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!!!!! BRS YR2 !!!!! > Derm - Skin Cancer > Flashcards

Derm - Skin Cancer Flashcards

1
Q

What is a melanoma?

A

malignant tumour arising from melanocytes

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2
Q

What are the worldwide statistics for melanomas?

A

leads to >75% of skin cancer deaths

rising incident rates observed world wide

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3
Q

What causes the central depigmented zone?

A

due to tumour regression

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4
Q

What are the main diagnostic tools for skin cancers?

A

imaging + skin biopsy

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5
Q

Where can melanomas arise?

A

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

even internal organs can be affected

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6
Q

What are the different categories fo risk factors for melanomas?

A
  • genetic factors
  • environmental factors
  • phenotypic
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7
Q

What are the genetic risk factors for melanomas?

A
  • Family history (CNKN2A mutations), MC1R variants
  • Lightly pigmented skin
  • Red hair
  • DNA repair defects (e.g. xeroderma pigmentosum)
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8
Q

What are the environmental risk factors for melanomas?

A
  • Intense intermittent sun exposure
  • Chronic sun exposure
  • Residence in equatorial latitudes
  • Sunbeds
  • Immunosuppression
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9
Q

What are the phenotypics risk factors for melanomas?

A
  • >100 Melanocytic nevi
  • Atypical melanocytic nevi

nevi = proliferations of melanocytes that are in contact with each other, forming small collections of cells known as nests

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10
Q

What pathway is important in melanoma molecular pathogensis? Why?

A
  • Mitogen-activated protein kinase (MAPK) [RAS-RAF-MEK-ERK] pathway
  • regulates cellular proliferation, growth and migration
  • mutations in this pathway contribute to melanoma growth
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11
Q

What are the different mutations that can lead to melanomas?

A
  • KIT mutation
  • NRAS gene
  • BRAF gene
  • CDKN2A mutations
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12
Q

What do KIT mutations lead to?

A
  • 30-40% of acral and mucosal melanomas
  • also melanomas from chronically sun-exposed skin harbour activating mutations or copy number amplifications of KIT gene
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13
Q

What melanomas do mutations in NRAS gene?

A

15-20% of melanomas

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14
Q

What do mutations in the BRAF gene cause?

A
  • 50-60% of melanomas
  • high in melanomas of skin with intermittent UV exposure
  • low in melanomas of skin with high cumulative UV exposure
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15
Q

What is the purpose of CDKN2A gene?

A
  • encodes P16 - tumour supressor
  • this binds to CDK4/6, preventing formation of cyclin D1-CDK4/6 complex
  • Cyclin D1-CDK4/6 complex phosphorylates Rb, inactivating it, leading to E2F release (once released, E2F promotes cell cycle progression)
  • therefore prevention of the complex stops cell cycle progression
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16
Q

Why do mutations in the the CDKN2A gene cause melanomas?

A

can’t encode p16, which stops progression of cell cycle

therefore cell cycle progresses and tumours ariseee

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17
Q

What is the host response to melanomas?

A
  • CD8+ T-cell recognise melanoma-specific antigens and if activated appropriately, are able to kill tumour cells.
  • CD4+ helper T-cells and antibodies also play a critical role
  • 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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18
Q

What immunotherapy is based on the CTLA-4 blokade?

A

ipilimumab

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19
Q

What are the checkpoint inhibitors in our immune system? What do they do?

A

PD-1, PDL1

they remove the signal “don’t kill cells” and let immune system kill cancer cells

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20
Q

What is the epidemiology of melanomas?

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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21
Q

What are the different subtypes of melanaomas?

A
  • Superficial spreading
  • Nodular
  • Lentigo maligna
  • Acral lentiginous
  • Unclassifiable
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22
Q

What percentage of melanomas are superfical spreading?

A

60-70%, most common type in fair-skinnned individuals

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23
Q

Where do superficial spreading melanomas usually occur?

A
  • Most frequently seen on trunk of men and legs of women
  • Can arise de novo or in pre-existing nevus (without mole or form a pre-existing mole)
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24
Q

What are some characterisitics of superficial spreading melanomas?

