Evidence map›Paper›PMID 22791509›Full record

ReviewInternational journal of hematology2012

Molecular markers in acute myeloid leukaemia.

Andrea Kühnl, David Grimwade

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2012. 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
3.8field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Gene expression of carbonic anhydrase 9 (CA9) inJournal of medicine and life · 2022
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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 1 institution in 1 country.

Andrea KühnlDepartment of Medical and Molecular Genetics, King's College London School of Medicine, London, UK.
David Grimwade
King's College London · GB

Funding

Department of Health RP-PG-0108-10093Medical Research Council MR/J006742/1
6 · The paper itself

Abstract

An increasing number of cytogenetic and molecular genetic aberrations have been identified in acute myeloid leukaemia (AML), highlighting the biological heterogeneity of the disease. Moreover, the characterisation of specific molecular abnormalities provides the basis for targeted therapies, such as all trans retinoic acid (ATRA) and arsenic trioxide treatment in acute promyelocytic leukaemia or tyrosine kinase inhibitors in AML with FLT3 mutations. Several cytogenetic and molecular genetic changes have been shown to be prognostically relevant and have been acknowledged in the latest WHO classification of AML as separate entities. A detailed marker assessment at diagnosis is crucial for risk-stratification of AML patients, allowing the identification of those at high risk of relapse, who may benefit from early allogeneic stem cell transplantation. Finally, molecular markers are important for the detection of minimal residual disease after initial therapy and during long-term follow-up, which enables a more tailored treatment approach for individual AML patients.

Indexed as

Biomarkers, TumorChromosome AberrationsEpigenesis, GeneticHumansLeukemia, Myeloid, AcuteNeoplasm, ResidualBiomarkers, Tumor

Identifiers

PMID22791509
OpenAlexW2080576274

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.