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Year 2 - MCD - Cancer > 15: Skin Cancer (27.02.2020) > Flashcards

15: Skin Cancer (27.02.2020) Flashcards

1
Q

Microanatomy of the skin

A

3 main layers:

  • epidermis
  • dermis (contains hair follicles)
  • hypodermis (contains fat, sebaceous glands)
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2
Q

Cells in the epidermis

A
  • keratinocytes
  • melanocytes
  • langerhaans cells (dendritic cells)
  • merkel cells (oval-shaped mechanoreceptors essential for light touch sensation)
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3
Q

Which cells are mainly affected in skin cancer?

A

keratinocytes

melanocytes

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4
Q

Examples of causes of skin cancer

A

Genetic syndromes

  • Gorlin’s syndrome
  • xeroderma pigmentosum (genetic defect in DNA repair, particularly after UV radiation)

Viral infections

  • HHV8 (human herpes) in Kaposi’s sarcoma
  • HPV in SCC (particularly in immunosuppressed patients)

UV light

  • BCC, SCC, malignant melanoma
  • main cause of skin cancer

Immunosuppression
- drugs, HIV, old age *by itself is an immunosuppressive condition), leukaemia

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5
Q

Keratinocyte derived skin cancer

A
  • basal cell carcinoma
  • squamous cell carcinoma
  • aka Non melanoma skin cancer (NMSC)
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6
Q

Melanocyte derived skin cancer

A

Malignant melanoma

or lentigo maligna = melanoma in situ / lentigo maligna melanoma

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7
Q

Vasculature derived skin cancer

A
  • Kaposi’s sarcoma

- angiosarcoma

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8
Q

Lymphocyte derived skin cancer

A
  • Mycosis fungoides
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9
Q

features of basal cell carcinoma

A
  • pinky greyish colour
  • small capillary blood vessles (looks a bit like their branching)
  • glistens/glows
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10
Q

Incidence of BSS

A

increasing

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11
Q

Different types of UV light

A

Sl 13 + 14

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12
Q

Incidence of BCC

A

increasing

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13
Q

Different types of UV light

A

UVC

  • wavelength 100-280 nm
  • stopped in the ozone layer/stratosphere

UVB

  • wavelength 280-310 nm
  • does not penetrate sea level

UVA

  • wavelength 310-00 nm
  • penetrates sea level, reaches Dead Sea level
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14
Q

Different types of UV light - what are their effects on the skin?

A

UVB
- most important wavelength in skin carcinogenesis

UVA

  • 100 times more UVA penetrates to the Earth’s surface
  • major cause of skin ageing
  • contributes to skin carcinogenesis
  • used therapeutically in PUVA therapy
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15
Q

UVB light

A
  • UVB directly induces abnormalities in DNA eg mutations

UVB induces photoproducts (mutations)
Affects pyrimidines ie Cytosine (C) and Thymine (T) bases
cyclobutane pyrimidine dimers eg T=T, T=C, C=C
6-4 pyrimidine pyrimidone photoproducts

Usually repaired quickly by nucleotide excision repair

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16
Q

UVB light

A
  • UVB directly induces abnormalities in DNA eg mutations

UVB induces photoproducts (mutations)

  • Affects pyrimidines ie Cytosine (C) and Thymine (T) bases
  • cyclobutane pyrimidine dimers eg T=T, T=C, C=C
  • 6-4 pyrimidine pyrimidone photoproducts
  • Usually repaired quickly by nucleotide excision repair
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17
Q

UV induced skin carcinogenesis

A

UV damage to DNA leads to mutations in specific genes

  • cell division
  • DNA repair
  • cell cycle arrest
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18
Q

UV induced skin carcinogenesis

A

UV damage to DNA leads to mutations in specific genes

  • cell division
  • DNA repair
  • cell cycle arrest
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19
Q

Repair of UV induced DNA damage

A

Photoproducts are removed by a process called Nucleotide Excision Repair

Xeroderma pigmentosum

  • Genetic condition with defective Nucleotide Excision Repair
  • develop cancer at a very young age, don’t need much exposure.
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20
Q

Mutations that cause cancer

A
  1. Mutations that stimulate uncontrolled cell proliferation
    - Eg abolishing control of the normal cell cycle (p53 gene)
  2. Mutations that alter responses to growth stimulating / repressing factors
  3. Mutations that inhibit programmed cell death (apoptosis)
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21
Q

Xeroderma pigmentosum

A

Mutation in a gene repair gene.

Causes very high susceptibility to skin cancer because UV induced mistakes (i.e. base dimers) cannot be fixed.

