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Breast Flashcards

1
Q

Classify papillary lesions of the breast

A

Papilloma
Papilloma with ADH or DCIS
Papillary DCIS
Encapsulated papillary CA
Solid papillary CA (in situ and invasive)
Invasive papillary CA

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2
Q

Features of solid papillary carcinoma

A

In situ or invasive carcinoma with solid growth pattern and delicate fibrovascular cores
Frequently shows neuroendocrine differentiation
ER/PR+ HER2-
Unless conventional invasion, typically indolent and staged as pTis regardless of myoeps

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3
Q

Papilloma with ADH vs papilloma with DCIS

A

Papilloma with atypia and loss of myoeps
ADH <3mm
DCIS >/=3mm

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4
Q

Intraductal papilloma vs encapsulated papillary CA

A

Papilloma - well developed fibrovascular cores, 2 cell types, often have apocrine change, myoeps present, nipple discharge
EPC - delicate fibrovascular cores, 1 cell type, atypical epithelial cells, absent myoeps, usually presents as a mass

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5
Q

IHC of encapsulated papillary CA

A

Neg for myoeps
CK5/6 neg
ER/PR+

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6
Q

Recommended management for papillary lesion diagnosed on core needle biopsy

A

If radiologic concordance and lesion appears benign on biopsy, clinical follow up
In some centres, local excision may be recommended

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7
Q

Definition of invasive papillary carcinoma

A

Invasive mammary CA with predominantly papillary morphology (>90%) and infiltrative growth pattern

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8
Q

Grading of invasive papillary carcinoma

A

Nottingham grading system

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9
Q

Differential diagnosis of mammary paget disease

A

Paget disease
Bowen disease
Melanoma in situ
Toker cell hyperplasia

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10
Q

IHC to differentiate DDx of mammary paget disease

A

Paget: CK7+ Cam5.2+ EMA+ HER2+, may express mucins
Bowen: HMWK+
MIS: MelanA+
toker cell hyperplasia: CK7+, may be Cam5.2+St

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11
Q

Staging of paget disease

A

If not associated with underlying invasive CA, then pTis
If associated with underlying invasive CA, staged by that

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12
Q

Prognosis of pagets disease

A

Determined by variables of associated carcinoma

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13
Q

Classify mesenchymal tumors of the breast

A

Fibroepithelial/biphasic: fibroadenoma, phyllodes
Fibro/myofibroblastic: myofibroblastoma, PASH, nodulart fasciitis, fibromatosis, IMT
Adipocytic: lipoma, angiolipoma, liposarc
Smooth muscle: leiomyoma, meiomyosarcoma
Neural: Granular cell tumor, neurofibroma, schwannoma
Vascular: hemangioma, angiomatosis, atypical vascular lesion, angiosarc

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14
Q

Gross and histologic characteristics of a phyllodes

A

Gross - well-circumscribed, gray-white cut surface, solid with cystic areas, fleshy leaflike processes
Histo - stromal hypercellularity, expansile stroma and benign epithelial elements, leafy architecture

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15
Q

Features that differentiate benign and malignant phyllodes tumor

A

Increased stromal mitoses (5/10hps is borderline, 10/10hpfs is significant)
Marked stromal hypercellularity
Stromal atypia
Stromal overgrowth (one 4x field without epithelium)
Infiltrating margin
Tumor necrosis
Malignant heterologous elements even in the absence of other criteria EXCEPT WDLS

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16
Q

Differentiate phyllodes tumor from fibroadenoma

A

Phyllodes - expansile, hypercellular, mitotically active stroma, leaflike architecture

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17
Q

Treatment for phyllodes

A

Malignant - local excision with wide margin
Benign - local excision preferably with wide margin
Borderline - local excision with wide margin

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18
Q

Differentiate malignant phyllodes from metaplastic CA

A

Look for epithelial lined clefts
Phyllodes stroma should be negative for epithelial markers and positive for CD34 and BCL-2
Broad panel of epithelial markers for metaplastic CA

