CasaD - Skin Cancer Flashcards by Rama Jha

3 main leys of the skin and explain what one of the layers is made up of

3 main layers:
• epidermis
• dermis
• hypodermis (fat layer)

Epidermis is compromised of (superficial --> deep) :
 o	Stratum corneum
  – dead keratinocytes
o	Stratum lucidum
o	Stratum granulosum
o	Stratum spinosum
 – dendritic cells.
o	Stratum basale 
 – melanocytes, merkel cells, dividing cells

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What are the different types of skin cancers?

 Keratinocyte derived
• e.g. BCC (Basal Cell Carcinoma), SCC (Squamous Cell Carcinoma)
• aka – Non-Melanoma Skin Cancer (NMSC)

 Melanocyte derived
• e.g. Malignant melanoma

 Vasculature derived
• e.g. Kaposi’s sarcoma,
angiosarcoma

 Lymphocyte (lymphoma) derived
• e.g. Mycosis fungoides

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What is the main cause of skin cancer?

Accumulation of genetic proliferation

• uncontrolled cell proliferation

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Example of causes of skin cancer

o Genetic syndromes
• Gorlin’s syndrome, Xeroderma pigmentosum

o Viral infections
• HHV8 (Kaposi’s sarcoma), HPV (SCC)

o UV light
• BCC, SCC, malignant melanoma

o Immunosuppression
• drugs, age, HIV, leukaemia

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Explain what MM looks like and its epidemiology

Malignant Melanoma:
• has an irregular margin
• dark-coloured

Epidemiology:
• incidence highest in WHITE and lowest in BLACK
• incidence highest in SW England

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Explain what B-C C looks like and its epidemiology

Basal-Cell Carcinoma:
• pearly appearance
• dilated vessels on surface

Epidemiology:
• incidence increasing in men & women (due to increasing ages and more exposure)

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What is the different parts that makes up the UV Spectrum?

UVA
• 310-400nm
• penetrates to deep sea level

UVB
• 280 - 310nm
• penetrates to ground level

UVC
• 100-280nm
• does NOT penetrate ozone

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Which is the most important UV that contributes to skin cacrinogenesis?

UVB

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Explain how UVB contributes to skin carcinogenesis?

Most important in skin carcinogenesis:
• Induces direct abnormalities in skin DNA – e.g. mutations.
• Induces photoproducts – affects PYRIMIDINES (C, T) bases, e.g :
o Cyclobutane pyrimidine dimers (e.g. T=T, T=C, C=C).
o 6-4 pyrimidine pyrimidone photoproducts.

 Photoproducts are usually repaired quickly by nucleotide excision repair.

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Explain how UVA contributes to skin carcinogenesis

 100x more penetrating than UVB

 Major cause of skin AGEING and contributes to skin carcinogenesis.
• Also forms Cyclobutane pyrimidine dimers BUT less efficiently than UVB
• Forms free radicals to damage DNA and cell membranes

 Used therapeutically in PUVA therapy – treats psoriasis etc.

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How is UV damage repaired?

Nucleotide Excision Repair
• photoproducts removed

Xeroderma Pigmentosum
• genetic condition with defective Nucleotide Excision Repair

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Mutations that cause cancer?

Mutations that:
(1) stimulate uncontrolled cell proliferation (e.g. abolishing control of normal cell cycle via. p53 gene)

(2) alter responses to growth stimulating/repressing factors
(3) inhibit programmed cell death (apoptosis)

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What happens in sun burn?

UV light –>
• leads to keratinocyte apoptosis

• apoptosis removes UV damaged cells in skin which might otherwise become cancerous

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Explain the immunomodulatory effects of UV light

UVA/B effect expression of genes:

deplete Langerhans cells in the epidermis
= decreased skin immunocompetance & immunosurveillance
= basis for using UV phototherapy to treat psoriasis BUT also further increases cancer chances

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Explain photocarcinogenesis

Leads to DNA damage in kerainocytes
• can REPAIR or if damage to severe then can enter APOPTOSIS

BUT if also have
p53 mutations
CAN lead to skin cancer

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What determines host reponse to UV?

By genetic influences especially SKIN PHOTOTYPE

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What are the different skin phototypes?

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Fitzpatrick Phototypes:
 o	1 – always burns, never tans.
 o	2 – usually burns, sometimes tans.
 o	3 – sometimes burns, usually tans.
 o	4 – never burns, always tans.

o 5 – moderate
constitutive pigmentation – Asian.
o 6 – moderate constitutive pigmentation – Afrocaribean.

Where is melanin produced and where does it go?

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 Melanin:
• produced by melanocyte (from tyrosine)
• within the BASAL LAYER of the EPIDERMIS
• packed into melanosomes

It is then:
• transported UP SPINES to the keratinocytes where it passes into the cells
• here it then COATS the nuclei within the cells to protects from UV damage.

