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The Public (Y2) > Cancer > Flashcards

Cancer Flashcards

1
Q

Over 40% of cancers are preventable. True or false?

A

True

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2
Q

Nitrogen mustard is more toxic than sulphur mustard. True or false?

A

False

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3
Q

Nitrogen mustard is no longer used clinically. True or false?

A

False - used clinically in combination with other drugs

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4
Q

What is the mechanism of action of alkylating agents (mustards)?

A

They attach an alkyl group to DNA (guanine base)

This causes linkages between the DNA strands, inhibiting DNA synthesis

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5
Q

Alkylating agents only attack cancerous cells. True or false?

A

False - also attack normal cells that divide frequently - i.e. cells of GIT, bone marrow etc

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6
Q

What is the least toxic alkylating agent that is used in chemotherapy?

A

Chlorambucil

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7
Q

What are 3 ways in which toxicity of alkylating agents can be reduced?

A

Only form the electrophile slowly in the tumour
Attach alkylating agent to an “amino acid”
Pro-drug

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8
Q

Why do tumours require amino acids?

A

For protein synthesis - so making a chemotherapeutic drug look like an amino acid, will allow it to be taken up by the cancerous cell

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9
Q

Which alkylating agent gets taken up into the tumour cell by a phenylalanine amino acid transporter?

A

Melphalan

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10
Q

Name an alkylating agent that is a prodrug

A

Mitomycin C

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11
Q

Alkylating agents contain highly nucleophilic groups. True or false?

A

False - electrophilic

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12
Q

Alkylating agents form hydrogen bonds with nucleophilic DNA bases. True or false?

A

False - covalent bonds

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13
Q

Alkylating agents are carcinogenic themselves. True or false?

A

True - they produce long term side effects

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14
Q

Name 3 alkylating agents

A

Chlorambucil
Mitamycin C
Melphalan

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15
Q

Name a drug that involves the binding of metal complexes to DNA.

A

Cisplatin

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16
Q

How do metal complexes that bind to DNA work?

A

Neutral inactive molecule acting as a prodrug
Platinum covalently binds to chloro-groups
Ammonia molecules act as ligands
Activated in cells with low chloride concentration
Chloride substituents are replaced with neutral water ligands, producing positively charged species

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17
Q

Cisplatin binds to regions in DNA that are rich in cytosine. True or false?

A

False - guanine

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18
Q

Doxorubicin is an alkylating agent. True or false?

A

False - intercalating agent

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19
Q

What is the mechanism of action of doxorubicin?

A

the planar tetracyclic chromophore is inserted between adjacent pairs and is stabilised by electrostatic interactions between DNA phosphate groups and the positively charged amino group of the sugar. As a result inhibits action of topoisomerase II
Also generates oxygen free radicals which leads to DNA damage

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20
Q

Which drug can be used to reduce the cardiotoxicity of doxirubicin?

A

Dexrazoxane

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21
Q

Explain the action of topoisomerase II

A

It relieves the strain in the DNA helix by temporarily cleaving the DNA chain and crossing an intact strand through the broken strand.
Tyrosine (in the topoisomerase enzyme) are involved in the chain breaking process and form covalent bond with DNA

22
Q

Name a topoisomerase II inhibitor and outline its mechanism of action

A

Etoposide - forms a ternary complex with DNA and topoisomerase II and prevents the re-ligation of DNA and so the double strand breaks

23
Q

Which chemotherapeutic drug is a semi-synthetic derivative of podophyllotoxin poison, extracted from the Mandrake plant?

A

Etoposide

24
Q

Which drug is only effective in chemo-sensitive tumours such as leukaemias, testicular cancer and small cell lung cancer?

A

Etoposide

25
Q

Etoposide has less major long term irreversible organ specific toxicity compared to doxorubicin and cisplatin. True or false?

A

True

26
Q

What are the effects of vincristine and vinblastine on mitosis?

A

Prevent polymerisation of microtubules

27
Q

What is the effect of taxol on mitosis?

A

Binds and stabilises microtubules

28
Q

How do anti-metabolites work?

A

they interfere with the production of nucleic acids

29
Q

Give an example of an anti-metabolite drug

A

5-FU

Methotrexate

30
Q

What are the advantages of antisense therapy?

A

Has the same effects as enzyme inhibitors or receptor antagonists (i.e. same as conventional drugs)
It is highly specific where the oligonucleotide is 17 nucleotides or more
Smaller doses are required compared to inhibitors or antagonists

31
Q

What are the disadvantages of antisense therapy?

A

‘Exposed’ sections of mRNA must be targeted
Instability and polarity of oligonucleotides
Short lifetime of oligonucleotides and poor absorption across cell membranes

32
Q

What are the advantages of micro-RNA therapy?

A

siRNAs have potential to be used in gene therapy
Greater efficiency in silencing mRNA than conventional antisense therapy
One siRNA could lead to cleavage of many mRNA molecules

33
Q

What are the disadvantages of micro-RNA therapy?

A

siRNAs need to be metabolically stable
Difficult to reach target cells
Devise a mechanism to ensure entry to target cells

34
Q

What is micro-RNA?

A

short segments of double stranded RNA - recognised by RISC to to produce siRNA

35
Q

What are the 3 essential domains of tyrosine kinase receptors?

A 
ligand binding site (extracellular domain)
transmembrane domain (alpha helix)
domain with tyrosine kinase activity (cytosolic)
36
Q

Name 2 drugs which target kinases by disrupting ligand-receptor interactions

A

Bevacizumab

Trastuzumab (Herceptin)

37
Q

How does bevacizumab work?

A

It binds to a growth factor (VEGF) therefore preventing its binding to TK receptors. This interferes with tumour blood vessel development

38
Q

Which drug is used first line for colorectal cancers?

A

Bevacizumab

39
Q

How does trastuzumab work?

A

targets HER2 receptor which is over expressed in late stage breast cancers. It prevents binding of EGF to the HER2 receptor and therefore prevents signal transduction

40
Q

Herceptin works on all cancers. True or false?

A

False - only HER2 positive cancers as it only works on tumours where this protein is over expressed

41
Q

Name 2 drugs which target kinases by blocking ATP binding

A

Imatinib

Gefitinib

42
Q

How does imatinib work?

A

Blocks ATP from binding to bcr/abl fusion protein

43
Q

How does gefitinib work?

A

Prevents ATP binding to EGFR

44
Q

EGFR is overexpressed in many solid tumours. True or false?

A

True - that is why it is a target for cancer therapy as binding of EGF to EGFR receptor causes dimerisation and tyrosine is phosphorylated as a result -> signalling

45
Q

What is one way in which oestrogen secretion can be reduced?

A

Surgery

46
Q

What drug can reduce oestrogen secretion?

A

Tamoxifen

47
Q

Tamoxifen is a non-competitive inhibitor. True or false?

A

False - competitive inhibition of oestrogen binding to its receptor

48
Q

Which two drugs can inhibit MAPK signalling?

A

Dabrafenib and vemurafenib

49
Q

What are the two ways in which inflammation in cancer can be targeted?

A

Inhibiting pro-tumour inflammation

Promoting anti-tumour inflammation

50
Q

Name the monoclonal antibody that is a CTLA4 inhibitor

A

Ipilimumab

51
Q

Name the monoclonal antibody that is a PD-1 inhibitor

A

Nivolumab

The Public (Y2) (35 decks)

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