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cancer > Cancer as a disease: Skin Cancer > Flashcards

Cancer as a disease: Skin Cancer Flashcards

1
Q

What are the 3 main layers of the skin

A

§ There are 3 main layers to the skin – epidermis, dermis and hypodermis (fat layer).

BM separates epidermis from dermis
Muscles found below hypodermis.

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2
Q

Which layer of the skin do most skin cancers arise from

A

The epidermis

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3
Q

What are the four cell types that make up the epidermis

A

Keratinocytes
Melanocytes
Merkel cells
Dendritic cells (e.g Langerhans cells).

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4
Q

Summarise the different layers of the epidermis

A

§ The epidermis is comprised of (superficial à deep):

o Stratum corneum – dead keratinocytes- where they then shed off.

o Stratum lucidum.

o Stratum granulosum.

o Stratum spinosum – dendritic cells.

o Stratum basale – melanocytes, merkel cells, dividing cells - will also see tactile cells (with sensory nerve endings going into the dermis).

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5
Q

Which epidermis cell types are most commonly inflicted in skin cancers

A

Keratinocytes- mature and differentiate as they go move up form the stratum basale to the stratum corneum- so exposed to UV-Radiation.
Melanocytes- also exposed to UV radiation (they sit on the BM between the epidermis and the dermis).

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6
Q

Describe the keratonicoyte derived skin cancers

A

Keratinocyte derived
eg basal cell carcinoma (most common)
squamous cell carcinoma
aka Non melanoma skin cancer (NMSC)

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7
Q

Describe the melanocyte derived skin cancers

A

Melanocyte derived

eg Malignant melanoma

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8
Q

Describe some other types of skin cancer that may arise

A

Vasculature derived
eg Kaposi’s sarcoma (common in patient’s with AIDS)., angiosarcoma

Lymphocyte derived
eg Mycosis fungoides

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9
Q

Ultimately, what is the cause of skin cancer

A

Accumulation of genetic mutations —– uncontrolled cell proliferation

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10
Q

Describe the genetic syndromes that can lead to breast cancer

A

Inherited (genetic) predisposition to developing cancers

Gorlin’s syndrome- tendency to develop BCC- due to defects in the PTCH1 gene

xeroderma pigmentosum- genetic defect in DNA repair- so can't repair DNA damage by UV-Radiation- – increased risk of BCC, SCC and malignant melanoma
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11
Q

Describe how viral infections can cause skin cancers

A

Viral infections
HHV8 in Kaposi’s sarcoma
HPV in SCC- particuarly in the immunosuppressed.

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12
Q

Describe how UV light can cause skin cancers

A

Most significant cause- most common cause in patients

BCC, SCC, malignant melanoma

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13
Q

Describe how immunosuppression can cause skin cancers

A

drugs (immunosuppressants- organ transplants)., HIV, old age, leukaemia

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14
Q

What tool can be used to look at skin lesions more effectively

A

A dermatoscope (essentially a torch with a magnifying glass).

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15
Q

How will a lesion of malignant melanoma look under a dermatoscope

A

Irregular borders
Assymetrical
Blue/darkish in the middle/

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16
Q

Describe the epidemiology of malignant melanoma

A

o Incidence is highest in white people and lowest in blacks (increasing in whites).

o Incidence is highest in the south-west of England.

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17
Q

Describe the appearance of a skin lesion of basal cell carcinoma

A

§ Has a pearly appearance (pinky, reddish, greyish, glistens) and has dilated vessels (telangiectasia) on the surface

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18
Q

Describe the epidemiology of basal cell carcinoma

A

§ Epidemiology:

o Incidence is increasing in men and women – due to increasing ages and more exposure

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19
Q

What are the different types of UV radiation (from longest wavelength to the shortest)

A

UVA- 310-400nm
UVB- 280-310 nm
UVC- 100-280 nm

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20
Q

Describe how the sunlight is essential for life

A

Essential for photosynthesis (plants)
Infrared spectra provide warmth
Effect on human mood
Stimulates the production of vitamin D in the skin

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21
Q

Describe the difference in properties of the different types of UV radiation in terms of the depths that they penetrate

A

UV-C -stratosphere (ozone layer)
UV-B- sea level
UV-C- dead sea level

Longer wavelengths can penetrate more.

