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imed3003 > Malignant Breast Diseases > Flashcards

Malignant Breast Diseases Flashcards

1
Q

How common is breast cancer?

A

Invasive breast carcinoma is the most common cancer in women

BC is the second most common cause of cancer related death in women.

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2
Q

What is the 5 year survival of invasive breast carcinoma?

A

95%

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3
Q

What are the risk factors for invasive breast carcinoma?

A

Gender (>99% occur in women)

Age (77% over 50 years of age)

Previous breast carcinoma and other benign proliferative breast disease

Oestrogen exposure

Nulliparity and older age at first pregnancy

Family History/Genetics

Breast density

Radiation

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4
Q

What causes oestrogen exposure that is a risk factor in breast carcinoma?

A

Young age at menarche

Older age at menopause

Obesity

OCP/HRT

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5
Q

How can risk of breast cancer be estimated?

A

Using the breast cancer risk assessment tool (by US national cancer institute)

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6
Q

Which gene mutations increase potential for development of breast cancer? How?

A

BRCA1/BRCA2 mutations.

They are tumour suppressor genes that function to maintain DNA integrity. When mutated they cause cancer.

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7
Q

What is the lifetime risk of breast cancer in someone with a BRCA1/BRCA2 mutation?

A

50 - 85%

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8
Q

What inheritance pattern do BRCA1/BRCA2 mutations follow?

A

They are highly penetrant autosomal dominant genes.

They rarely arise sporadically

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9
Q

What percentage of heritable breast cancer syndromes are BRCA1/BRCA2 related?

A

47%

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10
Q

What mutations are well characterised in breast cancer?

A

BRCA1/BRCA2

TP53

ATM

PTEN

STK11

CHEK2

PALB2

45% involve unidentified or multiple genes.

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11
Q

What are the characteristics of hereditary breast cancers?

A

They present at a younger age and are bilateral

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12
Q

What happens to risk of breast cancer in the presence of proliferative breast disease without atypia?

A

Mild increased risk of BC 1.5 - 2x above general population.

no increased risk from: Inflammatory conditions, fibrocystic change. Adenoma, PASH, fibroadenoma.

Increased risk in: Usual hyperplasia, complex sclerosing lesion/radial scar, intraductal papilloma, columnar cell change

Magnitude of risk is related to degree of histological atypia.

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13
Q

What happens to risk of breast cancer in the presence of proliferative breast disease with atypia?

A

Associated with moderate increased risk of BC

4 - 5x above general population

Includes: Atypical papilloma, columnar cell change with atypia, atypical hyperplasia.

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14
Q

What is breast carcinoma in situ?

A

A premalignant carcinoma.

Malignant BC cells confined to the ductal-lobular system without invasion. Thus they resemble invasive carcinomas.

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15
Q

How is breast carcinoma in situ classified?

A

Ductal (DCIS)

Lobular (LCIS)

Different biology, clinical presentation, pathology and management.

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16
Q

How much is the risk of breast carcinoma increased in someone with a breast carcinoma in situ?

A

10x above general population.

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17
Q

What does DCIS look like?

A

BC cells confined within duct spaces, occasionally lobular spaces.

Identical morphological features to BC. Very similar genetic alterations.

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18
Q

What should be done with DCIS?

A

Theoretically it is curable. No invasion and no metastatic potential.

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19
Q

How is DCIS discovered?

A

Calcifications on MMG

Background finding in biopsy for invasive.

Histology: Malignant cells, variable growth pattern, necrosis, calcifications

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20
Q

What is prognosis of DCIS based on? (time to recurrence, invasive recurrence, metastasis)

A

Based on:

Grade

Extent of lesion

Completeness of excision

21
Q

How is DCIS treated?

A

Surgical excision with clear margins +/- radiotherapy

22
Q

How is low, intermediate, and high grade DCIS different?

A

Low grade DCIS: Cribiform calcifications

Intermediate grade DCIS: Solid pattern (more nuclear atypia)

High grade DCIS: Solid pattern with necrosis due to high mitotic rate (high need for blood supply)

23
Q

What is paget’s disease of the nipple?

A

High grade DCIS develops and cells move through the duct to the epidermis of the nipple and start to replicate.

24
Q

What are the clinical and histopathological symptoms of paget’s disease of the nipple?

A

Clinical: Red, weeping, eczematous nipple

Histopathology: BC cells admixed with keratinocytes in epidermis, DCIS in lactiferous ducts (commonly high grade)

25
Q

How is paget’s disease of the nipple treated and what is prognosis?

A

Management is surgical excision with clear margins including associated DCIS (+/- invasive)

Prognosis depends on features of the DCIS and whether or not it has invaded.

