Evidence map›Paper›PMID 27308409›Full record

ArticleMolecular & cellular oncology

Alternative end joining, clonal evolution, and escape from a telomere-driven crisis.

Eric A Hendrickson, Duncan M Baird

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular oncology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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 at 2 institutions in 3 countries.

Eric A HendricksonDepartment of Biochemistry; Molecular Biology, and Biophysics ; University of Minnesota Medical School ; Minneapolis, MN USA.
Duncan M BairdInstitute of Cancer and Genetics; School of Medicine ; Cardiff University, Heath Park ; Cardiff, UK.
Cardiff University · GBInstitute of Molecular Biology and Biophysics · RU

Funding

The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cellsR01GM088351 · NIGMS · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2010 to 2018
$2.3M
Ku regulates non-homologous end joining pathways in human somatic cellsR01CA154461 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA154461NIGMS NIH HHS R01 GM088351
6 · The paper itself

Abstract

Telomere dysfunction and fusion play key roles in driving genomic instability and clonal evolution in many tumor types. We have recently described a role for DNA ligase III (LIG3) in facilitating the escape of cells from crisis induced by telomere dysfunction. Our data indicate that LIG3-mediated telomere fusion is important in facilitating clonal evolution.

Indexed as

cancerDNA repairligase IIInon-homologous end joiningtelomerasetelomere

Identifiers

PMID27308409
PMCPMC4905247
OpenAlexW1980679031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.