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Z Year 2 BRS MSK > Skin cancers > Flashcards

Skin cancers Flashcards

1
Q

What is melanoma?

A

Malignant tumour arising from melanocytes

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2
Q

Why is melanoma dangerous?

A
  • Leads to >75% of skin cancer deaths

- Rising incidence rates observed worldwide

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3
Q

What can melanoma arise on?

A

on mucosal surfaces (e.g. oral, conjunctival, vaginal) and within uveal tract of eye

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4
Q

What are the genetic factors that lead to melanoma?

A
  1. Family history (CNKN2A mutations), MC1R variants
  2. Lightly pigmented skin
  3. Red hair
  4. DNA repair defects (e.g. xeroderma pigmentosum)
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5
Q

What are the environmental factors that lead to melanoma?

A
  1. Intense intermittent sun exposure
  2. Chronic sun exposure
  3. Residence in equatorial latitudes
  4. Sunbeds
  5. Immunosuppression
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6
Q

What are the phenotypic causes of melanoma?

A
  1. > 100 Melanocytic nevi

2. Atypical melanocytic nevi

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7
Q

What does the MAPK pathway regulate?

A

regulates cellular proliferation, growth and migration

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8
Q

When are KIT mutations present?

A
  1. 30-40% of acral and mucosal melanomas
  2. also melanomas from chronically sun-exposed skin harbour activating mutations or copy number amplifications of KIT gene
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9
Q

When are activation mutations present?

A
  1. NRAS gene (15-20% of melanomas)
  2. BRAF gene (50-60%) – high in melanomas of skin with intermittent UV exposure, yet low in melanomas of skin with high cumulative UV exposure.
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10
Q

What do BRAF gene mutations do?

A

BRAF mutations substitution leads to activation of mitogen-activated protein kinase (MAPK) pathway

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11
Q

What else can cause MAPK pathway activation?

A

Inherited CDKN2A mutations

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12
Q

What is P16 tumour suppressor encoded by?

A

CDKN2A

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13
Q

What does P16 tumour suppressor bind to?

A

CDK4/6, p16 prevents formation of cyclin D1-CDK4/6 complex

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14
Q

What does the cyclin D1-CDK4/6 complex phosphorylates?

A

Rb, inactivating it, leading to E2F release (once released, E2F promotes cell cycle progression)

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15
Q

What is the host response to melanoma?

A
  1. CD8+ T-cell recognise melanoma-specific antigens and if activated appropriately, are able to kill tumour cells
  2. CD4+ helper T-cells and antibodies also play a critical role
  3. Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) is natural inhibitor of T-cell activation by removing the costimulatory signal (B7 on APC to CD28 on T-Cell)
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16
Q

How do you treat melanoma?

A
  1. Immunotherapy based on CTLA-4 blockade – ipilimumab

2. Also checkpoint inhibitors (PD-1, PDL1)

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17
Q

What is the epidemiology of melanoma?

A
  • Increasing worldwide
  • Develops predominantly in Caucasian populations
  • Incidence low amongst darkly pigmented populations
  • 10-19/100,000 per year in Europe
  • 60/100,000 per year in Australia / NZ
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18
Q

What are the subtypes of melanoma?

A
  1. Superficial spreading
  2. Nodular
  3. Lentigo maligna
  4. Acral lentiginous
  5. Unclassifiable
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19
Q

What is the are 60-70% of all melanoma?

A
  • Most common type in fair-skinned individuals

- superficial spreading

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20
Q

Where is melanoma mostly?

A

seen on trunk of men and legs of women

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21
Q

When do melanoma arise?

A

•Can arise de novo or in pre-existing nevus

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22
Q

When does regression happen in superficial spreading?

A

In up to 2/3 of tumours, regression (visible as grey, hypo-or depigmentation), reflecting the interaction of host immune system with tumour

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23
Q

What is the process of superficial spreading?

A
  1. After a slow horizontal (radial) growth phaselimited to epidermis
  2. more rapid vertically oriented growth phase, which presents clinically with development of nodule
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24
Q

What is nodular melanoma?

A

2nd most common type of melanoma in fair skinned individuals

25
Q

What are 15-30% of all melanomas?

A

15-30%

26
Q

Where does nodular melanoma happen?

A
  • Most commonly trunk, head and neck

* M>F

27
Q

How does nodular melanoma present?

A
  1. Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding
  2. Develops rapidly
28
Q

Where does nodular melanoma arise?

A
  1. arise as a de novo vertical growth phase without the pre-existing horizontal growth phase
  2. Tend to present more advanced stage, with poorer prognosis.
29
Q

What is lentigo maligna?

A
  • Minority of cutaneous melanomas (around 10%) and is >60 years old
  • chronically sun-damaged skin, most commonly on the face
30
Q

How does lentigo maligna progress?

