Evidence map›Paper›PMID 21423218›Full record

ArticleOncogene2011

Genomic evolution in Barrett's adenocarcinoma cells: critical roles of elevated hsRAD51, homologous recombination and Alu sequences in the genome.

J Pal, R Bertheau, L Buon, A Qazi, R B Batchu, S Bandyopadhyay, R Ali-Fehmi, D G Beer, D W Weaver, R J Shmookler Reis and 4 more

Abstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  18. Article
  19. RAD51 regulates CHK1 stability via autophagy to promote cell growth in esophageal squamous carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  20. Review
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

14 authors at 7 institutions in 1 country.

J PalDepartment of Adult Oncology, Dana Farber Cancer Institute, Boston, MA 02132, USA.
R Bertheau
L Buon
A Qazi
R B Batchu
S Bandyopadhyay
R Ali-Fehmi
D G Beer
D W Weaver
R J Shmookler Reis
R K Goyal
Q Huang
N C Munshi
M A Shammas
Dana-Farber Cancer Institute · USWayne State University · USThe Barbara Ann Karmanos Cancer Institute · USVA Boston Healthcare System · USCentral Arkansas Veterans Healthcare System · USHarvard University · USUniversity of Michigan–Ann Arbor · US

Funding

Homologous Recombination Mediates Genomic Instability and Progression in MyelomaR01CA124929 · NCI · DANA-FARBER CANCER INST · PI MUNSHI, NIKHIL C. · 2008 to 2012
$1.8M
Telomerase And Homologous Recombination As Targets In Barrett's AdenocarcinomaR01CA125711 · NCI · WAYNE STATE UNIVERSITY · PI SHAMMAS, MASOOD A · 2008 to 2012
$1.7M
NCI NIH HHS R01 CA124929NCI NIH HHS R01 CA125711NCI NIH HHS R01CA125711PHS HHS P01-78378PHS HHS P50-100007PHS HHS R01-1375555
6 · The paper itself

Abstract

A prominent feature of most cancers including Barrett's adenocarcinoma (BAC) is genetic instability, which is associated with development and progression of disease. In this study, we investigated the role of recombinase (hsRAD51), a key component of homologous recombination (HR)/repair, in evolving genomic changes and growth of BAC cells. We show that the expression of RAD51 is elevated in BAC cell lines and tissue specimens, relative to normal cells. HR activity is also elevated and significantly correlates with RAD51 expression in BAC cells. The suppression of RAD51 expression, by short hairpin RNA (shRNA) specifically targeting this gene, significantly prevented BAC cells from acquiring genomic changes to either copy number or heterozygosity (P<0.02) in several independent experiments employing single-nucleotide polymorphism arrays. The reduction in copy-number changes, following shRNA treatment, was confirmed by Comparative Genome Hybridization analyses of the same DNA samples. Moreover, the chromosomal distributions of mutations correlated strongly with frequencies and locations of Alu interspersed repetitive elements on individual chromosomes. We conclude that the hsRAD51 protein level is systematically elevated in BAC, contributes significantly to genomic evolution during serial propagation of these cells and correlates with disease progression. Alu sequences may serve as substrates for elevated HR during cell proliferation in vitro, as they have been reported to do during the evolution of species, and thus may provide additional targets for prevention or treatment of this disease.

Indexed as

Alu ElementsGenome, HumanRecombination, GeneticAdenocarcinomaBarrett EsophagusCell Line, TumorEsophageal NeoplasmsHumansLoss of HeterozygosityMutationRad51 RecombinaseRAD51 protein, humanRad51 Recombinase

Identifiers

PMID21423218
PMCPMC3406293
OpenAlexW2030797511

What OpenQuestion holds

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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.