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22
Q

Which type of UV is most important in skin carcinogenesis

A

UVB

most important wavelength in skin carcinogenesis

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23
Q

Summarise the key properties of UVA

A

UVA
100 times more UVA penetrates to the Earth’s surface
major cause of skin ageing (penetrates to the deeper levels of the skin and effects collagen).
contributes to skin carcinogenesis (but UVB more important for skin carcinogenesis)
used therapeutically in PUVA therapy

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24
Q

How does UVB damage DNA

A

UVB directly induces abnormalities in DNA eg mutations

UVB induces photoproducts (mutations)
Affects pyrimidines ie Cytosine (C) and Thymine (T) bases- cross-linking between bases
The following photoproducts are formed:

cyclobutane pyrimidine dimers eg T=T, T=C, C=C
6-4 pyrimidine pyrimidone photoproducts

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25
Q

How is damage by UV radiation normally repaired

A

Usually repaired quickly by nucleotide excision repair

Nucleotides removed- then correct ones added with DNA polymerase.

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26
Q

Describe the carcinogenesis of UVA

A

Also promotes skin carcinogenesis

DNA forming cyclobutane butane pyrimidine dimers but less efficiently than UVB

free radicals which damage DNA and cell membrane

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27
Q

Ultimately, in which 3 gene types does UV radiation cause mutations in

A

UV damage to DNA leads to mutations in specific genes
cell division
DNA repair
cell cycle arrest

This leads to unregulated cell proliferation

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28
Q

Summarise the 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

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29
Q

What are the key features of xermoderma pigmentosum

A

Increased risk of BCCs, SCCs and melanoma
Photosensitivity and dry skin
Increased freckling
Skin cancers at early age- don’t need much sun exposure to overcome faulty DNA repair process

If suspected- genetically screen all future sibilings
Can be managed with sun avoidance

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30
Q

Summarise the key mutations that can lead to skin cancers

A

Mutations that stimulate uncontrolled cell proliferation
Eg abolishing control of the normal cell cycle (p53 gene)

Mutations that alter responses to growth stimulating / repressing factors

Mutations that inhibit programmed cell death (apoptosis)
- apoptosis normally occurs to get rid of cells with faulty DNA.

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31
Q

Outline a scheme for photocarcinogensis

A

UV light (B/A) penetrates into the cell
If this cell has a p53 mutation or an inactivated wild type- then this will lead to skin cancer.
However, in a normal cell, the damage will be repaired
However, sometimes, the damage can be so severe that the cell is unable to repair it- so it undergoes apoptosis.

32
Q

Summarise the dendritic cells of the skin

A

Found in the epidermis and the dermis

Called langerhans cells in the epidermis.

33
Q

Describe the 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

34
Q

Describe UV phototherapy for inflammatoery dermatoses such as Psoriasis

A

UVA or UVB used
Psoralen UVA/B PUVA/PUVB
Place patient in a light box- dampens down immune response and inflammation
But it will increase your risk of skin cancer.

35
Q

What happens to the keratinocytes in sun burn

A

The UV damage leads to keratinocyte apoptosis

The apoptotic cells in UV overexposed skin are called sun burn cells

36
Q

Describe the consequences of a depletion of langerhan cells

A

UV light damages cells and causes malignant transformation- Langerhans cells would normally recognise these cells and clear them in the immune response (cell death).
However, if the Langerhans cells have been damaged by UV light, this immune response is lost and you get skin cancer.

37
Q

Which system is used to categorise people based on their skin type and sensitivity to UV?

A

Fitzpatrick’s phototypes:

The host response to UV light is determined by genetic influences, especially skin phototype.

