Evidence map›Paper›PMID 20410925›Full record

ArticleLeukemia2010

High-density single nucleotide polymorphism array analysis and ASXL1 gene mutation screening in chronic myeloid leukemia during disease progression.

J Boultwood, J Perry, R Zaman, C Fernandez-Santamaria, T Littlewood, R Kusec, A Pellagatti, L Wang, R E Clark, J S Wainscoat

Abstract read
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In one paragraph

Article in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Systematic review of pre-clinical chronic myeloid leukaemia.International journal of hematology · 2018
    Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. The Functions and Mechanisms of PR-DUB in Malignancy.Frontiers in molecular biosciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Haematologica · 2019
    Article
  14. Review
  15. Article
  16. Disruption ofDisease models & mechanisms · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Epigenetic Reprogramming and Emerging Epigenetic Therapies in CML.Frontiers in cell and developmental biology · 2019
    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

10 authors at 4 institutions in 2 countries.

J BoultwoodLRF Molecular Haematology Unit, NDCLS, University of Oxford, John Radcliffe Hospital, Oxford, UK. jacqueline.boultwood@ndcls.ox.ac.uk
J Perry
R Zaman
C Fernandez-Santamaria
T Littlewood
R Kusec
A Pellagatti
L Wang
R E Clark
J S Wainscoat
John Radcliffe Hospital · GBUniversity of Oxford · GBRoyal Liverpool University Hospital · GBKlinička bolnica Merkur · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have undertaken a genome-wide single nucleotide polymorphism (SNP) array analysis of 41 chronic myeloid leukemia (CML) patients. In total, 44 regions of uniparental disomy (UPD) >3 Mb were identified in 24 of 32 patients in chronic phase (CP), and 21 regions of UPD >3 Mb were identified in 13 of 21 patients in blast crisis (BC). Chromosome 8 had the highest frequency of UPD regions in both CP and BC samples. Eight recurrent regions of UPD were observed among the 41 patients, with chromosome 8 showing the highest frequency. Ten regions of copy number change (CNC) >3 Mb were observed in 4 of 21 patients in BC, whereas none were observed in CP. We have identified several recurrent regions of UPD and CNC in CML that may be of pathogenetic importance. Overrepresentation of genomic aberrations (UPD and copy number gain) mapping to chromosome 8 was observed. Selected candidate genes mapping within the aberrant genomic regions were sequenced and mutation of the TP53 gene was observed in one case in BC and of the ASXL1 gene in 6 of 41 cases in CP or BC. Mutation of ASXL1 represents an important new molecular abnormality in CML.

Indexed as

Blast CrisisDisease ProgressionGene DosageGenome, HumanHumansKaryotypingLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMutationOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideRepressor ProteinsTumor Suppressor Protein p53Uniparental DisomyASXL1 protein, humanRepressor ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID20410925
OpenAlexW2076142320

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.