Evidence map›Paper›PMID 21653938›Full record

ArticleBlood2011

Dynamics of chronic myeloid leukemia response to long-term targeted therapy reveal treatment effects on leukemic stem cells.

Min Tang, Mithat Gonen, Alfonso Quintas-Cardama, Jorge Cortes, Hagop Kantarjian, Chani Field, Timothy P Hughes, Susan Branford, Franziska Michor

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-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

31 citing papers in PubMed, 68 citations in OpenAlex.

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  18. Molecular monitoring in chronic myeloid leukemia-how low can you go?Hematology. American Society of Hematology. Education Program · 2016
    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

9 authors at 5 institutions in 2 countries.

Min TangDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, and Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA.
Mithat Gonen
Alfonso Quintas-Cardama
Jorge Cortes
Hagop Kantarjian
Chani Field
Timothy P Hughes
Susan Branford
Franziska Michor
The University of Texas MD Anderson Cancer Center · USDana-Farber Cancer Institute · USUniversity of Adelaide · AUMemorial Sloan Kettering Cancer Center · USSouth Australia Pathology · AU

Funding

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

Abstract

Treatment of chronic myeloid leukemia (CML) with the tyrosine kinase inhibitors (TKIs) imatinib mesylate and nilotinib represents a successful application of molecularly targeted anticancer therapy. However, the effect of TKIs on leukemic stem cells remains incompletely understood. On the basis of a statistical modeling approach that used the 10-year imatinib mesylate treatment response of patients with CML and a patient cohort receiving first-line nilotinib therapy, we found that successful long-term therapy results in a triphasic exponential decline of BCR-ABL1 transcripts in many patients. Within our framework, the first slope of -0.052 ± 0.018 (imatinib mesylate) and -0.042 ± 0.015 (nilotinib) per day represents the turnover rate of leukemic differentiated cells, whereas the second slope of -0.0057 ± 0.0038 (imatinib mesylate) and -0.0019 ± 0.0013 (nilotinib) per day represents the turnover rate of leukemic progenitor cells. The third slope allows an inference of the behavior of immature leukemic cells, potentially stem cells. This third slope is negative in most patients, positive in others, and not observable in some patients. This variability in response may be because of insufficient follow-up, missing data, disease heterogeneity, inconsistent compliance to drug, or acquired resistance. Our approach suggests that long-term TKI therapy may reduce the abundance of leukemic stem cells in some patients.

Indexed as

AlgorithmsBenzamidesFusion Proteins, bcr-ablHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveModels, BiologicalMolecular Targeted TherapyNeoplastic Stem CellsPiperazinesProtein Kinase InhibitorsPyrimidinesReverse Transcriptase Polymerase Chain ReactionTime FactorsTranscription, GeneticTreatment OutcomeBenzamidesFusion Proteins, bcr-ablImatinib MesylatenilotinibPiperazinesProtein Kinase InhibitorsPyrimidines

Identifiers

PMID21653938
PMCPMC3156048
OpenAlexW2058201897

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.