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FIBROCYSTIC CHANGES
NON PROLIFERATIVE
Cysts and fibrosis
PROLIFERATIVE
Innocuous/atypical ductular epithelial cell hyperplasia
Sclerosing adenosis
EPITHELIAL HYPERPLASIA
Mild and orderly
Ducts filled by orderly cuboidal cells and small glandular pattern within
Ductal papillomatosis
Atypical lobular hyperplasia
Monomorph8ic cells with complex architectural patterns
Dosent often produce discrete breast mass. But produce microcalcifications
SCLEROSING ADENOSIS
Gross
Hard rubbery similar to ca breast
Microscopy
Proliferation of lining epithelial cells and myoepithelial cells in small ducts
Glandular pattern within fibrous stroma
Stromal fibrosis
Can resemble invasive scirrhous ca breast
TUMORS
BENIGN
TUMOR
CAUSE
FIBROADENOMA Increased
PHYLLODES
TUMOR
INTRADUCTAL
PAPILLOMA
MORPHOLOGY
Gross
estrogen
Firm, freely movable
level
nodule(1-10 cm)
White on cut section with
yellow specs of glandular area
Micro
Loose fibroblastic stroma with
duct like epithelial lined specs
Pericanalicular- open duct
space
Intracanalicular- slit like duct
space
Periductal
Gross
stroma
Large
proliferation Leaf like clefts and slits on
section due to lobulation and
cysts
Increased stromal cellularity,
anaplasia and mitotic activity
Principal
Small, solitary
lactiferous
Multiple papillaeducts/sinuses
Central connective tissue
Cuboidal or columnar cell
lining
Frequently double layered
epith,
basal layermyoepithelial
C/F
Monoclonal
cells
Never become
malignant
Benign
Localized and
cured by
excision
Most
malignant may
metastasise
Benign
Multiple
papillomas in
several ducts
and absence of
myoepithelium
indicates
malignancy
CARCINOMA
CAUSES
Hormone replacement therapy for osteoporosis
OCPs
Ionizing radiations
Genetic
HER2/NEU
RAS, MYC amplification
RB, p53 mutation
5 subtypes based on gene profiling
Luminal A
Luminal B
HER2/NEU overexpressing
Basal like
Normal breast like
CLASSIFICATION
Non invasive
DCIS
LCIS
Invasive
IDC (Scirrous tumor)
ILC
Medullary carcinoma
Colloid carcinoma
Tubular carcinoma
Other types
NON INVASIVE
DCIS
Terminal duct lobular unit
Origin
Fill distort, unfold lobules involved and
Gross
Histology
Nuclear
grade
Hormone Positive
receptors
Prognosis Excellent
C/F
LCIS
Terminal duct lobular unit
Expand, but dosent alter the
underlying str
Uniform
Loosely cohesive clusters
Signet ring cells
Low
----High chance for invasive
carcinoma and developing
in both breasts
Clinical and radiological
follow up
Bilateral prophylactic
mastectomy
Often incidential finding
No masses or calcification
PAGETS DISEASE
Extension of DCIS to lactiferous ducts and contiguous skin around nipple
Disrupt epidermal barrier
Unilateral crusting
INVASIVE CARCINOMA
TYPE
MORPHOLOGY
Gross
DUCTAL
Produce desmoplastic
response
Microscopy
Heterogeneous
LOBULAR
Gross
Bilateral and multicentric
more frequently than others
Microscopy
Cells identical to LCIS
Allined in strands or chains
Bulls eye pattern occationally
PROGNOSIS RECEPTORS
Vary according
to type. But
generally poor
2/3 have
hormone
receptors
1/3 have
HER2/NEU
Metastasise
Hormone
more frequently receptors
to CSF, ovary,
serosa, uterus,
GIT, BM
COMMON FEATURES
1)Tendency to become adherent to pectoral fascia, muscles and skin
2) Dimpling of skin,
3) lymphedema
SPREAD
Lymphatic and hematogenous
Metastasis mainly to lungs, skeleton, adrenals, liver and less commonly to brain and
pituitary
COURSE
Solitary, movable painless mass
2-3 cm when palpable and 1 cm when just detectable by mammography
PROGNOSIS
TNM
Grade well differentiated, moderate differentiated, poorly differentiated based on
Tubule formation
Nuclear grade
Mitotic rate
Histology
Presence of hormone receptors is a slightly better prognosis
Proliferation rate
Aneuploidy
Overexpression of HER2NEU is bad prognosis
STAGING
STAGE 1
STAGE 2
STAGE 3
STAGE 4
87%
75%
46%
13%