Evidence map›Paper›PMID 23799845›Full record

ArticleBritish journal of cancer2013

BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistance.

W T Parker, A L Yeoman, B A Jamison, D T Yeung, H S Scott, T P Hughes, S Branford

Abstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Leukemia & lymphoma · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Return of the malingering mutants.British journal of cancer · 2013
    Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

W T ParkerDepartment of Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, South Australia, Australia.
A L Yeoman
B A Jamison
D T Yeung
H S Scott
T P Hughes
S Branford

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBCR-ABL1 mutation analysis is recommended for chronic myeloid leukaemia patients. However, mutations may become undetectable after changing therapy, and it is unknown whether they have been eradicated.

methodsWe examined longitudinal data of patients with imatinib-resistant mutations, which became undetectable by Sanger sequencing to determine whether mutations could reappear, and the related circumstances.

resultsIdentical imatinib- and nilotinib-resistant mutations reappeared following further therapy changes in five patients, and was associated with subsequent nilotinib resistance in four.

conclusionThe data suggest that some BCR-ABL1 mutations may persist at undetectable levels for many years after changing therapy, and can be reselected and confer resistance to subsequent inhibitors.

Indexed as

MutationAdultAgedBenzamidesDrug Resistance, NeoplasmFemaleFusion Proteins, bcr-ablHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLongitudinal StudiesMaleMiddle AgedPiperazinesProtein Kinase InhibitorsPyrimidinesBCR-ABL1 fusion protein, humanBenzamidesFusion Proteins, bcr-ablImatinib MesylatenilotinibPiperazinesProtein Kinase InhibitorsPyrimidines

Identifiers

PMID23799845
PMCPMC3776970

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Registered trials

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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.