PATHOLOGY OF BREAST

KELOMPOK 7 :
LINA PANDU BOBBY MARTHIN - MARSELLA
NORMAL BREAST
Breast profile
A ducts
B lobules
C dilated section of duct to hold milk
D nipple
E fat
F pectoralis major muscle
G chest wall/rib cage
2
Enlargement
A normal duct cells
B basement membrane (duct wall)
C lumen (center of duct)
Illustration Mary K. Bryson
NORMAL BREAST
BREAST GLAND
4
Each breast has 15 to 20 sections (lobes)
arranged like the petals of daisy
Inside each lobe are many smaller structures
called lobules
At the end of each lobule are tiny sacs
(bulbs) that can produce milk
PHYSIOLOGIC CHANGES
at birth male and female breasts
- active secretion (transplacental passage of maternal
hormones) bilateral breast enlargement
- recedes several months postpartum
after menopause gradual and progressive involution (lobular
atrophy, increased fat, cystic dilatation of ducts)
Macromastia
diffuse enlargement of both breasts
adolescence or pregnancy
exaggerated response to hormonal stimulation
Pubertal (Virginal) Macromastia
1669 - 23-year-old woman - breasts enlarged "overnight" to a combined weight
of 104 pounds
Pregnancy
1 in 100,000 pregnancies - erythematous, edematous, painful
PHYSIOLOGIC CHANGES
DEVELOPMENTAL ABNORMALITIES
Aplasia and hypoplasia
uncommon associated with overdevelopment of the contralateral
breast
acquired (irradiation chest wall tumors)
unilateral or bilateral amastia (absence of a nipple, breast ducts,
pectoralis major muscle) sex-linked recessive inheritance
Ectopic breast
supernumerary breast (from ectopic breast tissue along the milk lines
(midaxillae normal breasts medial groin and vulva)
1 6 % of adult women, much less often in men
unilateral axillary breast tissue
Polythelia
Supranumerary Nipple
Aberrant Breast
beyond the usual anatomic extent (no nipple or areola)
DEVELOPMENTAL ABNORMALITIES
INFLAMMATORY AND REACTIVE CONDITIONS
Fat necrosis
can simulate carcinoma clinically and mammographically
history of antecedent trauma, prior surgical intervention
Characterized by a central focus of necrotic fat cells with lipid-laden
macrophages and neutrophils
fibrosis, calcifications, egg shell on mammography
INFLAMMATORY AND REACTIVE CONDITIONS
Hemorrhagic necrosis with coagulopathy
Warfarin treatment shortly after initiation
edema, hemorrhage, necrosis (thrombi in small blood vessels )
protein C deficiency
Breast augmentation
foreign materials (shellac, glazier's putty, spun glass, epoxy resin, beeswax,
and shredded silk, silicone)
thinwalled silicone bag capsule disfiguration
Puerperal mastitis
early stages (2
nd
and 3
rd
W) of lactation
stasis of milk in distended ducts + staphylococci
abscess formation (ATB, incision and drainage)

