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cancer > clinical oncology 3: skin cancer > Flashcards

clinical oncology 3: skin cancer Flashcards

1
Q

epidemiology of skin cancer:

A
  • commonest cancer to affect man
  • incidence is rising
  • main aetiological agent is sunlight
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2
Q

what are the important factors for development of skin cancer?

A
  • sunlight
  • ionising radiation
  • viruses
  • tissue scarring
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3
Q

what are the most common types of skin cancer?

A
  • basal cell carcinoma (most common, least deadly)
  • squamous cell carcinoma
  • melanoma (least common, most deadly)
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4
Q

what is basal cell carcinoma?

A

tumours arise from pluripotent stem cells in epidermis

  • almost always found on sun-exposed body parts
  • locally destructive but rarely metastatic
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5
Q

what is squamous cell carcinoma?

A

tumours arise from basal keratinocytes

  • usually tumours of elderly on sun-exposed areas
  • often metastatic -> spread to lymph nodes + other organs, particularly lungs
  • can arise from other lesions eg solar keratoses
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6
Q

what is melanoma?

A

tumours arise from epidermal melanocytes (or sometimes dermal)

  • tumour of young age
  • associated with intermittent, intense sun exposure
  • unusually found in sun-exposed areas
  • associated with systemic immunosuppression
  • highly metastatic
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7
Q

what are the risk factors for melanoma?

A
  • family history
  • presence of dysplastic naevae (abnormal moles) or >50 naevae
  • childhood radiotherapy
  • higher socioeconomic background (sunny holidays)
  • occupational hazards eg ionising radiation of airline pilots
  • frequent tanning beds
  • other cancer
  • transplants
  • certain melanocortin-1 receptor variant alleles
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8
Q

what are the 4 clinical subtypes of melanoma?

A

superficial spreading: horizontal growth phase through epidermis followed by vertical invasion

nodular: more aggressive, no horizontal growth phase

lentigo maligna: from precusor lesion of same name

acrolentigenous: start on feet/hands, tent to be due to trauma not sun exposure

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9
Q

what are the 4 types of precursor lesion for melanoma?

A
  • junctional / compound-acquired melanocytic naevae
  • dysplastic naevae
  • dermal naevae
  • ginat bathin trunk naevae
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10
Q

what are the types of UV light and how do they contribute to skin cancer?

A

UVA: main cause of skin agein
UVB: can’t penetrate glass -> more important than UVA
UVC: very little penetrates atmosphere so is less relevant even tho is strongest

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11
Q

what interactions happen between UVB & DNA?

A

DNA acts as a chromophore for UVB -> photoproducts eg cyclobutane butane pyrimidine dimers + thymine dimers
- thymine dimers can be repaired via base excision but if damage is irreparable cell apoptoses -> sunburn (mediated by Bax protein)

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12
Q

how does UVA damage DNA?

A

mainly causes indirect DNA damage by formation of xinglet oxygens + free radicals

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13
Q

what are Langerhans cells?

A

specialised dendritic cells that have migrated to superbasilar layer of skin
- recognise tumour-associated antigens on skin -> present to T cells -> mutatnts killed before cancer develops

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14
Q

how does Langerhans cell function change with UV exposure?

A

function decreases proportionally

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15
Q

what is the Fitzpatrick classification of skin types?

A 
I: always burns, never tans  
II: usually burns, sometimes tans  
III: sometimes burns, usually tans  
IV: never burns, always tans   
V: moderate constitutive pigmentation   
VI: marked constitutive pigmentation
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16
Q

what does melanin do?

A

responsible for skin pigmentation

  • acts as crhomophore for UV light -> absorbs UV -> provides protection for more sensitive layers of skin underneath
  • also traps electrons & free radicals
17
Q

how is melanin produced?

A

from tyrosine via DOPA

18
Q

what are the types of melanin?

A

eumelanin: black/brown, insoluble, useful
phaeomelanin: yellowish-reddish brown, soluble in alkalis, useless
neuromelanin: present only in the substantia nigra of brain, function unknown
- number of melanocytes relatively constant in everyone so colour is determined by amount & type of melanin

19
Q

what are melanocortins?

A

group of peptides derived from pro-opiomelanocortin (POMC) MSH (melanocyte stimulating hormone)

  • ACTH
  • endorphins
  • liptrophins
20
Q

what does MCIR do?

A

highly polymorphic melanocortin-1 receptor

  • regulates skin & hair pigmentation phenotype
  • promotes a switch from phaeomelanin to eumelanin production -> therefore alleles which don’t work as well are associated with ginger hair and hence skin cancer
21
Q

what are the 2 ways in which tanning occurs?

A

immediate: UVA -> alteration & redistribution of melanin -> making you look tanned but affording you no extra protection eg tanning booth, first day at beach
delayed: UVB increases production of melanin but effects depend on MCIR variant

22
Q

what is another effect of sun exposure?

A

epidermal thickening

23
Q

what is an epidermal melanin unit?

A

each melanocyte is associated with 36 keratinocytes

- melanocytes pass melanosomes via dendrites to keratinocytes -> phagocytose melanosome

24
Q

what is Gorlin’s syndrome?

A

development of hundreds of basal cell carcinomas on face and trunk age 10-20

  • autosomal dominant
  • casued by mutation of both alleles of Patched gene -> loss of suppression of Smoothened gene -> production of transcription factor that casues cell proliferation
  • Patched & Smoothed gene part of sonic hedgehog pathway
25
Q

what is Xeroderma pigmentosum?

A

defective base excision repair mechanisms -> very early solar ageing & get BCCs, SCCs & melanomas before age 10

  • autosomal/sex-linked recessive
  • usually death age 10-30
26
Q

what is epidermodysplasia verruciformis?

A

mild immunodeficiency -> skin gets infected by opportunistic HPV -> thousands of warts beofre age 10 -> develop into SCCs on UV exposure

  • autosomal recessive
  • HPV’s E6 protein disrupts DNA repair following UV exposure and inactivates p53
27
Q

what is FAMM syndrome?

A

famial atypical mole/melanoma syndrome - patients have multiple dysplastic naevae -> multiple melanomas
- 40-50% have CDKN2A mutation -> less p16 (a cyclin-dependent kinase inhibitor) produced -> cell proliferation

28
Q

which type of skin cancer are transplant patients more likely to get and why?

A

10x more likely to get SCC than BCC due to EV-causing HPV strains

29
Q

60% of melanomas have a ____ mutation

A

BRAF mutation

  • BRAF is part of Raf family of protein kinases in MAPK pathway downstream of Ras
  • mutation resulst in constitutive activation of BRAF without need for Ras stimulation -> cell proliferation
  • 90% of mutations are replacement of valine by glutamate at position 600 (BRAF V600E mutation)
30
Q

what is vemurafenib?

A

small molecule inhibitor selective for BRAV V600E mutants

  • taken orally
  • reversible
  • ATP-competitive
31
Q

how can immunotherapy be used to treat melanoma?

A

CTLA-4 receptor on T cells is negative regulator, important in self-tolerance to prevent autoimmunity
- ipilimumab (IgG mAb to CTLA-4 receptor) removes inhibition -> T cells react better

32
Q

how can skin cancer be prevented?

A
  • sun-block
  • sun-protective clothing
  • increasing public awareness of UV exposure dangers -> protective behaviour
  • increasing public awareness of skin cancer identification -> early diagnosis
33
Q

what does SPF mean?

A

sun protection factor = time needed in sun with sun-block before skin redness develops after 24h / time needed in sun without sun-block before skin redness develops 24h later

cancer (22 decks)

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