Evidence map›Paper›PMID 31000418›Full record

ArticleEBioMedicine2019

Assessment of epigenetic mechanisms and DNA double-strand break repair using laser micro-irradiation technique developed for hematological cells.

Danielle P Johnson, Gabriella S Spitz-Becker, Korak Chakraborti, Srividya Bhaskara

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Targeting DNA Repair Pathways in Hematological Malignancies.International journal of molecular sciences · 2020
    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

4 authors at 2 institutions in 1 country.

Danielle P JohnsonDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA.
Gabriella S Spitz-BeckerDepartment of Radiation Oncology, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA.
Korak ChakrabortiDepartment of Radiation Oncology, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA.
Srividya BhaskaraDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA; Department of Radiation Oncology, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT, USA. Electronic address: srividya.bhaskara@hci.utah.edu.
University of Utah · USHuntsman Cancer Institute · US

Funding

Histone deacetylases 1,2 and DNA repairR01CA188520 · NCI · UNIVERSITY OF UTAH · PI BHASKARA, SRIVIDYA · 2015 to 2019
$1.7M
NCI NIH HHS R01 CA188520
6 · The paper itself

Abstract

backgroundCertain tumors rely heavily on their DNA repair capability to survive the DNA damage induced by chemotherapeutic agents. Therefore, it is important to monitor the dynamics of DNA repair in patient samples during the course of their treatment, in order to determine whether a particular drug regimen perturbs the DNA repair networks in cancer cells and provides therapeutic benefits. Quantitative measurement of proteins and/or their posttranslational modification(s) at DNA double strand breaks (DSBs) induced by laser microirradiation provides an applicable diagnostic approach to examine DNA repair and its dynamics. However, its use is restricted to adherent cell lines and not employed in suspension tumor cells that include the many hematological malignancies.

methodsHere, we report the development of an assay to laser micro-irradiate and quantitatively measure DNA repair transactions at DSB sites in normal mononuclear cells and a variety of suspension leukemia and lymphoma cells including primary patient samples.

findingsWe show that global changes in the H3K27me3-ac switch modulated by inhibitors of Class I HDACs, EZH2 methyltransferase and (or) H3K27me3 demethylases do not reflect the dynamic changes in H3K27me3 that occur at double-strand break sites during DNA repair.

interpretationResults from our mechanistic studies and proof-of-principle data with patient samples together show the effectiveness of using the modified micro-laser-based assay to examine DNA repair directly in suspension cancer cells, and has important clinical implications by serving as a valuable tool to assess drug efficacies in hematological cancer cells that grow in suspension.

Indexed as

DNA Breaks, Double-StrandedEpigenesis, GeneticLasersBlood CellsCell Line, TumorChromatinDNA DamageDNA RepairHistonesHumansLow-Level Light TherapyLymphoma, Large B-Cell, DiffuseChromatinHistonesCancerChromatin modifiersDNA repairHematological cellsHistone deacetylasesLaser damage

Identifiers

PMID31000418
PMCPMC6562062
OpenAlexW2939250074

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.