Targeted Cancer Therapy Flashcards

1
Q

Targeted therapy

A

Treatment that targets specific molecules driving cancer growth and progression

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2
Q

What is adjuvant targeted therapy

A

Targeted therapy in combo with surgery/chemo/radio

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3
Q

Why do targeted therapies have less adverse reactions than other treatments

A

Less likely to affect molecules involved in other functions and healthy tissues

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4
Q

What can biomarkers from molecular profiling be used to assess

A

Prognosis
Diagnosis
Predict Drug sensitivity/resistance
Predict adverse effects

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5
Q

What is used to individualise treatment plans to specific mutations and cancers

A

Molecular signatures

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6
Q

Advantages of treatments targeted to individual patients

A

Improve diagnosis
Decr side effects
Decr use of ineffective drugs
Incr survival
Incr quality of life
Decr costs

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7
Q

Where are the best targets for targeted therapy found

A

In cancer cells but not in normal cells

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8
Q

What happens after a growth factor binds to a tyrosine kinase receptor

A

Receptor dimerises and kinase activated

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9
Q

What is the most important tyrosine kinase receptor involved in cancer

A

HER2

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10
Q

What is the most important oncogenic driver

A

MAPK pathway

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11
Q

How do targeted therapies targeting growth factors or tyrosine kinase receptors treat cancers

A

Inactivate MAPK and PI3 pathways decreasing cell growth, proliferation, and angiogenesis

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12
Q

What are the main targets of targeted therapies

A

Receptors on plasma membrane
Kinase activity within cells
RAS RAF - kinases

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13
Q

2 main types of targeted therapy

A

Antibodies
Small molecule kinase inhibitors

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14
Q

Why do antibodies only have targets on the cell surface membrane

A

Too big to enter cells

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15
Q

Antibodies or small molecule kinase inhibitor more selective

A

Antibodies

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16
Q

How are antibody targeted therapies administered

17
Q

How are small molecule kinase inhibitor targeted therapies administered

18
Q

What part of tyrosine kinase receptors do small molecule kinase inhibitors bind to

A

ATP binding site

19
Q

How can antibody targeted therapies disrupt tyrosine kinase receptors

A

Bind to regions preventing ligand binding, receptor dimerisation, or ATP binding

20
Q

How can monoclonal antibodies kill tumour cells directly

A

Inhibit ligand binding blocking signalling and inducing apoptosis
Deliver toxic drugs conjugated to the antibody

21
Q

How do monoclonal antibodies kill tumour cells via immune mediated mechanisms

A

Induce phagocytosis
Complement dependent cytotoxicity
Antibody dependent cell cytotoxicity

22
Q

How can monoclonal antibodies kill tumour cells by vascular or stromal ablation

A

Antagonise VEGF

23
Q

What type of targeted therapy is cetuximab and what is its MOA

A

monoclonal antibody
Binds to EFGR kinase receptor preventing dimerisation

24
Q

Kadcycla/trastuzumab emtansine MOA

A

enters cell bound to antibody -> antibody degraded -> kadcycla causes apoptosis, mitotic arrest, and mitotic catastrophe

25
Do patients become resistant to kadcycla or herceptin first
Herceptin
26
Kinase inhibitor targets
Transcription Receptor tyrosine kinase signalling Proto oncogenes
27
What causes drug resistance to targeted therapies
Mutations to target molecules
28
Why do most HER2 cancer pts eventually become resistant to herceptin
HER2 becomes truncated and the binding site for herceptin is lost but kinase activity is still switched on
29
Which receptor do erlotinib, gefitinib, afatinib, and osimertinib target
EGFR
30
Why is osimertinib used after erlotinib
Pts become resistant to erlotinib
31
Targeted therapy side effects
Acneform Skin rashes EGFR Dry skin Itchy skin Hand foot syndrome VEGF Hair changes Dry or red eyes Red and tender eyelids High blood pressure Slow wound healing and blood clotting
32
Which targeted therapy side effects are specifically associated with EGFR targeting drugs
Skin rashes Slow wound healing and blood clotting
33
Which targeted therapy side effects are specifically associated with VEGF targeting drugs
Hand foot syndrome High blood pressure
34
Why must cardiac function be assessed before and every 3 months during trastumazab use
Cardiomyopathy is side effect
35
Why does trastuzumab cause cardiomyopathies
Inhibiting HER2 damages cardiomyocytes
36
What type of heart failure is caused by trastuzumab
Congestive