A
  • assymetry, border irregularity, colour variation, increased diameter
  • 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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25
Q

How do superficial spreading melanomas grow?

A

horizontal growth first (this is where all the visibal echaracteristics show e.g. assymmetry)

then vertical growth (this where you get the appearance of a nodule or bump)

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26
Q

What percentage of melanomas do nodular ones represent?

A

15%-30% of all melanomas

2nd most common type of melanoma of fair-skinned individuals

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27
Q

Where does it usually appear? What is the demographic?

A

most commonly trunk, head, neck

more present in M than F

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28
Q

What are the characteristics of a nodular melanoma?

A
  • Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding
  • Develops rapidly
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29
Q

What is a nodular melanoma with no pigment called?

A

amelanotic melanoma

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30
Q

How do nodular melanomas grow?

A

only has vertical growth phase

therefore the characteristics features of horizontal growth (e.g. assymmetry, border irregularity, etc.) are not present or not obvious)

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31
Q

What percentag eof melanomas do lentigo maligna make up?

A

minority of cutaneous melanomas (around 10%)

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32
Q

What is the demographic of occurence of lentigo maligna? Where does it commonly occur?

A
  • over 60 year olds
  • occurs in chronically sun-damaged skin
  • most commonly on the face
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33
Q

What do lentigo maligna melanomas look like?

A

Slow growing, asymmetric brown to black macule with colour variation and an irregular indented border

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34
Q

What are lentigo malignas usually precursors for?

A

Invasive Lentigo Maligna Melanoma arises in a precursor lesion termed lentigo maligna

therefore a precursor for invasive melanoma

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35
Q

What percentage of lentigo malignas progress?

A

5% progress to invasive melanomas

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36
Q

What are some of the characteristics of lentigo maligna under dermatoscope?

A
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37
Q

What percentage of all melanomas are acral lentiginous?

A

relatievly uncommon, around 5% of all melanomas

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38
Q

When are acral lentiginous melanaomas usually diagnosed?

A

most freqeuntly in 7th decade of life

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39
Q

Where do acral lentiginous melanomas typically appear?

A

palms and soles or in and around the nail apparatus

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40
Q

What is the incidence like across all demgraphics?

A
  • Incidence similar across all racial and ethnic groups
  • 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%)
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41
Q

What do acral lentiginous melanomas look like?

A

a black or brown discoloration that appears on the sole of the foot or palm of the hand. It may resemble a bruise or stain, but over time it grows in size

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42
Q

What do acral lentiginous melanomas look like in the nail? What are the characteristics?

A

melanonychia = brown-black discoloration of the nail plate and the pigment referred to is conventionally melanin

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43
Q

What is an amenalotic melanoma?

A
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44
Q

What is key to early detection of melanomas?

A

self-detection - looking for history of change in colour, shape, or size of a pigmented skin lesion

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45
Q

What does the ABCDE public awareness acronym for self-detection stand for?

A

A = asymmetry

B = border irregularity

C = colour variation

D = diameter greter than 5mm

E = evolving

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46
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

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47
Q

What can be some diffrential diagnosis for melanomas?

A

basal cell carcinoma

seborrhoeic keratosis = harmless skin lesions that increase in number wiht age

dermatofibroma = harmless benign skin lesion

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48
Q

What are poor prognostic features of melanomas?

A
  • Increased Breslow thickness >1mm
  • Ulceration
  • Age
  • Male gender
  • Anatomical site – trunk, head, neck
  • Lymph node involvement

Stage 1A melanoma have 10 year survival of >95% whereas thick melanomas >4mm and ulceration pT4b have a 10 year survival rate of 50%

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49
Q

How is Breslow thickness measured

A

measurment hitological from granular layer to bottom of tumour

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50
Q

What invetigative tools are used ot identify melanomas?

A

dermoscopy

  • allows you to see through stratum corneum, negating all the refraction that happens at that level
  • allows you to observe features that can’t be seen with the naked eye
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51
Q

What are some global features of melanomas on dermoscopy?

