Evidence map›Paper›PMID 22157291›Full record

ReviewCancer journal (Sudbury, Mass.)

Development of an effective therapy for chronic myelogenous leukemia.

David W Woessner, Carol S Lim, Michael W Deininger

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Cancer journal (Sudbury, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Current and future of targeted therapies against BCR::ABL kinases.Journal of the Egyptian National Cancer Institute · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. CML in Elderly: Does Age Matter?Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2020
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

David W WoessnerDepartments of Pharmacology and Toxicology, College of Pharmacy, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Carol S Lim
Michael W Deininger
Huntsman Cancer Institute · US

Funding

TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THALL, PETER F · 1990 to 2014
$41.8M
Biology of Imatinib-Resistant Mutants of BCR-ABLR01HL082978 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DEININGER, MICHAEL W. · 2005 to 2009
$1.5M
Converting an Oncogene to an Apoptotic Factor by Manipulating Signal SequencesR01CA129528 · NCI · UNIVERSITY OF UTAH · PI LIM, CAROL S. · 2008 to 2012
$1.4M
Howard Hughes Medical InstituteNCI NIH HHS CA04963920A2NCI NIH HHS CA129528NCI NIH HHS P01 CA049639NCI NIH HHS R01 CA129528NHLBI NIH HHS HL082978-01NHLBI NIH HHS R01 HL082978
6 · The paper itself

Abstract

Targeted small-molecule drugs have revolutionized treatment of chronic myeloid leukemia (CML) during the last decade. These agents interrupt a constitutively active BCR-ABL, the causative agent for CML, by interfering with adenosine 5' triphosphate-dependent ABL tyrosine kinase. Although the efficacy of tyrosine kinase inhibitors (TKIs) has resulted in overall survival of greater than 90%, TKIs are not curative. Moreover, no currently approved TKIs are effective against the T315I BCR-ABL variant. However, a new generation of TKIs with activity against T315I is on the horizon. We will highlight the clinical utility of historical CML therapeutics, those used today (first- and second-generation TKIs), and discuss treatment modalities that are under development. Recent advances have illuminated the complexity of CML, especially within the marrow microenvironment. We contend that the key to curing CML will involve strategies beyond targeting BCR-ABL because primitive human CML stem cells are not dependent on BCR-ABL. Ultimately, drug combinations or exploiting synthetic lethality may transform responses into definitive cures for CML.

Indexed as

Drug Resistance, NeoplasmHumansLeukemia, Myeloid, Chronic-PhaseProtein Kinase InhibitorsProtein-Tyrosine KinasesProtein Kinase InhibitorsProtein-Tyrosine Kinases

Identifiers

PMID22157291
PMCPMC3251313
OpenAlexW2077171467

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.