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Novel cancer treatments Flashcards

(23 cards)

1
Q

What are examples of targeted therapy and what does it treat?

A

BRAF-melanoma
ckit/PDFGR-GIST
EGFR-adenocarcinoma, lung cancer

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2
Q

Are the above targeted therapies intravaneous or tablets?

A

Tablet

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3
Q

Examples of immunotherapies and what do they treat? Are they intravaneous or tablets?

A

provenge- prostate cancer
t-vec-melanoma
Checkpoint inihibitors for renal, head and bladder cancer

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4
Q

Why have targeted and
immunotherapies been
developed?

A

Because chemotherapies are toxic to rapidly dividing normal cells affecting bone marrow, GI mucosa, skin, hair and don’t work on every cancer type.

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5
Q

What do targeted therapies target? What’s rationale behind it?

A

Overexpressed receptors or signalling pathways. Tumour cells are reliant on these pathways or receptors so blocking it will kill the tumour

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6
Q

What’s the problem with using vemurafenib to treat melanoma? How did this happen? What are the side effects?

A

It’s not that effective, MEK activation becomes more through another mechanism making the tumour more aggresive.
Diahrrea, fatigue, joint pain cutaneous scc, hyperkeratosis, rashes

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7
Q

What is a more effective drug than vemurafenib monotherapy and why? What are the side effects?

A

dabrafenib and trametinib combination therapy because it targets both MEK and raf decreasing activity of the signalling pathway.
Less cutaneous toxicity, cardiac damage, pyrexia

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8
Q

Which exon mutations in c-kit has the highest response when treating with imatinib? How about wildtype c-kit?

A

exon11 and then exon 9

no response

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9
Q

What does imatinib target?

A

ABL kinase,BCR ABL fusion, c-kit, PDGFR

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10
Q

What toxicity is associated with imatinib?

A

Fluid retention, nausea, fatigue, rash, diahrrea

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11
Q

What kinds of resistance mechanism are there and give an example of each?

A

Primary resistance-BRAF,ras,SDHB muations
Secondary mutations-reactivation of kit phosphorylation
interference iwth imatinib binding
dedifferentiation
activation of other pathway such MET
New mutations arising

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12
Q

Where does mutations occur in EGFR? And what subpopulation is this seen in?

A

Catalytic domain

Adenocarcinoma, non smokers, women, asians

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13
Q

What is the 1st line of treatment for lung cancer patients with EGFR mutations? How about the patients without EGFR muations?

A

Gefitinib

Carboplatin plus paclitaxel

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14
Q

What are the side effects of EGFR treatment?

A

rash,diahrrea, nausea, anorexia

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15
Q

What’s the problem with EGFR treatment?

A

Primary mutation
Secondary mutation- T790 mutation which increases ATP binding
Activation of other suvival pathway-MET

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16
Q

What’s the rationale for using immunotherapy?

A

Spontaneous regression, abscopal effect, response to IL-2&interferon

17
Q

What’s the first line of treatment for melanoma? What’s the perks and downsides of using this? How to treat the porblem?

A

pembroluzimab monotherapy and ipilumimab/nivolumab
No neutropenic sepsis, oral mucositis,hair loss
autoimmunity, with immunosupprssion steroid

18
Q

What part of the immune cycle does ipilimumab target?

A

the priming and activation of t-cells at the lymph node

19
Q

What is a better substitute to ipilimumab and why?

A

nivolumimab and pembrolizumab, because they work at the tumour site therefore less toxicity(more specific)

20
Q

What happens if you combine both nivolumimab and ipiliumimab ?

A

It is slightly more better than nivolumimab monotherapy but the toxicity is substantial(50-60% grade 3-4 toxicity)

21
Q

What’s the objective response of the combination treatment?

22
Q

What is the prognosis of lung cancer patients treated with pembrolizumab?

A

Hyperprogression-progression at a rapid rate compared ti before treatment

23
Q

Who to give nivolumab monotherapy and who to give combination therapy(nivolumab and ipilumimab)?

A

PDL1 positive tumours give nivolumab monotherapy but PDL1 negative tumours give combination therapy