The document discusses several benign breast lesions and conditions:
- Mammary duct ectasia, which involves ectasia and thickening of large ducts with accumulation of debris, calcification, and chronic inflammation.
- Fibrocystic changes and sclerosing lesions, which present as multiple nodules involving glandular proliferation and compression.
- Columnar cell lesions, including simple columnar cell change, columnar cell hyperplasia, and lesions with atypia, the earliest neoplastic changes.
- Inflammatory conditions such as fat necrosis, mastitis, and granulomatous lobulitis. These can mimic carcinoma clinically and mammographically.
2. An increased number or enlargement of
glandular components.
Physiological/simple
Sclerosing adenosis
Radial scar and complex sclerosing lesion
Tubular adenosis
Microglandular adenosis
Blunt duct adenosis/ ccc/cch
3.
4.
5.
6.
7.
8.
9.
10.
11.
12. Multiple nodules-rounded and well defined
Retention of lobular architecture
Numeric increase in the glandular elements
Stromal proliferation
Glandular compression and distortion-more
towards centre of lesion
Tubules retain the two cell layers
Microcalcification+/-
13. Fibrous stroma dense ,hyalinized with elastic
tissue
Lacks atypical features
Apocrine metaplasia+/_
14. Sclerosing adenosis lesion with superimposed
apocrine metaplasia
Atypia may be moderately severe -
distinction from apocrine DCIS (with lobular
cancerisation) may be difficult
Immunostaining will demonstrate an intact
myoepithelial layer and basement membrane
Follow up of patients showed no greater
cancer risk than other atypical lesions
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26. Glands lined by a monolayer of bland epithelial
cells –no outer myoepithelial mantle.
Tubules –haphazard, small, regular, rounded
without angulation.
Lumens contain PAS positive,diastase resistant
secretory material .
Myoepithelial layer absent but dense basement
membrane present
Epithelial cells cuboidal or flattened without
apical snouts, cytologically benign.
Cells- vacoulated and contain PAS positive
material.
BM- PAS neg. reticulin –complete ring
Type IV Collagen
27. The cells show positive immuno staining with
S100, CK 8/18 & EGFR and negative staining
for ER, PGR & Her-2
Immuno stains for Collagen IV or laminin are
usually positive indicating an intact bounding
basement membrane
There is an association with atypical
proliferations and malignancy in up to 50% of
cases
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40. Histologically complex with adenosis
epithelial hyperplasia and frequent cyst
formation.
Usually not palpable
Often multiple
Frequently bilateral
Incidental findings in specimens and
mammography
41. Usually detected as stellate shadows on
mammograms
Therefore common in screening
Radiologically very similar to cancers
Note: both low grade cancers (especially tubular
cancers) and radial scars may remain unchanged
between screening rounds so a lack of growth is
no guarantee that the lesion is a radial scar
> 10mm called "Complex sclerosing lesions
42. Gross:
firm chalky white lesions with irregular outline
like head of a flower
Microscopy :
Lobular architecture is distorted
Centre of lesion –sclerosis and elastosis
Entrapped epithelial structure mimics carcinoma
Surrounded by epithelial sructures showing
dilation ,adenosis, and epithelial hyperplasia.
43. Haphazard arrangement of irregular small
tubules
Two cell layers
Apocrine metaplasia+/_
Calcification+/-
Associated sclerosing adenosis+/-
44. Benign lesion.
But associated with ADH,DCIS.-thus increased
risk of breast ca.
72. ‘presumably neoplastic intraductal
alteration, characterised by the replacement
of native epithelial cells by a single layer or
three to five layers of mildly atypical cells’.
By Simpson’s classification, FEA would
pertain to categories 4 and 6
Only low grade cytological atypia
No architectural atypia
No high grade atypia.
88. .
