Abstract
We have investigated the possibility that structural alterations of the 'nuclear' oncogene family (c-myc, N-myc, L-myc, fos, myb and p53) leading to aberrant expression might, as in several other tumour types, play a role in the multi-stage development of tumorigenesis in the human thyroid follicular cell. Direct analysis of expression by slot and Northern blot RNA hybridisation showed that normal thyroid expresses surprisingly high levels of fos, and to a lesser extent c-myc, c-myc expression was markedly increased in all tumours, both benign and malignant, but no increase was seen in any other nuclear oncogene. fos expression was reduced specifically in one type of malignant tumour-follicular carcinoma-in inverse correlation with differentiation. Southern blot analysis showed no evidence of rearrangement or amplification of c-myc, or of any other 'nuclear' oncogene in any thyroid tumour. We conclude that there is no evidence that a primary abnormality of these genes plays a role in thyroid follicular cell tumorigenesis and suggest that the observed changes in expression can be adequately explained as secondary consequences of the tumour phenotype.
Highlights
Tumours were homogenised in a Waring blender, and DNA extracted as described by Kunkel et al (1977), modified by the addition of sodium perchlorate after the proteinase K digestion step
Total RNA from tumour and normal thyroid samples was first analysed by slot blot hybridisation
The level of expression of each oncogene was compared to that of the housekeeping gene hypoxanthine phosphoribosyltransferase (HPRT), the expression of which can be assumed to be independent of proliferative rate or neoplastic phenotype, to control for unavoidable variations in amount of RNA loaded between samples
Summary
We analysed the following thyroid follicular cell tumours Received 10 March 1989; and in revised form 17 May 1989. Criteria-Hedinger, 1974): 15 adenomas (8 of macrofollicular, 7 of microfollicular histological pattern); 17 differentiated carcinomas (5 follicular, 12 papillary); four anaplastic carcinomas. All tumours were obtained fresh from surgery, frozen in liquid nitrogen and stored at -70'C. Tumours were homogenised in a Waring blender, and DNA extracted as described by Kunkel et al (1977), modified by the addition of sodium perchlorate (to 1M) after the proteinase K digestion step. DNAs prepared from peripheral blood leukocytes of normal subjects were used as controls
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