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Cancer - Vicki > Malignant Melanoma > Flashcards

Malignant Melanoma Flashcards

1
Q

What are the 3 main types of skin cancer?

A

Malignant melanoma

Non-melanoma skin cancers: BCC/Basal cell carcinoma. SCC/Squamous cell carcinoma.

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2
Q

Who does skin cancer mainly affect?

A

White-skinned people.

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3
Q

Where is melanoma most common?

A

Aus and NZ

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4
Q

What are the risk factors for melanoma?

A

Sun exposure.
Number of moles.
Skin type: fair skin.
Family history.

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5
Q

How is melanoma diagnosed?

A

Pts presents.
Dermascope examination.
Excisional biospy: removal of entire lesion.
Histopathology: examination of lesion and analysis.

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6
Q

Where does melanoma tend to spread?

A

Lymph nodes.
Liver
Brain
Lungs

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7
Q

How are stage 0-3 melanomas treated?

A

Stage 0-3 tumours: excision followed by wide local excision to remove good margin of healthy tumour.

> 50% of stage 3 tumours recur.

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8
Q

What percentage of stage 3 tumours will recur?

A

> 50%

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9
Q

How are stage 4 melanomas treated?

A

Stage 4: chemotherapy, biological therapies e.g. ipilimumab, pembrolizumab, vemurafenib, dabrafenib.

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10
Q

How can melanomas be identified?

A 
ABCDEF
Asymmetry
Border
Colour
Diameter
Evolution/elevation
Funny looking
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11
Q

What does ABCD(EF) refer to?

A 
Way to identify tumours:
Asymmetry
Border
Colour
Diameter
Evolution/elevation
Funny looking
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12
Q

For stage 4 melanoma, what is the 10 year survival?

A

<10%

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13
Q

Ipilimumab was the first agent to show what?

A

An increase in overall survival in advanced/unresectable MM.

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14
Q

What is ipilimumab? (structure)

A

Recomb human monoclonal antibody that binds to CTLA-4 (cytotoxic T-lymphocyte associated antigen 4).

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15
Q

How does Ipilimumab function as a chemotherapeutic agent?

A

Blocks interaction of CTLA-4 and its ligands, CD80 and CD86.

Normally, CTLA-4 serves as an immune checkpoint that down-regulates pathways of T-cell activation and prevents autoimmunity. By blocking this function, Ipilimumab potentiates the antitumour T-cell response, resulting in unrestricted T-cell proliferation.

Thus, the mechanism of action of ipilimumab in pts with melanoma is indirect, possibly through T-cell mediated antitumour immune responses.

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16
Q

What are the side effects associated with ipilimumab?

A 
diarrhoea
Rash
Pruritus
Fatigue
Nausea &amp; vomiting
Decreased appetite
Abdominal pain
Colitis
Hepatitis
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17
Q

Ipilimumab is licensed for the treatment of

A

Previously untreated advanced MM or after prior therapy.

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18
Q

What does Ipilimumb bind to?

A

CTLA-4 -> cytotoxic T-lymphocyte associated antigen 4.

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19
Q

How much does Ipilimumab cost?

A

£25,000 for 1 dose, given every 3 weeks for 4 weeks in total.

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20
Q

What class of drug is Vemurafenib?

A

BRAF inhibitor.

Oral tyrosine kinase inhibitor.

21
Q

The ligands which Ipilimumab blocks CTLA-4 from interacting with.

A

CD80, CD86.

22
Q

A recombinant monoclonal antibody that binds to CTLA-4.

A

Ipilimumab.

23
Q

What route must Ipilimumab be given by?

A

IV

24
Q

What route can Vemurafenib be given by?

A

Oral.

It is an orally active tyrosine kinase inhibitor.

25
Q

What is BRAF?

A

A gene that is mutated in 60% of melanomas and becomes constitutively active causing cell proliferation and tumour growth.

26
Q

What patients can be given Vemurafenib?

A

Only those with the BRAF V600 mutation.

Pos 600, glutamate becomes valine.

27
Q

What percentage of pts have tumour regression quickly with vemurafenib?

A

~90%

28
Q

What are the main side effects of vemurafenib?

