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derm > 1B skin cancer > Flashcards

1B skin cancer Flashcards

1
Q

What do these photos show?

A

Melanoma

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2
Q

What cells does melanoma arise from?

A

Melanocytes

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3
Q

How deadly are melanomas?

A

Causes >75% of skin cancer deaths

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4
Q

Where on the body can melanocytes arise?

A
  • Mucosal surfaces (e.g. oral, conjunctival, vaginal)
  • Within uveal tract of eye
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5
Q

What genetic factors are there for melanoma?

A
  • Lightly pigmented skin
  • Red hair
  • Family history (CDKN2A mutations), MC1R variants
  • DNA repair defects (e.g. xeroderma pigmentosum)
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6
Q

What environmental factors are there for melanoma?

A
  • Intense intermittent/chronic sun exposure
  • Sunbeds
  • Immunosuppression
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7
Q

What phenotypic risk factors are there for melanoma?

A
  • > 100 melanocytic nevi (moles)
  • Atypical melanocytic nevi (moles)
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8
Q

What does the mitogen-activated protein kinase (MAPK) [RAS-RAF-MEK-ERK] pathway regulate?

A
  • Cellular proliferation
  • Growth
  • Migration
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9
Q

What is a KIT mutation and what melanomas is it present in?

A
  • A mutation along the MAPK pathway
  • Is in 30-40% of acral and mucosal melanomas
  • Activating mutations or copy number amplifications of KIT gene found in melanomas from chronically sun-exposed skin
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10
Q

What 2 other common genes are activation mutations present in in a lot of melanomas?

A
  • NRAS gene (15-20% of melanomas)
  • BRAF gene (50-60%)
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11
Q

What type of melanomas is BRAF gene low in?

A

Low in melanomas of skin with high cumulative UV exposure

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12
Q

Explain how CDKN2A mutations can cause MAPK pathway activation leading to melanoma

A
  • CDKN2A codes for tumour suppressor P16
  • P16 binds to CDK4/6 and prevents formation of cyclin D1-CDK4/6 complex
  • This complex phosphorylates Rb, inactivating it, leading to E2F release
  • once released, E2F promotes cell cycle progression
  • Therefore a mutation will mean that P16 can’t stop the complex forming which goes on to release E2F and progress the cell cycle
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13
Q

What is CTLA-4?

A

Cytotoxic T-lymphocyte-associated antigen-4

It is a natural inhibitor of T cell activation by removing the costimulatory signal (B7 on APC and CD28 on T cell)

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14
Q

How does CTLA-4 influence immunotherapy for melanoma?

A

It’s based on a CTLA-4 blockade e.g. ipilimumab

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15
Q

What other type of immunotherapy other than CTLA-4 blockade do we have?

A
  • There are also checkpoint inhibitors (PD-1, PDL1)
  • PD1 is a signal to our immune system to not kill a certain cell (usually to prevent autoimmunity)
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16
Q

What are the subtypes of melanoma?

A
  • Superficial spreading
  • Nodular
  • Lentigo maligna
  • Acral lentiginous
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17
Q

How common is superficial spreading in melanomas?

A

60-70% of melanomas

Most common in fair skinned people

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18
Q

Where is superficial spreading seen on the body most frequently?

A

Trunk of men and legs of women

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19
Q

How can superficial spreading arise?

A

de novo or in pre-existing nevus

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20
Q

How is regression seen and why does it happen?

A
  • In 2/3 of tumours, regression is visible as grey or hypopigmentation
  • Shows interaction of host immune system with tumour
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21
Q

Describe the growth pattern of superficial spreading melanoma

A
  • Initially there’s horizontal (or radial) growth where you see the 4 characteristic features
  • Then you have vertical growth phase
    • Clinically shows the appearance of a nodule or bump
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22
Q

What are the four characteristic features of superficial spreading?

A
  • Asymmetry
  • Border irregularity
  • Colour variation
  • Increased diameter
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23
Q

How common is nodular in melanomas?

A

15-30% of all melanomas

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24
Q

Which group of people are nodular melanomas common ni?

A
  • 2nd most common type of melanoma in fair skinned individuals
  • More common in men than women
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25
Q

Which body parts are nodular melanomas most common in?

A

Trunk, head and neck

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26
Q

How do nodular melanomas present?

A
  • Usually as blue to black, sometimes pink to red nodule (so a pigmented nodule)
  • May be ulcerated, bleeding
  • Develops rapidly
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27
Q

What does amelanotic mean?

A

When a nodule has no pigment

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28
Q

Describe the growth of nodular melanomas

A
  • There is no radial (horizontal growth phase)
  • Only vertical growth phase
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29
Q

What does lack of horizontal and only vertical growth phase for nodular melanomas mean clinically?

