Endocrine Abstracts

The Chernobyl accident in 1986 resulted in a release of radioiodine that contaminated large areas of what are now Belarus, Northern Ukraine and a neighbouring area of Russia. The major health consequence of the accident to date has been a large increase in thyroid cancer in those who were children or adolescents at the time of exposure. The increase is mostly restricted to an increase in papillary carcinoma, of a particular subtype (the solid follicular variant) and associated with a specific rearrangement of the ret oncogene (PTC3). However, there is evidence that the morphological type of papillary carcinoma is changing with time, and that this may be associated with a change in molecular biological profile. Recent evidence suggests that the age group that shows the highest risk for the development of papillary cancer also exhibits an increase in follicular adenoma incidence at later time points. In general, there do not appear to be major differences with respect to the frequencies of involvement of individual molecular biological markers between Chernobyl-related and sporadic thyroid cancers.
In order to maximise the amount of molecular biological information that could be learnt from studying a group of human tumours for which the aetiological agent is known together with the time of that exposure, the Chernobyl Tissue Bank (CTB: www.swansea.ac.uk/nisctb) was established. The CTB permits multiple analyses of different oncogenes on RNA or DNA extracted from the same samples of tumour/normal pairs that have been assigned an agreed diagnosis by a panel of internationally recognised, expert pathologists. Some of the recent studies using material from the CTB have suggested that ret rearrangement may occur in a subset of cells within the tumour and that this may not always correlate with expression of the rearranged gene. We hope that detailed pathological analysis linked to multiple analyses on RNA extracted from the same sample of tumour will provide a better understanding of cooperation between oncogenes in carcinogenesis.