Evidence map›Paper›PMID 18214391›Full record

ReviewImmunologic research2008

DNA damage and repair during lymphoid development: antigen receptor diversity, genomic integrity and lymphomagenesis.

Nahum Puebla-Osorio, Chengming Zhu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Nahum Puebla-OsorioDepartment of Immunology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77054, USA.
Chengming Zhu

Funding

Preventing Tumorigenesis in Developing LymphocytesR01CA116933 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ZHU, CHENGMING · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA116933
6 · The paper itself

Abstract

Lymphocyte maturation requires generation of a large diversity of antigen receptors, which involves somatic rearrangements at the antigen receptor genes in a process termed V(D)J recombination. Upon encountering specific antigens, B-lymphocytes undergo rearrangements in the constant region of the immunoglobulin genes to optimize immune responses in a process called class switch recombination. Activated B-cells also undergo somatic hypermutation in the variable regions of the immunoglobulin genes to enhance their antigenic affinity. These somatic events are initiated by the infliction of DNA lesions within the antigen receptor genes that are strictly confined to a specific developmental window and cell-cycle stage. DNA lesions are then repaired by one of the general DNA repair mechanisms, such as non-homologous end-joining. Mutations in key factors of these pathways lead to the interruption of these processes and immunodeficiency, making it possible to study the mechanisms of cellular response to DNA lesions and their repair. This review briefly summarizes some of the recently developed animal models with focus on current advances in the understanding of the mechanism of DNA end-joining activities, and its role in the maintenance of genomic stability and the prevention of tumorigenesis.

Indexed as

DNA DamageDNA RepairAnimalsB-LymphocytesGene Rearrangement, B-LymphocyteImmunoglobulin Class SwitchingLymphomaMutationReceptors, Antigen, B-CellRecombination, GeneticReceptors, Antigen, B-Cell

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.