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19
Q

Classify lymphomas of the breast

A

Primary breast lymphoma
Disseminated lymphoma with breast involvement
Recurrent lymphoma (?)
Breast implant associated anaplastic large cell lymphoma

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20
Q

Most common types of lymphomas seen in the breast

A

Most common DLBCL
Burkitt lymphoma when bilateral

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21
Q

Clinical and pathologic features of breast implant associated anaplastic large cell lymphoma

A

Rare CD30+ ALK- ALCL associated with breast implants (specifically textured ones)
Usually develops 7-10y after placement of textures surface implant, present with unilateral effusion with unremarkable or erythematous overlying skin

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22
Q

Handling of specimens from patients with clinical concern for breast implant associated anaplastic large cell lymphoma

A

Seroma fluid should be taken for cytopathology with cell block preparation, flow cytometry, C&S (if sufficient)
Capsulectomy specimens must be sampled thoroughly and mapped
Lymph nodes and capsular masses submitted fresh for lymphoma protocol

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23
Q

Which breast tumors should be tested for hormone receptors and HER2

A

All primary invasive breast CAs
All recurrent breast CAs
All metastatic breast CAs

24
Q

Optional breast biomarkers

A

Ki67
Multigene expression assays
PD-L1

25
% of ER+ breast CAs
~80%
26
% of HER2+ breast CAs
~10-20%
27
Clinical uses for HER2 testing
Prognostic - associated with worse prognosis Predictive - sensitivity to anti-HER2 therapy
28
Methods for HER2 testing
IHC for protein overexpression ISH to detect gene amplification
29
Interpretation for IHC of HER2 testing
Positive 3+: complete, intense, circumferential membrane staining in >10% of invasive tumor cells Equivocal 2+: incomplete and/or weak moderate circumferential membrane staining in >10% of invasive tumor cells or complete, intense, circumferential staining in 10% invasive tumor cells Negative 0: no staining or incomplete faint/barely perceptible membrane staining in
30
Interpretation of HER2 ISH
Group 1 (Positive, amplified) - HER2/CEP17 ratio >/=2 AND average HER2 copy number >/=4 signals/cell Group 2 ( nonamplified) - HER2/CEP17 ratio >/=2 AND average HER2 copy number <4 signals per cell Group 3 (Amplified) - HER2/CEP17 ratio <2 AND average HER2 copy number >/=6 signals per cell Group 4 (non amplified) - HER2/CEP17 ratio <2 AND average HER2 copy number 4-6 Group 5 (negative, nonamplified) - HER2/CEP17 ratio <2 AND average HER2 copy number <4 signals per cell
31
Which HER2 ISH groups require additional workup
Group 2, 3, 4
32
Preanalytic variables for reporting biomarkers as per ASCO and CAP guidelines
Cold ischemia time Duration of fixation Type of fixative Treatment of tissue that can potentially alter immunoreactivity (eg decal) Status of internal and external controls Adequacy of sample for evaluation Primary antibody clone used Regulatory status
33
Reporting of ER and PR status
Positive - percentage of cells with nuclear positivity and average intensity of staining Negative - status of internal control
34
Cutoff for positivity of ER and PR biomarker testing
1%
35
Factors that impact results of ER/PR staining
Exposure of tumor cells to heat Delay in fixation Under or over fixation Type of fixative Quality, freshness, concentration of antibodhy Nonoptimized method of antigen retrieval Decal Method of antigen retrieval Dark hematoxylin counterstain obscuring faintly positive staining
36
Reasons for false positive ER, PR, or HER2 result
Use of impure antibody that cross-reacts with another antigen Edge artifact Misinterpretation of entrapped normal cells or in situ component Analysis by an image analysis device that mistakenly counts overstained nuclei Cytoplasmic positivity Overstaining, potentially due to improper antibody titration
37
Factors impact ability to obtain results for HER2 testing by FISH
Prolonged fixation Fixation in nonformalin fixatives Procedures or fixation involving acid (eg decal) Insufficient protease treatment of tissue
38
Issues to be addressed by pathologist on H&E or HER2 IHC slide prior to FISH testing