Granulomatous Lobular Mastitis
etiology unknown, suggests carcinoma

Mammary duct ectasia
- Poorly defined periareolar mass; can be confused
clinically/radiologically with carcinoma
- Can also present as a thick, intermittent cheesy nipple discharge
- Periductal chronic inflammation destruction and dilation of
the ducts with fibrosis
SIGNS
13
Most common: lump
or thickening in
breast. Often
painless
Change in color or
appearance of areola
Redness or pitting of skin
over the breast, like the skin
of an orange
Discharge or
bleeding
Change in size or
contours of breast
SIGNS
Fibrocystic changes: Lumpiness, thickening and swelling, often
associated with a womans period
Cysts: Fluid-filled lumps can range from very tiny to about the size
of an egg
Fibroadenomas: A solid, round, rubbery lump that moves under skin
when touched, occuring most in young women
Infections: The breast will likely be red, warm, tender and lumpy
Trauma: a blow to the breast or a bruise can cause a lump
14
BENIGN PROLIFERATIVE LESIONS
pathologic spectrum of seemingly related clinically benign breast
abnormalities
palpably irregular and painful breasts
discrete lumps, multiple nodules, cystically dilated ducts, apocrine
metaplasia, interlobular and intralobular fibrosis
intraductal epithelial proliferation
fibrocystic disease, fibrocystic changes
extremely common (58% F)
BENIGN PROLIFERATIVE LESIONS
Adenosis
elongation of the terminal ductules Characterized by #acini +
stromal fibrosis within lobules
- sclerosing adenosis
- apocrine adenosis
- tubular adenosis
nonpalpable lesion, recognized in mammograms
microcalcifications
BENIGN TUMORS
Fibroadenoma
proliferation of epithelial and stromal elements, occurs mainly in large ducts
most common breast tumor in adolescent and young adult women (peak age =
third decade)
higher incidence in black patients
well-circumscribed, freely movable, nonpainful mass
regress with age if left untreated
Papillae are fibrovascular stalks lined by layers of proliferating epithelial and
myoepithelial cells
Most patients present with a serous or bloody nipple discharge
Tubular adenoma
far less common than fibroadenomas
young women, discrete, freely movable masses
uniform sized ducts
Lactating Adenoma
enlarging masses during lactation or pregnancy
prominent secretory change
Intraductal papilloma
in the mammary ducts, subareolar lactiferous ducts
periductal inflammation, duct sclerosis
serous or bloody nipple discharge
fibrosis, infarction, squamous metaplasia
CYSTOSARCOMA PHYLLODES
(PHYLLODES TUMOR)
initial description - over 150 years ago - fleshy tumor, leaf-like pattern
and cysts on cut surface
circumscribed, connective tissue and epithelial elements (fibroadenomas =
overgrowth connective tissue cellularity), 1-15 cm
less than 1 % of breast tumors
benign, malignant

metastases are hematogenous
low grade

high grade
BREAST CARCINOMA
most frequent malignant tumor in females (followed by cervix and colon)
highest incidence developed countries (USA 84,8/100 000F/Y, Western Europe
64,7/100 000F/Y)
2
nd
killer among cancers (1
st
= lung ca)
risk factors: genetic predisposition (breast ca in close (1
st
degree) relatives),
proliferative changes, early menarche, late menopause, history of ca (breast, ovary,
endometrium)
importance of preventive controls - early diagnosis - better prognosis
BREAST CARCINOMA - CLASSIFICATION
> 95 % breast malignancies ADENOCARCINOMAS
BREAST CARCINOMA
INVASIVE
Penetrated
through the BM
into the stroma.
IN SITU Neoplastic
cells limited
within the
ducts,lobules by
BM.
CLASSIFICATION BREAST CARCINOMA
NON-INVASIVE/IN SITU
CARCINOMA
Intraductal carcinoma
Lobular carcinoma in situ

INVASIVE CARCINOMA
Infiltrating ( invasive ) duct carcinoma
NOS
Infiltrating ( invasive ) lobular carcinoma
Medullary carcinoma


Colloid (mucinous)
carcinoma
Papillary carcinoma
Tubular carcinoma
Adenoid cystic carcinoma
Secretory carcinoma
Inflammatory carcinoma
Carcinoma with metaplasia

