Studies summarize promising innovations in molecular diagnosis of thyroid cancer
Two recently released studies, one written by a pair of Greek endocrinologists and the other by an American pathologist, summarize the latest advancements made into the molecular analysis and diagnosis of thyroid cancer.
In a report appearing in the Journal of Thyroid Research (JTR), researchers from Athens noted that a number of genetic mutations, molecular markers and epigenetic modifications can help doctors detect an increased risk of abnormal thyroid cell growth.
The other paper, written by a physician at the University of Pittsburgh Medical Center and published in the journal Modern Pathology, addressed similar subject matter, though its scope was limited to genetic mutations.
Both papers pointed to chromosomal rearrangement as a budding field of thyroid cancer-related inquiry. For instance, researchers have found that the REarranged during Transfection (RET) proto-oncogene confers a substantial risk of medullary or papillary thyroid cancer.
The RET proto-oncogene is a strip of DNA that, when spontaneously rearranged, can increase the growth, differentiation and migration of thyroid cells. RET rearrangements often occur after exposure to intense radiation, according to the JTR report.
Both studies also discussed the molecular detection of RAt Sarcoma (RAS) oncogenes. When mutations occur in a specific area of a person's DNA that controls RAS subfamily proteins, cells can experience radical growth. This phenomenon occurs because RAS proteins help control the signals between a cell's nucleus and its organelles. Point mutations in the genes that control these proteins can increase the risk of thyroid cancer, although these same mutations may be detected through genetic testing.
Finally, the JTR study touched on epigenetic modifications. All DNA is coiled into a tight structure called chromatin. Molecules called methyl groups, which lie on the outside of DNA strands, help keep genes bunched together in this way.
However, accidental modifications to the placement of these methyl groups can lead to whole sections of DNA being inaccessible to transcribing proteins. These epigenetic changes can prevent thyroid cells from limiting their own growth.
In a report appearing in the Journal of Thyroid Research (JTR), researchers from Athens noted that a number of genetic mutations, molecular markers and epigenetic modifications can help doctors detect an increased risk of abnormal thyroid cell growth.
The other paper, written by a physician at the University of Pittsburgh Medical Center and published in the journal Modern Pathology, addressed similar subject matter, though its scope was limited to genetic mutations.
Both papers pointed to chromosomal rearrangement as a budding field of thyroid cancer-related inquiry. For instance, researchers have found that the REarranged during Transfection (RET) proto-oncogene confers a substantial risk of medullary or papillary thyroid cancer.
The RET proto-oncogene is a strip of DNA that, when spontaneously rearranged, can increase the growth, differentiation and migration of thyroid cells. RET rearrangements often occur after exposure to intense radiation, according to the JTR report.
Both studies also discussed the molecular detection of RAt Sarcoma (RAS) oncogenes. When mutations occur in a specific area of a person's DNA that controls RAS subfamily proteins, cells can experience radical growth. This phenomenon occurs because RAS proteins help control the signals between a cell's nucleus and its organelles. Point mutations in the genes that control these proteins can increase the risk of thyroid cancer, although these same mutations may be detected through genetic testing.
Finally, the JTR study touched on epigenetic modifications. All DNA is coiled into a tight structure called chromatin. Molecules called methyl groups, which lie on the outside of DNA strands, help keep genes bunched together in this way.
However, accidental modifications to the placement of these methyl groups can lead to whole sections of DNA being inaccessible to transcribing proteins. These epigenetic changes can prevent thyroid cells from limiting their own growth.
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