A
  • Features resulting from radial growth phase (e.g. asymmetry, border irregularity, colour variation) aren’t present or not v obvious
  • It invades earlier and tends to present at a more advanced stage with a worse prognosis
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30
Q

What do these photos show?

A

Nodular melanomas

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31
Q

How common are lentigo malignas?

A

Minority of cutaneous melanomas (around 10%)

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32
Q

Which group of people are lentigo malignas seen most commonly in?

A
  • > 60 year olds
  • Occurs in chronically sun-damaged skin, most commonly on the face
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33
Q

What does the term ‘lentigo maligna’ refer to?

A

Pre-invasive slow growing, asymmetric brown to black macule with colour variation and an irregular indented border

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34
Q

When do we call lentigo maligna ‘lentigo maligna melanoma’?

A
  • When lentigo maligna becomes invasive
  • Around 5% of lentigo maligna lesions progress to invasive melanoma
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35
Q

What do these photos show?

A

Lentigo maligna

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36
Q

How common is acral lentiginous?

A

5% of all melanomas

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37
Q

Which group is acral lentiginous diagnosed most frequently in?

A

People in their 60s

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38
Q

Where in the body does acral lentiginous occur?

A

Typically occurs on palms and soles or in and around the nail apparatus

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39
Q

What is the incidence of acral lentiginous in different racial groups?

A
  • Similar across all racial and ethnic groups
  • As more darkly pigmented Africans and Asians do not typically develop sun-related melanomas
    • ALM represents disproportionate % of melanomas diagnosed in Afro-Caribbean (up to 70%) or Asians (up to 45%)
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40
Q

What are these photos of?

A

Acral lentiginous

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41
Q

What are these photos of?

A

Melanonychia

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42
Q

How are patients instructed to detect melanomas early?

A

Look for history of change in colour, shape or size of a pigmented skin lesion

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43
Q

What is the ABCDE public awareness campaign?

A
  • Asymmetry- one half does not match
  • Border- uneven borders
  • Colour- variety of colours
  • Diameter- larger than a pencil eraser
  • Evolution- change in size, shape, colour → most important one
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44
Q

What is Garbe’s rule?

A

If a patient is worried about a single skin lesion, don’t ignore their suspicion and have a low threshold for performing a biopsy

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45
Q

How do we diagnose melanoma?

A

Skin biopsy

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46
Q

What are the differential diagnoses for melanoma?

A
  • Basal cell carcinoma- can be pigmented
  • Seborrheic keratosis- harmless skin lesions that increase in number with age
  • Dermatofibroma- harmless benign skin tumour
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47
Q

What are poor prognostic features for melanoma?

A
  • Increased Breslow thickness >1mm
  • Ulceration
  • Age
  • Male gender
  • Anatomical site- head, neck, trunks
  • Lymph node involvement
48
Q

How is Breslow thickness measured?

A

Measured histologically from stratum granulosum downwards

49
Q

What are the survival rates of melanoma?

A
  • Stage 1A melanoma has 10 year survival rate of >95%
  • Thick melanoma >4mm and ulceration pT4b has 10 year survival rate of 50%
50
Q

What technique do we use to investigate melanoma?

A

Dermoscopy- can improve correct diagnosis of melanoma by nearly 50%

51
Q

What do we do if in doubt for diagnosing melanoma?

A

Excise the lesion for histological assessment because clinical features aren’t specific for us not to have a low threshold for excision

52
Q

What are the stages of excision of a melanoma?

A
  • Primary excision → down to subcutaneous fat and 2mm peripheral margin
  • If there’s melanoma, then a wide excision is done
    • Margin determined by Breslow depth
    • 5mm for in situ
    • 10mm for ≤1mm
  • Prevents local recurrence or persistent disease
53
Q

What does excision prevent?

A

Local recurrence or persistent disease

54
Q

How do we stage melanoma?

A
  • Pathological staging occurs then clinical exam
  • TNM staging happens in some instances
55
Q

What is a sentinel lymph node?

A
  • The first node within a nodal basin that lymphatic drainage goes to
  • These are the nodes most likely to contain metastatic disease
56
Q

What types of TNM tumours is sentinel lymphoma node biopsy available for?

A

Currently offered for pT1b and more advanced

57
Q

What would extracapsular spread on lymph node biopsy require?

A

Lymph node dissection

58
Q

What 2 types of imaging are available for melanoma?

A
  • PET-CT
  • MRI Brain
59
Q

What stages of melanoma are PET-CT/MRI brain available for?

A
  • Stage IIc without SLNB (sentinel lymph node biopsy)
  • Stage III
  • Stage IV
60
Q

What is a major prognostic factor in metastatic melanoma?

A

LDH

61
Q

What are 2 ways we can treat unresectable or metastatic melanomas?

