Evidence map›Paper›PMID 22493298›Full record

ArticleBlood2012

Chronic myelogenous leukemia stem and progenitor cells demonstrate chromosomal instability related to repeated breakage-fusion-bridge cycles mediated by increased nonhomologous end joining.

Sujata Chakraborty, Jeremy M Stark, Can-Lan Sun, Hardik Modi, WenYong Chen, Timothy R O'Connor, Stephen J Forman, Smita Bhatia, Ravi Bhatia

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Roles of SIRT1 in leukemogenesis.Current opinion in hematology · 2013
    Review
  14. Cancer Stem Cells: A Moving Target.Current pathobiology reports · 2013
    Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Sujata ChakrabortyDivision of Hematopoietic Stem Cell and Leukemia Research, City of Hope National Medical Center, Duarte, CA 91010, USA.
Jeremy M Stark
Can-Lan Sun
Hardik Modi
WenYong Chen
Timothy R O'Connor
Stephen J Forman
Smita Bhatia
Ravi Bhatia
Centre for Cancer Biology · AULeukemia Research Foundation · USCity Of Hope National Medical Center · US

Funding

Transplant for Lymphoma:Therapy-Related LeukemiaP50CA107399 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI FORMAN, STEPHEN J, KWAK, LARRY W · 2004 to 2022
$35.5M
Roles of SIRT1 in normal hematopoietic and leukemic stem cellsR01CA143421 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHEN, WENYONG · 2011 to 2015
$1.5M
NCI NIH HHS P50 CA107399NCI NIH HHS P50CA107399NCI NIH HHS R01 CA143421
6 · The paper itself

Abstract

Chromosomal aberrations are an important consequence of genotoxic exposure and contribute to pathogenesis and progression of several malignancies. We investigated the susceptibility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exposure to ionizing radiation. In normal progenitors, ionizing radiation induced both stable and unstable chromosomal lesions, but only stable aberrations persisted after multiple divisions. In contrast, radiation of chronic phase CML progenitors resulted in enhanced generation of unstable lesions that persisted after multiple divisions. CML progenitors demonstrated active cell cycle checkpoints and increased nonhomologous end joining DNA repair, suggesting that persistence of unstable aberrations was the result of continued generation of these lesions. CML progenitors demonstrated enhanced susceptibility to repeated cycles of chromosome damage, repair, and damage through a breakage-fusion-bridge mechanism. Perpetuation of breakage-fusion-bridge cycles in CML progenitors was mediated by classic nonhomologous end joining repair. These studies reveal a previously unrecognized mechanism of chromosomal instability in leukemia progenitors because of continued generation of unstable chromosomal lesions through repeated cycles of breakage and repair of such lesions.

Indexed as

Chromosome BreakageAntigens, CD34Cell Cycle CheckpointsCell Line, TumorChromosomal InstabilityDNA DamageDNA End-Joining RepairGene FusionHumansIn Situ Hybridization, FluorescenceLeukemia, Myelogenous, Chronic, BCR-ABL PositiveModels, BiologicalNeoplastic Stem CellsRadiation, IonizingRecurrenceAntigens, CD34

Identifiers

PMID22493298
PMCPMC3383199
OpenAlexW1967031426

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.