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Cancer > 15. Cancer as a disease - skin cancer > Flashcards

15. Cancer as a disease - skin cancer Flashcards

1
Q

Name the 5 layers of the epidermis.

A

Come Lets Get Sun Burn

  • Stratum Corneum
  • Stratum Lucidum
  • Stratum Granulosum
  • Stratum Spinosum
  • Stratum Basale
  • The basal layer of keratinocytes is resting on the basement membrane
  • The keratinocytes proliferate and as they move up through the layers of the epidermis, they differentiate and eventually end up in the stratum corneum
    • ​The stratum corneum is a layer of keratinocytes that have lost their nuclei and mainly consist of keratin - it forms the barrier function of the skin
  • Main cell types of the epidermis
    • Keratinocytes
    • Melanocytes - sit on the basement membrane and produce melanin
    • Langerhans cells - APCs found within the epidermis
    • Merkel cells - involved in sensation
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2
Q

Name the types of skin cancer.

A
  • Keratinocyte derived:
    • ​Basal cell carcinoma (BCC)
    • Squamous cell carcinoma (SCC)
    • Collectively know as non-melanoma skin cancer (NMSC)
  • Melanocyte derived:
    • ​Malignant melanoma
  • Vasculature derived:
    • ​Kaposi’s sarcoma - arises from the endothelium of the lymphatics
    • Angiosarcoma - arises from the endothelium of blood vessels
  • Lymphocyte derived:
    • ​Mycosis fungoides - lymphoma that is specific to the skin
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3
Q

Name causes of skin cancer.

A
  • Genetic Syndromes
    • ​Gorlin’s Syndrome
      • ​Autosomal dominant condition where the individual has a defect in the PTCH gene
      • They have a germline mutation in this gene so only require one more mutation to develop BCC
      • RESULT: these patients have multiple BCCs throughout their lives.
    • Xeroderma pigmentosum
      • Rare condition caused by a mutation in a gene involved in DNA repair
      • Nucleotide excision repair is faulty in these patients, so they go on to develop multiple skin cancers
  • Viral Infections
    • ​HHV8 (human herpes virus 8) in Kaposi’s Sarcoma
    • HPV in SCC
  • UV light
    • ​BCC (been rising)
    • SCC
    • Malignant Melanoma (rising in white population)
  • Immunosuppression
    • ​Drugs e.g. azathioprine, cyclosporin
    • HIV
    • Old age
    • Leukaemia
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4
Q

Describe the types of UV light and their relevance in cancer.

A
  • UVC doesn’t penetrate the stratosphere so isn’t relevant to us on the earth surface
  • UVB will reach sea level
  • UVA will reach dead sea level
  • UVB is more significant for skin cancer development but the dose of UVB that reaches the earth surface is much lower than UVA
  • UVA also has an effect on skin cancer development but to a much lesser extent than UVB
  • UVA is the major cause of skin ageing
  • UVA is used therapeutically to treat psoriasis with PUVA therapy
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5
Q

Explain the effect of UVB and UVA.

A
  • UVB directly induces abnormalities in DNA e.g. mutations
  • UVB induces the formation of photoproducts(mutations) Particularly affects the pyrimidines(cytosine and thymine) - causes cross-linking
    • Cyclobutane pyrimidine dimers (e.g. T=T, T=C and C=C)
    • 6-4 pyrimidine pyrimidine photoproducts
  • These are usually repaired quickly by nucleotide excision repair
  • UVA can also promote skin carcinogenesis:
    • 100 times more penetrative to the Earth’s surface.
    • Major cause of skin ageing
    • Contributes to skin carcinogenesis
    • Forming cyclobutane pyrimidine dimers but less effectively than UVB
    • It also generated free radicals, which can damage DNA and the cell membrane
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6
Q

What is the link between UV and skin damage?

A
  • UV damage to DNA leads to mutations in specific genes:
    • Cell division
    • DNA repair
    • Cell cycle arrest
  • Photoproducts are normally removed by a process called nucleotide excision repair
  • Xeroderma pigmentosum - genetic condition with defective nucleotide excision repair
    • When DNA is not being repaired properly, patients tend to develop cancer at a very young age and at a high frequency
    • They will develop BCCs, SCCs and melanomas
    • They are also photosensitive and their skin gets very dry
    • They sometimes also have ocular and neurological problems
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7
Q

What happens in a sun burn?

