE
FIBROADENOMA
Morphology
Gross Appearance
Pale well-circumscribed mass
- Tumor sharply delimited by fibrous capsule
Histopathology
Fibroblastic stroma enclosing
Glandular and cystic spaces lined by glandular epithelium
PHYLLODES TUMOR
Morphology
Gross Appearance
Large lesions often have bulbous leaflike protrusions
Histopathology
Differentiated from fibroadenomas by presence of:
- Increased cellularity, mitotic rate, pleomorphism
Morphology
Composed of multiple branching papillae
Consisting of a connective tissue axis covered by
- Myoepithelial and epithelial cells
BREAST PATHOLOGY
EPITHELIAL HYPERPLASIA
Morphology
Usually not grossly evident
Solid masses extending into duct lumen
Fenestrations can usually be seen
Classified into:
Hyperplasia Without Atypia
No increase to small increase in risk
Atypical Hyperplasia
Cellular atypia and architectural distortion
Histologically can resemble ductal or lobular carcinoma in situ
- Atypical ductal and lobular hyperplasia respectively
More than two fold increase in risk of developing carcinoma
SCLEROSING ADENOSIS
Morphology
Increased number of acini per terminal duct
Acini compressed by stromal fibrosis can create appearance of cords or strands of cells
Mimicking carcinoma