Treatment:

  • remove all skin cancer (lesions)
  • very strict protective measures
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22
Q

Sun burn

A
  • too much sun exposure
  • skin goes very red
  • develop keratinocytes that apoptose

UV leads to keratinocyte cell 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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23
Q

Photocarcinogenesis

A

UV light causes DNA damage

  • > a) p53 mutaation, inactivated wild type -> skin cancer
  • > b) DNA damage
    - repair of DNA
    - damage too severe, unable to repair -> cell death - apoptosis
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24
Q

Immunomodulatory effects of UV Light

A
  • UVA and UVB effect the expression of genes involved in skin immunity
  • Depletes Langerhans cells in the epidermis
  • Reduced skin immunocompetence and immunosurveillance
  • Basis for UV phototherapy for eg psoriasis
  • Further increases the cancer causing potential of sun exposure
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25
Q

What does Host Response to UV light depend on?

A

Determined by genetic influences especially skin phototype

-> Fitzpatrick phototypes

26
Q

Fitzpatrick Phototypes

A

1 - Always burns never tans

II - Usually burns, sometimes tans

III - Sometimes burns, usually tans

IV - Never burns, always tans

V - Moderate constitutive pigmentation - Asian

VI - Marked constitutive pigmentation - Afrocaribean

  • 1+2 are most susceptible to skin cancer
  • 3-6 tend not to get skin cancer.
27
Q

What is melanin?

A
  • Melanin pigmentation is responsible for skin colour
  • Produced by melanocytes within 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)
  • > in people with darker skin, melanocytes make more melanin
28
Q

How do melanocytes work?

A
  • sit on the basement membrane in the epidermis
  • dendritic appearance
  • comunicate with keratinocytes
  • after UV exposure keratinocytes have paracrine effects: secrete MSH which will affect the adjacent melanocyte and make it produce more malenin
  • melanin will go down dendritic processes and go to the keratinocyte
  • keratinocytes take up the melanin and places it around the nucleus, protecting it from UC exposure
  • this is what happens in tanning.

Generally 1 melanocute for every 5 keratinocytes, dependant on the skin type.

29
Q

What are the different types of melanin?

A
  • Eumelanin – brown or black
  • Phaeomelanin – yellowish or reddish brown
  • Melanin is formed from tryosine via a series of enzymes
  • in skin types 2 and 3 there is a ratio between the 2 melanin types.
  • MCR1 gene
    >20 gene polymorphisms
    Variation in eumelanin : phaeomelanin produced
    Explains different hair colour and skin types

Melanin dictates skin sensitivity to UV damage

30
Q

MCR1 gene

A

> 20 gene polymorphisms
Variation in eumelanin : phaeomelanin produced
Explains different hair colour and skin types

31
Q

Malignant melanoma

A
  • most dangerous kin cancer
  • Malignant tumour of melanocytes
  • Melanocytes become abnormal
  • Atypical cells and architecture

Caused

  • by UV exposure
  • Genetic factors

Risk of metastasis

32
Q

Lentigo maligna

A
  • (melanoma in situ)
  • one of the hallmarks of melanoma:
  • Proliferation of malignant melanocytes within the epidermis (confined to the epidermis)
  • No risk of metastasis
  • quite common in elderly patients
  • flat, dark irregular patches.
  • Irregular shape
    Light & dark brown colours
    Size usually >2.0 cm
  • treatment can be excision
33
Q

Lentigo maligna melanoma vs lentigo maligna vs. superficial spreading MM

A

Lentigo maligna melanoma is invasive, lentigo maligna is not.

  • lentigo maligna melanoma is derived from lentigo maligna, SSMM is not.
34
Q

How does MM spread?

A
  • Lateral proliferation of malignant melanocytes
  • Invade basement membrane
  • Risk of metastasis
35
Q

Diagnosis of superficial spreading malignant melanoma

A

ABCD rule

  • Asymmetry
  • Border irregular
  • Colour variation (dark brown-black)
  • Diameter >0.7mm and increasing
  • Erythema
36
Q

What does it mean if a lesion loses pigmentation?

A
  • If a lesion seems to have lost pigmentation -> regression -> immune system has fought it off
  • You think this is a good sign, however, the lesion may have spread already.
37
Q

Regression of melanoma

A
  • Regression describes an area where it appears there had been melanoma cells, but these have been destroyed by the immune system and replaced with inflammation or scar tissue.
  • you would think that it is a good sign, however, the cancer may have already spread? find out more here
38
Q

Nodular malignant melanoma

A
  • Vertical proliferation of malignant melanocytes
    (no previous horizontal growth)
  • Risk of metastasis
39
Q

Nodular melanoma arising within a superficial spreading melanoma

A
  • Downward proliferation of malignant melanocytes
    FOLLOWING PREVOIUS HORIZONTAL GROWTH (vs. nodular melanoma)
  • Nodule developing within irregular plaque
  • Prognosis will become WORSE
40
Q

Acral lentiginous melanoma

A
  • specific type of melanoma that appears on the palms of the hands, the soles of the feet, or under the nails.
  • these are most common skin cancer in dark skin types
41
Q

Amelanotic melanoma

A
  • the malignant cells have little or no pigment (truly amelanotic (no pigment at all) is quite rare)
  • many hypopigmented lesions are labelled as amelanotic
42
Q

List 5 different types of malignant melanomas

A 
Superficial spreading
Nodular
Lentigo maligna melanoma
Acral lentiginous
Amelanotic
43
Q

Prognosis of melanoma

A

Breslow thickness

-> measurement from granular layer to the bottom of the tumour.

