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PATH3309 > 17 - Breast Cancer > Flashcards

17 - Breast Cancer Flashcards

1
Q

Most common cancer in woman excluding non melanoma skin cancer

A

Invasive breast carcinoma

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2
Q

5 year survival of breast cancer

A

95%

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3
Q

Risk factors

A
  • Gender
  • Age (over 50)
  • Previous breast carcinoma
  • Oestrogen exposure
  • Nulliparity
  • Older age at first pregnancy
  • Genetics
  • Radiation
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4
Q

Estimating risk

A

Breast Cancer Risk Assessment Tool

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5
Q

Hereditary Breast Cancer

A
  • 5-10% of all BC
  • Younger at age, bilateral
  • BRCA1/BRCA2
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6
Q

BRCA1/BRCA2

A
  • Tumour suppressor genes
  • Most common (47% of heritable BC syndromes)
  • Highly penetrant, autosomal dominant pattern
  • Lifetime risk of BC 50-85%
  • Increased risk of other cancers (BRCA1- ovarian, colon, prostate; BRCA2- ovary, pancreas, prostate)
  • Mutations rare in pathogenesis of sporadic BC
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7
Q

Well characterised heritable mutations beside BRCA1/BRCA2

A
  • TP53
  • ATM
  • PTEN
  • STK11
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8
Q

Benign lesions

A
  • More common than BC
  • Non proliferative and many proliferative breast disease have no increased risk, some do
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9
Q

Proliferative breast disease without atypia

A
  • Associated with mild increase of BC (2x above general pop)
  • Includes epithelial hyperplasia, columnar cell change, papilloma, radial scar
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10
Q

Proliferative breast disease with atypia

A
  • Associated with moderate increased risk of BC (4-5x above general pop)
  • Includes atypical papilloma, columnar cell change with atypia, atypical hyperplasia
  • Exist toward the ‘benign’ end of a biologic continuum with low grade in situ and low grade invasive BC
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11
Q

Breast carcinoma in situ (CIS)

A
  • Malignant BC cells confined to ductal lobular system without basement membrane invasion into stroma
  • Cells are morphologically and genetically identical to invasive BC
  • Associated with high risk of invasive BC (10x above general pop)
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12
Q

Classification of CIS

A
  • Ductal (DCIS)
  • Lobular (LCIS)
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13
Q

Difference between DCIS and LCIS

A

Different biology, clinical presentation, pathology and management

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14
Q

DCIS

A
  • BC cells confined within duct spaces, occasionally lobular spaces
  • Exist toward the ‘malignant’ end of a biologic continuum with ductal type BC
  • No invasion thus no metastatic potential
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15
Q

DCIS histopathology

A
  • Malignant cells
  • Variable growth pattern (solid, cribriform, micropapillary etc)
  • Necrosis
  • Calcifications
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16
Q

DCIS prognosis

A
  • Grade
  • Extent of lesion
  • Completeness of excision
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17
Q

Management of DCIS

A

Surgical excision with clear margins +/- radiotherapy

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18
Q

Paget’s disease of the nipple

A
  • BC cells within epidermis of nipple
  • Associated with underlying high grade DCIS, cells spread up lactiferous ducts
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19
Q

Clinical symptoms of Paget’s disease of the nipple

A

Red, weeping, “eczematous” nipple

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20
Q

Histopathology of Paget’s disease of the nipple

A

BC cells admixed with keratinocytes in epidermis

21
Q

Management of Paget’s disease of the nipple

A

Surgical excision with clear margins including associated DCIS

22
Q

Prognosis of Paget’s disease of the nipple

A

Dependant on features of associated DCIS (+/- invasive)

23
Q

LCIS

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
  • Exist toward the ‘malignant’ end of a biologic continuum with
    lobular type BC
  • Risk of subsequent BC is bilateral and the invasive BC may or may not be lobular type
24
Q

