Evidence map›Paper›PMID 20600922›Full record

ReviewSeminars in cancer biology2010

All y'all need to know 'bout retroelements in cancer.

Victoria P Belancio, Astrid M Roy-Engel, Prescott L Deininger

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
24.4field-weighted citation impact, top 1% of its field
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

104 citing papers in PubMed, 187 citations in OpenAlex.

  1. Trial
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  8. Review
  9. DNA damage and repair in age-related inflammation.Nature reviews. Immunology · 2023
    Review
  10. Article
  11. Article
  12. An EpigeneticInternational journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Role of Cell-Free DNA and Deoxyribonucleases in Tumor Progression.International journal of molecular sciences · 2021
    Review

44 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Victoria P BelancioTulane University, Department of Structural and Cellular Biology, School of Medicine, Tulane Cancer Center and Tulane Center for Aging, New Orleans, LA 70112, USA.
Astrid M Roy-Engel
Prescott L Deininger
Tulane University · US

Funding

UNCOVERING THE MECHANISMS OF OSTEOSARCOMA METASTASIS SUPPRESSION BY MTBPP20RR020152 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2004 to 2011
$17.0M
Sine RetrotranspositionR01GM045668 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 1993 to 2014
$4.2M
Regulatory effects of LINE components on SINE mobilizationR01GM079709 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI ENGEL, ASTRID M · 2008 to 2012
$1.4M
L 1 element as an inrinsic factor of mammalian agingK01AG030074 · NIA · TULANE UNIVERSITY OF LOUISIANA · PI BELANCIO, VICTORIA PEREPELITSA · 2008 to 2012
$504k
NCRR NIH HHS P20 RR020152NCRR NIH HHS P20RR020152NIA NIH HHS 5K01AG030074NIA NIH HHS K01 AG030074NIGMS NIH HHS R01 GM045668NIGMS NIH HHS R01 GM079709NIGMS NIH HHS R01GM079709ANIGMS NIH HHS R01GM45668
6 · The paper itself

Abstract

Genetic instability is one of the principal hallmarks and causative factors in cancer. Human transposable elements (TE) have been reported to cause human diseases, including several types of cancer through insertional mutagenesis of genes critical for preventing or driving malignant transformation. In addition to retrotransposition-associated mutagenesis, TEs have been found to contribute even more genomic rearrangements through non-allelic homologous recombination. TEs also have the potential to generate a wide range of mutations derivation of which is difficult to directly trace to mobile elements, including double strand breaks that may trigger mutagenic genomic rearrangements. Genome-wide hypomethylation of TE promoters and significantly elevated TE expression in almost all human cancers often accompanied by the loss of critical DNA sensing and repair pathways suggests that the negative impact of mobile elements on genome stability should increase as human tumors evolve. The biological consequences of elevated retroelement expression, such as the rate of their amplification, in human cancers remain obscure, particularly, how this increase translates into disease-relevant mutations. This review is focused on the cellular mechanisms that control human TE-associated mutagenesis in cancer and summarizes the current understanding of TE contribution to genetic instability in human malignancies.

Indexed as

AnimalsBase SequenceGene Expression Regulation, NeoplasticGenomic InstabilityHumansKnowledgeModels, BiologicalMutagenesis, InsertionalNeoplasmsPolymorphism, GeneticRetroelementsRetroelements

Identifiers

PMID20600922
PMCPMC2943028
OpenAlexW2001961555

What OpenQuestion holds

Textmetadata
LicenceTDM
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.