Classifications of Anti- CANCER drugsI. According to mechanism:Alkylating agents:Example: Including drugs such as nitrogen mustard and cyclophosphamide.Mechanism: these are highly reactive molecules which bind irreversibly to macromolecules in the cell, notably DNA, RNA and proteins.Antimetabolites:Mechanism: these are closely related analogues of normal components intermediary metabolism or DNA synthesis.Example: Methotrexate inhibits folic acid metabolism. 6-mercaptopurine) inhibit DNA synthesis.
Natural products: A wide range of drugs has been developed from plants, bacteria, yeasts and fungi.Examples and mechanisms:Mitosis inhibitors: as vincristine .Antibiotics: as actinomycin D.Steroid hormones and antihormones:Mechanisms: These are widely used in cancer management, not only for the treatment of malignant disease, but also for the treatment of symptoms such as anorexia and hypercalcaemia.Examples: prednisolone, tamoxifen and cyproterone acetate.Others: Several drugs have been identified, often by random synthesis and screening, whose, Mechanism of action is not fully established but are thought to interact with DNA synthesis or replication. They include , dacarbazine, and cis-platinum.
II. According to their effect on the cell cycle:• Actively dividing cells pass through several phases. Mitosis is followed by a gap or delay (G1) then a synthetic phase (s) a second gap (G2) and mitosis again (M). Cells may cycle continuously or enter a quiescent phase (G0). Some drugs act at all phases of the cell cycle, others exert effects specifically at certain phase.
Class 1 drugs are non-specific and act on cells whether or not they are actively dividing, e.g. nitrogen mustard.Class 2 drugs act only at specific phases of the cell cycle, e.g. vincristine and methotrexate.Class 3 drugs act on cells in division and at all phase of the cycle, e.g. cyclophosphamide and actinomycin, D. Most cytotoxic drugs act by interfering with the synthesis and replication of DNA.•
Adverse effects:•Reactions to cancer chemotherapy are secondary to cell death both in the tumour and in other rapidly dividing cells of bone marrow, gastrointestinal tract, germinal epithelium etc. These can be divided into:
A. General adverse effects:Nausea and vomiting:may be severe and related to the direct actions of cytotoxic drugs on the chemoreceptor trigger zone or secondary to extensive tissue damage as occurs in radiation sickness.Metoclopramide (antiemetics) and the cannabinoid nabilone can be used to control nausea and vomiting.Alopecia:is a common adverse effect of cytotoxic drugs. Hair re-grows after the drugs are withdrawn.
Hyperuricaemia:Very high levels of plasma uric acid with precipitation of clinical gout or renal failure may complicate treatment of leukaemias and Iymphomas. Allopurinol, the xanthine oxidase inhibitor, may be used to prevent gout.Diarrhoea and malabsorption:occur as a result of cytotoxic effects on gut mucosal cell turnover.
Bone marrow depression:The bone marrow is particularly sensitive to cytotoxic drugs. Neutropenia or thrombocytopenia is common. They result in an increased risk of infection and haemorrhage respectively.Opportunistic infections:occur as a result of neutropenia and immunosuppressant therapy, which interfere with humoral and cell-mediated responses. Unusual infection with fungi and protozoa in addition to common pathogenic bacteria and viruses occur.
Drug Interactions:With many cytotoxic drugs in use, often in combination, it is not surprising that adverse interactions occur.Methotrexate and salicylates:As methotrexate is highly protein bound it is readily displaced from the binding site by aspirin and other salicylates. This may increase the risk of adverse effects of methotrexate.
6-Mercaptopurine and allopurinol:These two drugs are frequently used together. Allopurinol is a competitive inhibitor of xanthinc oxidase and also inhibits the breakdown of 6-mercaptopurine. The dose of 6-mercaptopurine must be reduced by at least 50%.
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