A
  • Immunotherapy
  • Mutated oncogene targeted therapy
62
Q

How does immunotherapy work?

A
  • CTLA-4 inhibition e.g. ipilimumab
  • PD-L1 (programmed cell death ligand) inhibitors e.g. nivolumab
  • Combination immunotherapy leads to 60% response vs 20% monotherapy alone
63
Q

What is mutated oncogene targeted therapy?

A

Combination of a BRAF inhibitor (e.g. encorafenib, vemurafenib, dabrafenib) and MEK inhibitor (e.g. trametinib)

64
Q

What groups of people do keratinocyte dysplasia or carcinoma affect mostly and how?

A

Predominantly pale skin types via solar induced UV damage

65
Q

What are the stages of development of keratinocyte dysplasia?

A
  • Actinic keratoses
  • Bowen’s disease
  • Squamous cell carcinoma
  • Basal cell carcinoma
66
Q

What is actinic keratoses?

A

Atypical dysplastic keratinocytes that are confined to the epidermis

67
Q

Where do actinic keratoses develop?

A
  • On sun-damaged skin
  • Usually head, neck, upper trunk and extremities
68
Q

How do actinic keratoses present?

A
  • Macules or papules
  • Red or pink
  • Usually some scale - may be thick
69
Q

When would a biopsy be needed for actinic keratoses?

A

The distinction of an actinic keratosis from SCC is sometimes difficult so a biopsy would be needed

70
Q

What is there a risk of in actinic keratoses?

A

Progression to SCC- 0.025-16% per year for any single lesion

71
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ

72
Q

How does Bowen’s disease present?

A

Erythematous scaly patch or slightly elevated plaque

73
Q

How may Bowen’s disease arise?

A

De novo or from pre-existing AK

74
Q

What may Bowen’s disease resemble?

A
  • Actinic keratoses
  • Psoriasis
  • Chronic eczema
75
Q

What is the treatment for actinic keratoses and Bowen’s disease?

A
  • 5-fluorouracil cream
  • Cryotherapy
  • Imiquimod cream
  • Photodynamic therapy
  • Curettage and cautery
  • Excision
76
Q

What is squamous cell carcinoma?

A
  • Invasive atypical keratinocytes
  • potential for metastasis/death
77
Q

What skin do SCC arise in?

A

Background of sun-damaged skin

78
Q

What different ways can SCC look?

A
  • Erythematous (red) to skin coloured
  • Papule or bump
  • Plaque-like- raised area
  • Exophytic- like a mushroom
  • Hyperkeratotic- scaly
  • Ulceration
79
Q

What type of keratinocyte carcinoma is there that doesn’t metastasise?

A

Basal cell carcinoma

80
Q

What is a significant risk factor for BCC?

A

UV radiation

81
Q

What is BCC dependent on?

A

Stroma produced by dermal fibroblasts

82
Q

What happens between tumour cells and mesenchymal cells of stroma?

A
  • Cross talk occurs, including with platelet derived growth factor (PDGF)
  • Receptors for PDGF are upregulated in stroma but PDGF is upregulated in tumour cells
83
Q

What kind of activity does BCC have and how does that help it?

A
  • Proteolytic activity e.g. metalloproteinases and collagenases
  • Degrade pre-existing dermal tissue and facilitate spread of tumour cells
84
Q

What signalling pathway is important for BCC progression and something we can target for treatment?

A
  • Loss of function in chromosome 8q (PTCH gene) is important here
85
Q

What other type of mutation is important in BCC pathogenesis and why?

A

p53 mutations- majority are missense mutations that carry a UV signature

86
Q

How does the epidemiology of BCC compare with SCC?

A
  • BCC is most common skin cancer
  • BCC to SCC is 4:1
  • Both commoner in pale skin types
  • Both more common in men vs women (2 or 3:1)
  • Median age of diagnosis of BCC is 68
87
Q

What are the main 6 subtypes of BCC?

A
  • Nodular
  • Micronodular
  • Superficial
  • Morphoeic
  • Basisquamous
  • Infiltrative
88
Q

How does nodular BCC present?

A
  • Typically presents as shiny, pearly papule or nodule
  • On dermoscopy you can see arborizing (branching) blood vessels
89
Q

How common is nodular BCC?

A
  • Most common subtype
  • Accounts for approx 50% of BCC
90
Q

What other subtype does micronodular BCC resemble and how is it different?

A
  • Resembles nodular BCC clinically
  • More destructive behaviour though- high rates of recurrence and subclinical spread
91
Q

How does superficial BCC present?

A

Well-circumscribed, erythematous macule/patch

or thin papule/plaque

92
Q

How does morphoeic BCC present?

