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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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Mitogens and the Cell Cycle02:38

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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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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Related Experiment Video

Updated: Jan 3, 2026

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

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Functional Enhancers Shape Extrachromosomal Oncogene Amplifications.

Andrew R Morton1, Nergiz Dogan-Artun2, Zachary J Faber1

  • 1Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Case Comprehensive Cancer Center, Cleveland, OH 44106, USA.

Cell
|November 26, 2019
PubMed
Summary
This summary is machine-generated.

Cancer gene amplifications often include non-coding DNA, particularly enhancers near oncogenes like EGFR. These regions, crucial for cell fitness, are maintained on extrachromosomal DNA in glioblastoma.

Keywords:
EGFRMYCMYCNdouble minuteenhancerepigeneticextrachromosomal DNAglioblastomaoncogene amplification

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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
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Author Spotlight: FISH as a Tool for Precise Gene Amplification Assessment in Cancer Specimens
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Related Experiment Videos

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Author Spotlight: FISH as a Tool for Precise Gene Amplification Assessment in Cancer Specimens
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Author Spotlight: FISH as a Tool for Precise Gene Amplification Assessment in Cancer Specimens

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Area of Science:

  • Genomics
  • Cancer Biology
  • Epigenetics

Background:

  • Non-coding DNA regions adjacent to amplified oncogenes are frequently overlooked.
  • Understanding the role of these non-coding elements in cancer progression is critical.

Purpose of the Study:

  • To investigate the co-amplification patterns of non-coding DNA with oncogenes across various cancer types.
  • To explore the functional significance of co-amplified non-coding regulatory elements, specifically enhancers, in glioblastoma.

Main Methods:

  • Computational analysis to identify co-amplification signatures of non-coding DNA.
  • CRISPR interference screening to assess the impact of regulatory elements on cell fitness.
  • Analysis of chromatin topology and extrachromosomal DNA amplifications.

Main Results:

  • Significant co-amplification of non-coding DNA beyond oncogene boundaries was observed in five cancer types.
  • In glioblastoma, EGFR was co-amplified with its cell-type-specific enhancers, which were preserved on extrachromosomal DNA.
  • CRISPR screening identified diverse elements impacting cell fitness, mirroring rearrangements and chromatin rewiring on amplicons.

Conclusions:

  • Oncogene amplifications are influenced by regulatory dependencies within the non-coding genome.
  • Co-amplified non-coding elements, including enhancers, play a significant role in cancer cell fitness.
  • Extrachromosomal amplifications maintain the functional integrity of these regulatory elements and their associated chromatin topology.