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PATH FINAL > Breast PATH > Flashcards

Breast PATH Flashcards

1
Q

Most common non-skin malignancy in the world ?

A

BREAST CANCER*
By age 90, one in eight women will get breast cancer.

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2
Q

Breast cancer RFs

A
  • Age: Increasing age.
  • Family: 1st degree relatives with breast cancer, and their age at diagnosis. BRCA or other familial
    syndromes.
  • Lifestyle: Higher socioeconomic status, obesity, lack of exercise.
  • Oestrogen exposure: Early menarche, late menopause, high age at first live birth or nulliparity,
    exogenous oestrogen exposure.
  • Breast Factors: Dense breasts, never breastfed, previous breast cancer or atypia, previous irradiation.
  • (Note: no clear link with smoking)**
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3
Q

Breast cancer associatitions

A
  • BRCA1 and 2.
  • Hamartoma syndromes: Cowden and Peutz-Jegher
  • High risk germline mutations: Li-Fraumeni (p53) Ataxia Telangiectasia (ATM gene)
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4
Q

Breast cancer can arise without a pre-cursor, T or F ?

A

T
- Known precursor lesion is DCIS with a 1% per year conversion to IDC. Carcinoma may also arise on its own.

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5
Q

DCIS morphology..any invasion?

A

Tumour cells limited to ducts and lobules by the basement membrane.

Microinvasion <1 mm is allowed.

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6
Q

DCIS 2 types

A

Comedo
- central necrosis
- calcifications in ducts

Non-comedo
- Solid
- Cribiform
- Micropapillary
- Papillary

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7
Q

Define paget’s disease

A

DCIS
- If they go out the ducts to the skin but still don’t breach the basement membrane it is called Paget disease of the nipple.
- Pagets often signals underlying invasive carcinoma.

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8
Q

DCIS cancer progression risk, and how many bilateral ?

A
  • Progress to cancer at 1% per year.
  • Bilateral in 10-20% of cases
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9
Q

Define LCIS (Lobular Carcinoma in Situ)

A

Dyscohesive malignant cells with loss of E-cadherin adhesion protein (same for ALH, LCIS, ILC).

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10
Q

LCIS cancer risk increase % ?

A

May or may not be a precursor lesion (Robbins 8th edition says 1% per year progress to cancer too). But
increases risk of cancer in both breasts 8 – 12 times. Bilateral in 20-40%.

The invasive cancer may be lobular or ductal (mostly IDC)*

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11
Q

LCIS mammogram ?

A
  • Incidentally discovered as they are invisible on mammography.
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12
Q

ILC (invasive lobular carcinoma) morphology ?

A
  • may be diffusely infiltrating with no mass, only palpable firmness, or a mass lesion with poorly defined margins
  • dyscohesive, single filed (indian file)
  • Signet ring mucin cells common*
  • Luminal A*
  • Rate of bilaterality is controversial. Traditionally thought to be increased. Now thought similar to normal IDC at 5-10% (Robbins).
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13
Q

Which type of Inavsive ductal carcinoma has the worst prognosis ?

A
  • NOS (Luminal A, same as ILC)
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14
Q

Which subtype of invasive ductal carcinoma has the best prognosis ?

A
  • Tubular
  • Malignant cells arranged in well formed tubules lacking the myoepithelial layer (ie just epithelial cells
    then basement membrane).
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15
Q

Tubular carcinoma association ?

A
  • Often associated low grade DCIS, and associated with radial scars
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16
Q

Medullary Carcinoma epi?

A
  • Younger people with BRCA1
17
Q

Medullary Carcinoma micro ?

A

o Solid syncytial growth pattern (cells connected to each other) with a lymphocytic infiltrate.

o Over-expression of E-cadherin explains why the cells are all stuck together and this limits spread somewhat so it has a slightly better prognosis than IDC NST.

18
Q

Mucinous (Colloid) Carcinoma epi ?