A
  1. Slow growing, asymmetric brown to black macule

2. with colour variation and an irregular indented border

31
Q

When does invasive lentigo maligna melanoma arise?

A

in a precursor lesion termed lentigo maligna (in situ melanoma) in sun damaged skin)

32
Q

How many lentigo maligna progress to invasive melanoma?

A

estimated that 5%

33
Q

How common is Acral lentiginous?

A

~5% of all melanomas

34
Q

When is acral lentiginous diagnosed?

A

frequently in 7th decade of life

35
Q

Where does acral lentiginous occur?

A

palms and soles or in and around the nail apparatus

36
Q

What is the epidemiolgy of acral lentiginous?

A
  1. Incidence similar across all racial and ethnic groups
  2. As more darkly pigmented Africans and Asians do not typically develop sun-related melanomas, ALM represents disproportionate percentage of melanomas diagnosed in Afro- Caribbean (up to 70%) or Asians (up to 45%)
37
Q

What early detection of melanoma?

A

History of change in colour, shape or size of a pigmented skin lesion

38
Q

What is the public awareness campaign ABCDE for melanoma self detection?

A
  1. Asymmetry
  2. Border irregularity
  3. Colour variegation
  4. Diameter greater than 5mm
  5. E evolving
39
Q

What is Garbe’s rule?

A

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

40
Q

What are the differential diagnosis of melanoma?

A
  1. Basal cell carnoma
  2. seborrhoeic keratosis
  3. dermatofibroma
41
Q

What are poor prognostic features of melanoma?

A
  1. Increased Breslow thickness >1mm
  2. Ulceration
  3. Age
  4. Male gender
  5. Anatomical site – trunk, nhead, neck
  6. . Lymph node involvement
42
Q

What is stage 1A melanoma?

A

10 year survival of >95% whereas thick melanomas >4mm and ulceration pT4b have a 10 year survival rate of 50%

43
Q

What is breslow thickness?

A

measurement from granular layer to bottom of tumour

44
Q

What is dermoscopy?

A

can improve correct diagnosis of melanoma by nearly 50%

45
Q

What are the global features of melanoma?

A
  1. Asymmetry
  2. Presence of multiple colours
  3. Reticular, globular, reticular-globular, homogenous
  4. Starburst
  5. Atypical network, streaks, atypical dots or globules, irregular blood vessels, regression structures, blue-white veil
46
Q

What should you do if you are unsure if it is melanoma?

A
  1. Dermoscopic findings should not be considered n isolation
  2. History and risk factor status are important
  3. Excise lesion for histological assessment if in any doubt
  4. “If in doubt, take it out”
47
Q

What is the management of a melanoma?

A
  1. Primary excision

2. Wide excision

48
Q

What is a primary excision?

A
  • down to subcutaneous fat

- 2mm peripheral margin

49
Q

What is a wide excision?

A
  1. Margin determined by Breslow depth
  2. 5mm for in situ
  3. 10mm for =1mm
    - Prevents local recurrence or persistent disease
50
Q

What is the staging of melanoma?

A
  1. Pathological

2. TNM

51
Q

What is the management of melanoma?

A

Sentinel lymphoma node biopsy

52
Q

What happens in a sentinel lymphoma node biopsy?

A
  1. Lymphatic drainage of finite regions of skin drain specifically to an initial node within a given nodal basin - the ‘sentinel node’
  2. Represent most likely nodes to contain metastatic disease
53
Q

What is the imaging of melanoma?

A

-Stage III, IV
And Stage IIc without SLNB
•PET-CT
•MRI Brain

54
Q

What is a major prognostic factor in metastic melanoma?

A

LDH

55
Q

When is sentinel lymphoma biopsy offered?

A
  1. Currently offered for pT1b+

2. Extracapsular spread on lymph node biopsy – needs lymph node dissection

56
Q

What immunotherapy used in melanoma management?

A
  1. CTLA-4 inhibition – unresectable or metastatic BRAF negative melanoma (Ipilimumab)
  2. PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)
  3. Combination immunotherapy not much better than ingle agent in
  4. Combination immunotherapy leads to 60% response vs 20% monotherapy alone
57
Q

What is mutated oncogene targeted therapy in melanoma management?

A
  • Combination of aBRAFinhibitor (e.g. encorafenib, vemurafenib, dabrafenib)
  • MEK inhibitor (e.g. trametinib)
58
Q

What is the growth of melanoma superficial spreading?

A

horizontal growth (asymmetry, border irregualrity and colou variation) (limited to epidermis) then vertical growth (more invasive)

59
Q

What is the growth of nodular melanoma?

A

only vertical growth

Z Year 2 BRS MSK (18 decks)

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