Evidence map›Paper›PMID 24236822›Full record

ReviewExpert review of anticancer therapy2013

Tyrosine kinase inhibition: a therapeutic target for the management of chronic-phase chronic myeloid leukemia.

Elias J Jabbour, Jorge E Cortes, Hagop M Kantarjian

Abstract readReview
In one paragraph

Review in Expert review of anticancer therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. The roles of KLHL family members in human cancers.American journal of cancer research · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Review
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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

3 authors.

Elias J JabbourThe University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Jorge E Cortes
Hagop M Kantarjian

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a hematologic neoplasm with a progressive, ultimately terminal, disease course. In most cases, CML arises owing to the aberrant formation of a chimeric gene for a constitutively active tyrosine kinase. Inhibition of the signaling activity of this kinase has proved to be a highly successful treatment target, transforming the prognosis of patients with CML. New tyrosine kinase inhibitors continue to improve the management of CML, offering alternative options for those resistant to or intolerant of standard tyrosine kinase inhibitors. Here we review the pathobiology of CML and explore emerging strategies to optimize the management of chronic-phase CML, particularly first-line treatment.

Indexed as

Antineoplastic AgentsBenzamidesDrug Resistance, NeoplasmHumansImatinib MesylateLeukemia, Myeloid, Chronic-PhaseMolecular Targeted TherapyPiperazinesProtein Kinase InhibitorsProtein-Tyrosine KinasesPyrimidinesTreatment OutcomeAntineoplastic AgentsBenzamidesImatinib MesylatePiperazinesProtein Kinase InhibitorsProtein-Tyrosine KinasesPyrimidines

Identifiers

PMID24236822
PMCPMC4181370

What OpenQuestion holds

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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.