A 
Fatigue
Joint pain (painkillers, heat/ice packs)
Rash (emollient, antihistamine or painkillers) 
Sensitivity to sun (SPF 30-50 needed in all weathers, wear long sleeves, apply a UV resistant film to windows)
Nausea 
Alopecia
Pruritus
Headache
29
Q

What are the main distinguishing side effects of vemurafenib?

A

Sensitivity (SPF30-50) to sun, uv films on windows.

Can ironically cause cutaneous squamous cell carcinomas have been reported in 20% of patients (minor cancers), patients need to be aware to check for any new/changing skin lesions.

30
Q

When should vemurafenib be taken and how?

A

With food twice a day, orally as it is in tablet form.

Major advantage over Ipilimumab.

31
Q

Vemurafenib is a _______ inhibitor which is approved by NICE for patients with _________ __ who have the ____ _____ mutation.

A

CTLA-4 inhibitor.
Advanced MM.
BRAF V600.
Glutamine to valine mutation.

32
Q

Why does Vemurafenib have many interactions with other drugs?

A

It is metabolised by cytochrome p450 enzymes and has many drug interactions.

33
Q

What does Dabrafenib have in common with Vemurafenib?

A

Also a BRAF inhibitor.
NICE approved in same pts.
IT is used more often.

34
Q

What are the side effects of dabrafenib? what type of drug is it?

A 
Fever (pts report >38 - not infectious)
Fatigue
Joint pain
Rash
Headache
Nausea
Diarrhoea
Cutaneous squamous cell carcinomas have been reported in 10% of patients. 
Uveitis in 1% of patients - pts report any eye redness.
35
Q

Cutaneous squamous cell carcinoma have been reported in 10% of patients taking which advanced MM treatment?

A

Dabrafenib

36
Q

What route can dabrefenib be given by?

A

Oral. Again many drug interactions as it is metabolised by CYP450

37
Q

Pembrolizumab is one of the first of a new generation of immuno-oncology therapies called anti-___s

A

One of the first of a new generation of immuno-oncology therapies called anti-PD-1s (programmed death receptor-1)

38
Q

What is Pembrolizumab, how is it given and how does it work?

A

Humanized monoclonal antibody given by IV infusion that blocks the interaction between PD-1 (programmed death receptor-1) found on T cells and its ligands, PD-L1 and PD-L2.

By blocking the interaction with the receptor ligands, pembrolizumab releases the PD-1 pathway mediated inhibition of the immune response, including the anti-tumour immune response (i.e. it “takes the brakes off the immune system”).

39
Q

Which treatment for advanced MM can cause uveitis?

A

Dabrafenib

40
Q

How does pembrolizumab take the breaks off the immune system?

A

It blocks the interaction between PD-1 (programmed death receptor 1) found on T cells and its ligands, PD-L1 and PD-L2. This releases the PD-1 pathway mediated inhibition of the immune response, including anti-tumour immune response.

41
Q

Humanized monoclonal antibody given by IV infusion that blocks the interaction between PD-1 (programmed death receptor-1) found on T cells and its ligands, PD-L1 and PD-L2.

A

Pembrolizumab

42
Q

What is the overall survival at 18 months post initiation of Pembrolizumab treatment and what is the overall response rate to treatment?

A

18 months = 62%

Overall response rate = 24%.

43
Q

One of the first of a new generation of immuno-oncology therapies called anti-PD-1s (programmed death receptor-1)

A

Pembrolizumab

44
Q

What is the inidication for Pembrolizumab use?

A

Indicated for previously untreated advanced MM or following ipilimumab/BRAF inhibitor

45
Q

What are the important side effects of pembrolizumab?

A

Decreased appetite

Immune-mediated adverse reactions such as pneumonitis, colitis and hepatitis.

46
Q

What are the first line treatment options for advanced/unresectable MM with no BRAF V600 mutation?

A

Either Ipilimumab (expensive) or Pembrolizumab.

Second line: whichever wasnt used first line.

47
Q

What are the 1st line treatment options for BRAF V600 mutation MM?

A

Vemurafenib/dabrefenib.

48
Q

What are the second line treatment options for BRAF V600 mutation MM?

A

Ipilimumab/pembrolizumab.

Cancer - Vicki (12 decks)

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