PAGETS DISEASE OF THE NIPPLE
BREAST CARCINOMA RISK FACTORS
Incidence increases with age Peaks at
75 80 yrs. Age
Only 1 % incidence men.
Gender
Early menarche, Late menopause
increased risk.
Age at menarche &
menopause
Nulliparous women /Late pregnancy
proliferation of cells with pre neoplastic
changes.
Age at first live birth -
Mother,sister increased risk.
First-Degree Relatives
with Breast Cancer -
BREAST CARCINOMA RISK FACTORS
In previous biopsies => increased risk.
Proliferative breast changes without
atypia smaller risk.
Atypical Hyperplasia
Non-Hispanic white women highest rates
of breast cancer. Race / Ethnicity
Increases the risk of breast cancer.
Postmenopausal hormone
replacement therapy
High breast density --d/t less complete involution
of lobules at the end of each menstrual cycle
increases no. of cells potentially susceptible to
neoplastic transformation.
Breast Density
To chest - d/t cancer therapy, atomic
bomb exposure, or nuclear accidents.
Radiation Exposure
BREAST CARCINOMA RISK FACTORS
1% of women with breast cancer second
contralateral breast carcinoma / year. Risk - higher for
women with germline mutations in BRCA1 and BRCA2
Carcinoma of the Contralateral
Breast or Endometrium.
United States and Europe higher
incidence.
Geographic Influence
Alcohol consumption higher estrogen levels
and lower folate levels.
Diet
Postmenopausal obese women increased synthesis
of estrogens in fat depots. Obesity
The longer women breastfeed, the greater the
reduction in risk
Breastfeeding
Organochlorine pesticides estrogenic
Environmental Toxins
Increased risk.
Tobacco & cigarette smoking
HORMONAL
EXPOSURE
(SPORADIC)
GENETIC FACTORS
(HEREDITARY)
Major risk
factors of Breast
Carcinoma
PATHOGNESIS GENETIC FACTORS
Most common genes
implicated in Breast
carcinoma
BRCA1 BRCA2
p53 CHEK2
PATHOGENESIS HORMONAL FACTORS
Excess Hormonal exposure Sporadic
cancers.
Post menopausal women sporadic
cancers ER positive.
Hormones breast growth during puberty,
menstrual cycles, pregnancy cycles of
proliferation cells at risk for DNA
damage.
If premalignant or malignant cells are
present, hormones - stimulate their growth +
growth of normal epithelial and stromal cells
tumour development.
Metabolites of estrogen mutations /
generate DNA-damaging free radicals.

Stage T: Primary Cancer Lymph Nodes (LNs) M: Distant Metastasis 5-Year Survival (%)
0 DCIS or LCIS No metastases Absent 92
I
Invasive carcinoma 2
cm
No metastases Absent 87
II Invasive carcinoma >2
cm
No metastases Absent 75
Invasive carcinoma <5
cm
1 to 3 positive LNs Absent
III Invasive carcinoma >5
cm
1 to 3 positive LNs Absent 46
Any size invasive
carcinoma
4 positive LNs
Absent
Invasive carcinoma
with skin or chest wall
involvement or
inflammatory
carcinoma
0 to >10 positive LNs. Absent
IV Any size invasive
carcinoma
Negative or positive
lymph nodes
Present 13
PROGNOSTIC FACTORS - MAJOR
Outcome in breast CA varies widely.

Prognosis determined by pathologic
examination of primary carcinoma & axillary
lymph nodes.


American Joint Committee on Cancer (AJCC)
staging system divides patients into five
stages (O to IV) correlated with survival.

Major prognostic factors strongest
predictors of death.
1) Invasive vs insitu CA.
2) Distant metastasis
3) Lymph node metastasis
4) Tumour size
5) Locally advanced ds.
6) Inflammatory CA.


PROGNOSTIC FACTORS - MINOR
Histologic
Type & Grade
Gene
expression
profiling
NORMAL MALE BREAST



Consists of the nipple and a rudimentary
duct system ending in terminal buds without
lobule formation.
GYNAECOMASTIA
Enlargement of male breast.
Puberty/very aged/hyperestrinism.
Cirrhosis of liver, Increased adrenal estrogens as
androgenic functions of testis fail in very aged, Drugs
alcohol, marijuana, heroin, ART, anabolic steroids
used by atheletes & body builders, Klinefelter
syndrome.
Imbalance between estrogens, stimulate breast
tissue and androgens which counteract these
effects
Unilateral or bilateral
Button-like subareolar enlargement.


