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Canc > Cancer 15: Skin cancer > Flashcards

Cancer 15: Skin cancer Flashcards

(73 cards)

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1
Q

Outline the microanatomy of the skin

A

Epidermis:

  • stratum corenum
  • stratum granulosum
  • stratum spinosum
  • stratum basale

Dermis (contains glands and hair follices)

Hypodermis (blood vessels)

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2
Q

Where do most cancers aruse from in the skin

A

Epidermis

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3
Q

Which cells are present in the epidermis

A

Keratinoytes… prolferate and move up the epidermis until they become the stratum corneum- so stem cells in stratum basale

Melanocytes

Merkel cells (mecahnoceptors detecting light touch)

Langerhans cells (dendritic cells- prominent in stratum spinosum)

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4
Q

Outline the cancers derived from keratinocytes

A

Non-melanocyte skin cancer:

basal cell carcinoma
squamous cell carcinoma

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5
Q

Outline melanocyte derived cancer

A

Malignant melanoma

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6
Q

List vasculature derived tumours

A

Kaposi’s sarcoma, angiosarcoma

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7
Q

List a type of lymphocyte derived cancer

A

Mycosis fungoides

NOT fungal infection (a skin lymphoma)

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8
Q

Cause of skin cancer

A

Accumulation of genetic mutations

leads to
uncontrolled cell proliferation

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9
Q

Examples of causes of skin cancer

A

Genetic syndromes
Viral infection
UV light
Immunosuppression

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10
Q

Examples of genetic syndromes leading to skin cancer

A

Gorlin’s syndrome (Basal cell)

xeroderma pigmentosum (DNA repair system malfunction)

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11
Q

Examples of viruses leading to skin cancer

A

HHV8 in Kaposi’s sarcoma

HPV in SCC

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12
Q

Examples of UV light causing skin cancer

A

BCC, SCC, malignant melanoma

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13
Q

Examples of immnosuppression causing skin cancer

A

drugs, HIV, old age, leukaemia

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14
Q

Look at malignant melaona

Compare to squamous cell

A

Malignant melanoma (streaks/different coloured areas)

Swuamous cell pearly and veins on surface

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15
Q

What skin type is malignant melanoma most common in

A

White people and increasing

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16
Q

What is happenng t BCC

A

Increasing

Common on face
Has increased since people stopped wearing hats

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17
Q

Which UV rays are we exposed to

A

UVA and UVB

UVA most penetrative can go down to sea level

UVB most important for for skin cancer

UVC filtered out by the ozone layer

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18
Q

What is the spectrum of visible light

A

400-700

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19
Q

Why is UV 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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20
Q

Why are UVB and UVA important

A

UVB:
most important wavelength in skin carcinogenesis

UVA:major cause of skin ageing
contributes to skin carcinogenesis
used therapeutically in PUVA therapy

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21
Q

How does UVB usually affect DNA

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

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22
Q

Why is UVB normally not a problem for DNA

A

The damage is usually repaired quickly by nucleotide excision repair

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23
Q

Outline affect of UVA on skin carcinogenesis

A

Also promotes skin carcinogenesis

DNA forming cyclobutane butane pyrimidine dimers but less efficiently than UVB

free radicals which damage DNA and cell membrane (including langerhans)

