ReviewAdvances in immunology2010
The role of mechanistic factors in promoting chromosomal translocations found in lymphoid and other cancers.
Review in Advances in immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
70 citing papers in PubMed, 116 citations in OpenAlex.
- Visualization and quantification of rDNA instabilities in mammalian cells and mouse models.Nucleic acids research · 2026Article
- Building a neural network model to define DNA sequence specificity in V(D)J recombination.Nucleic acids research · 2025Article
- Multiscale reorganization of the genome following DNA damage facilitates chromosome translocations via nuclear actin polymerization.Nature structural & molecular biology · 2023Article
- The high toxicity of DSB-clusters modelling high-LET-DNA damage derives from inhibition of c-NHEJ and promotion of alt-EJ and SSA despite increases in HR.Frontiers in cell and developmental biology · 2022Article
- Chromosome Folding Promotes Intrachromosomal Aberrations under Radiation- and Nuclease-Induced DNA Breakage.International journal of molecular sciences · 2021Article
- Preclinical Evaluation of Gilteritinib on NPM1-ALK-Driven Anaplastic Large Cell Lymphoma Cells.Molecular cancer research : MCR · 2021Article
- Long-Range Control of Class Switch Recombination by Transcriptional Regulatory Elements.Frontiers in immunology · 2021Review
- Genome-Wide Analysis IdentifiesFrontiers in cell and developmental biology · 2021Article
- Repair of G1 induced DNA double-strand breaks in S-G2/M by alternative NHEJ.Nature communications · 2020Article
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- DNA-PKcs phosphorylation at the T2609 cluster alters the repair pathway choice during immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The nucleoskeleton protein IFFO1 immobilizes broken DNA and suppresses chromosome translocation during tumorigenesis.Nature cell biology · 2019Article
- Review
- Translocation Breakpoints Preferentially Occur in Euchromatin and Acrocentric Chromosomes.Cancers · 2018Article
- The Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- Riches in RAGs: Revealing the V(D)J Recombinase through High-Resolution Structures.Trends in biochemical sciences · 2017Review
- Expressed alleles of imprinted IGF2, DLK1 and MEG3 colocalize in 3D-preserved nuclei of porcine fetal cells.BMC cell biology · 2016Article
- The structure of ends determines the pathway choice and Mre11 nuclease dependency of DNA double-strand break repair.Nucleic acids research · 2016Article
- Defining chromosomal translocation risks in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Chromosomal Translocations in the Parasite Leishmania by a MRE11/RAD50-Independent Microhomology-Mediated End Joining Mechanism.PLoS genetics · 2016Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Recurrent chromosomal abnormalities, especially chromosomal translocations, are strongly associated with certain subtypes of leukemia, lymphoma and solid tumors. The appearance of particular translocations or associated genomic alterations can be important indicators of disease prognosis, and in some cases, certain translocations may indicate appropriate therapy protocols. To date, most of our knowledge about chromosomal translocations has derived from characterization of the highly selected recurrent translocations found in certain cancers. Until recently, mechanisms that promote or suppress chromosomal translocations, in particular, those responsible for their initiation, have not been addressed. For translocations to occur, two distinct chromosomal loci must be broken, brought together (synapsed) and joined. Here, we discuss recent findings on processes and pathways that influence the initiation of chromosomal translocations, including the generation fo DNA double strand breaks (DSBs) by general factors or in the context of the Lymphocyte-specific V(D)J and IgH class-switch recombination processes. We also discuss the role of spatial proximity of DSBs in the interphase nucleus with respect to how DSBs on different chromosomes are justaposed for joining. In addition, we discuss the DNA DSB response and its role in recognizing and tethering chromosomal DSBs to prevent translocations, as well as potential roles of the classical and alternative DSB end-joining pathways in suppressing or promoting translocations. Finally, we discuss the potential roles of long range regulatory elements, such as the 3'IgH enhancer complex, in promoting the expression of certain translocations that are frequent in lymphomas and, thereby, contributing to their frequent appearance in tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.