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M1 Cancer > Anti-cancer Drugs > Flashcards

Anti-cancer Drugs Flashcards

1
Q

What are the 6 types of cytotoxic drugs?

A

1) Alkylating agents
2) Platinum Analogues
3) Anti-metabolites
4) Cytotoxic Antibodies
5) Microtubule inhibitors
6) Topoisomerase inhibitors

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2
Q

What are the different treatment options for cancers?

A

1) Surgery
2) Radiotherapy
3) Pharmacotherapy/chemotherapy
4) Cryotherapy
5) Thermotherapy
6) Molecular targeted therapy
7) Biological response modifiers (eg. immuno-oncology)
8) Combination/multimodality therapies

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3
Q

What are the 7 roles of cancer pharmacotherapy?

A

1) Induction
2) Curative
3) Neo-adjuvant
4) Adjuvant
5) Maintenance
6) Palliative
7) Combination w radiotherapy (as radiation sensitiser)

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4
Q

Do chemotherapy drugs generally have a low or high TI?

A

Low TI (narrow therapeutic window)

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5
Q

What is the log-kill hypothesis?

A

Cytotoxic drugs demonstrate 1st order kinetics in killing tumour cells (fixed % die/cycle)
1 log kills 90%, 2 log kills 99%, 3 log kills 99.9%

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6
Q

What is growth fraction?

A

Growth fraction of tumor refers to the percentage of cells engaged in proliferation vs G0 phases at any given point in time

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7
Q

What are the differences between phase-specific and phase-non-specific drugs?

A

Phase-specific only kill during a specific phase of the cell cycle and are effective for high growth fraction tumours.

Phase-non-specific drugs work throughout the cell cycle and are effective for BOTH low and high growth fraction malignancies.

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8
Q

Why are nausea, vomiting, and colon ulceration common side effects of chemotherapy?

A

The epithelium of the GIT is highly proliferative

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9
Q

What form of toxicity is commonly found later in chemotherapy treatment?

A

Late organ toxicity (eg. cardio/pulmonary/nephro/neurotoxicity)

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10
Q

What is the MOA for Alkylating drugs?

A

Alkylates DNA, causing it to crosslink and unable to unwind for replication and transcription. It can also cause ss and dsDNA breaks.

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11
Q

Are Alkylating drugs phase-specific or phase-non-specific?

A

phase-non-specific (both replication and transcription disrupted)

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12
Q

What are some examples of Alkylating drugs?

A

1) Nitrogen mustards (eg. Cyclophosphamide, Chlorambucil)
2) Nitrosoureas (eg. Camustine, Lomustine, Semustine)
3) Alkyl sulfonates (eg. Busulfan)
4) Ethylenimines (eg. Thiotepa)
5) Triazenes (eg. Decarbazine, Procarbazine)

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13
Q

How can tumours develop resistance to Alkylating agents?

A

1) Increased efflux and decreased influx from cell
2) Inactivation of agent
3) Enhanced DNA repair (of lesions by alkylation)

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14
Q

Are Platinum analogues phase-specific or phase-non-specific?

A

Act like Alkylating agents: phase-non-specific (both replication and transcription disrupted)

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15
Q

What is the MOA for Platinum analogues?

A

Similar to Alkylating agents –> DNA adducts causing intra-strand crosslinks (< interstrand than alkylating) –> unable to unwind for replication and transcription.

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16
Q

What are some examples of Platinum analogues?

A

“-platin”
1st Gen: Cisplatin (** CI in Creatinine CL <60ml/min)
2nd Gen: Carboplatin
3rd Gen: Oxaliplatin

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17
Q

When are Platinum Analogues contraindicated?

A

Renal impairment

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18
Q

Are Anti-metabolites phase-specific or phase-non-specific?

A

Highly phase specific

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19
Q

What is the MOA of Anti-metabolites?

A

They prevent DNA replication by inhibiting purine and pyrimidine synthesis and incorporate into DNA to produce stress signals.

20
Q

What is the MOA of Methotrexate and when is it used clinically?

A

Methotrexate is an anti-metabolite which inhibits dihydrofolate reductase (DHFR), preventing thymidine monophosphate synthesis.
It is used in many tumours eg. breast cancer, lymphoma

21
Q

What is the MOA of 5-Fluorouracil?

A

5-Fluorouracil is an anti-metabolite which inhibits thymidylate synthase, and DNA synthesis

It is used in colorectal cancer

22
Q

What are some examples of Anti-metabolites?

A

**Methotrexate (MTX) **
5-Fluorouracil (5-FU)
6-Thioguanine
6-mercaptopurine
Gemcitabine
Cytosine arabinoside

23
Q

Are Cytotoxic Antibodies phase-specific or phase-non-specific?

A

phase-non-specific (both replication and transcription disrupted)

24
Q

What are 4 MOAs for Cytotoxic Abs?