A
  • Slightly elevated or depressed area of induration
  • Usually light-pink to white in colour
  • Aggressive behaviour- can cause extensive local tissue destruction
93
Q

What are the histological features of basisquamous carcinoma

A

Histological and clinical behaviour is a mix of both BCC and SCC

Can metastasise

94
Q

How can we investigate BCC?

A
  • Often clinical diagnosis sufficient
  • Diagnostic biopsy can be taken if doubt
95
Q

What differentials are there for BCC?

A
  • SCC
  • Adnexal (sebaceous) carcinoma
  • Merkel cell carcinoma
96
Q

What treatments for BCC are there?

A
  • Standard surgical excision
  • Mohs micrographic surgery
  • Topical therapy e.g. 5-fluorouracil, imiquimod for superficial BCC only
  • Photodynamic therapy for superficial BCC only
  • Curettage for superficial BCC
  • Radiotherapy- only above age of 70 though because it can cause SCC
  • Vismodegib- selectively inhibits abnormal signalling in Hedgehog (Hh) pathway
97
Q

What is Mohs micrographic surgery used for?

A
  • Recurrent BCC
  • Aggressive subtype e.g. morphoeic/infiltrative/micronodular
  • Critical site
98
Q

What is bread loafing?

A

When you send a histological specimen for analysis, it’s sectioned using bread loafing technique

Sometimes after an excision when you’re checking to see if there’s any carcinoma left, the section doesn’t analyse a specific part of skin where there is some left so you get a falsely reassuring report

99
Q

How does Mohs micrographic surgery avoid false negative problems in bread loafing?

A
  • You remove the tumour
  • Then you take thin onion skin layers from the margin and examine them repeatedly until you see there’s healthy tissue there
100
Q

Why can’t Mohs micrographic surgery be used for everyone?

A

Because it takes hours for a single lesion to be removed

101
Q

What is a significant risk factor for SCC?

A

UV radiation

102
Q

What causes SCC to develop?

A
  • Develops through a series of genetic alterations
  • Alterations in p53 are most common
  • CDKN2A alterations also common
103
Q

What other signalling pathway other than p53 plays a role in SCC pathogenesis?

A

NOTCH1 or NOTCH2 (Wnt/β-catenin signalling)

104
Q

What high risk features for SCC are there?

A
  • Localisation:
    • trunk and limbs >2cm
    • Head/neck >1cm
    • Periorificial zones
  • Ill defined margins
  • Rapidly growing
  • Immunosuppressed patients
  • Previous radiotherapy or site of chronic inflammation
  • Histological features
105
Q

What histological features are a high risk feature for SCC?

A
  • Poorly differentiated
  • Acantholytic, adenosquamous, demosplastic subtypes
  • Tumour thickness → Clark level >6mm, Clark IV, V
  • Invasion beyond subcutaneous fat
  • Perineural, lymphatic or vascular invasion
106
Q

How do we investigate SCC?

A
  • Often clinical diagnosis is sufficient
  • Diagnostic biopsy may be taken if diagnosis is uncertain
  • Ultrasound of regional lymph nodes, maybe with fine needle aspiration, if there’s concerns of regional lymph node metastasis
107
Q

What differentials are there for SCC?

A
  • BCC
  • Viral wart
  • Merkel cell carcinoma
108
Q

What is the treatment for SCC?

A
  • Examination of rest of skin and regional lymph nodes
  • Excision (4-6mm margin)
  • Radiotherapy if unresectable or high risk features e.g. perineural invasion
  • Cemiplimab (PD1 inhibitor) for metastatic SCC
  • Secondary prevention e.g. skin monitoring and sun protection advice, because they are at high risk of developing another SCC
109
Q

What is a keratoacanthoma?

A

A rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with a keratotic core

110
Q

Why is keratoacanthoma so difficult to classify?

A

Difficult to distinguish clinically and histologically from SCC

Can only really tell it was keratoacanthoma if/when it resolves

111
Q

How is keratoacanthoma treated?

A

It resolves slowly over months to leave atrophic scar

112
Q

Where does keratoacanthoma occur on the body?

A

Most occur on head or neck or sun-exposed areas

113
Q

What is merkel cell carcinoma?

A

Malignant proliferation of highly anaplastic cells which share structural and immunohistochemical features with various neuroectodermally derived cells, including Merkel cells

114
Q

What are aetiological factors for MCC?

A
  • 80% are associated with polyomavirus
  • UV exposure
115
Q

How does merkel cell carcinoma present?

A
  • Solitary, rapidly growing nodule
  • Pink-red to violaceous, firm, dome shaped
  • Ulceration can occur
116
Q

How does merkel cell carcinoma behave?

A
  • Aggressive, malignant behaviour
  • > 40% develop advanced disease

derm (3 decks)

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