Oncology Pharmacology - lecture

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lee.staite
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270884
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Oncology Pharmacology - lecture
Updated:
2014-04-17 07:20:28
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mechanism chemotherapy radiotherapy
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How treatments for cancer work
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  1. What are the main functions of chemotherapy which cause the common ADR?
    Affects rapidly proliferating cells - GI tract, hair follicles, bone marrow, gonads (infertility men), fetus.
  2. What are the classes of chemotherapy agents?
    • Alkylating agents
    • Anthracyclins
    • Camptothecins
    • Etoposide
    • Bleomycin
    • Anti-metabolites
    • "Anti-folate"
    • Purines and Pyrimadines
    • Microtubule polymerisation regulators
    • Platinum drugs
    • Hormonal therapy: Anti-oestrogen
    • Hormonal therapy: Anti-androgens
  3. How do alkylating agents work?
    e.g. Cyclophosphamide
    Cross link strands of DNA together or excision of base or ring opening or incorrect base pairing.

    If occurs in an essential gene causes cell death.

    Mutations in normal cells may cause mutation.

    Occur at nucleophilic sites: guanine N-7 and O-6
  4. How do Anthracyclins work?
    e.g. Doxorubicin, Epirubicin
    Interchelate between DNA strands. Prevents topoisomerase from cleaving DNA to allow unraveling to prevent supercoil.

    Risk of cardiac toxicity. esp. doxo (generates free-radicals)
  5. How do Camptothecins work?
    e.g. Topotecan, Irinotecan
    Stabilise the DNA:Topoisomerase 1 complex. Thus preventing rejoining
  6. How does Etoposide work?
    Stabilise the DNA:Topoisomerase 2 complex. Thus preventing rejoining
  7. How does Bleomycin work?
    Chelates Fe2+, cleaves DNA strand
  8. How do Anti-metobolites work?
    Mercaptopurine, Thioguanine
    Inhibits the production of nucleotides
  9. How do anti-folate work?
    Methotrexate
    Prevent the production of folate by interfering with enzymes involved in the pathway.

    • Aspirin and NSAIDs inhibit excretion
    • Penicillin inhibits renal excretion, reduce dose.
  10. How do purines and pyrimidines work?
    Are incorporated into DNA and cause functional changes that are vital to cells survival.

    • Thioguanine: inhibits transcription and replication
    • Fludarabine: (purine) cause chain termination
    • Cladribine: Causes strand breaks.
    • Gemcitabine: Inhibit riboneucleotide, interferes with replication
    • 5-azacytidine (cytidine analogue) Isn't methylated, alters gene expression
    • Cytrabine (cytidine analogue) Cause chain termination.
  11. How do microtubule polymerisation regulators work?
    Microtubules have a key role in mitosis during chromosome segregation.

    • Vinca alkaloids - inhibit polymerisation
    •    vinblastine
    •    vincristine
    •    vinrelbine
    •    vindesine

    • Taxanes - inhibit depolymerisation - Mpahse arrest and apoptosis
    •    Docetaxel
    •    Paclitaxel
  12. How do platinum drugs work?
    Carboplatin, Cisplatin, Oxaliplatin
    Similar to cisplatin but also cause other damage to DNA strand such as bending and coiling as well as chelation.

    Vomiting common, use 5HT3

    Cisplatin oto.nephro-toxic. Less common with carboplatin.
  13. Hormonal therapy: anti-oestrogens
    Useful in breast cancer.

    • Oestrogen receptor antagonists
    • -Tamoxifen: partial antagonist (active metabolite 4-hydroxytamoxife) ER positive breast cancer cells (oestrogen receptor, hormone depending tumour growth. May become independent)
    • -Fluvestrant: oestrogen receptor antagonist

    • Aromatase inhibitors - aromatase is an enzyme that hydroxylates steroids during oestrogen synthesis.
    • -Anastrozole
    • -Letrozole
  14. Hormonal therapy: anti-androgens
    Useful in prostate cancer

    • Androgen receptor antagonist
    • - Bicalutamide (casodex)

    GnRH super-agonnist. reduces the regulation of LHRH receptor, inhibits production of LH and FSH, therefore androgens too.

    LHRH => LH, FSH => Testosterone

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