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07:01
An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
The clonal origin of thyroid nodules and adenomas
G A Thomas1, D Williams, E D Williams
1Department of Pathology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom.
The American Journal of Pathology
|January 1, 1989
Summary
Thyroid adenomas in mice heterozygous for glucose-6-phosphate dehydrogenase (G6PD) deficiency were monoclonal, while nodules were polyclonal. This suggests distinct cellular origins for different thyroid lesion types.
Area of Science:
- Oncology
- Genetics
- Endocrinology
Background:
- Studying the clonal origin of tumors is crucial for understanding cancer development.
- X-linked enzyme deficiencies, like glucose-6-phosphate dehydrogenase (G6PD), can be used as genetic markers to trace cellular lineage.
- Thyroid lesions, including adenomas and nodules, present distinct histological features.
Purpose of the Study:
- To determine the clonal origin of thyroid adenomas and nodules in mice.
- To investigate the role of genetic markers (G6PD deficiency) in assessing tumor monoclonality versus polyclonality.
- To explore the potential involvement of stromal components in the development of thyroid lesions.
Main Methods:
- Utilized female mice heterozygous for G6PD deficiency as a model system.
- Employed enzyme histochemistry to differentiate cellular phenotypes based on G6PD activity.
- Developed a method to quantify the degree of cellular phenotype mingling in normal tissue.
- Analyzed 453 induced thyroid lesions (adenomas and nodules) in experimental mice.
Main Results:
- Thyroid adenomas (128) were predominantly monophenotypic (84%), indicating monoclonal origin.
- Thyroid nodules (75) showed a significant proportion of monophenotypic lesions (33%), but also a variegated pattern suggesting polyclonal origin.
- A method to assess cellular phenotype mingling indicated that a quarter of adjacent cells were of unlike phenotype.
Conclusions:
- Thyroid adenomas arise from a single cell (monoclonal).
- Thyroid nodules originate from multiple cells (polyclonal).
- The prominent stroma in nodules suggests a potential causative role in their polyclonal development.
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