Morphology : Increase in dense collagenous
connective tissue, marked micropapillary
epithelial hyperplasia of the duct lining.
Individual epithelial cells fairly regular,
columnar to cuboidal cells with regular nuclei.
Lobule formation is rare.
38
EVALUATION
A. Clinical Manifestation:
B. Physical Examination:
39
EVALUATION
Radiological Examination:
A positive result is only suggestive of carcinoma
1. Mammography (Screening):
Uses low dose of radiation (0.1 rad), not proven to escalate breast CA
Complementary study, can not replace biopsy
(+) fine stippling of calcium suggestive of CA
Early detection of an occult CA before reaching 5 mm.
Recommended Program of Using Mammography:
1. Daily breast examination after 20y/o
2. Baseline mammography 35-40y/o
3. Annual mammography > 40 y/o
40
MAMMOGRAPHY
41
EVALUATION
Radiological Examination:
2. Computed Tomography or Magnetic Resonant Imaging:
Too expensive
For detection of vertebral metastasis
3. Ultrasonography
No radiation exposure
Can differentiate cystic lesions from solid mass
Can not detect less than 5mm.
42
PET SCAN
PET scan Normal
43
PET scan abnormal
PET in woman with breast CA
that has spread to bone
44
EVALUATION
Radiological Examination:
4. Interventional Technique:
Ductography:
Inject radio-opaque contrast
media into the mammary duct
Biopsy: positive result is diagnostic
1. Excision biopsy
2. Incision biopsy
3. True-cut or core biopsy (Vim-
Silverman)
4. Fine needle biopsy
THANK YOU

CARCINOMA IN SITU
Malignant clonal population of cells limited to
ducts & lobules by the basement membrane.

DUCTAL CARCINOMA IN SITU

Most DCIS detected by
calcifications on
mammography/mammograp
hic density - periductal fibrosis
surrounding a DCIS/rarely
palpable mass/ nipple
discharge/incidental finding
on a biopsy for another lesion.

Spreads through ducts &
lobules extensive lesions
entire sector of a breast.

DCIS involves lobules acini
distorted, unfolded appear
as small ducts.
DCIS 5 ARCHITECTURAL SUBTYPES
CRIBRIFORM
COMEDO
CARCINOMA
PAPILLARY
MICRO
PAPILLARY
SOLID
COMEDOCARCINOMA
Solid sheets of pleomorphic
cells with high grade
hyperchromatic nuclei.

Areas of central necrosis +nt.

Necrotic cell membranes
calcify clusters/linear &
branching microcalcifications
on mammography.

Periductal concentric fibrosis &
chronic inflammation.

Extensive lesions palpable as
vague nodularity.




NONCOMEDO DCIS
Monomorphic cell
population nuclear
grades low to high.
CRIBRIFORM DCIS
Intra-epithelial spaces
evenly distributed, regular
in shape.

COOKIE CUTTER LIKE

SOLID DCIS
Completely fills the
involved spaces.
NONCOMEDO DCIS
PAPILLARY DCIS
Grows into spaces along
fibrovascular cores lack
myoepithelial cell layer.

MICROPAPILLARY DCIS
Bulbous protrusions without
a fibrovascular core
arranged in complex
intraductal patterns.

Calcifications assoc.with
necrosis/form on
intraluminal secretions.
PAGETS DISEASE OF NIPPLE
Rare manifestation of breast CA.
U/l erythematous eruption, Pruritus.
Malignant cells/PAGET CELLS
Extend from DCIS within ductal system
via lactiferous sinuses nipple skin
without crossing the BM.
Tumour cells disrupt tight squamous
epithelial barrier ECF seeps out onto
nipple surface oozing scaly crust.
Pagets cells detected by nipple
Bx/cytological preparation of the
exudate.
Palpable mass 50 60 % of women
=> invasive CA.
No palpable mass => DCIS
Poorly differentiated, ER Negative,
HER2/neu overexp.
Prognosis depends on features of
underlying Ca.
PAGETS DISEASE OF NIPPLE
DCIS WITH MICROINVASION
Area of invasion through
BM stroma - > 0.1 cm.