A
  • Asymmetry
  • Presence of multiple colours
  • Reticular, globular, reticular-globular, homogenous
  • Starburst
  • Atypical network
  • streaks
  • atypical dots or globules
  • irregular blood vessels
  • regression structures
  • blue-white veil
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52
Q

How important are dermosocpic lesions?

A

can improve diagnoses by 50%

but should not be taken in isolation

history + risk factor status are also important

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53
Q

What should be done if there are doubts about the melanoma?

A

• Excise lesion for histological assessment if in any doubt

IF IN DOUBT, TAKE IT OUT!

54
Q

How is a melanoma lesion taken out for histological assessment?

A

• Primary excision down to subcutaneous fat with 2mm peripheral margin

55
Q

What is done to remove a melanoma?

A

Wide excision, Margin determined by Breslow depth

  • 5mm for in situ
  • 10mm for =1mm

Prevents local recurrence or persistent disease

56
Q

How are melaonomas staged? What is it based on?

A
  • pathology
  • TMN
57
Q

What is a sentinel lymphoma node?

A
  • Lymphatic drainage of finite regions of skin drain specifically to an initial node within a given nodal basin - the ‘sentinel node’
  • Represent most likely nodes to contain metastatic disease
58
Q

When is a sentinel lymph node biopsy offered?

A

currently offered for pT1b+

59
Q

When is lymph node dissection done?

A

when there is Extracapsular spread on lymph node biopsy

60
Q

What different imaging is done for melanomas and at what stage?

A
  • Stage III, IV and Stage IIc without SLNB
  • PET-CT
  • MRI Brain
61
Q

What else is measured in progressing melanomas? Why?

A

LDH

mjor prognostic factor in metastatic melanomas

62
Q

How are unresectable + metastatic melanomas treated?

A
  • immunotherapy
  • mutated oncogene targeted therapy
63
Q

What immunotherapy is used to manage melanomas?

A

• CTLA-4 inhibition – unresectable or metastatic BRAF negative melanoma (Ipilimumab)

• PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)
Combination immunotherapy not much better than ingle agent in

  • Combination immunotherapy leads to 60% response vs 20% monotherapy alone
64
Q

What mutated oncogene targeted therapy can be used to manage melanomas?

A

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

65
Q

Who does keratinocyte dysplasia + carcinomas commonly occur in?

A

predominantly pale skin types

66
Q

What causes keratinocyte dysplasia / carcinomas?

A

solar induced UV damge

67
Q

What are some different types of keratinocyte dysplasia / carcinoma?

A

•Actinic keratoses

  • Dysplastic keratinocytes
  • Bowen’s disease (Squamous cell carcinoma in situ)
  • Squamous cell carcinoma
  • Potential for metastasis/ death

•Basal cell carcinoma

  • (Virtually) never metastasises
  • Locally invasive
68
Q

What contributes to basal cell carcinoma pathogensis?

A
  • UV radiation is significant risk factor
  • Dependent on stroma produced by dermal fibroblasts
  • Cross talk between tumour cells and mesenchymal cells of stroma
  • Receptors for PDGF are upregulated in Stroma but PDGF is upregulated in tumour cells
  • BCC has proteolytic activity e.g. metalloproteinases and collagenases – degrade pre-existing dermal tissue and facilitate spread of tumour cells
  • Loss of function in chromosome 8q (PTCH gene)
  • Sonic Hedgehog-Patched signalling pathway

/ SHH signalling is required for growth of established BCCs

• p53 mutations are also important – majority are missense mutations that carry a UV signature

69
Q

What contributes to the pathogenesis of squamous cell carcinomas?

A
  • UV radiation is significant risk factor
  • Develops through addition of genetic alterations – alterations in p53 are most common, CDKN2A also
  • NOTCH1 or NOTCH2 (Wnt / β-catenin signalling) also plays role
70
Q

What is the epidemiology of keratinocyte carcinomas?

A
  • Basal cell carcinoma is most common skin cancer
  • BCC:SCC 4:1
  • Both commoner in pale skin types
  • Both more common in men vs women (2-3:1)
  • Median age at diagnosis of BCC is 68
71
Q

What are the risk factors of keratinocyte carcinomas?

