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Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

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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DNA Damage can Stall the Cell Cycle02:36

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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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C4 Pathway and CAM01:27

C4 Pathway and CAM

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Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
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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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Translesion DNA Polymerases02:10

Translesion DNA Polymerases

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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DNA Topoisomerases02:02

DNA Topoisomerases

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Topoisomerases are enzymes that relax overwound DNA molecules during various cell processes, including DNA replication and transcription. These enzymes regulate positive and negative DNA supercoiling without changing the nucleotide sequence. DNA overwinding in a clockwise direction results in positively supercoiled DNA, whereas underwinding in a counterclockwise direction produces negatively supercoiled DNA.
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Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
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DNA damage pathways and B-cell lymphomagenesis.

Gero Knittel1,2, Tim Rehkämper1,2, Pascal Nieper1,2

  • 1Department I of Internal Medicine, University Hospital of Cologne.

Current Opinion in Hematology
|April 28, 2018
PubMed
Summary

Recent genomic studies reveal DNA repair defects in lymphomas, particularly ATM mutations in chronic lymphocytic leukemia (CLL). These findings identify new therapeutic targets for lymphoma treatment.

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Area of Science:

  • Genomics
  • Cancer Biology
  • Hematology

Background:

  • Lymphoma genome sequencing projects have elucidated the genomic landscape of indolent and aggressive lymphomas.
  • Understanding molecular mechanisms of mutations and translocations is crucial for lymphoma research.

Purpose of the Study:

  • Review recent genomic discoveries in lymphoma, focusing on acquired DNA repair defects.
  • Highlight actionable molecular vulnerabilities in chronic lymphocytic leukemia (CLL) as a model.
  • Discuss novel therapeutic interventions targeting DNA damage response pathways.

Main Methods:

  • Analysis of large lymphoma genome sequencing project data (CLL, T-PLL, DLBCL).
  • Alignment of discoveries with proposed mutation acquisition mechanisms in B-cell lymphomas.
  • Evaluation of novel autochthonous mouse models for CLL preclinical studies.

Main Results:

  • Identification of acquired DNA repair defects as selected events in lymphoma development.
  • ATM deficiency is linked to sensitivity to PARP1 and DNA-PKcs inhibitors.
  • Early clinical data show promise for compounds targeting DNA damage response in CLL.

Conclusions:

  • Genomic insights are advancing our understanding of lymphoma pathogenesis.
  • Targeting DNA repair defects presents a promising therapeutic strategy for lymphomas, especially CLL.
  • ATM mutations represent a key vulnerability for targeted therapies in CLL.