Assoc. with
comedocarcinoma.

Few microinvasion foci
prognosis similar to DCIS.
MANAGEMENT AND PROGNOSIS OF
DCIS
MASTECTOMY for DCIS
curative > 95 % pts.

Recurrence rare d/t
residual DCIS in ducts in
subcutaneous tissue
not removed during
surgery/ d/t occult foci
of invasion not
detected at diagnosis.

Breast conservation
can be done but slightly
higher risk of
recurrence.
Major risk factors for
recurrence:
1. Grade
2. Size
3. Margins

In ER + ve DCIS Post-
op. radiation +
Tamoxifen recurrence
risk low.

Death < 2 % DCIS.
LOBULAR CARCINOMA IN SITU
Incidental biopsy finding -no
calcifications /stromal
reactions mammographic
densities.

Bilateral - 20% to 40% .

Young women.

Loss of expression of E-
cadherin(transmembrane cell
adhesion protein cohesion
of normal breast epithelial
cells).


LOBULAR CARCINOMA IN SITU -
MORPHOLOGY
Dyscohesive round cells
with oval or round nuclei
and small nucleoli.
Absence of atypia,
pleomorphism, mitoti
activity, necrosis.

Involved acini
recognizable as lobules.

Mucin-positive signet-ring
cells.

ER and PR +ve.

LOBULAR CARCINOMA IN SITU
Invasive carcinoma 1% per
year.

Both breasts - increased risk.
Risk - slightly higher in the
ipsilateral breast.


Invasive carcinomas - lobular
type.

Treatment:
1. Bilateral prophylactic
mastectomy.
2. Tamoxifen.
3. Close clinical follow-up.
4. Mammographic screening.
INVASIVE CARCINOMA

INVASIVE CARCINOMA
CLINICALFEATURES
Palpable mass.

Axillary lymph node
metastases

Fixity to the chest wall / skin
dimpling.

Nipple retraction

Lymphatics - involved - block
the local area of skin
drainage lymphedema,
skin thickening.

Tethering of the skin to the
breast by Cooper ligaments
peau d'orange.

Mammography
Radiodense mass




INVASIVE CARCINOMA, NO SPECIAL
TYPE (NST; INVASIVE DUCTAL
CARCINOMA)
Majority (70% to 80%).

Gross appearance: Most
tumors - firm to hard
,irregular border . Less
frequently - well-
circumscribed border , softer
consistency.

When cut / scraped
characteristic grating
sound d/t small, central
pinpoint foci or streaks of
chalky-white elastotic stroma
and occasional small foci of
calcification.

INVASIVE CARCINOMA NST- HPE
Features Well diff. Ca Mod. diff.Ca Poorly diff. Ca.
Tubule formation Prominent Less,solid
clusters/single
infiltrating cells
Ragged
nests/solid sheets
of cells
Nuclei Small,round,mon
omorphic
Greater nuclear
pleomorphism
Nuclei
enlarged,irregula
r.
Mitotic figures Rare Present Numerous
Proliferation rate - - High
Tumour necrosis - - Present
INVASIVE LOBULAR CARCINOMA
Palpable mass/
mammographic density with
irregular borders. Sometimes -
tumor infiltrates the tissue
diffusely little desmoplasia, not
palpable, no mammographic
density. Metastases difficult to
detect.

Bilateral - 5 10 %.

Biallelic loss of expression of
(CDH1, encodes E-cadherin)
d/t mutations.



INVASIVE LOBULAR CARCINOMA
Morphology: Histologic
hallmark dyscohesive
infiltrating tumor cells, often
arranged in single file or in
loose clusters or sheets
INDIAN FILE APPEARANCE.

Tubule formation - absent.

Signet-ring cells containing
an intracytoplasmic mucin
droplet are common.

