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Related Concept Videos

Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Mutations01:39

Mutations

Overview
Biological Effects of Radiation02:59

Biological Effects of Radiation

All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they produce ions...
Other Unique Bacteria01:18

Other Unique Bacteria

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 and are commonly found near the...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids
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Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids

Published on: April 5, 2024

Cellular radiosensitivity: how much better do we understand it?

Penny Jeggo1, Martin F Lavin

  • 1Genome Damage and Stability Centre, Science Park Road, University of Sussex, Falmer, Brighton, East Sussex BN1 9RQ, UK. p.a.jeggo@sussex.ac.uk

International Journal of Radiation Biology
|December 10, 2009
PubMed
Summary
This summary is machine-generated.

Ionizing radiation damages DNA, with DNA double-strand breaks (DSBs) being the most critical lesion. Effective repair of DSBs, via homologous recombination (HR) or non-homologous end-joining (NHEJ), is crucial for cell survival and preventing genetic instability.

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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines

Published on: August 21, 2019

Area of Science:

  • Molecular Biology
  • Radiation Biology
  • Genetics

Background:

  • Ionizing radiation induces DNA lesions, leading to genetic instability, cancer, or cell death.
  • Radiation damage occurs through direct DNA interaction or indirect effects via water radiolysis and free radicals.
  • DNA double-strand breaks (DSBs) are the most detrimental lesions, significantly impacting cell fate.

Purpose of the Study:

  • To review the cellular response to radiation damage.
  • To explain the mechanisms determining cellular radiosensitivity.
  • To discuss the impact of radiation on cells and organisms.

Main Methods:

  • Literature review of studies on radiation damage and cellular response.
  • Analysis of DNA repair pathways, including homologous recombination (HR) and non-homologous end-joining (NHEJ).
  • Examination of genetic disorders associated with defects in DNA repair proteins.

Main Results:

  • Failure to recognize or repair DSBs dictates cellular radiosensitivity.
  • Mutations in HR and NHEJ proteins cause radiosensitivity and genome instability.
  • Defects in DNA repair proteins are linked to immunodeficiency, cancer predisposition, and neurodegeneration.

Conclusions:

  • Understanding of cellular radiation response has advanced significantly over 50 years.
  • Current knowledge integrates basic and sophisticated research approaches.
  • The review provides insights into factors determining an organism's response to radiation.