Biological Basis of Cancer Therapy Flashcards

1
Q

What are the four main anti-cancer modalities?

A

Radiotherapy
Chemotherapy
Surgery
Immunotherapy

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2
Q

List the different types of cytotoxic chemotherapy.

A
Alkylating agents  
Pseudoalkylating agents  
Antimetabolites 
Anthracyclines  
Vinca alkaloids and taxanes 
Topoisomerase inhibitors
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3
Q

What are the main types of targeted therapy for cancer?

A

Monoclonal antibodies

Small molecule inhibitors

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4
Q

What is the term used to describe chemotherapy that is given:

a. Following surgery
b. Before surgery

A

Adjuvant

Neoadjuvant

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5
Q

How do alkylating agents work?

A

They add an alkyl group to the guanine residues in DNA
This causes cross-linking of the DNA strands and prevents DNA from uncoiling at replication
This then triggers apoptosis (via a DNA checkpoint pathway)

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6
Q

How do pseudoalkylating agents work?

A

They have the same mechanism as alkylating agents but use platinum instead of alkyl groups

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7
Q

How do anti-metabolites work?

A

They masquerade as purine or pyrimidines leading to inhibition of DNA replication and transcription
They can also be folate antagonists (dihydrofolate reductase inhibitors)
This blocks DNA replication and transcription

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8
Q

How do anthracyclines work?

A

Insert between nucleotides in DNA/RNA so inhibits transcription and replication therefore BLOCKS DNA REPAIR creating FREE RADICALS that will damage the cells and cause APOPTOSIS

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9
Q

How do vinca alkaloids and taxanes work?

A

Vinca alkaloids inhibit assembly of microtubules
Taxanes inhibit disassembly of microtubules
This forces the cells into mitotic arrest

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10
Q

How do topoisomerase inhibitors work?

A

Topoisomerase is responsible for the unwinding of DNA and they induce temporary single and double strand breaks in the phosphodiester backbone
Topoisomerase inhibitors alter the binding of topoisomerase to DNA and allow permanent breaks in the DNA

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11
Q

What are the six hallmarks of cancer?

A
SPINAP 
Self-sufficient  
Pro-invasive and metastatic  
Insensitive to anti-growth signals  
Non-senescent
Anti-apoptotic  
Pro-angiogenic
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12
Q

Give three examples of receptors that are over-expressed in cancer.

A

EGFR
HER2
PDGFR

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13
Q

Give an example of a ligand that is over-expressed in some cancers.

A

VEGF

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14
Q

Give two examples of constitutive (ligand independent) receptor activation in cancer.

A

EGFR

FGFR

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15
Q

How do small molecule inhibitors work?

A

They mimic ATP and bind to the kinase domain of tyrosine kinase receptors within the cytoplasm and block autophosphorylation and downstream signalling

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16
Q

State some resistance mechanisms to targeted therapies.

A

Mutations in ATP binding domain
Intrinsic resistance
Intragenic mutations
Upregulation of downstream signalling pathways

17
Q

Side effects of all alkylating agents

A

Nephrotoxicity

Neurotoxicity

18
Q

Side effects of antimetabolites

A

Palmar-plantar erythrodysesthesia

19
Q

Side effects of anthracyclines

A

Cardiac toxicity

Red urine and red tears- Doxorubicin

20
Q

Side effects of vinca alkaloids

A

Neuropathy
Arthralgia
Allergy

21
Q

Side effects of taxanes

A

Neuropathy
Arthralgia
Allergy

22
Q

What are 3 things monoclonal antibodies can do

A

Ligand neutralisation
Prevent receptor dimerisation
Cause receptor internalisation

23
Q

What do small molecule inhibitors do

A

ATP-mimetics bind to kinase domains of tyrosine kinase in cytoplasm blocking the autophosphorylation therefore stop downstream kinase activation

24
Q

Expensive alternate cancer therapy

A

Anti-sense oligonucleotides
RNA interference
b-RAF inhibitor

25
Q

3 mechanisms of resistance to targeted therapy

A

DNA repair upregulated
ATP binding cassette transporters efflux drug
Altered target site

26
Q

Drug classes affected by upregulated DNA repair

A

Alkylating agents
Antimetabolites
Topoisomerase inhibitors

27
Q

Drug classes effluxed by ABC transporters

A

Pseudoalkylating agents

Vinca alkaloids

28
Q

Drugs affected by altered target site

A

Anthracyclines