Related Experiment Video
Updated: Mar 1, 2026
05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
2.3K
Epigenetic modifications in poorly differentiated and anaplastic thyroid cancer
Thanyawat Sasanakietkul1, Timothy D Murtha1, Mahsa Javid1
1Yale Endocrine Neoplasia Laboratory, Section of Endocrine Surgery, Yale School of Medicine, New Haven, CT 06520, USA; Department of Surgery, Section of Endocrine Surgery, Yale School of Medicine, New Haven, CT 06520, USA.
Molecular and Cellular Endocrinology
|May 30, 2017
Summary
Poorly differentiated thyroid carcinoma (PDTC) and anaplastic thyroid carcinoma (ATC) are aggressive. Epigenetic alterations in PDTC and ATC offer potential therapeutic targets for these challenging endocrine malignancies.
Area of Science:
- Endocrinology
- Oncology
- Epigenetics
Background:
- Well-differentiated thyroid cancer has a good prognosis, but poorly differentiated thyroid carcinoma (PDTC) and anaplastic thyroid carcinoma (ATC) are highly aggressive.
- PDTC and ATC represent a significant challenge in endocrine oncology due to their aggressive nature and poor outcomes.
Purpose of the Study:
- To review current understanding of epigenetic alterations in PDTC and ATC.
- To explore the therapeutic potential of targeting epigenetic dysregulation in these aggressive thyroid cancers.
Main Methods:
- Literature review of epigenetic modifications in thyroid cancer.
- Analysis of identified epigenetic candidates including specific genes and non-coding RNAs.
- Discussion of affected signaling pathways and their role in carcinogenesis.
Main Results:
- Identified key epigenetic dysregulations in PDTC and ATC involving Aurora group, KMT2D, PTEN, RASSF1A, ncRNAs, and SWI/SNF complex.
- Highlighted the role of these epigenetic alterations in driving thyroid carcinogenesis.
- Emphasized the potential for improved prognostic testing and development of epigenetic therapies.
Conclusions:
- Epigenetic alterations are crucial in the pathogenesis of PDTC and ATC.
- Targeting epigenetic dysregulation presents a promising avenue for novel therapeutic strategies in aggressive thyroid cancers.
Related Concept Videos
01:37Epigenetic Regulation
4.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
X-chromosome...
4.0K
01:46Epigenetic Regulation
34.1K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
34.1K
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
56
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
56
01:12Loss of Tumor Suppressor Gene Functions
6.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.2K
02:23Abnormal Proliferation
5.3K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K
02:53Adaptive Mechanisms in Cancer Cells
7.2K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.2K