A

•UV exposure

  • PUVA
  • Fair skin
  • Genetic syndromes
  • Xeroderma pigmentosum
  • Oculocutaneous albinism
  • Muir Torre syndrome
  • Nevoid basal cell carcinoma syndrome*
  • Nevus sebaceous
  • Porokeratosis
  • Organ transplantation (immunosuppressive drugs)
  • Chronic non-healing wounds
  • Ionising radiation
  • Airline pilots

•Occupational chemical exposures

  • Tar, polycyclic aromatic hydrocarbons,
72
Q

What are actinic keratoses? What are their characterisitics?

A
  • Atypical keratinocytes confined to epidermis
  • Erythematous macule or scale or both-> thick papules or hyperkeratosis or both, sometimes cutaneous horn
73
Q

Where do actinic keratoses usually develop?

A

develop on sun-damaged skin, usually head, neck, upper trunk or extremities

74
Q

How do you distinguish actinic keratoses from SCCs?

A

•Distinction from squamous cell carcinoma sometimes difficult – requiring biopsy

75
Q

What is the risk of progression for actinic keratoses into SCCs?

A

0.025–16% per year for any single lesion

76
Q

What is Bowen’s disease? What are the characteristics?

A
  • squamous cell carcinoma in situ (occupy the skin but haven’t invaded dermis)
  • Erythematous scaly patch or slightly elevated plaque
  • May arise de novo or from pre-existing AK
  • May resemble actinic keratoses, psoriasis, chronic eczema
77
Q

How are actinic keratoses and Bowen’s disease treated?

A
  • 5-fluorouracil cream =
  • Cryotherapy = freezing with liquid nitrogen
  • Imiquimod cream = stimulates immune system to attack them
  • Photodynamic therapy = apply porforin, sine, light, generate free radicals, cuasing apoptosis
  • Curettage and cautery = burning, etc.
  • Excision
78
Q

What do squamous cell carcinomas look like?

A
  • Erythematous to skin coloured
  • Papule
  • Plaque-like
  • Exophytic = describe an abnormal growth that sticks out from the surface of a tissue
  • Hyperkeratotic
  • Ulceration
79
Q

What are the high risk features of SCCs?

A
  • Localisation: Trunk and limbs > 2cm; Head / neck > 1cm; Periorificial zones
  • Margins: Ill-defined
  • Rapidly growing
  • Immunosuppressed patients
  • Previous radiotherapy or site of chronic inflammation
80
Q

What histological features of SCCs can identify them as high risk?

A
  • Grade of differentiation: poorly differentiated
  • Acantholytic, adenosquamous, demosplasticsubtypes
  • Tumour thickness - Clark level: >6mm, Clark IV, V
  • Invasion beyond subcutaneous fat
  • Perineural, lymphatic or vascular invasion
81
Q

What is a keratoacanthoma?

A
  • Rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with keratotic core
  • Resolves slowly over months to leave atrophic scar
  • Controversial entity : Pseudo-malignancy or variant of SCC?
82
Q

Where do keratoacanthomas normally occur?

A

most occur on the head or neck, sun-exposed areas

83
Q

How do you distinguish between keratoacanthomas and SCCs?

A

Difficult to distinguish clinically and histologically from squamous cell carcinoma

84
Q

How are SCCs investigated + diagnosed?

A
  • Often clinical diagnosis sufficient
  • Diagnostic biopsy may be taken if diagnostic uncertainty
  • Ultrasound of regional lymph nodes ± FNA (fine needle aspiration) if concerns regarding regional lymph node metastasis
85
Q

What are some diffrential diagnoses for SCCs?

A

basal cell carcinoma

viral wart

merkel cell carcinoma

86
Q

How are SCCs treated?

A
  • Examination of rest of skin and regional lymph nodes
  • Excision
  • Radiotherapy
  • Cemiplimab for metastatic SCC
  • Secondary prevention
87
Q

When is radiotherapy considered for SCCs?

A
  • Unresectable
  • High risk features e.g. perineural invasion
88
Q

What is a part of secondaey prevention for SCCs?

A
  • skin monitoring advice
  • sun protection advice
89
Q

What are the different subtypes of Basal cell carcinomas?