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24
Q

How can the UV damage to DNA lead to cancer i.e. which specific genes

A

UV damage to DNA leads to mutations in specific genes

cell division
DNA repair
cell cycle arrest

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25
How can the UV damage to DNA lead to cancer
UV damage to DNA leads to mutations in specific genes cell division DNA repair cell cycle arrest
26
Photoproducts are removed by what. When is this a problem
Photoproducts are removed by a process called Nucleotide Excision Repair Xeroderma pigmentosum =Genetic condition with defective Nucleotide Excision Repair
27
Mutations causing skin cancer more generally (i,e not just in UV)
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)
28
What happens in sun burn
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
29
Outline photocarcinogenesis
Usually skin cell with DNA damage due to UV rays will have DNA repaired, so it dosn't develop cancer phenotype If the damage is too severe it will apoptose, in a p53 mutation, there is inactivated wild type Skin cancer
30
As well as directly inducing DNA mutations, what other effect of UV light in the skin
IMMUNOMODULATORY
31
Outline the immunomodulatory effect of UV light
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
32
What is the use of UV light in psoriasis
Down regulating langerhans cells reduces skin immunocompetence and immunosurveilance (UV A and UVB) And this will reduce the inflammatory response
33
Outline photocarcinogenesis with regard to UV
So we had that UV induces mutations in key regions such as p53 and the other types of genes (cell division, DNA repair , cell cycle arrest) But normally and immune reponse would be mounted against this skin cancer But if there is UV damage to langer hans cells this will not happen so no cell death
34
What determines the host response to UV
Phototype Fitzpatrick (1-6) depends how dark you are
35
What determiens skin colour
Amount of melanin and the type of melanin
36
How is melanin produced
By melanocute in the stratum basale (dendritic cell) ..... FINISH
37
What happens in th eevent of sun exposure
Keratinocytes release MSH Stimuates melanocytes to release melanin from melanosomes wich then are released from dendrtic process of the melanocyte
38
T/F there is difference in the meanocyte number between light and dark skinned people
F
39
What are the two types of melanin
Eumelanin – brown or black Phaeomelanin – yellowish or reddish brown
40
What affects the expression of eumelanin or phaeomelanin
MCR1 gene >20 gene polymorphisms Variation in eumelanin : phaeomelanin produced Explains different hair colour and skin types
41
How is melanin produced
Melanin is formed from tryosine via a series of enzymes
42
what dictates skin sensitivity to UV damage
MELANIN
43
Outline malignant melanoma
Melanocytes become abnormal Atypical cells and architecture by UV exposure Genetic factors Risk of metastasis
44
What is lentigo maligna
Melanoma in situ Proliferation of malignant melanocytes within the epidermis No risk of metastasis Usually flat and dark
45
What is it called if lengigo is malignant FNISH
Lentigo maligna melanoma
46
What is a superficial spreading malignant melaonma
Lateral proliferation of malignant melanocytes Invade basement membrane Risk of metastasis
47
What is ABCDE rule
``` Asymmetry Border irregular Colour variation (dark brown-black) Diameter >0.7mm and increasing Erythema ```
48
Why can there be a white patch in the middle of the lesion.... good or bad
Immune response has been mounted against it Good bcause there is a immune response Bad because it might mean the melanoma has gone deeper
49
What is a nodular melanoma
Vertical proliferation of malignant melanocytes (no previous horizontal growth) Risk of metastasis
50
When is prognosis worse with malignant melaonma
Nodule developing within irregular plaque (i,e, nodular within superifical spreadng) Prognosis will become WORSE
51
Why could you get erythema in malingnat melanoma
......
52
What is acral lentiginous melanoma
Acral lentiginous melanoma (ALM) is a specific type of melanoma that appears on the palms of the hands, the soles of the feet, or under the nails
53
What is amelanotic melanoma
Amelanotic melanoma When the migantn cells lose ability to make melanin
54
Types of malignant melanoma
``` Superficial spreading Nodular Lentigo maligna melanoma Acral lentiginous Amelanotic ```
55
What is breslow thickness
How far down the melanoma goes affects the prognosis
56
Important risk factors for melanoma developent
``` Family hisotry Personal hostry Skin type I,II Sunburns during childhood Do they have lots of moles (atypical nervus syndrome) ```
57
What is keratocanthoma
Lumps which grow quickly and then fall off Benign
58
What could keratocanthoma look like SCC
.....
59
When is SCC worse
When worse differentiated (when the lump doesn't have a core) Having a horn or core is good
60
What us SCC
Malignant tumour of keratinocytes
61
Case of SCC
UV exposure HPV Immunosuppression May occur in scars or scarring processes
62
High risk site for SCC
Ears for men (not covered by hair) Lips Genital regions
63
What is a commons site of SCC for women
Legs (low risk malingancy)
64
What SCC is worse
If just a lump not horns or a core
65
What is basal cell carcinoma and cause, compare to SCC
Malignant tumour arising from basal layer of epidermis Sun exposure and genetics BCC invades tissue but DOES NOT METASTASISE, relatively slow growing
66
Why are basal cell carcinoma not havig horns or a core
Don't make keratin so not rough or horny
67
Where do basal cell carcinomas commonly occur
On the eye (incluidng eye lashes)
68
Outline the vascularitsation on basal cell carcinoma
Looks like a tree Arbarising telangiotectasia
69
T/f BCC can incade
Invades tissue, but does not metastasise Slow growing
70
Where are BCC common
Common on face
71
What will be seen under microscpe in mycosis fungoides
Lymphocytes in the dermis and epidermis.... CHECK slow progressive disease
72
What kaposis sarcoma
HIV and HHV8 associated Spread to gut liver and lung
73
What is epidermodysplasia veruciformis
Rare autosomal recessive condition | predisposition to HPV induced warts and SCCs

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