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The Public 2 - Sem 2 > Cancer > Flashcards

Cancer Flashcards

1
Q

Why can chemotherapy be problematic?

A

because it prevents cell growth, but some normal cells can also have rapid cell growth

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2
Q

Where do chemotherapy side effects usually occur?

A

areas with rapidly dividing cells

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3
Q

Why is immunosuppression a big issue for patients on chemotherapy?

A

affects cells in bone marrow which makes patients more susceptible to infection and will require regular blood tests for monitoring

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4
Q

Side effects of chemo can be dose limiting and impede efficacy, how can you combat this?

A

reduce dose, increase window between doses, give drugs such as anti-sickness meds to combat side effects and in some instances, treatment must be stopped

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5
Q

What are the 2 main modes of action of chemo?

A
  1. Direct interaction with DNA

2. Prevention of nucleic acid synthesis by inhibiting one or more of the enzymes involved in DNA/RNA synthesis

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6
Q

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

A

True

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7
Q

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

A

False

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8
Q

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

A

False

Used clinically in combination with other drugs

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9
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. They are also carcinogenic and can cause long term side effects and secondary cancer

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10
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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11
Q

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

A

Chlorambucil

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12
Q

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

A
  1. Only form the electrophile slowly in the tumour
  2. Attach alkylating agent to an amino acid
  3. Use a prodrug
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13
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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14
Q

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

A

Melphalan

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15
Q

Name an alkylating agent that is a prodrug

A

Mitomycin C

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16
Q

Alkylating agents contain highly nucleophilic groups. True or false?

A

false, electrophilic

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17
Q

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

A

False

Covalent bonds

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18
Q

1Name 3 alkylating agents

A

Chlorambucil, Mitomycin C. Melphalan

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19
Q

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

A

Cisplatin

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20
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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21
Q

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

A

False

Guanine

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22
Q

Doxorubicin is an alkylating agent. True or false?

A

False

Intercalating agent

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23
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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24
Q

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

A

Dexrazoxane

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25
Q

What are 4 side effects of Doxorubicin?

A

nausea/vomiting, myelosuppression, alopecia, cardiotoxicity

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26
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

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27
Q

Name a topoisomerase II inhibitor and outline its mechanism of action

A

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

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28
Q

Topoisomerase II inhibitors are cytotoxic because?

A

they cause errors in DNA synthesis

29
Q

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

A

Etoposide

30
Q

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

A

Etoposide

31
Q

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

A

True

32
Q

What are the effects of vincristine and vinblastine on mitosis?

A

Prevent polymerisation of microtubules

33
Q

What is the effect of taxol on mitosis?

A

Binds and stabilises microtubules

34
Q

How do anti-metabolites work?

A

they interfere with the production of nucleic acids by inhibiting production of deoxyribonucleoside triphosphates, the precursors of DNA synthesis & some are structurally similar to normal bases so get incorporated into RNA and DNA instead of the normal triphosphates

35
Q

Give an example of an anti-metabolite drug

A

5-FU & Methotrexate

36
Q

Describe the cell cycle

A

G1 (growth of cell and prep), S phase (synthesis, new copies of DNA made), G2 (another checkpoint, cell prepares to divide) and mitosis (nuclear division)

37
Q

What happens during mitosis?

A

2 genetically identical cells are formed form the division of a eukaryotic cell – purpose of this is for growth to and replace cells

38
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

39
Q

What are the disadvantages of antisense therapy?

A

‘Exposed’ sections of mRNA must be targeted/ Instability and polarity of oligonucleotides

Instability and polarity of oligonucleotides

Short lifetime of oligonucleotides and poor absorption across cell membranes

40
Q

What does antisense therapy involve?

A

downregulation of gene expression, blocks mRNA from being transcribed into a protein

41
Q

What is miRNA?

A

short segments of double stranded RNA which are recognised by enzyme complex RISC to produce single stranded RNA - small interfering or small inhibitory RNA (siRNA). Devised to ensure entry into target cells

42
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

43
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

44
Q

Describe the signal transduction process

A

receptor proteins bind signals with high affinity and Conformational changes in structure of receptor protein convert the external signal into one or more intra-cellular signals

45
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)

46
Q

RTKs can initiate a signalling cascade leading to changes in expression of genes that are important for what?

A

proliferation, evasion of apoptosis, induction of angiogenesis and generating metastasis

47
Q

How can a change in kinase activity be achieved?

A

through disruption of ligand receptor interactions and inhibition of kinase activity (blocking ATP binding)

48
Q

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

A

Bevacizumab, Trastuzumab (Herceptin)

49
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

50
Q

Which drug is used first line for colorectal cancers?

A

Bevacizumab

51
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

52
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

53
Q

Name 2 drugs which target kinases by blocking ATP binding

A

Imatinib & Gefitinib

54
Q

How does imatinib work?

A

Blocks ATP from binding to bcr/abl fusion protein

55
Q

How does gefitinib work?

A

Prevents ATP binding to EGFR

56
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

57
Q

What happens when EGFR dimerization doesn’t occur?

A

phosphorylation cannot take place and signaling inhibited

58
Q

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

A

Surgery

59
Q

What drug can reduce oestrogen secretion?

A

Tamoxifen

60
Q

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

A

False - competitive inhibition of oestrogen binding to its receptor

61
Q

Which two drugs can inhibit MAPK signalling?

A

Dabrafenib and vemurafenib

62
Q

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

A

Inhibiting pro-tumour inflammation & Promoting anti-tumour inflammation

63
Q

Name the monoclonal antibody that is a CTLA4 inhibitor

A

Ipilimumab

64
Q

What is CTLA4 and what do the inhibitors do?

A

a checkpoint for T cell activation, it’s a receptor found on the surface of T cell and its activation inhibits T cell function. Inhibitors block CTLA4 signaling, enabling anti-tumour T cell response

65
Q

Name the monoclonal antibody that is a PD-1 inhibitor

A

Nivolumab

66
Q

What is the PD-1/PD-L1 pathway?

A

PD-1 receptor and its ligand are expressed on surface of dendritic cells and macrophages, inhibitory factors, act as checkpoint for dendritic cell mediated response

67
Q

What do PD-1 inhibitors do?

A

release the inhibitory checkpoint allowing for T cell response and proliferation and also anti-tumour activity

68
Q

How do targeted therapies for inflammation work?

A

by switching off signalling that allows immune cells to help the cancer and switching on signalling which allows immune cells to attack the cancer (initiating a T cell response).

The Public 2 - Sem 2 (11 decks)

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