A
  • nodular
  • superficial
  • morpheic
  • infiltrative
  • basisquamous
  • micronodular
90
Q

What percentage of BCCs do nodular ones account for?

A

most common subtype

accoutns for approx. 50%

91
Q

What are the cahracteristsics of a nodular BCC?

A
  • Typically presents as shiny, pearly papule or nodule
92
Q

What are the characteristics of superficial BCCs?

A
  • Well-circumscribed, erythematous, macule / patch or thin papule /plaque
  • can resemble Bowen’s disease, actinin keratoses, etc.
93
Q

What are the characteristics of morphoeic BCC?

A
  • Less common
  • Slightly elevated or depressed area of induration
  • Usually light-pink to white in colour
  • More aggressive behaviour
  • Extensive local destruction
94
Q

What are the histological features of basisquamous BCCs?

A

Histological features of both basal cell carcinoma and squamous cell carcinoma

95
Q

What are the characteristsics of micronodular BCCs?

A
  • Resembles nodular basal cell carcinoma clinically
  • More destructive behaviour – high rates of recurrence and subclinical spread
96
Q

How are BCCs investigated + diagnosed?

A
  • Often clinical diagnosis sufficient
  • Diagnostic biopsy may be taken
97
Q

What are the diffrential diagnoses for BCCs?

A
  • SCCs
  • Adnexal (Sebaceous) carcinoma
  • Merkel cell carcinoma
98
Q

How do you treat BCCs?

A
  • Standard surgical excision
  • Mohs micrographic surgery
99
Q

When is Mohs micrograph surgery used on BCCs?

A
  • Recurrent basal cell carcinoma
  • Aggressive subtype (morpheic / infiltrative / micronodular)
  • Critical site
100
Q

What are some other ways to treat BCCs?

A

Suitable for superficial BCCs:

  • Topical therapy e.g. 5-Fluorouracil, Imiquimod
  • Photodynamic therapy
  • Curettage

Sutitable for patients over age of 70 due to risks of SCCs:

  • Radiotherapy

Suitable for rare BCCs metastases or unresectable BCCs

  • Vismodegib - selectively inhibits abnormal signalling in Hedgehog (Hh) pathway
101
Q

How does micrographic surgery work? Why is this done?

A
  • to preserve tissue that is healthy
  • to target the cancerous tissue specifically, rather than missing the tumours in thebread-loafing method or situation
  • however, is very time-comsuming, taking hours and hours to resct one tumour that could be done in 45 mins of standard surgery
102
Q

What percentage of cutaneous lymphomas are T-cell?

A

75%

103
Q

What are cutaneous T-cell lymphomas?

A

Heterogenous group of neoplasms of skin-homing T-cells that show considerable variation in clinical presentation, histological appearance, immunophenotype and prognosis

104
Q

What are the 2 most common subtypes?

A
  • Sézary syndrome
  • mycosis fungoides
105
Q

What is the underlying molecular pathogensis?

A

unknown

Inactivation of genes controlling cell cycle and apoptosis has been identified

106
Q

What is the epidemiology of cutaneous T-cell lymphoma?

A
  • Mycosis fungoides 0.4/100,000
  • Typically older adults (median age of diagnosis 55-60)
  • Sézary syndrome is rare - <5% of all CTCL
107
Q

What is mycosis fungoides?

A
  • Common variant of primary CTCL and accounts for 50% of all primary cutaneous lymphoma
  • Indolent clinical course
108
Q

How is a mycosis fungoides lymphoma diagnosed?

A

• Diagnosis requires skin biopsy

  • Diagnosis may take years as skin lesions may be present that are neither clinically nor histologically diagnostic for many years
  • lesions may present as eczema or psoriasis for yearss
109
Q

What can appear as mycosis fungoides?

A

Atypical T-cell infiltrates which can be found in lymphomatoid drug eruptions

110
Q

What is the progression of mycosis fungoides?

A
  • Patients progress from patch stage → plaque stage → (finally) tumour stage disease
  • Protracted clinical course over years → decades
111
Q

How can the early stages of MF be characterised?

