Evidence map›Paper›PMID 20875553›Full record

ReviewSeminars in hematology2010

The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?

Bing Z Carter, Duncan H Mak, Jorge Cortes, Michael Andreeff

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in hematology, 2010. 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
1.4field-weighted citation impact, top 18% 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, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. TPEN exerts selective anti-leukemic efficacy in ex vivo drug-resistant childhood acute leukemia.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
    Article
  6. Prosurvival kinase PIM2 is a therapeutic target for eradication of chronic myeloid leukemia stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Review
  8. Bcr-Abl regulation of sphingomyelin synthase 1 reveals a novel oncogenic-driven mechanism of protein up-regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Classic and molecular cytogenetic findings in leukemia patients from the Western part of Romania.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    Article
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

4 authors at 1 institution in 1 country.

Bing Z CarterSection of Molecular Hematology and Therapy, Department of Stem Cell Transplantation and Cellular Therapy, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA. bicarter@mdanderson.org
Duncan H Mak
Jorge Cortes
Michael Andreeff
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ARLINGHAUS, RALPH BERNARD · 1990 to 2014
$41.8M
NCI NIH HHS CA16672NCI NIH HHS P01 CA049639NCI NIH HHS P01 CA49639NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a clonal multistep myeloproliferative disease originating from and ultimately sustained by a rare population of BCR-ABL(+) cells with multilineage stem cell properties. Imatinib, the most successful of molecular targeted therapies, has revolutionized treatment of patients with CML. Despite this achievement, CML is often not curable, largely due to the innate insensitivity of CML stem cells, particularly when in a quiescent state. This failure of not only imatinib but also the second-generation tyrosine kinase inhibitors (TKIs) frequently leads to relapse upon drug discontinuation. Thus, any curative therapy must eliminate CML stem cells. A comprehensive understanding of the biological properties of CML stem cells and an elucidation of the molecular mechanisms and signaling pathways enabling these CML stem cells to self-renew, combined with insight into the regulation of apoptosis signaling and the mechanisms governing the interaction of CML stem cells with their bone marrow microenvironment, will facilitate the development of therapies for targeting these cells. Here, we discuss the biological properties of CML stem cells and potential strategies to eliminate them.

Indexed as

Antineoplastic AgentsBenzamidesHumansImatinib MesylateInterferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsPiperazinesProtein Kinase InhibitorsPyrimidinesSignal TransductionAntineoplastic AgentsBenzamidesImatinib MesylateInterferon-alphaPiperazinesProtein Kinase InhibitorsPyrimidines

Identifiers

PMID20875553
PMCPMC2948413
OpenAlexW2040981107

What OpenQuestion holds

Textmetadata
LicenceTDM
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.