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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Nucleotide Excision Repair01:38

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Fixing Double-strand Breaks02:04

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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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Base Excision Repair01:54

Base Excision Repair

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Medulloblastoma and the DNA Damage Response.

Leon F McSwain1, Kiran K Parwani2,3, Shubin W Shahab2

  • 1Department of Pediatrics, Emory University, Atlanta, GA, United States.

Frontiers in Oncology
|June 24, 2022
PubMed
Summary

Targeting DNA damage repair proteins offers a promising strategy for treating medulloblastoma (MB), the most common pediatric brain cancer. This approach could provide broad impact across all molecular subgroups of MB.

Keywords:
medulloblastomap53 statuspediatricsradiation oncologytherapeutic targeting

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Area of Science:

  • Pediatric Oncology
  • Cancer Genomics
  • Molecular Biology

Background:

  • Medulloblastoma (MB) is the most common malignant pediatric brain tumor.
  • Current treatments include surgery, radiation, and chemotherapy, often guided by histology rather than molecular profile.
  • Four distinct molecular subgroups (WNT, SHH, Group 3, Group 4) have been identified, yet treatment stratification remains limited.

Purpose of the Study:

  • To explore the potential of targeting DNA damage response (DDR) pathways in medulloblastoma.
  • To discuss the molecular basis of genomic instability in MB.
  • To identify novel therapeutic strategies for MB irrespective of molecular subgroup.

Main Methods:

  • Review of molecular underpinnings of genomic instability in medulloblastoma.
  • Analysis of DNA damage response (DDR) pathways relevant to cancer therapy.
  • Exploration of DDR inhibitors as potential therapeutic agents for MB.

Main Results:

  • Genomic instability is a key feature of medulloblastoma.
  • DNA damage response (DDR) proteins are critical for cancer cell survival.
  • DDR inhibitors show promise as monotherapy or in combination for various cancers.

Conclusions:

  • Targeting DNA damage repair mechanisms presents a viable therapeutic strategy for medulloblastoma.
  • Inhibitors of DDR proteins could offer a broad-impact approach across all MB molecular subgroups.
  • Further research into DDR inhibition is warranted for developing novel MB treatments.