A

1) Intercalate base pairs to prevent DNA replication and RNA synthesis
2) Create Fe-mediated free Oxygen radicals that dmg DNA and cell membranes
3) Inhibit Topoisomerase II
4) Alter membrane fluidity and ion transport

25
Q

What are some examples of Cytotoxic Antibodies?

A

Anthracyclines “-rubicin”: Doxorubicin, Daunorubicin, Idarubicin, Epirubicin
Others: Mitomycin C, Bleomycin

26
Q

Are Microtubule Inhibitors phase-specific or phase-non-specific?

A

phase-specific (disrupts mitosis)

27
Q

What are the 2 MOAs of Microtubule Inhibitors?

A

1) Vinca Alkaloids “Vin-“ bind to polymerising end to prevent microtubule elongation
2) Taxanes “-tax-“ bind and stabilise microtubule to prevent shortening/depolymerisation

28
Q

What are some examples of Microtubule Inhibitors?

A

1) Vinca Alkaloids “Vin-“: Vinblastine, Vincristine, Vinorelbine
2) Taxanes “-taxel”: Paclitaxel, Docetaxel, Carbazitaxel

29
Q

What adverse effect is especially associated with Taxane use.

A

Bradycardia

30
Q

Are Topoisomerase Inhibitors phase-specific or phase-non-specific?

A

phase-non-specific (both replication and transcription disrupted)

31
Q

What is the MOA of Topoisomerase Inhibitors

A

Inhibit Type I/II Isomerases to disrupt DNA supercoiling

32
Q

What are some examples of Topoisomerase Inhibitors?

A

Type I “-tecan”: Irinotecan, Topotecan
Type II “-poside”: Etoposide, Teniposide, Amsacrine

33
Q

What drug is used for Ph+ Chronic Myeloid Leukemia (CML)?

A

Imatinib (BCR-ABL TKI)

34
Q

What are 2 main receptors targeted with Tyrosine Kinase Inhibitors?

A

Constitutively active EGFR receptors (eg. Lung Cancer)
HER 2 Overexpression (eg. Breast cancer)

35
Q

What are the 5 approaches of molecular targeted therapy?

A

1) Blocking Abs (Growth factor)
2) Soluble receptors (Growth factor receptor)
3) Receptor kinase/chaperone protein inhibitors (Signal transduction to nucleus)
4) Inhibition of downstream signaling pathways (Signal transduction to nucleus)
5) Epigenetic modulators (Nuclear activity)

36
Q

What are the ideal characteristics for potential therapeutic antibodies targets?

A

They should be cell surface receptors or extracellular ligands that are (i) highly enriched and (ii) mediate essential tumour promoting pathways

37
Q

What are 4 types of therapeutic Abs?

A

1) Neutralising Abs (IgG/IgA)
2) Effector-mediated cytotoxicity: Complement system (IgM) or ADCC (IgG)
3) Ab-Drug Conjugates
4) Radio-labelled Abs

38
Q

What is the MOA of Avastin (Bevacizumab)?

A

Neutralising Ab.
Binds to VEGF before it binds to VEGFR to prevent angiogenesis

39
Q

What is the MOA of Ab-drug conjugates?

A

Ab with high affinity and specificity to tumour-specific Ag can be linked with drugs normally highly toxic on their own (low TI). Abs can bring the drug to the tumour where it is internalised and the linker is cleaved within, releasing the drug to take effect.

40
Q

What is an example of a Ab-drug conjugate?

A

Brentuximab (anti-CD30 mAb linked with mitotic inhibitor)

41
Q

What is the main concern of using molecular-targeted radiotherapy?

A

“Bystander” effect (potential destuction of adj cells)

42
Q

What are CAR T cells?

A

T cells engineers to express chimeric Ag receptors that recognise tumour cells

43
Q

What is the general structure of a CAR T cell?

A

1) Extracellular portion: recognises tumour Ag (CD19)
2) Intracellular portion: costimulatory signals (CD 26/134/137)

Newer gen CAR have >1 costimulatory signal for stronger activation (1st gen no costimulatory signal–> unsuccessful)

44
Q

What is the process of CAR T cell Therapy?

A

1) Extract T cells from px
2) Insert CAR gene into T cells via viral vector
3) Proliferate T cells invitro
4) Pre-condition px by lowering WBC
5) Insert engineered T cells into px

45
Q

What are immune checkpoint inhibitors?

A

Abs that are specific to Immune checkpoint receptors/ligands (eg. CTLA-4/B7, PD-1/PD-L1)

46
Q

What are some examples of Immune Checkpoint Inhibitors?

A

Ipilimumab (anti-CTLA-4)
Nivolumab and Pembrolizumab (PD-L1)

M1 Cancer (4 decks)

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