Evidence map›Paper›PMID 22427031›Full record

ArticleCurrent hematologic malignancy reports2012

Genomic instability in chronic myeloid leukemia: targets for therapy?

N Muvarak, P Nagaria, F V Rassool

Abstract read
PubMed Publisher
In one paragraph

Article in Current hematologic malignancy reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. The Downregulation of Both Giant HERCs,Journal of clinical medicine · 2022
    Article
  4. Review
  5. Review
  6. Article
  7. DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia.International journal of molecular sciences · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Expression of minichromosome maintenance 8 in chronic myelogenous leukemia.International journal of clinical and experimental pathology · 2015
    Article
  13. Genetic events other than BCR-ABL1.Current hematologic malignancy reports · 2014
    Review
  14. Review
  15. 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

3 authors at 1 institution in 1 country.

N MuvarakDepartment of Radiation Oncology, University of Maryland School of Medicine, Baltimore, MD 21230, USA.
P Nagaria
F V Rassool
University of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Philadelphia positive (Ph+) chronic myeloid leukemia (CML) is characterized by the occurrence of nonrandom genetic and cytogenetic abnormalities during disease progression. Many of these abnormalities are markers for genes which, when altered, can drive the blastic transformation process. Thus, such genetic alterations may be manifestations of an underlying genomic instability resulting from a compromised DNA damage and repair response, leading to advanced stages of CML and resistance to therapy. This article examines the molecular pathways that may lead to genomic instability in CML and the potential of these pathway constituents to be therapeutic targets.

Indexed as

Genomic InstabilityCell Transformation, NeoplasticDisease ProgressionDNA DamageHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMolecular Targeted TherapyReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID22427031
OpenAlexW2060312814

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.