• CCLs with atypia are the early precursor
lesions in the low grade neoplasia pathway
• CCL WITH ATYPIA
• ADH/LOW GRADE DCIS
• LOW GRADE
CARCINOMAS[TUBULAR/CRIBRIFORM/LOBUL
AR/TUBULILOBULAR/]
89. 44-51 yrs
Non palpable in 86%
Intraluminal calcifications detected
mammogaraphically -74% cases of CCL
90. TDLU
Enlarged
Epithelial proliferation and cystic dilatation
Variably dilated acini at low power
First terminal ductules are affected later acini
Interlobular stroma diminished
91. Simple columnar cell change
1-2 layers of uniformly distibuted cuboidal to tall
columnar cells
Apical snout
Nucleus
Large
Crowded
Perpendicular to BM
No atypia
calcification
92. More than 2 layers of uniformly distibuted
cuboidal to tall columnar cells
Tufts/ mounds can be seen
No true papillae or cribriforn structures
Apical snout+/- hobnailing
Nucleus
Large
Crowded/ nucleus overlaps
Perpendicular to BM
No atypia
calcification
93. The earliest morphologically identifiable
neoplastic alteration among CCLs.
Luminae-rigidly round [unlike irregular
outline in CCC and CCH without atypia.]
Cells-atypical- larger, taller, uniform, high
N:C ratio, hyperchroamtic
94. CCL s with low grade nuclear atypia= FLAT
EPITHELIAL ATYPIA
CCLs with high grade nuclear atypia= high
grade DCIS
CCLs with architectural atypia=ADH/ low
grade DCIS.
95.
96.
97. Acute inflammation with abcess.
Chronic granulomatous mastitis and its
differential diagnosis
Periductal mastitis /duct ectasia
Diabetic mastopathy and lymphocytic
mastopathy
98. Usually occurs in the lactating breast
Localised swelling/redness/tenderness
Pus drained on aspiration
Antibiotics effective
99.
100.
101.
102.
103.
104. Perilobular mastitis
c/f:
Breast mass in women of childbearing age
Usually parous women
Oten related to recent pregnancy
Mimics carcinoma
May be b/l
Strong tendency for persistence or recurrence
in more than half the cases
The cause remains unknown (obstruction and
hypersensitivity reaction have been suggested).
107. Granulomatous infections
Sarcoidosis
Mammary duct ectasia
Peurperal mastitis
Vasculitis
Foreign body reaction to polyvinyl plastic or silicone used for
mammaplasty can result in tumor-like masses, granulomas, and sinus
tracts
Granulomatous angiopanniculitis
Bacteria
Bartonella henselae (cat scratch disease)
Corynebacteria
Fungi
Actinomycosis
Blastomycosis
Cryptococcosis
Histoplasmosis
Mycobacterium tuberculosis
108.
109. Granulomatous angiopanniculitis
This lesion contains multiple non-
necrotic,noncaseous granulomas with a
giant cell component and lymphocytic
angiitis, which involves predominantly
the subcutis but can extend into the
breast tissue without affecting lobules or
ducts.
115. Often seen following conservation surgery for
breast cancer
May occur at any time after about 6 months
following treatment
Commonly presents as breast thickeneing
Less commonly as a lump
Changes include:
Hyalinisation of collagen and necrosis
Vascular changes
Characteristic radiation fibroblasts
116. 30 year old female - 2 month history of firm
non-tender lump in breast deep to areola
117.
118.
119.
120.
121.
122. Inflammatory breast lesion
Mimic carcinoma.
It likely has an autoimmune cause.
Association with diabetes, especially type 1
and less commonly type 2 (i.e., diabetic
mastopathy).
Identical lesions occur in nondiabetic
patients, often with other evidence of
autoimmune disease (e.g., Hashimoto’s
thyroiditis) or circulating autoantibodies.
123. Hard, painless, irregularly contoured,
movable masses.
Occur in men and women
Present as a solitary mass or bilateral
disease, and recur in either breast.
Recognition of the potential for recurrence
is important because it can spare patients
with documented diabetic mastopathy from
repeated breast biopsies.
Mammography reveals dense tissue
suggestive of malignant change.
125. Predominance of B lymphocytes
Expression of HLA-DR antigen in involved
lobular epithelium.
Frequent presence of circulating
autoantibodies associated with HLA DR3,
DR4, DR5.
