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Genetic and Epigenetic of Medullary Thyroid Cancer
Medullary thyroid carcinoma (MTC) is an infrequent calcitonin-producing neuroendocrine tumor that initiates from the parafollicular C cells of the thyroid gland. Several genetic and epigenetic alterations are collaterally responsible for medullary thyroid carcinogenesis. In this review article, we s...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Pasteur Institute
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889499/ https://www.ncbi.nlm.nih.gov/pubmed/29126344 http://dx.doi.org/10.22034/ibj.22.3.142 |
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author | Khatami, Fatemeh Tavangar, Seyed Mohammad |
author_facet | Khatami, Fatemeh Tavangar, Seyed Mohammad |
author_sort | Khatami, Fatemeh |
collection | PubMed |
description | Medullary thyroid carcinoma (MTC) is an infrequent calcitonin-producing neuroendocrine tumor that initiates from the parafollicular C cells of the thyroid gland. Several genetic and epigenetic alterations are collaterally responsible for medullary thyroid carcinogenesis. In this review article, we shed light on all the genetic and epigenetic hallmarks of MTC. From the genetic perspective, RET, HRAS, and KRAS are the most important genes that are characterized in MTC. From the epigenetic perspective, Ras-association domain family member 1A, telomerase reverse transcriptase promoter methylations, overexpression of histone methyltransferases, EZH2 and SMYD3, and wide ranging increase and decrease in non-coding RNAs can be responsible for medullary thyroid carcinogenesis. |
format | Online Article Text |
id | pubmed-5889499 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Pasteur Institute |
record_format | MEDLINE/PubMed |
spelling | pubmed-58894992018-05-01 Genetic and Epigenetic of Medullary Thyroid Cancer Khatami, Fatemeh Tavangar, Seyed Mohammad Iran Biomed J Review Article Medullary thyroid carcinoma (MTC) is an infrequent calcitonin-producing neuroendocrine tumor that initiates from the parafollicular C cells of the thyroid gland. Several genetic and epigenetic alterations are collaterally responsible for medullary thyroid carcinogenesis. In this review article, we shed light on all the genetic and epigenetic hallmarks of MTC. From the genetic perspective, RET, HRAS, and KRAS are the most important genes that are characterized in MTC. From the epigenetic perspective, Ras-association domain family member 1A, telomerase reverse transcriptase promoter methylations, overexpression of histone methyltransferases, EZH2 and SMYD3, and wide ranging increase and decrease in non-coding RNAs can be responsible for medullary thyroid carcinogenesis. Pasteur Institute 2018-05 /pmc/articles/PMC5889499/ /pubmed/29126344 http://dx.doi.org/10.22034/ibj.22.3.142 Text en Copyright: © Iranian Biomedical Journal http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Khatami, Fatemeh Tavangar, Seyed Mohammad Genetic and Epigenetic of Medullary Thyroid Cancer |
title | Genetic and Epigenetic of Medullary Thyroid Cancer |
title_full | Genetic and Epigenetic of Medullary Thyroid Cancer |
title_fullStr | Genetic and Epigenetic of Medullary Thyroid Cancer |
title_full_unstemmed | Genetic and Epigenetic of Medullary Thyroid Cancer |
title_short | Genetic and Epigenetic of Medullary Thyroid Cancer |
title_sort | genetic and epigenetic of medullary thyroid cancer |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5889499/ https://www.ncbi.nlm.nih.gov/pubmed/29126344 http://dx.doi.org/10.22034/ibj.22.3.142 |
work_keys_str_mv | AT khatamifatemeh geneticandepigeneticofmedullarythyroidcancer AT tavangarseyedmohammad geneticandepigeneticofmedullarythyroidcancer |