A
  • UV leads to keratinocyte apoptosis
  • ‘Sun burn’ cells are apoptotic cells in UV overexposed skin
  • Apoptosis removes UV damaged cells in the skin which might otherwise become cancer cells
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8
Q

Explain the immunomodulatory effects of UV light.

A
  • UVA and UVB affect the expression of genes involved in skin immunity
    • It depletes Langerhans cells in the epidermis
  • This causes reduction immunocompetence and immunosurveillance
  • This is the basis of using UV phototherapy to treat psoriasis - it immunocompromises the skin to the inflammatory condition gets better
  • However, this does further increase the cancer causing potential of sun exposure
  • Mechanism by which UV therapy increases the risk of skin cancer:
    • UV can act on keratinocytes and cause DNA damage that could lead to it becoming malignant cell
    • If the Langerhans cells are working properly, they will induce an immune response and cause cell death in the damaged cell
    • If the Langerhans cell have been depleted as a result of UV phototherapy, they will be unable to knock out the damaged cells and this could promote the development of cancer
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9
Q

Describe the Fitzpatrick Phototypes.

A
  1. Always burns, never tans
  2. Usually burns, sometimes tans
  3. Sometimes burns, usually tans
  4. Never burns, always tans
  5. Moderate constitutive pigmentation - Asian
  6. Marked constitutive pigmentation - Afrocaribean
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10
Q

What is the function of melanocytes?

A
  • Melanocytes produce melanin in the basal layer of the epidermis
  • Skin colour depends on the amount and type of melanin produced, NOT the density of melanocytes (which is fairly constant)
  • Melanocytes are dendritic and they interdigitate with about 30 or so keratinocytes
  • They produce melanin, which is packed into melanosomes
  • The melanosomes pass down the processes and are taken up by the keratinocytes
  • The keratinocytes put the melanosomes around their nucleus, which protects it from UV damage
  • In paler skin types, under the influence of UV light, the keratinocytes will make melanocyte stimulating hormone, which will have a paracrine effect on the melanocytes to make more melanin
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11
Q

What are the types of melanin?

A
  • TWO types of melanin are formed:
    • Eumelanin- brown/black
    • Phaeomelanin- yellowish or reddish-brown
  • Melanin is formed from tyrosine via the action of many enzymes
  • Red heads have more phaeomelanin- this doesn’t effectively protect against sun exposure
  • The relative amounts of melanin produced is regulated by the MCR1 gene
  • There are >20 gene polymorphisms in this gene
  • The polymorphism determines the eumelanin: phaeomelanin produced and the quantities
  • Melanin dictates skin sensitivity to UV damage
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12
Q

Describe melignant melanomas.

A
  • Malignant tumour of melanocytes
  • Melanocytes become abnormal and have atypical cells and atypical architecture
  • It can be caused by:
    • UV exposure
    • Genetic factors
  • Risk of metastasis
  • This is the type of skin cancer with the highest mortality
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13
Q

Describe lentigo maligna (melanoma in situ)

A
  • Proliferation of malignant melanocytes within the epidermis
  • Normally, the melanocytes are found along the basal layer but here they are distributed throughout the epidermis
  • This has no risk of metastasis at this stage (as it hasn’t reached the basement
  • PICTURE: This is considered a premelanoma state
    • They normally have an irregular shape and irregular borders with light and dark brown colours
    • Usually > 2.0 cm
  • Sometimes you can have a large area of lentigo maligna and then you can develop an area within it that becomes invasive - this is lentigo maligna melanoma
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14
Q

Describe superficial spreading malignant melanomas.

A
  • Lateral proliferation of malignant melanocytes
  • They invade the basement membrane
  • It is invasive and it grows outwards
  • This has a risk of metastasis because the melanoma is below the basement membrane
  • Diagnosis of superficial spreading malignant melanoma:
  • ABCDE
    • Asymmetry
    • Border irregularity
    • Colour variation (dark brown-black)
    • Diameter >0.7 mm and increasing
    • Erythema
  • PICTURE:
    • Pale area in the middle - area of regression
    • The tumour has disappeared either because it has burned itself out or the immune system has got rid of it - usually associated with a higher risk of metastasis.
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15
Q

Describe nodular malignant melanomas.

