Evidence map›Paper›PMID 26593906›Full record

ReviewInternational journal of molecular sciences2015

DNA Repair--A Double-Edged Sword in the Genomic Stability of Cancer Cells--The Case of Chronic Myeloid Leukemia.

Elzbieta Pawlowska, Janusz Blasiak

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?International journal of molecular sciences · 2021
    Review
  7. Curcumin: reclaiming the lost ground against cancer resistance.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. A Preliminary Study: Human Fibroid Stro-1Reproductive sciences (Thousand Oaks, Calif.) · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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 1 country.

Elzbieta PawlowskaDepartment of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland. elzbieta.pawlowska@umed.lodz.pl.
Janusz BlasiakDepartment of Molecular Genetics, University of Lodz, 90-236 Lodz, Poland. jblasiak@biol.uni.lodz.pl.
Medical University of Lodz · PLUniversity of Łódź · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability is a common feature of cancer cells, which can result from aberrant DNA damage reaction (DDR). We and others showed that the well-known BCR-ABL1 fusion oncogene, the cause of chronic myeloid leukemia, induced an increased production of reactive oxygen species (ROS) and conferred therapeutic drug resistance by suppression of apoptotic signaling, prolonged G2/M arrest and stimulation of several pathways of DNA repair. However, to protect from apoptosis, cancer cells may tolerate some DNA lesions, which may increase genomic instability. Moreover, BCR/ABL1-stimulated DNA repair might be faulty, especially non-homologous end joining in its alternative forms. Normal DNA repair can remove DNA damage and prevent mutations, reducing genome instability, but on the other hand, due to its imprecise nature, it may increase genomic instability by increasing the ratio of mutagenic DNA lesions. The example of BCR-ABL1-expressing cells shows that DNA repair can both increase and decrease genomic instability of cancer cells and understanding the mechanism of the regulation of these opposite effects would be helpful in anticancer strategies.

Indexed as

DNA RepairGenomic InstabilityAnimalsAntineoplastic AgentsCell Transformation, NeoplasticDNA DamageDNA End-Joining RepairDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMutagenesisProtein Kinase InhibitorsReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsFusion Proteins, bcr-ablProtein Kinase InhibitorsReactive Oxygen SpeciesBCR-ABL1chronic myeloid leukemiaDNA repairgenomic instability

Identifiers

PMID26593906
PMCPMC4661907
OpenAlexW2177617854

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.