44
Q

Risk Factors for the development of melanoma

A
  • UV irridation
  • sunburns during childhood
  • skin types 1 and 2
  • more the burin got skin then sunlight exposure in general (intermittent burning exposure in unacclimatised fair skin)
  • personal history of melanoma
  • FH of dysplastic nevi or melanoma
  • atypical/dysplastic nevus synrome
45
Q

Keratoacanthoma

A
  • skin lesion that erupts in sun-damaged skin, rather like a little volcano.
  • grows for a few months; then it may shrink and resolve by itself
  • considered to be a variant of the keratinocyte or non-melanoma skin cancer, (SCC).
  • As it cannot be clinically reliably distinguished from more severe forms of skin cancer, keratoacanthomas are usually treated surgically.
  • generally excisable
46
Q

SCC

A
  • Malignant tumour of keratinocytes (e.g. horn. growing out of the lump)
  • Caused by
    UV exposure
    HPV
    Immunosuppression
    May occur in scars or scarring processes
  • may appear on the lips, ears, legs (in women mainly because of sun exposure)
  • Risk of metastasis (but much much less than melanoma, for a poorly differentiated one perhaps 10%)
  • makes keratin if well differentiated
47
Q

How does a well differentiated SCC look?

A
  • e.g. horn of keratin growing out of the lump
48
Q

BCC

A

= basal cell carcinoma

  • Malignant tumour arising from basal layer of epidermis
  • Caused by
    sun exposure
    Genetics
  • Slow growing
  • Invades tissue, but does NOT metastasise
  • Common on face but can occur elsewhere.
  • can be flat (superficial BSS), some have edge?
  • can appear on eyelid, lost eyelashes on that spot (loss of eyelashes is usually a tumour)
  • blood vessles with small branches like a tree (arborising)
49
Q

vascular feature of BCC

A

arborising (branching like trees) small blood vessles

50
Q

What are some rather rare types of SC?

A
  • Mycosis fungoides

- Kaposi’s sarcoma

51
Q

Mycosis fungoides

A
  • type of cutaneous or skin lymphoma
  • slowly progressing disease (can take decades to progress)
  • A sign of mycosis fungoides is a red rash on the skin.
  • can be controlled through various waays
52
Q

Kaposi’s sarcoma

A
  • associated with HIV and HHV8 infections
  • purplish
  • orientation of the plaque often goes along ht lines of the skin
  • sometimes on palate
  • treatment by
    • treating the HIV
    • chemo/radiotherapy
53
Q

Epidermodysplasia veruciformis

A
  • Rare autosomal recessive condition

- predisposition to HPV induced warts and SCCs

54
Q

Summary

A
  • Incidence of Melanoma and NMSC increasing in Western Countries
  • Mainly pale skin people effected
  • UV exposure a significant risk factor
  • UVB most important for carcinogenesis – mutations in key genes
  • Other factors involved in skin cancer development
    • HPV infection
    • immunosuppression
    • age
    • genetics eg MCR1 polymorphisms
  • Treatment is still mainly surgical
55
Q

What are the layers of the epidermis

A

(dermis)

  • stratum basale
  • stratum spinous
  • stratum granulosum
  • stratum lucidum
  • stratum cornea (dead keratinocytes, those on the surface flake off)
56
Q

Gorlin’s syndrome

A
  • Gorlin syndrome, also known as nevoid basal cell carcinoma syndrome, is a condition that affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumors.
  • the type of cancer diagnosed most often is BCC, which is the most common form of skin cancer. - Individuals with Gorlin syndrome typically begin to develop basal cell carcinomas during adolescence or early adulthood.
  • These cancers occur most often on the face, chest, and back.
  • The number of basal cell carcinomas that develop during a person’s lifetime varies among affected individuals.
  • Some people with Gorlin syndrome never develop any basal cell carcinomas, while others may develop thousands of these cancers.
57
Q

p53

A
  • tumour suppressor gene
  • regulates the cell cycle
  • important in suppressing cancer in multicellular organisms
58
Q

How do numbers of melanocytes differ in individuals in people with different skin types?

A
  • the numbers fo melanocytes don’t really differ

- what differs is how much melanin they produce.

59
Q

How is melanin formed? (chemicals)

A

Tyrosine -> DOPA -> Dopaquinone -> Eumelanin or Pheomelanin -> Melanin

60
Q

Subcategories of BCC

A
  • superficial BCC

- nodular BCC

Year 2 - MCD - Cancer (15 decks)

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