Identification of invasive carcinoma and area to be scored Identification of DCIS (oftentimes will show amplification when the invasive component will not)
39
Reasons Ki67 not currently recommended for breast CA
Lack of consensus on scoring Lack of consensus on definition of low versus high expression Lack of an appropriate cut point for positivity Lack of consensus on which part of the tumor should be tested (eg leading edge, hotspot, average) Paucity of data on effect of preanalytic variables
40
Features to distinguish sclerosing adenosis from invasive ductal carcinoma
Lobulated clustered arrangement Compressed and distorted tubular lumens Fibrous stroma compressing tubules Tubules lined by 2 cell layers Tubules invested by basement membrane
41
Describe characteristic features of microglanular adenosis
Haphazard proliferation of small round tubules Tubules have open lumens Tubules lined by single layer of epithelial cells Lumen contains colloid-like secretory material Dense fibrous stroma Multilayered basement membrane on EM Epithelial cells positive for S100 and CKs Lack expression of ER/PR
42
Clinical significance and management of MGA
May be mass forming or associated with microcalcs Is a benign proliferation, but atypical forms and carcinomas arising from MGA can occur (triple negative) May be nonobligate precursor of basal-type breast carcinoma Should be excised with clear margins
43
Benign breast lesions and relative risk of developing invasive carcinoma
Nonproliferative changes: 1x Proliferative without atypia: 1.5-2x Proliferative with atypia: 4-5x CIS: 8-10x
44
Histologic features of radial scar
Stellate configuration Central elastosis and fibrosis Entrapped distorted ductules in central scar Dilated ductules at the periphery with various patterns of epithelial hyperplasia Tubules lined by 2 layers of cells IHC for some myoep markers may be aberrrant in ducts within central nidus size < 1cm
45
Clinical significance of radial scar
Benign mimic of cancer Relative risk akin to proliferative without atypia Management remains controversial
46
Radial scar vs complex sclerosing lesion
Radial scar <1cm Complex sclerosing lesion >1cm
47
Histologic features of UDH
Architectural: peripheral elongated clefts, intraductal secondary spaces irregular in size, shape, location, steaming, tufts and mounds projecting into lumen, irregularly shaped/twisted bridges Cellular: 2 cell types, lack of atypia, heterogeneous population, indistinct cell borders, apocrine metaplasia, absence of necrosis IHC: heterogeneous expression of ER and CK5/6 mosaic
48
IHC to differentiate UDH from ADH/LGDCIS
UDH: CK5/6 mosaic positive, ER patchy ADH/DCIS: CK5/6 negative, ER diffuse pos
49
Definition of ADH
Epithelial proliferative lesion with cytologic and architectural features similar to low grade CIS but less developed in extent. Partial involvement of multiple duct spaces OR uniformly involved duct spaces but no more than 2-3mm.
50
Benign DDx for invasive breast CA
complex sclerosing lesion/radial scar Sclerosing adenosis Microglandular adenosis Sclerotic papilloma
51
Malignant lesions that mimic collagenous spherulosis
Adenoid cystic CA DCIS, cribriform
52
WHO classification of columnar lesions
Columnar cell change Columnar cell hyperplasia FEA
53
Clinical significance of columnar cell lesions
Can be associated with calcs Nonobligate precursors of ADH, low grade DCIS and low grade invasive CA Clear margins for any columnar cell lesion is not required
54
Clinical and histologic features of nipple adenoma
Clinical - nipple discharge, swelling of the nipple with or without erosion Histologic - well circumscribed, haphazardly arranged proliferating tubular structures with myoeps, varying degrees of epithelial hyperplasia, fibrous stroma, areas of papillary architecture are possible
55
Explain next steps for when a core biopsy for calcs does not show any calcs
Check patient ID and labels Check radiographs for calcs polarize to search for calcium oxalate crystals Cut deepers Can take X rays of the block, cut to the level of the calcs If no calcs, have the X rays reviewed by radiology to confirm presence or absence of calcs If no calcs in block but confirmed in patient radiographs, report as is - calcs may have fallen out of the block during trimming
56

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