Targeted therapy in cancer

• Autores: Philip Charlton, James Spicer
• Localización: Medicine, ISSN-e 1357-3039, Vol. 44, Nº. 1, 2016, págs. 34-38
• Idioma: inglés
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• Resumen

  • The historical use of chemotherapy relied on the systemic use of cytotoxic agents to disrupt mitosis in rapidly dividing cancer cells, with foreseeable dose-limiting haematological toxicities. Targeted therapies affect specific cellular molecular mechanisms promoting cancer cell survival and proliferation, enabling treatment tailored to specific tumour characteristics. The key pathways include the hormonal axis, growth factor receptor-mediated tyrosine kinases and cellular immune system. Monoclonal antibodies can target extracellular ligands or cell surface growth factor receptors. Tyrosine kinase inhibitors prevent signal transduction from the intracellular portion of the receptors. Immune checkpoint inhibiting antibodies facilitate immune recognition and destruction of cancer cells by cytotoxic T cells. Various agents are used to reduce hormone synthesis or block activation of intracellular hormone receptors. These newer agents have a different pattern of adverse effects, but offer an improved therapeutic ratio for many patients. The highly targeted mechanism of activity means that an individualized pre-treatment characterization of the patient's tumour molecular profile is increasingly needed.