ReviewBMC genomics2010
Mechanisms of chromosomal rearrangement in the human genome.
Review in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 89 citations in OpenAlex.
- An Overview of EGFR Mechanisms and Their Implications in Targeted Therapies for Glioblastoma.International journal of molecular sciences · 2023Review
- Analysis of complex chromosomal rearrangements using a combination of current molecular cytogenetic techniques.Molecular cytogenetics · 2022Article
- First Comprehensive Characterization of Phayre's Leaf-Monkey (Frontiers in genetics · 2022Article
- Chromoanagenesis from radiation-induced genome damage in Populus.PLoS genetics · 2021Article
- Classical, Molecular, and Genomic Cytogenetics of the Pig, a Clinical Perspective.Animals : an open access journal from MDPI · 2021Review
- Mechanisms of receptor tyrosine kinase activation in cancer.Molecular cancer · 2018Review
- An efficient and tunable parameter to improve variant calling for whole genome and exome sequencing data.Genes & genomics · 2018Article
- AID and Reactive Oxygen Species Can Induce DNA Breaks within Human Chromosomal Translocation Fragile Zones.Molecular cell · 2017Article
- Accurate quantification of homologous recombination in zebrafish: brca2 deficiency as a paradigm.Scientific reports · 2017Article
- Article
- Genetic and biochemical evidences reveal novel insights into the mechanism underlyingJournal of biosciences · 2016Article
- Holliday junction trap shows how cells use recombination and a junction-guardian role of RecQ helicase.Science advances · 2016Article
- Childhood Leukemia and Primary Prevention.Current problems in pediatric and adolescent health care · 2016Article
- Mechanisms of human lymphoid chromosomal translocations.Nature reviews. Cancer · 2016Review
- RNA Polymerase Collision versus DNA Structural Distortion: Twists and Turns Can Cause Break Failure.Molecular cell · 2016Review
- Combined deletion of Xrcc4 and Trp53 in mouse germinal center B cells leads to novel B cell lymphomas with clonal heterogeneity.Journal of hematology & oncology · 2016Article
- Methylation of CpG sites in BCL2 major breakpoint region and the increase of BCL2/JH translocation with aging.Age (Dordrecht, Netherlands) · 2015Article
- CRISPR-Cas9: A Revolutionary Tool for Cancer Modelling.International journal of molecular sciences · 2015Review
- Article
- Human lymphoid translocation fragile zones are hypomethylated and have accessible chromatin.Molecular and cellular biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many human cancers are associated with characteristic chromosomal rearrangements, especially hematopoietic cancers such as leukemias and lymphomas. The first and most critical step in the rearrangement process is the induction of two DNA double-strand breaks (DSB). In all cases, at least one of the two DSBs is generated by a pathologic process, such as (1) randomly-positioned breaks due to ionizing radiation, free radical oxidative damage, or spontaneous hydrolysis; (2) breaks associated with topoisomerase inhibitor treatment; or (3) breaks at direct or inverted repeat sequences, mediated by unidentified strand breakage mechanisms. In lymphoid cells, one of the two requisite DSBs is often physiologic, the result of V(D)J recombination or class switch recombination (CSR) at the lymphoid antigen receptor loci. The RAG complex, which causes the DSBs in V(D)J recombination, can cause (4) sequence-specific, pathologic DSBs at sites that fit the consensus of their normal V(D)J recombination signal targets; or (5) structure-specific, pathologic DSBs at regions of single- to double-strand transition. CSR occurs specifically in the B-cell lineage, and requires (6) activation-induced cytidine deaminase (AID) action at sites of single-stranded DNA, which may occur pathologically outside of the normal target loci of class switch recombination regions and somatic hypermutation (SHM) zones. Recent work proposes a seventh mechanism: the sequential action of AID and the RAG complex at CpG sites provides a coherent model for the pathologic DSBs at some of the most common sites of translocation in human lymphoma - the bcl-2 gene in follicular lymphoma and diffuse large B-cell lymphoma, and the bcl-1 gene in mantle cell lymphoma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.