38
Q

State the Fitzpatrick phototypes

A

1 - Always burns never tans ( ginger)
II - Usually burns, sometimes tans (blond, blue eyes)
III - Sometimes burns, usually tans (brown eyes, olive skin)
IV - Never burns, always tans
V - Moderate constitutive pigmentation - Asian
VI - Marked constitutive pigmentation - Afrocaribean

1 and II more likely to get skin cancers both (non-melanomas and melanomas)

39
Q

What is the function of melanin and where is it made

A

Melanin pigmentation is responsible for skin colour

Produced by melanocytes within the basal layer of the epidermis

40
Q

What does a person’s skin colour depend on

A

Skin colour depends on the amount and type of melanin produced not the density of melanocytes (which is fairly constant)
Normally one melanocyte for every 5/6 keratinocytes along the basal layer of the epidermis.

41
Q

Describe the cross-talk between keratinocytes and melanocytes for melanin production

A

UV light reaching keratinocytes stimulates them to release Melanocyte Stimulating Hormone (MSH) which has a paracrine effect on the melanocytes (who’s digits come into contact with the keratinocytes). This results in the melanosome producing melanin- which travels up the spinous processes of the melanocyte and is taken into the keratinocyte by phagocytosing the tip of the melanocyte
The melanin then wraps around the nucleus to protect it.

42
Q

How can we stain for melanocytes and melanin

A

Melanocytes- black

Melanin- brown on H and E stain

43
Q

What happens to the melanin once it is produced by the melanocytes

A

It is packaged into melanosomes and it passes along the processes of the melanocytes and is taken up by the keratinocytes
The keratinocytes put the melanosomes around their nuclei, which protects the nuclei from DNA damage

44
Q

What are the two different types of melanin

A

Two types of melanin are formed:
Eumelanin – brown or black
Phaeomelanin – yellowish or reddish brown (fair haired people)
Melanin is formed from tryosine via a series of enzymes

45
Q

Which gene is responsible for the production of melanin

A

MCR1 gene
>20 gene polymorphisms
Variation in eumelanin : phaeomelanin produced (based on the polymorphism you have)
Explains different hair colour and skin types
Phototypes 2 and 3 will have a more mixed ration of eumelanin: phaeomelanin

46
Q

Ultimately, what does melanin dictate

A

Melanin dictates skin sensitivity to UV damage

47
Q

Outline the production of melanin

A

Produced by the Golgi and RER of melanocytes:

Tyrosine – DOPA (tyrosinase)
DOPA- dopaquinone (tyrosinase)

Dopaquinone — Eumelanin/Phaeomelanin

Eumelanin/Phaeomelanin – Melanin

Melanocyte secretory function- melanin packaged in melanosomes and transported to the keratinocytes

Keratinocytes take up melanin by melanosome transfer

48
Q

Which type of skin cancer is the most aggressive

A

Malignant melanomas- can invade and metastasise

49
Q

Summarise malignant melanoma

A

Malignant tumour of melanocytes
Melanocytes become abnormal
Atypical cells and architecture

Caused
by UV exposure
Genetic factors

Risk of metastasis

50
Q

Describe lentigo maligna (melanoma in situ)

A

Proliferation of malignant melanocytes within the epidermis (pagetoid spread- move upwards in the epidermis- normally confined to stratum basale)- abnormal melanocytes with abnormal architecture

No risk of metastasis (bound within epidermis)

Treatment is excision and replacement with skin graft.

51
Q

Describe the features of lentigo maligna

A

Irregular shape
Light & dark brown colours
Size usually >2.0 cm
Often occur in elderly patients- in sun-exposed areas (e.g face)

52
Q

What is it the name given to a large area of lentigo maligna that has a smaller area within it that has become invasive

A

Lentigo maligna melanoma

53
Q

Describe the features of a superficial spreading malignant melanoma

A

Lateral proliferation of malignant melanocytes (radial growth phase) pagetoid spread and vertical growth phase (downward growth into the dermis)

Invade basement membrane

Risk of metastasis

54
Q

Describe the ABCDE rule for the diagnosis of malignant melanomas (particularly superficially spreading MMs)

A

ABCD rule

Asymmetry
Border irregular
Colour variation (dark brown-black)
Diameter >0.7mm and increasing
Erythema
55
Q

