gms | German Medical Science

27. Deutscher Krebskongress

Deutsche Krebsgesellschaft e. V.

22. - 26.03.2006, Berlin

Interactions of chemotherapy, hormones or exogenous traumata with ionising radiation

Meeting Abstract

Suche in Medline nach

  • corresponding author presenting/speaker Wolfgang Dörr - Medizinische Fakultät Carl Gustav Carus, Dresden, Deutschland

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocIS026

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Veröffentlicht: 20. März 2006

© 2006 Dörr.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



The effects of ionising radiation can be either deterministic in nature, resulting in clinically manifest pathological changes, or stochastic, inducing of e.g. mutations or tumours. For deterministic radiation effects, early tissue reactions, occurring within 3 months after exposure, have to be differentiated from late effects, which are seen at months to many years after exposure. The latent time to tumour manifestation is several years for leucaemia to decades for solid tumours. In general, interaction of endogenous parameters, like hormones or growth factors, or exogenous factors, likechemotherapy, or additional trauma, with the effects of ionising radiation must be considered.

Early radiation reactions are based on cell kill of proliferating cells and consequent impairment of cell production in tissues with permanent cell turnover, like haematopoietic system or surface epithelia, which results in progressive loss of functional cells. Additional cell kill, e.g. by cytostatic drugs or by additional trauma, usually accelerates and aggravates the reactions. Little is known about the impact of hormonal treatment. Late radiation effects follow a more complex pathogenesis, with contribution from organ-specific cells as well as of vasculo-connective tissues. Like for early effects, additional cytotoxic treatment can exacerbate the radiation sequelae, as well as additional trauma at later time points. Importantly, additional traumata can also be based on severe early reactions in the same organ, if these are associated with an impairment of the barrier function of epithelia, hence resulting in consequential late effects. In some instances, an impact of hormonal treatment on late radiation effects has been reported, e.g. for tamoxifen and radiation pneumonitis.

Two mechanisms must be differentiated with regard to induction of tumours after radiation exposure: chronic inflammatory changes on the basis of deterministic reactions, e.g. in large intestine, and true mutagenic effects. Radiation, however, causes mainly gross DNA damage, and hence may be clearly less effective than chemotherapeutic drugs, which can cause more subtle changes in the genetic information. Further clinical studies are required to answer the question of tumour risk after radiation versus cytostatic or cytotoxic drugs.