Desmoplasia - minimal or
absent

INVASIVE LOBULAR CARCINOMA
Well-differentiated and
moderately differentiated
carcinomas diploid, ER
positive, HER2/neu
overexpression - rare

Poorly differentiated carcinomas
aneuploid, lack hormone
receptors, may overexpress
HER2/neu.

Different pattern of metastasis
than other breast cancers.
Metastasis peritoneum
,retroperitoneum, the
leptomeninges (carcinoma
meningitis), the gastrointestinal
tract, ovaries and uterus.


MEDULLARY CARCINOMA
MC - 6
th
decade.

May closely mimic a
benign lesion clinically and
radiologically/ present as a
rapidly growing mass.

MORPHOLOGY : Well
circumscribed,soft,fleshy
mass - little desmoplasia
more yielding on palpation
and cutting. (medulla
=>marrow).

MEDULLARY CARCINOMA - HPE
1. Solid, syncytium-like
sheets of large cells with
vesicular, pleomorphic
nuclei, prominent nucleoli
> 75% of the tumor
2. Frequent mitotic figures;
3. Moderate to marked
lymphoplasmacytic
infiltrate surrounding and
within the tumor.
4. Pushing (noninfiltrative)
border.

Poorly differentiated.

MEDULLARY CARCINOMA
High nuclear grade,
aneuploidy, hormone
receptors - nt, HER2/neu
overexpression nt.

Lymph node metastases -
infrequent.

Syncytial growth pattern and
pushing borders - d/t
overexpression of adhesion
molecules intercellular cell
adhesion molecule and E-
cadherin limit metastatic
potential.


MUCINOUS/COLLOID CARCINOMA
Older women (median age
71) grow slowly - many
years.

Morphology: Tumor
soft/rubbery . Consistency &
appearance of pale gray-
blue gelatin. Borders -
pushing / circumscribed.


MUCINOUS CARCINOMA - HPE
Tumor cells - arranged in
clusters and small islands
within large lakes of mucin.

Mucinous carcinomas
diploid, well to moderately
differentiated, and ER
positive.

Lymph node metastases -
uncommon.

Overall prognosis is slightly
better.

TUBULAR CARCINOMA
Small irregular mammographic
densities - late 40s.

Uncommon.

Morphology: Well-formed
tubules + nt, myoepithelial cell
layer, BM - nt tumor cells in
direct contact with the stroma.
Apocrine snouts -
typical.Calcifications - within
the lumens.

> 95% of all tubular carcinomas
- diploid, ER + ve,HER2/neu ve
.

Well differentiated. Excellent
prognosis.

INVASIVE PAPILLARY &
MICROPAPILLARY CARCINOMA
Rare - 1% or fewer of all
invasive cancers.
More commonly seen in
DCIS.
INVASIVE PAPILLARY CA.
ER positive.
Favorable prognosis.
INVASIVE MICROPAPILLARY
CA.
ER negative,HER2 positive.
Lymph node metastases -
very common
Prognosis is poor.

INFLAMMATORY CARCINOMA
Tumors swollen,
erythematous breast - caused
by extensive invasion and
obstruction of dermal
lymphatics by tumor cells.

Underlying carcinoma -
diffusely infiltrative - does not
form a discrete palpable mass
confusion with true
inflammatory conditions a
delay in diagnosis.

Many patients metastases
at diagnosis / recur rapidly.

Overall prognosis poor.

METAPLASTIC CARCINOMA
Includes a variety of rare
types of breast cancer (<1%
of all cases) matrix-
producing carcinomas,
squamous cell carcinomas,
and carcinomas with a
prominent spindle cell
component.

ER-PR-HER2/neu triple
negative.

Lymph node metastases -
infrequent.