Resemble benign lymphoepithelial lesions of
the salivary gland and in Hashimoto’s
thyroiditis.
126. The epithelioid stromal cells in sclerosing
lymphocytic lobulitis can sometimes be so
prominent and abundant that the possibility of
an infiltrating carcinoma or granular cell tumor
is seriously considered.
Ashton and colleagues reported that the stromal
cells have features of Myofibroblasts, reacting
with antiactin.
These cells were negative for antibodies to
keratin (AE1/3), S-100 protein, desmin, MAC-
387, factor XIIIa, CD20 (L26), and CD45RO, but
they reacted with anti-CD68, suggesting some
lysosome formation.
127.
128.
129. Often involves the superficial subcutaneous
tissue rather than the breast parenchyma
itself.
A history of trauma can be elicited in about
half the cases, usually 1 to 2 weeks before
diagnosis.
Cases of mammary fat necrosis have also
been reported after radiation therapy and
as a local manifestation of Weber-Christian
disease
130. The disease can simulate carcinoma because
of skin retraction and the scirrhous (stellate
scarlike) nature of the reparative response.
Traumatic fat necrosis shows variable and
irregular stellate fibrosis around areas of
necrotic, variably vacuolated fat, with
abundant admixed foamy macrophages.
131.
132.
133.
134.
135.
136.
137.
138.
139.
140.
141.
142. varicocele tumor, comedomastitis, periductal
mastitis, plasma cell mastitis, stale milk
mastitis, chemical mastitis, granulomatous
mastitis, and mastitis obliterans.
143. The earliest lesions are characterised by the
accumulation of foamy macrophages
between the basement membrane and the
epithelium and also within duct lumens.
Later lesions show periductal chronic
inflammation whilst the most advanced
lesions show marked periductal scarring.
Superimposed (dystrophic) calcification may
be seen.
144. Most cases occur in premenopausal parous
women, possibly caused by duct obstruction
or triggered by different components of
stagnant colostrum.
It may produce retraction or inversion of the
nipple, and nipple discharge is present in
about 20% of cases
145. There is ectasia of the large ducts, with
accumulation of detritus in the lumen and
fibrous thickening of the wall, which contains an
increased amount of elastic fibers.
Calcification is common, producing tubular,
annular, and linear shadows on the mammogram.
There is no epithelial hyperplasia or apocrine
metaplasia.
If there is epithelial denudation, the luminal
material may escape from the duct, resulting in
a florid inflammatory reaction that is rich in
macrophages and plasma cells
146. In advanced stages, fibrous obliteration of
the ducts can occur.
Mammary duct ectasia is probably unrelated
to fibrocystic disease, but duct ectasia may
be related to breast abscess, which usually
results from the rupture of mammary ducts.
Abscesses occur most often during lactation
but can also occur independently of it.
Abscesses may be located deep within the
parenchyma or periareolar region.
147. Microscopic examination shows a central
cavity filled with neutrophils and secretion
surrounded by inflamed and eventually
fibrotic breast parenchyma, with obliteration
of the lobular pattern.
Clinically, a localized abscess may simulate
carcinoma.
Periareolar abscess associated with squamous
metaplasia of lactiferous ducts is referred to
as Zuska’s disease.
Squamous metaplasia of lactiferous ducts
requires surgical excision for cure
148.
149.
150.
151.
152.
153. Very uncommon in the breast
May be identified incidentally in a patient
with systemic amyloidosis
May very rarely present as a mass lesion -
amyloid tumour
Mimics carcinoma mammographically as well as histologically
Usually incidental but may be a mass lesion
Often associated calcs - picked up on screening
May be confused with cancers histologically
Low power view critical to make correct diagnosis.....
note the nodular arrangement of crowded acini
The edge of a focus may be apparently infiltrative but less so than many low grade carcinomas
At high power the glands are very crowded and may be cytologically atypical
Around some glands at least you should be able to see a compressed myoepithelial layer
Immunostaining shows an intact myoepithelial layer e.g. with CK 5/6
Awareness of this condition is important, because surgical therapy is suboptimal for recurrent disease, which requires antibiotics and even corticosteroids before resolution occurs. In fact, resolution may require several years of therapy
Destructive, necrotizing, granulomatous inflammation involving numerous polymorphonuclear leukocytes, multinucleated giant cells,lymphocytes ,plasma cells and focal lipogranuloma-like changes.