What is it called when a pale area appears in the middle of a melanoma

A

Area of regression- melanoma been cleared by immune cells- bad- usually means melanoma has invaded deeper and metastasised

56
Q

Describe the features of a nodular malignant melanoma

A

Vertical proliferation of malignant melanocytes
(no previous horizontal growth)

Risk of metastasis

Can arise from a mole or can arise de novo

57
Q

Describe the features of a nodular melanoma arising with a superficial spreading melanoma

A

Downward proliferation of malignant melanocytes

Following previous horizontal growth

Nodule developing within irregular plaque

Prognosis will become WORSE

Lesion can lose pigmentation (not be fully pigmented)- erythmatous (redden areas)- amelanotic areas

58
Q

Describe Acral lentiginous melanoma

A

Melanomas on the soles and palms
May appear as flat pigmented plaques or pigmented lumps
These melanomas are most common in dark skin types

59
Q

What are non-pigmented melanomas called

A

Amelanotic melanoma

§ A melanoma where the cancer cells have lost the ability to create melanin.

60
Q

State the different types of malignant melanomas

A 
Superficial spreading
Nodular
Lentigo maligna melanoma
Acral lentiginous
Amelanotic
61
Q

Summarise the ABCD recognition of melanomas

A

Asymmetry
Border
Colour
Diameter

62
Q

What is the prognosis for melanoma based on

A

Note – Breslow thickness (measured from granular layer to bottom of tumour) states that the deeper the melanoma, the worse the prognosis.
>1- small
1-4- intermediate
>4- large

63
Q

What are the risk factors for the development of a melanoma

A 
Genetic markers (CDKN2A mutations)
Number (>50) and size (>5mm) of melanocytic nevi (moles)
Congenital nevi
Number of atypical nevi (>5)
High socioeconomic status
Equatorial latitudes
DNA repair defects (xermoderma pigmentosum)
Immunosuppression

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

64
Q

What is the most important risk factor for the development of melanoma

A

Sunburn in fair skinned people

65
Q

What is a keratocanthoma

A

It is either a benign lesion or a benign version of an SCC
It grows rapidly but then disappears
There is no risk of metastasis
Tends to involute on itself.

66
Q

Describe squamous cell carcinomas

A 
Malignant tumour of keratinocytes
Caused by 
	UV exposure
	HPV
	Immunosuppression
	May occur in scars or scarring processes
Risk of metastasis
67
Q

How can you tell whether an SCC is well differentiated

A

If the lesion has a keratin horn then it shows that the keratinocytes can still produce keratin and so they are well differentiated

68
Q

Where do SCCs commonly occur

A

Lips- smoking
Face
Ears- more protuberant and exposed to sun in Men
Lower legs- more exposed in women

69
Q

What are BCCs a tumour of

A

Keratinocytes

70
Q

Summarise basal cell carcinomas

A 
Malignant tumour arising from basal layer of epidermis (SCCs more superficial)
Caused 
	sun exposure
	Genetics
Slow growing
Invades tissue, but does not metastasise
Common on face
71
Q

Describe the appearance of BCCs

A

They are pearly, have a rolled edge and often have arborising telangiectasia
Can be nodular or superficial
Can occur on the eyelids- lose eyelashes- sign of destruction

72
Q

Describe mycosis fungoides

A

§ Not a fungal condition – miss-classified.
§ This is a lymphoma that affects the skin-resident T-lymphocytes (cutaneous T cell lymphoma)
§ This can be fatal and has internal organ involvement

Starts as a flat lesion, then plaque, then tumour- dissemination
Looks like psoriasis .

73
Q

Describe Kaposi’s sarcoma

A

HIV and HHV8 associated
§ A tumour of the endothelial cells of the lymphatics.
§ Can occur in non-HIV patients and can occur internally

Always caused by HHV8

74
Q

Describe epidermodysplasia veruciformis

A

Rare autosomal recessive condition
predisposition to HPV induced warts and SCCs
Can become incredibly keratotic

75
Q

What is the treatment for many skin cancers based on

A

Surgery

cancer (15 decks)

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