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biology of cancer > Melanomas > Flashcards

Melanomas Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is the definition of a melanoma?

A

a malignant tumor of melanocyctes

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2
Q

where are the potential sites of a melanoma?

A
  • skin; cutaneous (common)
  • eye; ocular melaona (rare)
  • melanoma of mucous membranes (rare)
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3
Q

lifetime risk of melanoma in the UK

A
  • females 1 in 47
  • males 1 in 36
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4
Q

what does the melanocyte do?

A

in epidermis
- transfer of melanosomes, mainly to basal keratinocytes

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5
Q

types of melanomas and moles

A
  1. benign naevus; harmless mole
  2. dyplastic naevus; atypical mole
  3. radial growth phase (RGP); melanoma
  4. vertical growth face (VGP); capable of metastasis
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6
Q

what makes a mole atypical?

A

3 or more of these features
- size >5mm diameter
- ill defined or blurred borders
- irregular margin/unusual shape
- varying shades of colour
- flat and bumpy components

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7
Q

what are the two layers of the dermis?

A
  • papillary dermis; dermal papillae and below, fine collagen fibres, very few cells (fibroblasts, blood vessels)
  • reticular dermis; coarse collagen fibres
  • in healthy dermis; no clusers of cells, just single fibroblasts, leucocytes and blood vessels.
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8
Q

RGP characteristics

A
  • thin ‘early’
  • in epidermis and papillary dermis only
  • typically no lymphatic spread
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9
Q

VGP characteristics

A
  • thick ‘advanced’
  • cell proliferating in reticular dermis
  • typically lymphatic spread
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10
Q

what is clark level?

A

staging system that describes the depth of melanoma as it grows in the skin

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11
Q

breslow thickness

A
  • height from granular layer of epidermis to base of melanoma
  • easier in practice than the clark system
  • strong association with prognosis
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12
Q

melaonma; rapid progression

A
  • early detection is important
  • a melanoma of >1mm thick may have already spread and potentially fatal
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13
Q

what is epidemiology?

A

study of the distribution, patterns and correlates of disease conditions in defined populations

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14
Q

whatis aetiology?

A

study of the causes and mechanisms of disease
- epidemiology provides evidence about aetiology

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15
Q

what is unusual about melanoma cases?

A

longstanding rise in incidence

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16
Q

sun-related risk factors

A
  • fitzpatrick skin type (never tans) vs
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17
Q

what skin type has the heighest risk of melanoma?

A
  • FItzpatrick skin type (never tans)
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18
Q

what is the association between sunlight/ UV and melanoma?

A
  • skin type
  • sun exposure habits
  • melanomas are rare in areas rarely or never exposed to sunlight

AETIOLOGY: the main carcinogen appears to be UV radiation

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19
Q

three wavebands of solar UV

A

UVA= longest wavelength
UVB
UVC
ozone blocks all UVC, some UVB and UVA

20
Q

why is there increasing incidences of melanomas?

A
  • ozone changes
  • changes in behaviour; more sunbanthing and sunny holidays
21
Q

which waveband is more worrying?

A

both UVB and UVA;
- epidermis absorbs more UVB than UVA. UVB is more carcinogenic per photon but nearly all UV that reaches melanocytes is UVA

22
Q

experimental data on UVA and UVB

A
  • UVA can induce DNA damage as well as UVB
  • DNA damage can kill cells (large amounts), induce cell senescence (medium) or be repaired (small).
  • UVA can interact with melanin to relase ROS especially with pheomelanin. ROS can cause DNA damage.
23
Q

why is sunscreen important?

A
  • definitely protects against non-melanoma skin cancer but evidence is weaker for melanomas
24
Q

what is the MC1R gene variant?

A

present in those with red or fair hair
- encodes the melanocortin 1-receptor (MSH receptor).
- required in suntanning
- variants are proven risk factors

24
Q

how do benign naevi (moles) happen?

A
  • partly genetic and partly reflecting UV exposure
25
Q

dyplastic moles and melanoma

A

major risk factor for melanoma
- dyplastic naevi and family history of melanoma = 100-400x relative risk

26
Q

what is FAMMM syndrome?

A

familial atypical moles and malignant melanoma.
- melanoma susceptibility genes
- most often CDKN2A gene mutation
- biggest known risk factor

27
Q

what does CDKN2A encode for?

A

encodes the senescence effector p16

28
Q

TSGs involved in sporadic human cutaneous melanomas

A
  • CDKN2A (p16, ARF)
  • APAF1
  • CDKN28 (p15)
  • PTE
  • APC
  • TP53 (p53)

types of changes; deletion, methylation, mutation

29
Q

oncogenes involved in sporadic human cutaneous melanomas

A
  • TERT
  • BRAF
  • TBX2
  • MYC
  • PTPRD
  • NRAS
  • PREX2

types of changes; amplification, activating mutations, promoting overexpression

30
Q

what is p16?

A

aka; INK4A. CDKN2A, MTS1
- product of the most common mutated gene in familial melanoma ; CDKN2A
- most commonly defective/ silenced in sporadic melanoma

31
Q

what does p16 do?

A

cause cell senescence

32
Q

moles contain senescent melanocytes

A
  • p16
  • b-galactosidase
33
Q

what are some other senescence markers?

A
  • DNA damage markers
  • histone H2AFY
  • PML
  • H3K9Me
  • large nucleoli, multinucleacy
34
Q

how do melanomas escape cell senescence?

A
  • lack of p16
  • reactivation of TERT expression (catalytic subunit of telomerase)
35
Q

ABCDE checklist for suspected melanoma

A
  • Asymmetry
  • Border; is irregular
  • Colour; areas of varying colour
  • Diameter; >6mm
  • Expansion
36
Q

Primary melanoma (stage 0-2)

A
  • surgical excision with wide margins and sometimes lymph nodes
  • if invasive; further investigation
  • sentinel (specific draining) lymph node biopsy used increasingle. If found to contain melanoma cells, remove lovcal nodes.
  • cure frequent for thin lesions
37
Q

Local/lymph node metstasis (Stage 3)

A
  • surgery (/laser ablation) where possible
  • further investigation for distant metastasis (x-ray, liver scan)
38
Q

metastatic melanoma (stage 6)

A
  • no adjuvant therapies of proven benefit
  • palliative treatment only
  • dacarbazine (UK)
  • interferon a2b (USA)
39
Q

Ipilimumab

A

antibody to CTLA4 (cytotoxic T-lymphocyte associated antigen 4).
- CTLA4 involved in tolerance where immune response to the cancer fails

40
Q

Vemurafenib

A

inhibits oncogene BRAF(V600E) = VE mutant RAF inhibitor.
- oncogenic BRAF mutation found in 50% melanomas
- only useful for patients with oncogenic BRAF mutation
- 99% relapse

41
Q

Dabrafenib and Trametinib

A

BRAF inhibitor + MEK inhibtor
- MEK is downstream of BRAF in signalling pathway.
- helps delay the appearance of resistance

42
Q
A
43
Q

Nivolumab

A

antibody to PD-1 (programmed death-1)
- PD-1 expressed on lymphocytes and involved in tolerance to cancers

44
Q
A
45
Q

Prospects of treatment

A
  • many trials in progress
  • molecular understanding of cancer biology and genetics.
  • cost still a problem

biology of cancer (13 decks)

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