Centered on the segmental ducts and attached lobules, yielding a lobulocentric disease pattern.
Lobulocentric abscesses develop in adjacent segmental ducts and TDLUs, with relative sparing of interlobular stroma
Granulomatous lobular mastitis is distinct from variants of duct ectasia or periductal mastitis, which involve dilated large ducts rather than lobules.
Infection must always be considered with necrotizing granulomatous disease.
Indeed, histoplasmosis can cause a granulomatous lobular mastitis–like pattern of inflammation.
Mycobacterial, fungaland parasitic diseases and cat-scratch disease should also be considered and ruled out with appropriate stains
Lymphocytic lobulitis (i.e., mature lymphocytes and plasma cells surrounding acini and invading across basement membranes), “lymphocytic vasculitis” (mature lymphocytes surrounding small venules), and dense keloid-like fibrosis, which in 75% of cases is characterized by peculiar epithelioid cells embedded in dense fibrous tissue.
According to some reports, the lobulitis and vasculitis can be found in nondiabetic patients, but the epithelioid fibroblasts appear to be much better developed, and possibly unique, in those with diabetes.
However, others question the specificity of this feature because of identical findings in both patients with type 2 diabetes and nondiabetic patients
predominance of B lymphocytes in most cases and expression of HLA-DR antigen in involved lobular epithelium.
These immunologic features closely resemble those found in benign lymphoepithelial lesions of the salivary gland and in Hashimoto’s thyroiditis.
Schwartz and Strauchen speculated about an association between sclerosing lymphocytic lobulitis and an increased incidence of lymphoma development, much like that observed with Sjögren’s syndrome and Hashimoto’s thyroiditis.
The resulting lymphomas are thought to be related to mucosaassociated lymphoid tissue (MALT).
However, with insufficient follow-up, these authors were unable to reach a conclusion.
Other investigators have concluded that primary breast lymphomas may show features characteristicof MALT lymphoma (e.g., presence of lymphoepithelial lesions, tendency to remain localized or recur at other MALT sites, low-grade cytology, indolent behavior) arising from other organs such as the stomach, salivary glands, and thyroid. Moreover, Aozasa and colleagues found enough histologic and immunologic evidence to suggest that most mammary lymphomas are B-cell tumors and are associated with coexisting or antecedent lymphocytic mastopathy.
In fact, histologic evidence of lymphocytic mastopathy in mammary tissue apart from lymphoma was found in 11of 19 patients, and evidence of lymphocytic mastopathy was confirmed in 10 of the 11.
The so-called lymphoepithelial lesion, a characteristic finding of MALT lymphoma, was observed in 42% of their breast lymphomas. Others, however, dispute the existence of MALT features in breast lymphoma.
A variety of pseudolymphomas (lymphoid hyperplasias) of the breast have been reported, but they may actually represent either florid cases of sclerosing lymphocytic lobulitis or undetected early, low-grade (B-cell) MALT lymphomas.
The epithelioid stromal cells in sclerosing lymphocytic lobulitis can sometimes be so prominent and abundant that the possibility of an infiltrating carcinoma or granular cell tumor is seriously considered.
Ashton and colleagues reported that the stromal cells have features of Myofibroblasts, reacting with antiactin.
These cells were negative for antibodies to keratin (AE1/3), S-100 protein, desmin, MAC- 387, factor XIIIa, CD20 (L26), and CD45RO, but they reacted with anti-CD68, suggesting some lysosome formation.
These stains are important because lymphoepithelioma- like carcinoma of the breast can occur (rarely), and the lymphoid infiltrate could simulate lymphocytic lobulitis and obscure the underlying carcinoma
Duct ectasia with a central calcified keratin plug and associated giant cell inflammatory response