26
Q

What is LCIS? How is it different to DCIS?

A

BC cells confined within lobular spaces, occasionally duct spaces.

The biologic nature and potential of classical LCIS is less clear cut than for DCIS.

27
Q

What does LCIS indicate about breast cancer risk?

A

It is a risk factor for increased chance of getting invasive BC. The invasive BC may or may not be lobular.

28
Q

What are the clinical symptoms of LCIS?

A

Usually an incidental finding that rarely goes unnoticed and is 20 - 40 % bilateral and often multifocal.

29
Q

What are the histological features of LCIS?

A

Expansion of lobules by discohesive, uniform neoplastic cells, loss of E-cadherin expression.

30
Q

How is LCIS managed?

A

Isolated in core biopsy - increased surveillance (high level surveillance needed because it is often multifocal and bilateral)

Associated with mod-high risk lesion - dictated by the mod-high lesion

Anti-oestrogen risk reducing medication

Bilateral mastectomy is no longer recommended.

31
Q

What stain is used to visualize LCIS?

A

Negative E-cadherin stain

32
Q

What are the clinical features of breast cancer?

A

Discrete mass/lumpiness

Pain

Nipple changes/discharge

Skin changes

33
Q

What is done to diagnose breast cancer?

A

Examination - breast, axilla, general

Pathology - FNA or core biopsy

Radiology - MMG, US, MRI

34
Q

How are malignant cancer cells classified?

A

Type, grade, and stage

Biomarker expression +/- molecular profile

35
Q

What are the histological types of breast cancer?

A

> 80% of cases are invasive ductal carcinoma (IDC) of ‘no special type’

10% are invasive lobular carcinoma (ILC)

Remainder are relatively uncommon ‘special’ types of carcinoma, most considered variants of IDC

36
Q

What are the ‘special’ types of carcinoma?

A

Mucinous carcinoma

Tubular carcinoma

Micropapillary carcinoma

Basal-like carcinoma

37
Q

What is used to define histological grade of a tumour?

A

Score out of 3 for the following:

Tubule formation

Nuclear atypia

Mitotic rate

The sum is split into grade 1 (3, 4, 5) grade 2 (6,7) and grade 3 (8,9) with increasingly worse prognosis

38
Q

How are cancers staged?

A

Staging is by the AJCC system

aka TNM system

39
Q

How is lymphedema in the arm prevented during a biopsy?

A

Axillary dissection leads to lymphedema. So to avoid this a biopsy is taken from the sentinel node and evaluated because sentinel node is the first lymph node that the breast drains into.

40
Q

How is a sentinel node biopsy conducted?

A

Dye is placed on tumour and then it goes to sentinel node which is then biopsied when identified

41
Q

What biomarkers are used to detect breast cancer?

A

BC - ER, PR, HER2

42
Q

What are biomarkers and how are they assessed?

A

A biomarker is a measurable biological characteristic, indicator of normal/pathological process, prognosis, or predictor of response to treatment.

They are assessed by immunohistochemistry (ER + PR) or in situ hybridisation (HER2).

43
Q

Why are hormone receptors used as biomarkers?

A

They promote growth and proliferation in cancer cells.

ER is overexpressed in ~80% of breast cancers

PR is overexpressed in ~65% of breast cancers

These are detected via immunohistochemistry.

Effectiveness of anti-oestrogen therapy (tamoxifen) can be determined from expression of these receptors as well in addition to its diagnostic value.

44
Q

What is HER2?

A

A transmembrane tyrosine kinase protein.

It binds ligands (Growth factors), forms heterodimers with other HER family proteins, and activates intracellular signals. (RAS-MAPK and PI3K pathway)

RAS-MAPK activates proliferation and invasiveness

PI3K inhibits cell death.

For this reason this protein is overexpressed in malignant cells and allows them to survive for a long time.

45
Q

Why is HER2 used as a biomarker?

A

HER2 is amplified and overexpressed in 15 - 30% of BCs.

HER2 positive BC have poor survival so it provides a prognostic indicator.

HER2 is a strong predictor of response to anti-HER2 therapies such as trastuzumab.

46
Q

What is molecular profiling?

A

Early gene expression profiling studies examined gene up and down regulation across genome

47
Q

What are the limitations to molecular profiling?

A

Impractical to perform routine genome wide expression profiling.

48
Q

How is breast cancer managed?

A

Surgical excision with clear margins - mastectomy or wide local excision.

Axillary surgery - SLN biopsy with axillary clearance if SLN positive

Radiotherapy to chest wall if locally advanced disease. Radiotherapy is also done to axilla or supraclavicular nodes if there is high nodal burden.

Chemotherapy - If high risk clinicopathological features.

imed3003 (48 decks)

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