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Related Concept Videos

Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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Adaptive Mechanisms in Cancer Cells02:53

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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.
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Cancer02:18

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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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.
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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Telomeres and Cancer.

Hueng-Chuen Fan1,2,3,4, Fung-Wei Chang5, Jeng-Dau Tsai6,7

  • 1Department of Pediatrics, Tungs' Taichung Metroharbor Hospital, Wuchi, Taichung 435, Taiwan.

Life (Basel, Switzerland)
|December 24, 2021
PubMed
Summary

Telomeres protect chromosome ends, and their maintenance is crucial for preventing diseases like cancer. Dysfunctional telomere regulation, particularly telomerase reverse transcriptase (TERT) activation, drives cancer development and offers therapeutic targets.

Keywords:
CSTpromoter mutationsshelterintelomerasetelomerase reverse transcriptase

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Telomeres are essential chromatin structures at eukaryotic chromosome ends, vital for genome stability and replication.
  • Telomere length is regulated by telomerase, shelterin, and CST complexes, interacting with DNA replication, repair, and RNA metabolism pathways.
  • Telomere dysfunction and aberrant telomerase activation are implicated in human diseases, notably cancer.

Purpose of the Study:

  • To review the fundamental functions of telomeres and their regulatory mechanisms.
  • To elucidate the role of telomere maintenance modulators in genome protection.
  • To emphasize the implications of telomere dysregulation and telomerase activation in cancer development and explore therapeutic avenues.

Main Methods:

  • This review synthesizes existing research on telomere biology and its clinical relevance.
  • It analyzes the molecular mechanisms of telomere length regulation by key protein complexes.
  • The review examines the link between telomere maintenance, telomerase activity, and oncogenesis.

Main Results:

  • Telomere length maintenance involves a complex interplay of protein complexes and cellular pathways.
  • Cancer cells often exhibit activated telomerase, contributing to replicative immortality.
  • Telomerase reverse transcriptase (TERT) has oncogenic roles beyond telomere elongation.

Conclusions:

  • Understanding telomere dynamics and the multifaceted roles of telomerase is critical for cancer research.
  • Targeting telomere maintenance pathways presents promising therapeutic opportunities for cancer treatment.
  • Further investigation into telomere protection mechanisms can yield novel strategies against cancer.