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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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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.
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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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lncRNA - Long Non-coding RNAs02:39

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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Genetics and epigenetics in conventional chondrosarcoma with focus on non-coding RNAs.

Albert Roessner1, Sabine Franke1, Julian Schreier1

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Pathology, Research and Practice
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Summary

Mutations in isocitrate dehydrogenase 1 and 2 (IDH 1/2) drive chondrosarcoma by producing D-2-hydroxyglutarate (D-2HG), which disrupts epigenetic regulation. Non-coding RNAs (ncRNAs) further promote cancer by interacting with these epigenetic regulators.

Keywords:
Cartilage TumorsChondrosarcomaEpigenomeIsocitrat DehydrogenaseMolecular PathologyNon-coding RNAs

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Isocitrate dehydrogenase 1 and 2 (IDH 1/2) mutations are key drivers in chondrosarcoma, a rare mesenchymal tumor.
  • Mutant IDH 1/2 produces D-2-hydroxyglutarate (D-2HG), a metabolite that inhibits α-ketoglutarate (α-KG) dependent enzymes.

Purpose of the Study:

  • To review the molecular mechanisms of chondrosarcoma development, focusing on IDH mutations and epigenetic dysregulation.
  • To highlight the role of non-coding RNAs (ncRNAs) in chondrosarcoma pathogenesis and their interaction with epigenetic regulators.

Main Methods:

  • Review of existing literature on IDH mutations, D-2HG production, and epigenetic alterations in chondrosarcoma.
  • Analysis of the role of α-KG-dependent enzymes, including TET and Jumonji families, in regulating DNA methylation and histone modification.
  • Examination of the involvement of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in chondrosarcoma progression.

Main Results:

  • IDH mutations lead to D-2HG accumulation, causing aberrant DNA methylation and histone modifications by inhibiting TET and Jumonji enzymes.
  • ncRNAs, including miRNAs and lncRNAs, interact with α-KG-dependent epigenetic regulators, contributing to malignant transformation.
  • These interactions disrupt cellular signaling pathways, promoting the development of aggressive cellular traits in chondrosarcoma.

Conclusions:

  • IDH mutations and subsequent D-2HG production are central to the epigenetic reprogramming in chondrosarcoma.
  • ncRNAs play a critical oncogenic role by modulating epigenetic landscapes in conjunction with genetic mutations.
  • Understanding these complex genetic, epigenetic, and ncRNA interactions is crucial for developing targeted therapies for chondrosarcoma.