What does skin colour depend on?

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Skin colour depends upon AMOUNT and TYPE of melanin produced

NOT density

What are the different types of melanin?

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Types – encoded by MCR1 gene has that has >20 polymorphisms and describes the variations in melanin

Variation in eumelanin:phaeomelanin produced:
 Eumelanin – brown or black.
 Phaeomelanin – yellowish or reddish.

How is melanin produced?

Study These Flashcards

1• Tyrosine 
2• DOPA 
3• Dopaquinone 
4• Eumelanin or Phaeomelanin 
5• Melanin

What does melanin dictate?

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Skin sensitivity to UV damage

Explain what MM is and what causes it

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Malignant Melanoma
• malignant tumours of melanocytes

Melanocytes become:
• abnormal
• & have atypical cells & atypical architecture

Caused by:
• UV exposure
• Genetic factors

Risk of METASTASIS
• so skin cancer with HIGHEST MORTALITY

Summary of the Types of MM?

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(1) Lentigo MM (in situ)
(2) Superficial Spreading MM
(3) Nodular MM
(4) Nodular MM arising within SSMM
(5) Acral Lantiginous MM
(6) Amelanotic MM

Explain (1) L MM

Lentigo MM: • melanoma in situ  Proliferation of malignant melanocytes within the EPIDERMIS.  No risk of metastasis. ``` Features: o Considered premelanoma state o Irregular shape. o Light & dark colours. o Size usually >2.0cm. ```

Explain (2) SS MM

(2) Superficial Spreading MM  Lateral proliferation of malignant melanocytes.  Invasion of the BM (= grows outwards)  Risk of metastasis. ``` Diagnosis rule of SSMMs – ABCD: o A – Asymmetry. o B – Border irregularity. o C – Colour variation. o D – Diameter >0.7mm and increasing. o (E – Erythema). ```

Explain (3) N MM

(3) Nodular MM  VERTICAL proliferation of MMs with no previous horizontal growth.  Risk of metastasis (as growing downwards)  Usually much darker in appearance.

Explain (4) N MM arising within SSMM

(4) N MM arising within SSMM  Downward proliferation of MMs FOLLOWING previous horizontal growth.  Prognosis will become worse (as nodule growing within an irregular plaque).  Some may have areas of ERYTHEMA • usually when the tumour has lost ability to produce melanin so instead starts to looka erythematous

Explain (5) AL MM

(5) Acral Lentiginous MM  A malignant melanoma affecting the palms and soles of the feet.  Occur in darker skinned people more often than lighter coloured skin people.

Explain (6) A MM

(6) Amelanotic MM  A melanoma where the cancer cells have lost the ability to create melanin.

What is the prognosis of Melanoma determined by?

Breslow thickness! Measured from granular layer to bottom of tumour • states that the deeper the melanoma (>1mm), the worse the prognosis.

Risk factors for the development of Melanoma?

 Family history  Intermittent burning exposure  Skin types 1, 2.  UV light exposure  Atypical nevus syndrome  Sunburns during childhood  Personal melanoma history

Dysplastic nevi?

Moles that are a little atypical but are NOT melanomas

What are keratoacanthomas?

Either a benign lesion OR version of an SCC  grows rapidly but then DISAPPEARS  NO RISK of metastasis

Explain SCC

Squamous Cell Carcinoma:  Malignant tumour of keratinocytes. ``` Caused by: • UV • HPV • immunosuppression • scarring processes ```  Risk of metastasis (but not as high as in MMs)  “Horny” descriptors indicate well differentiation and the cell has retained the ability to create keratin.

Explain BCC

Basal Cell Carcinoma:  Malignant tumour arising from the basal layer of the epidermis. Caused by: • sun exposure • genetics Features: o Slow growing. o Invades tissues but does NOT metastasise. o Common on the face.  Can be nodular (has a telangiectasia) or superficial

Telangiectasia?

Localised collection of distended blood capillary vessels It is a KEY FEATURE of BCC

Explain MF

Mycosis Fungoides:  Not a fungal condition – miss-classified.  This is a lymphoma that affects the skin-resident T-lymphocytes • red patches make it look like psoriasis BUT is not  This can be fatal and has internal organ involvement.

Explain KS

Kaposi's Sarcoma:  HIV and HHV8 associated.  A tumour of the endothelial cells of the lymphatics.  Can occur in non-HIV patients and can occur internally.

Explain EV

Epidermodysplasia Verruciformis:  Rare autosomal condition.  Gives a predisposition to HPV-induced warts and SCCs.

What is the treatment for many of these skin cancers?

SURGICAL

CasaD - Skin Cancer Flashcards

(41 cards)