Clinical features of LCIS

A
  • Usually incidental finding
  • 20-40% bilateral, often multifocal
25
Q

Histopathology of LCIS

A

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

26
Q

Management of LCIS

A
  • Isolated in core biopsy (–> increased surveillance)
  • Associated with mod-high risk lesion (e.g. DCIS) (–> dictated by the mod-high risk lesion)
  • In surgical margins in excision (–>no action required)
  • Consider anti-oestrogen risk reducing medication
27
Q

Breast cancer

A
  • Invasion of malignant epithelial cells beyond basement membrane into stroma
  • Access to vessels and lymphatics leads to potential metastasis
28
Q

Clinical features of BC

A
  • Lump
  • Pain
  • Nipple change/discharge
  • Skin changes (ulceration)
29
Q

BC workup

A
  • Examination (breast, axilla)
  • Pathology (Fine needle aspiration or core biopsy)
  • Radiology (MMG, US, MRI)
30
Q

Pathology of BC

A
  • Malignant cells, invasive into stroma
  • Classifiers constitute important BC prognostic and predictive factors
31
Q

How are BCs classified

A
  • Type, grade, stage (degree of spread)
  • Biomarker expression
  • +/- molecular profile
32
Q

‘special’ types of breast carcinoma with good prognosis

A
  • Mucinous carcinoma
  • Tubular carcinoma
33
Q

‘special’ types of breast carcinoma with bad prognosis

A
  • Micropapillary carcinoma
  • Basal like carcinoma
34
Q

Grading of BC

A
  • Nottingham grade
  • Based on Tubule formation, nuclear atypia and Mitotic rate
35
Q

Staging of BC

A
  • TNM
  • Tumour size
  • Nodal burden (number and size of deposits in draining nodes)
  • Metastases
36
Q

BC spread via lymphatics

A

Will usually manifest as axillary node deposit

37
Q

Biomarkers

A
  • Measurable biological characteristic
  • Indicator of normal/pathologic process
  • Prognosis or predictor of response to treatment
  • Assessed by IHC or ISH
38
Q

Three biomarkers in routine use in BCs

A
  • ER (oestrogen receptor)
  • PR (progesterone receptor)
  • HER2
39
Q

ER/PR pathways

A

Oestrogen and progesterone bind to ER/PR in cytoplasm, migrate to nucleus, transcribe DNA to protein and exert physiological effects

40
Q

Physiological effects of ER/PR

A
  • Promote growth and differentiation in normal
    breast tissue
  • Promotes a growth advantage for overexpressing malignant cells
41
Q

ER/PR prognostic and predictive

A
  • ER+/PR+ BC improved survival vs ER-/PR- due to response to anti-oestrogen therapy (80% vs 10% response)
  • ER in ~80% invasive BC
  • PR in ~65% invasive BC
42
Q

Example of anti-oestrogen therapy

A

tamoxifen

43
Q

Her2

A
  • Transmembrane tyrosine kinase (TK) protein
  • Binds ligand (growth factors), forms heterodimers with other HER family proteins, activates
    intracellular signals
  • Promote growth and differentiation in normal
    breast tissue
  • Promotes a growth and survival advantage for overexpressing malignant cells
44
Q

Intracellular signals activated by Her2

A
  • Upregulates the RAS-MAPK pathway –> proliferation
    and invasiveness
  • Upregulates the PI3K pathway –> inhibits cell death
45
Q

Her2 prognostic and predictive

A
  • Her2 positive BC poor survival vs Her2 negative BC
  • Strong predictor of response to
    anti-HER2 therapies (e.g Trastuzumab)
46
Q

Four distinct BC subsets

A
  • Luminal A
  • Luminal B
  • HER2 enriched
  • Basal like
47
Q

MC management

A
  • Surgical excision with clear margins (Mastectomy or wide local excision)
  • +/- axillary surgery
  • +/- radiotherapy
  • +/- chemotherapy (if high risk clinicopathological features)
48
Q

+/- radiotherapy

A
  • To the chest wall (if WLE or positive margins on mastectomy)
  • To the axilla or supraclavicular nodes (if high nodal burden)

PATH3309 (12 decks)

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