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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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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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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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Magnetic bacteria exhibit a directed movement called magnetotaxis, driven by structures called magnetosomes. These magnetosomes consist of chains of magnetic particles made of either magnetite (Fe₃O₄) or greigite (Fe₃S₄) and are organized in a linear conformation by a protein scaffold within invaginations of the cell membrane. The bacteria align along the north–south magnetic field lines, much like a compass needle. They are typically microaerophilic or anaerobic...
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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
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DNA Damage Repair Classifier Defines Distinct Groups in Hepatocellular Carcinoma.

Markia A Smith1, Sarah C Van Alsten2, Andrea Walens3

  • 1Department of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.

Cancers
|September 9, 2022
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Summary

Hepatocellular carcinoma (HCC) tumors show varied DNA repair expression. High DNA repair activity, especially with liver regeneration, indicates aggressive tumors and poorer patient survival outcomes.

Keywords:
DNA repairHCChepatocellular carcinomaliver regenerationp53

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • DNA repair pathways influence hepatocellular carcinoma (HCC) clinical outcomes.
  • Mechanisms linking DNA repair variability to liver regeneration and HCC characteristics are not well understood.

Purpose of the Study:

  • To identify DNA repair expression classes in HCC.
  • To evaluate associations between these classes, liver features, and clinicopathologic variables.

Main Methods:

  • Curated a panel of 199 genes from 15 DNA repair pathways.
  • Analyzed The Cancer Genome Atlas (TCGA) HCC dataset.
  • Classified HCCs into low- or high-DNA repair expression groups.

Main Results:

  • Identified two main HCC groups: low-repair (lower grade, retained liver markers) and high-repair (aggressive features, increased p53 mutant-like genes, high liver regeneration).
  • The low-repair group comprised three subgroups (L1, L2, L3), with L3 showing high DNA repair and worse survival.
  • High-repair HCCs demonstrated significantly worse outcomes compared to L1 and L2 subgroups.

Conclusions:

  • Hepatocellular carcinoma exhibits diverse DNA repair expression profiles.
  • A subset of HCCs with high liver regeneration and high DNA repair expression is linked to poor prognosis and disrupted liver biology.