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Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
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Functions of Thyroid Hormones01:18

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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
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Loss of Tumor Suppressor Gene Functions01:12

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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...
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Mutagenicity and Carcinogenicity01:25

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Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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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...
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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Molecular Alterations in Thyroid Carcinoma.

Mohamed Rizwan Haroon Al Rasheed1, Bin Xu1

  • 1Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.

Surgical Pathology Clinics
|November 2, 2019
PubMed
Summary
This summary is machine-generated.

Thyroid carcinoma, the most common endocrine cancer, is driven by genetic alterations like RAS and BRAF mutations. These molecular changes in the mitogen-activated protein kinase pathway are key targets for new tyrosine kinase inhibitor therapies.

Keywords:
Anaplastic thyroid carcinomaBRAFPapillary thyroid carcinomaPoorly differentiated thyroid carcinomaRASTERT promoter mutationThyroid carcinoma

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Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid carcinoma is the most prevalent endocrine system malignancy.
  • Next-generation sequencing has advanced understanding of thyroid cancer's molecular basis.
  • Constitutive activation of the mitogen-activated protein kinase (MAPK) pathway is crucial in thyroid tumorigenesis.

Purpose of the Study:

  • To provide a concise and updated summary of the primary genetic alterations in thyroid carcinoma.
  • To highlight the role of specific mutations and fusions in thyroid cancer development.
  • To discuss the implications of these molecular findings for targeted therapies.

Main Methods:

  • Review of recent advances in next-generation sequencing.
  • Analysis of molecular pathogenesis of thyroid cancer.
  • Identification of key genetic alterations and molecular signatures.

Main Results:

  • RAS mutations, BRAF mutations, and RET-PTC fusions are central to MAPK pathway activation and tumorigenesis.
  • TERT promoter and TP53 mutations are linked to tumor progression.
  • These genetic alterations offer potential targets for tyrosine kinase inhibitor therapy.

Conclusions:

  • Understanding the genetic landscape of thyroid carcinoma is critical for diagnosis and treatment.
  • Targeting activated molecular pathways presents a promising therapeutic strategy.
  • Continued research into molecular signatures will refine prognostication and treatment selection.