Prognosis - poor.
Stage
T: Primary
Cancer
Lymph Nodes
(LNs)
M: Distant
Metastasis
5-Year Survival
(%)
0 DCIS or LCIS No metastases Absent 92
I Invasive
carcinoma 2
cm
No metastases Absent 87
II Invasive
carcinoma >2
cm
No metastases Absent 75
Invasive
carcinoma <5
cm
1 to 3 positive
LNs
Absent
III Invasive
carcinoma >5
cm
1 to 3 positive
LNs
Absent 46
Any size
invasive
carcinoma
4 positive LNs Absent
Invasive
carcinoma with
skin or chest
wall
involvement or
inflammatory
carcinoma
0 to >10 positive
LNs.
Absent
IV Any size
invasive
carcinoma
Negative or
positive lymph
nodes
Present 13
PROGNOSTIC FACTORS - MINOR
Histologic
Type & Grade
Gene
expression
profiling
STROMAL TUMOURS
TYPES OF STROMAL TUMORS

FIBROADENOMA
PHYLLODES TUMOUR
INTRALOBULAR
STROMA
LIPOMAS
ANGIOSARCOMAS
PSEUDOANGIOMATOUS STROMAL
HYPERPLASIA
FIBROUS TUMOURS
MYOFIBROBLASTOMA


INTERLOBULAR
STROMA
TUMOURS OF INTRALOBULAR
STROMA
FIBROADENOMA
MC benign tumor - 2 nd & 3 rd
decade.Multiple, bilateral.
Young women palpable mass.
Older women mammographic
density / calcifications.
Epithelium hormonally reponsive
increase in size during lactation
complicated by inflammation,
infarction mimics CA.
Stroma - densely hyalinized after
menopause -may calcify. Large
lobulated (popcorn)
calcifications characteristic
mammographic appearance.
Small calcifications - clustered -
require biopsy to exclude
carcinoma.

GROSS: Spherical,
sharply circumscribed,
rubbery, grayish white,
freely movable nodules -
bulge above the
surrounding tissue and
contain slitlike spaces.
< 1 cm large tumors.

FIBROADENOMA - HPE
Stroma delicate,
cellular,myxoid-resembles
normal intralobular
stroma.
Epithelium - surrounded
by stroma - compressed
& distorted by it.
Risk of malignancy
assoc. with Complex
fibroadenomas cysts >
0.3 cm. in size, sclerosing
adenosis, epithelial
calcifications, papillary
apocrine change.



FIBROADENOMA - TYPES
INTRACANALICULAR PERICANALICULAR
In pericanalicular histologic pattern, the glands
maintain their round or oval profiles. There is no
prognostic or clinical significance attached to the
pericanalicular and intracanalicular patterns. Both may
be seen within the same lesion.
PHYLLODES TUMOUR
HPE: Greater cellularity,
mitotic rate, nuclear
pleomorphism, stromal
overgrowth, and infiltrative
borders.

Recur locally, rare
metastases.

Majority Low-grade
lesions
Rare High-grade lesions.

Phyllodes tumors - excised
with wide margins /
mastectomy to avoid local
recurrences.

MALE BREAST
INVASIVE CARCINOMA
Invasive ductal carcinoma
largest group (65 to 80 % of mammary carcinomas)
mid to late fifties
stellate, white, firm (desmoplasia)
less often circumscribed, soft (medullary ca)
hormonally dependent (estrogen, progesterone)
Invasive lobular carcinoma
uniform cells, infiltrative growth (linear arrangement -
indian file pattern)
other types: tubular, mucinous, medullary,
inflammatory together about 10 % of breast ca

metastases: regional lymph nodes (axillary,
parasternal), lungs, liver, bone marrow, brain
treatment: surgery (radical mastectomy, breast
conserving surgery lumpectomy),
radiotherapy
antihormonal therapy (Tamoxifen)
chemotherapy
INVASIVE CARCINOMA
PAGETS DISEASE OF THE
NIPPLE
result of intraepithelial spread of intraductal
carcinoma
large pale-staining cells within the epidermis of the
nipple
limited to the nipple or extend to the areola
pain or itching, scaling and redness, mistaken for
eczema
ulceration, crusting, and serous or bloody discharge