major discovery! Proposed a new theory of thyroid tumor production August 16, 2016 Source: Bio Valley Autonomously functioning thyroid adenoma (autonomous thyroid adenoma, ATA) is the most common benign thyroid tumors. Mutations in both genes result in approximately 70% of ATA cases. Now, in a new study, researchers from the University of Würzburg, Germany, found another key trigger. The results of the study were published in the Journal of Clinical Investigation on August 8, 2016 under the heading "Recurrent EZH1 mutations are a second hit in autonomous thyroid adenomas". 2022 New Laser Distance Sensor
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Thyroid hormones are involved in controlling many functions of the body: they affect sugar, lipid and protein metabolism, regulate body temperature, heart rate, blood circulation and more. In children, they also control brain and nerve development as well as bone growth. It is no wonder that hyperthyroidism has several deleterious effects on affected patients. Typical features include persistent restlessness, irritability, puzzling weight loss, excessive sweating, and increased pulse pressure. Hyperthyroidism can have serious consequences when left untreated, including, most importantly, higher cardiovascular mortality.
Looking for mutations as a cause
In many cases, this hyperactivity is caused by thyroid tumors, most of which are benign. Among thyroid tumors, the so-called ATA accounts for the vast majority. In general, its origins are well understood: “We know that certain mutations in certain genes cause about 70% of ATA,†said Dr. Davide Calebiro, the first author of the paper and a researcher at the University of Würzburg School of Pharmacology and Toxicology. .
Specifically, activating mutations in the TSHR gene (encoding thyroid stimulating hormone receptor) have been found in up to 70% of ATA. In addition, a small portion of ATA undergoes activating mutations on the GNAS gene (encoding the Gs protein alpha subunit).
However, prior to this, it was not clear whether these mutations alone were sufficient to promote the increase of thyroid cells and the production of excess hormones, or whether other factors must be present. In addition, it is unclear which factors are involved in the remaining 30% of ATA cases.
Published in the journal
Among the other causes of ATA, an international team led by Davide Calebiro, Luca Persani from the University of Milan, Italy, and Ralf Paschke from the University of Calgary, Canada, are now successful.
Calebiro described their approach. "As far as our research is concerned, we have studied 19 ATA cases using full exon sequencing." This technique does not study the whole genome of cells, but rather studies the exons of genes. That is, a DNA fragment that is truly translated into a protein. Generally, these exons (exome) account for 1-2% of total DNA. Calebiro further explained, "We can confirm that a significant number of ATAs in these ATAs are mutated in a gene involved in controlling cell proliferation and differentiation."
Gene mutation leads to increased cell proliferation
The scientific name for this gene is EZH1 (Enhancer of Zeste Homolog 1). The EZH1 gene mutation works in concert with other known mutations, resulting in ATA production. Furthermore, functional studies have confirmed that EZH1 gene mutations cause changes in the signaling pathway leading to thyroid cell proliferation.
Calebiro concludes, "We have confirmed that a hotspot mutation in the EZH1 gene is the second most common genetic defect in ATA." In his view, EZH1 mutations are often associated with mutations that occur in previously known genes. Together, this suggests that there is a “two-strike modelâ€. Accordingly, the first gene mutation increases the susceptibility to ATA, and the second gene mutation triggers the disease process.
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