Targeted radiotherapy

The biological properties of the tumour itself provide the basis for selective irradiation. In principle, this strategy should be capable of eradicating tumour cells anywhere in the body, but it is currently at an early stage of development for many sites.

♦ Iodine (well differentiated thyroid carcinomas)

♦ Monoclonal antibodies to cancer cell surface antigens (B-cell lymphoma)

♦ Catecholamine precursor analogue meta-iodo-benzl-guanine (MIBG) (neuroblastoma)

♦ Somatostatin (neuroendocrine tumours)

Until recently, the nuclides used in targeted radiotherapy were selected because of their availability and low cost rather than on account of their physical or radiobiological properties. Considerable experience has been gained with p emitters such as iodine-131 and yttrium-90, but short lived a emitters (e.g. astatine-211 or bismuth-212) or Auger-emitting radionuclides (e.g. iodine-125) are more potent cell killers and may find a clinical role. Targeting strategies to improve clinical results include:

♦ Improving the specificity of the existing targeting agents

♦ Regional targeting (e.g. intraperitoneal therapy)

♦ Multiple treatments

♦ Decreasing side-effects (myelosuppression due to a radiation of bone marrow is the most important) by using peripheral blood stem cell support or haemopoietic growth factors

♦ Combination of targeted radiotherapy with other treatments

The effectiveness of targeted radiotherapy is strongly dependent on the extent to which a sufficient dose may be delivered to critical clusters of tumour clonogens, and micodosimetric studies have shown that fluctuations in dose uniformity can adversely affect treatment outcome. The optimal strategy may be to use 'cocktails' of radionuclides, or to supplement targeted radiotherapy with external-beam irradiation.

Boron neutron capture therapy is a specialized approach to targeted therapy in which non-radioactive boron atoms are selectively incorporated into tumour cells. When exposed to a beam of 'slow' neutrons the boron emits a particles locally within the tumour, causing dense ionizations and DNA damage. So far, clinical experience in brain tumours has produced controversial results.

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