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Dermatology > Photocarcinogenesis > Flashcards

Photocarcinogenesis Flashcards

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Dermatology Board Prep flashcards
1
Q

Describe how a cancer cell emerges from multi-step gene damage

A

series of mutations accumulate in successive generations (clonal evolution)

a cell accumulates enough mutations to become cancerous

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2
Q

What are the Hallmarks of Cancer?

A 
Sustained proliferative signalling
Evading growth suppressors
Acting Invasion and Metastasis
Enabling Replicative immortality
Inducing angiogenesis
Resisting cell death
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3
Q

What are the Emerging Hallmarks of cancer?

A

Deregulating cellular energetics

Avoiding immune destruction

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4
Q

What are the enabling characteristics of cancer?

A

Tumour-promoting inflammation

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5
Q

What is an oncogene?

A

Over-active form of a gene that positively regulates cell division
Drives tumour formation when activity or copy number is increased

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6
Q

Give examples of oncogenes

A

Ras, Raf, growth factor receptors

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7
Q

What is a Proto-oncogene?

A

normal, not yet mutated, form of an oncogene

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8
Q

What is a tumour suppressor?

A

Inactive or non-functional form of a gene that negatively regulates cell division
Prevents the formation of a tumour when functioning normally

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9
Q

Give examples of tumour suppressors

A

p53

Rb

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10
Q

What is different in the Ras pathway when a mutation occurs?

A

Ras is constantly on and stimulating cell division

usually it has the ability to turn off and halt this process

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11
Q

What happens when there is a lack of p53

A

DNA damage is unrepaired in the G1 checkpoint, therefore mutations are carried down during cell division

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12
Q

How many different Fitzpatrick Skin Types are there?

A 
Skin type I - always burns, never tans
Skin type II - usually burns, can tan
Skin type III - can burn, but usually tans
Skin type IV - always tans, never burns
Skin type V - ‘brown’ skin
Skin type VI - ‘black’ skin
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13
Q

What type of melanin can be found in Skin Type 1 that is responsible for freckling?

A

Pheomelanin

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14
Q

What occupational chemical exposures can increase the risk of non-melanoma skin cancer?

A 
Coal tar pitch
Soot
Creosote
Petroleum products, such as mineral oil or motor oil
Shale oils
Arsenic
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15
Q

By what percentage do IBD conditions increase the risk of skin cancer?

A

Ulcerative colitis 23% higher risk of malignant melanoma

Crohn’s disease 80% higher risk of malignant melanoma

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16
Q

Can UVA or UVB penetrate through glass?

A

UVA

17
Q

Does UVA or UVB cause sunburn?

A

UVB

18
Q

Does UVA or UVB cause pigmentation and skin ageing?

A

Both UVA and UVB

19
Q

What is the difference in damage caused by UVA and UVB

A

UVB causes DIRECT DNA damage

UVA causes INDIRECT oxidative damage

20
Q

What is the range of wavelengths for UVA?

A

320-400nm

21
Q

What si the range of wavelengths for UVB?

A

290-320nm

22
Q

What variation of DNA damage is typical of UV damage?

A

Pyrimidine Dimer (T=T)

23
Q

What are the 2 major types of UVB induced DNA lesion?

A

cyclobutane pyrimidine dimers (CPDs)
MORE COMMON

pyrimidine–pyrimidone (6–4) photo-products
MORE DAMAGING

Both = formed by covalent bonding between adjacent pyrimidines on the same DNA strand

24
Q

Name a common oxidation of a DNA base caused by UVA

A

deoxyguanosine to form 8-oxo-deoxyguanosine

this can then incorrectly base pair as G-A instead of the usual G-C

25
Q

How does chronic UV exposure cause immunosuppression?

A

Keratinocytes secrete IL-10 and other immunosuppressive molecules

LC lose antigen presenting ability

Dermal DC secrete IL-10

Regulatory CD4 T cells
predominate

26
Q

What is usually the driver mutation in basal cell carcinoma?

A

PTCH

encodes for a protein which acts as a tumour suppressor

27
Q

When is hedgehog signalling important?

A

This is switched on when we grow new hair

**important as BCCs can often look like little hair growths

28
Q

What mutations are common in melanoma?

A

Ras/Raf/MAPK

29
Q

What percentage of melanomas have a BRAF mutation?

A

> 50% melanomas have an activating
B-Raf mutation, mostly V600E
V600K, V600R, V600M, V600D

30
Q

WHat treatments are used to target BRAF mutations?

A

Vemurafenib and Dabrafenib

patients can become resistant to these

31
Q

If patients become resistant to a BRAF inhibitor, what other treatment can be used?

A

Tramatenib targets MEK

32
Q

How quickly can Vemurafenib clear metastases in skin cancer?

A

2 week’s

33
Q

What genes are usually involved in familial melanoma?

A

CDKN2A (tumour suppressor)

CDK4 (oncogene)

34
Q

What other treatment is combined with Ipilimumab for 80% effectiveness?

A

PD-1 Inhibitor

although many people don’t respond adequately

Dermatology (18 decks)

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