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Cards (15)

  • Antimetabolitesdrugs used in cancer chemotherapy. Interfere with enzymes for DNA synthesis. Has similar structure to substrate. They replace the substrate that would be used normally. They do not form the product.
  • Cancer cells replicate quickly than normal cells. These drugs affect cancer cell replication compared to normal cell.
  • Folate antagonistsantifolates: interfere with the nucleotide synthesis and folic acid use.
    Methotrexate replaces folic acid. Doesn't form nucleotide.
  • Fluorouracil has similar structure – forms false product by acting as false substrate. Interacts with thymidylate synthase and not form functional nucleotide TTP. Results in DNA inhibition only.
  • 5fluorouracil – an antimetabolite. Made based on tumor requirement of thymidine from uracil. Metabolite imitates uracil and intereferes with DNA synthesis. Stops cancer cell division that relies on thymidine.
  • Thymidylate synthase catalyzes dUMP to dTMP reaction.
  • Thymidylate permanently remains alkylated due to no elimination occuring since fluroine will not generate F+
  • Thymidylate synthase inhibition by 5FU
    Thymidine binds to thymidylate synthase and tetrahydrofolic acid. 5th position hydrogen removed from thymidine. Replaced by fluorine atom. Because fluorine is stable, does not release ion like hydrogen. Prevents normal dissociation process.
    DNA synthesis prevented due to thymidylate synthase not functioning properly.
  • Breast cancer hormones (anti - oestrogen) – oestrogen receptor activation leads to further replication of tumour cells in breast cancer.
    Tamoxifen competes for oestrogen receptors with endogenous oestrogen. Prevents transcription of oestrogen responsive genes.
  • Breast cancer that relies on estrogen for growth needs agents (tamoxifen) to counteract estrogen effect. 17B-estradiol is hormone which promotes growth of certain tissue. Tamoxifen partially activates estrogen receptors after binding. Prevents growth by blocking 17B –estradiol binding.
  • Monoclonal antibodiescancer cells have overexpressed antigens. Target for antibodies. Monoclonal antibodies made for attacking tumors. They start by trigerring immune response to attack cancer cells.
    Monoclonal antibodies are used in combo with anticancer drugs for max effectiveness. It offers highly targeted therapy where it spares healthy cells and targets cancer cells.
  • Monoclonal antibodies work by 2 principles.
    M1 - Antibody bidning trigers bodys immune mechanism. Cancer cell killed by complement-mediated lysis/killer T cells.
    M2antibody attach and inactivate growth factors preventing survival and results in apoptosis.
  • R chop is a combination therapy. First line of treatment for non-hodgkins lymphoma.
  • RCHOP: has 6-8 sessions. 21 days apart.
    Rituximab – boost immune system to attack B cells
    Cyclophosphamideguanine alkylating agent
    Doxorubicintopoisomerase II poison and DNA intercalator
    Vincristinemitotic inhibitor
    Prednisoloneimmunosuppressing and anti inflammatory properties.
  • chloromethine analogues are better than chlormethine as it has better properties than chloromethine in terms of less toxicity which reduces the side effects. This is because of teh presence of teh electron withdrawing group which decreases the nucleophilicity of the N thus making it a less reactive alkylating agent.