A
  • Older women in 70s
  • Good prognosis
  • Clustered of floating mucin
19
Q

Luminal A features

A

Luminal A
- ER, PR positive
- HER2 negative
- Most common type
- Low grade, best prognosis
- Most likely to have bone mets
- use Tamoxifen which blocks oestrogen
- use Letrozole blocks conversion into oestrogen

20
Q

Luminal B features

A

Luminal B
- ER, PR positive
- HER2 variable
- mets to bone too
- worse prognosis than A

21
Q

Basal-like features

A
  • Triple negative
  • High grade tumour with worst prognosis
  • Most associated with BRCA mutations
  • Mets to lungs, brain, etc
22
Q

HER-2 enriched features

A
  • ER, PR negative
  • HER2 positive
  • mid to high grade tumors
  • Treated with Herceptin
23
Q

Fibroadenoma RFs ?

A
  • Cyclosporin* (renal transplant commonly)
  • HRT
  • Fibrocystic change
  • Increase in size with Lactation, Pregnancy, Infarction
24
Q

Composition of Fibroadenoma

A
  • Biphasic tumour with stromal and epithelial elements
  • Arise from loose intralobular septa
  • Stromal elements: monoclonal (neoplastic)
  • Glandular elements: Polyclonal
  • Epithelial component: Hormone sensitive
25
Q

Fibroadenoma macro appearance ?

A
  • Greyish looking cut surface with slit like spaces.
  • Expanded stroma, similar to intralobular stroma, Growth pattern may be intracanalicular (stroma invaginates into the ducts) or pericanalicular where the stroma surrounded the ducts.
  • No mitoses
26
Q

Prognosis / Complication of Fibroadenoma

A

Even after biopsy proven, should follow up for 6-12 months to ensure no rapid growth. If this is seen, the
lesion may actually be a Phyllodes tumour (StatDx).

Accurate differentiation between the two based on a needle biopsy is 85-95%.

Rarely foci of cancer can develop within a fibroadenoma. Slightly increased risk of carcinoma, esp if complex features.

Phyllodes may also develop from FA sometimes.

27
Q

Phyllodes benign or malignant

A

They exist on a spectrum – the majority are benign (>75%), but can be borderline or malignant. High grade
tumours resemble malignant sarcomas.

Leaf like growths

28
Q

Epi of Phyllodes vs Fibro

A

Fibroadenoma
- 20-30

Phyllodes
- 45-50, asian

29
Q

Phyllodes microscopy

A

The 2 key features of PT are:
- Stromal hypercellularity
- Presence of benign glandular elements.

It is the amount and cellularity of the stromal component that determines whether the neoplasm is called a fibroadenoma or a phyllodes tumour.

30
Q

Treatment of Phyllodes

A

Treated with wide local excision. Main risk is local recurrence.
No need for nodal dissection. Radiation reduces risk of recurrence. No role for chemotherapy.

31
Q

What are Prolfierative lesions with increased relative risk of cancer

A

WITHOUT atypia = 1.5 – 2 x increased risk
 Usual ductal hyperplasia
 Sclerosing adenosis
 Complex sclerosing lesion / radial scar
 Papilloma

WITH atypia > 4 x incresed risk
 ADH
 ALH
 Classic LCIS

32
Q

Sclerosing adenosis can mimic what histologically ?

A

mimic invasive cancer histologically

33
Q

Radial scar associated with trauma ?

A

Not associated with trauma or surgery.

34
Q

Precursor lesions:
These are non-obligate precursors and most will not become cancer left untreated

A
  1. Atypical ductal hyperplasia :
    - Resembles DCIS but only partly fills ducts and measures <2mm
    - Presents as calcification on mammo
    - Requires excision biopsy to confirm the true extent (if >2mm it is DCIS)
  2. Atypical lobular hyperplasia :
    - Cells identical to LCIS but do not fill or distend more than 50% of acini in a lobule
    - Cells show loss of e-cadherin
35
Q

Lymphocytic Mastopathy (Sclerosing
Lymphocytic Lobulitis)
- mammo features
- associated with?

A
  • single or multiple hard palpable masses or mammographic densities.
  • areas of densely collagenized stroma, a feature that may make it difficult to obtain lesional tissue by needle biopsy.

Assoc:
- T1DM
- Autoimmune thyroid disease

36
Q

Which breast cancer is HER2 negative ?

A

Micropapillary / Papillary

37
Q

Which luminal type most associated with BRCA1 mutation ?

A

Basal-type (triple negative)
- Medullary breat cancer
- Majority BRCA1 are triple negative**

38
Q
A

PATH FINAL (12 decks)

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