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The role of genetic factors in the pathogenesis of thyroid neoplasms

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Ferenc T., Maciaszczyk K., Gesing A., Lewinski A.
Postępy Higieny i Medycyny Doświadczalnej
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1997
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vol. 51
|
issue 4
367-384
EN
This paper summarizes the current knowledge on the role of genetic factors in the development of thyroid neoplasms. The introduction of the methods and concepts of molecular genetics (as, e.g. recombinant DNA technology) have elucidated etiopathogenesis of the majority of thyroid tumours and, in the future, can make the diagnosis easier. Mutations of genes involved in the control of cellular growth and/or differentiation (ras, c-myc, RET, met) affect the development of thyroid neoplasms. Loss of heterozygosity (LOH) may suggest the presence of tumor suppressor genes and has been reported in thyroid follicular carcinomas. Activation of tyrosine kinase, whether by specific oncogene amplification or by rearrangement, appears to be highly specific for the transformation of thyroid follicular cells into papillary tumours. Cytogenetic studies have shown frequent clonal abnormalities in thyroid follicular adenomas and carcinomas.
2

Immunopathology of Grave's disease

100%
Baj Z., Ferenc T., Lewinski A.
Postępy Higieny i Medycyny Doświadczalnej
|
1997
|
vol. 51
|
issue 5
531-546
EN
The pathogenesis Graves' disease, an autoimmune disorder, is not fully understood. Immune disturbances, genetic predisposition and environmental factors, affecting thyroid gland, appear to play the main role in contribution and development of the disease. Autoreactive T lymphocyte infiltrates in the thyroid gland and/or in the retroorbital tissues and autoantibodies to TSH receptor detected in almost all of the patients, have been considered to be responsible for hyperthyroidism, ophtalmopathy, pretibial dermopathy and goiter. In this review, we describe some recent reports on the pathophysiological and immunological aspects of the thyroidal and extrathyroidal manifestations of the Graves' disease.
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