A
  • Early patch stage is characterised by variably sized erythematous, finely scaling lesions which may be mildly pruritic
  • Generally many years of nonspecific eczematous or psoriasiform skin lesions
112
Q

What is the median duration of onset of skin lesions to diagnosis?

A

4-6 years, but may vary from several months to more than 5 decades

113
Q

What si the pathogensis of MF?

A
  • Considered to be a stepwise accumulation of genetic abnormalities → clonal proliferation → malignant transformation → progressive and widely disseminated disease
  • Molecular events remain unidentified
  • Genetic abnormalities described – not constituting a patter
  • P53, CDKN2A, PTEN, STAT3 identified in advanced MF, but not early

e.g. likely secondary genetic events

• Persistent antigenic stimulation plays a crucial role in various lymphomas but no antigens known in MF

114
Q

How is MF evaluated + staged?

A
  • Type and extent of skin lesions
  • Presence of palpable lymph nodes
  • Skin biopsies
  • Complete blood counts and serum chemistries
115
Q

What is the treatment for MF?

A
  • Plaque / patch stage treatments include topical corticosteroids, phototherapy and radiotherapy
  • Systemic chemotherapy is only indicated in advanced stage when there is nodal or visceral involvement or in patients with rapidly progressive tumours unresponsive to less aggressive therapies
  • Brentuximab vedotin (anti-CD30)
116
Q

What is the prognosis of MF and what does it dpeend on?

A
  • Depends on stage
  • 10 year survival rates are:
  • > 95% in limited patch / plaque disease
  • 85% in generalised patch / plaque disease
  • 42% in tumour stage disease
  • 20% in those with histological lymph node involvement
117
Q

What are some diffrential diagnoses for MF?

A
  • psoriasis
  • eczema (discoid)
  • parapsoriasis
118
Q

What traid characterises Sezary syndrome?

A
  1. Erythroderma
  2. Generalised lymphadenopathy
  3. Presence of neoplastic T-cells (Sézary cells) in the skin, lymph nodes and peripheral blood
119
Q

What is the criteria for Sezary syndrome diagnosis?

A
  • Demonstration of a T-cell clone in peripheral blood by molecular or cytogenetic methods
  • Demonstration of immunophenotypical abnormalities an expanded CD4+ T-cell population – resulting in a CD4/ CD8 ratio of greater than 10 and / or aberrant expression of pan-T-cell antigens)
  • An absolute Sézary cell count of at least 1000 cells per microlitre
120
Q

How is Sezary syndrome treated?

A
  • Systemic treatment is required
  • Extracorporeal photophoresis = WBCs drained and UV light is used to make them undergo apoptosis
  • Chemotherapy can be used
  • Skin-directed therapies like PUVA or potent topical corticosteroids may be used as adjuvant therapy
121
Q

What is PUVA?

A

combination treatment consisting of taking a drug PSORALEN (P) and then exposing the skin to long-wave ultra- violet light (UVA)

122
Q

What is Kaposi Sarcoma? What characterises it?

A
  • multifocal systemic disease
  • Cutaneous lesions can vary from pink patches to dark violet plaques, nodules or polyps
123
Q

What causes kaposi sarcoma? What are the risk factors?

A

HHV8, form of the herpes virus

may be endemic, or related to immunosupression

124
Q

How is kapsoi sarcoma treated?

A

chemotherapy (vincristine, doxorubicin, etoposide, bleomycin) and / or radiation is favoured over surgery

125
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

126
Q

What are risk factors or causes for merkel cell carcinoma?

A
  • 80% are associated with polyomavirus
  • UV exposure is also an aetiological factor
127
Q

Where do merkel cell carcinomas occur?

A

•Predilection for the head and neck region of older adults

128
Q

What are the characteristsics of merkel cell carcinomas?

A

• Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped,

  • Ulceration can occur

• Aggressive, malignant behaviour

129
Q

What percentage of merkel cell carcinomas develop into advanced disease?

A

40%

130
Q

What are the treatments for merkel cell carcinomas?

A
  • Treated with surgery, radiation therapy
  • anti-PD1 (Pembrolizumab) / anti-PDL1 (Avelumab)
131
Q
A

!!!!! BRS YR2 !!!!! (72 decks)

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