The accident at Chernobyl and trisomy 21 in Finland.

Our objective was to explore whether the radiation fallout in Finland after the accident at the Chernobyl nuclear power plant in April 1986 led to an increased incidence of trisomy 21. In this geographic and temporal cohort study, the country was divided into three zones according to the amounts of radioactive fallout and internal radiation caused by two cesium isotopes. The 518 cytologically verified cases of trisomy 21 were divided into a control group (conceived before the accident), and a study group of children whose expected dates of birth were in the post-accident years 1987-1988, i.e., pregnancies commenced after May 1986. The cases were also divided into three subgroups according to the zones of radiation. There were no significant differences in prevalence of trisomy 21 between the control and study groups nor between the three zones in spite of the significant differences in the levels of radiation and in the body burden that prevailed throughout the study period. Power estimates showed that in the two zones of lower radiation, an increase of 0.5% in the prevalence would have been detected with a power of 0.85, and in the somewhat smaller zone of the highest radiation, with a power of 0.70. The study lends no further support to the view that the low radiation fallout in western Europe would have been causally associated with trisomy 21.     

Cysteine proteinases in chondrosarcomas

The aim of the present study was to define the role of cathepsins B, H, K, L and S in the pathogenesis of human chondrosarcomas. For this purpose 40 tumour samples obtained from 12 patients with the diagnosis of conventional chondrosarcoma were systematically investigated for the expression of cathepsin mRNAs by Northern hybridisation, and for immunohistochemical localisation of the proteins. Northern analysis demonstrated the highest levels of cathepsins B and L in a recurring grade 1 chondrosarcoma, and in a grade 3 chondrosarcoma and in fibrous histiocytomas. Increased expression of cathepsin K mRNA was seen in seven chondrosarcomas, as well as in control tumours; fibrous histiocytomas, osteosarcomas, enchondromas and a giant cell tumour of bone. Cathepsin L was immunolocalised within the large chondrocytes, while cathepsin K was predominantly localised in large multinucleated osteoclastic cells and in some hypertrophic chondrocytes. These results suggest that chondrosarcoma can be included in the growing list of tumours, where cathepsins may well be involved in tumour progression. The simultaneous upregulation of cathepsins B and L, together with matrix metalloproteinase-13, and the association of cathepsin K with negative prognostic parameters suggests that an aggressive biological behaviour of chondrosarcoma may be related to the synthesis of cysteine proteinases and activation of other proteolytic enzymes. If this turns out to be the case, cathepsin inhibitors could provide the much needed adjuvant therapy for chondrosarcomas.