A
  • VERTICAL proliferation of malignant melanocytes
  • There is no previous horizontal growth
  • As it is growing downwards, there is a high risk of metastasis
  • These can originate from pre-existing moles or they can originate de novo
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16
Q

Describe Nodular melanoma arising within a superficial spreading malignant melanoma.

A
  • This is a downward proliferation of malignant melanocytes that is following previous horizontal growth
  • If there is a nodule growing within an irregular plaque, the prognosis will become WORSE
  • Sometimes these melanomas have areas of erythema
  • This is usually when the tumour has lost the ability to produce melanin so instead it begins to look erythematous
17
Q

Describe the picture.

A
  • Acral Lentiginous Melanoma
  • These are the melanomas that occur on the palms and soles
  • These might occur in dark skin people
18
Q

Describe the picture.

A

Amelanotic Melanoma

Sometimes melanomas don’t produce pigments so it appears pink

This has also metastasised to the lymph nodes (arrow)

19
Q

Summarise the types of malignant melanomas

A
  • Superficial Spreading
  • Nodular
  • Lentigo Maligna Melanoma
  • Acral Lentiginous
  • Amelanotic
  • Simplified melanoma recognition:
    • Asymmetry
    • Border
    • Colour
    • Diameter
20
Q

Describe the prognosis of melanoma.

A
  • Prognosis of melanoma is determined using Breslow Thickness
  • This is the thickness of the tumour from top to bottom, measured in milimetres
  • < 1 mm= superficial tumour
  • > 1 mm= intermediate or deep tumour
  • This will determine how likely the tumour is to metastasise and cause death
21
Q

What are the risk factors for the development of melanoma

A
22
Q

Describe the picture.

A
  • Keratoacanthoma
  • This is thought to be either a benign lesion or a benign version of an SCC
  • It grows rapidly but then it disappears
  • It has NO risk of metastasis
23
Q

Describe squamous cell carcinomas (Causes, risk, areas affected)

A
  • Malignant tumour of keratinocytes
  • Caused by:
    • UV exposure
    • HPV
    • Immunosuppression
    • May occur in scars or scarring processes
  • Risk of metastasis- but not as high as in melanoma
  • Immunosuppression is significant - people who have organ transplants are at high risk of getting SCCs
  • PICTURE:
    • This is a well differentiated SCC because it has a keratin horn- it shows that the keratinocytes still have the ability to produce keratin
  • Women tend to get SCCs on the lower legs - presumably because they get more sun exposure there
  • Often occurs on the lips – smoking is a risk factor
  • On ears in men – specially on sticking out ears
  • Also on genital regions
24
Q

Describe Basal cell carcinomas (causes, risks, areas affected)

A
  • Malignant tumour arising from the basal layer of the epidermis
  • Causes:
    • Sun exposure
    • Genetics
  • These are slow growing
  • They invade tissues but they do not metastasise
  • They are common on the face
  • PICTURE:
    • It is pearly, it has a rolled edge and there is telangiectasia (a localised collection of distended blood capillary vessels)
    • A key feature of BCC is arborising telangiectasia - looks like branches of a tree
25
Q

Describe the picture

A
  • Mycosis Fungoides
  • This is a cutaneous T cell lymphoma- it specifically affects the skin
  • The red patches make it look like psoriasis but if a biopsy is taken, atypical lymphocytes can be seen
  • It is usually slowly progressiveover decades
  • Light treatment, chemotherapy or radiotherapy = treatment
26
Q

Describe the picture

A
  • Kaposi’s Sarcoma
  • HIV and HHV8 associated
  • It is a tumour of the endothelium of the LYMPHATICS
27
Q

describe the picture.

A
  • Epidermodysplasia Verruciformis
  • Rare autosomal recessive condition that predisposes to HPV induced warts and SCCs
  • The pale bits (left image) are the abnormal areas - they will be rough and warty
  • Sometimes these patients can develop abnormal warts on their hands and feet that become extremely keratotic (right image)

Cancer (15 decks)

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