Evidence map›Paper›PMID 29222245›Full record

ReviewHematology. American Society of Hematology. Education Program2017

Novel approaches to therapy in CML.

Ravi Bhatia

Abstract readReview
In one paragraph

Review in Hematology. American Society of Hematology. Education Program, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Novel targeted therapies in chronic myeloid leukemia.Pharmaceutical science advances · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. TARGETING LEUKEMIA STEM CELL RESISTANCE IN CHRONIC MYELOGENOUS LEUKEMIA.Transactions of the American Clinical and Climatological Association · 2019
    Article
  14. Review
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

1 author.

Ravi BhatiaDivision of Hematology/Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.

Funding

Resistance of CML stem cells to STI571 (Gleevec)R01CA095684 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BHATIA, RAVI · 2003 to 2017
$4.6M
Microenvironmental Regulation of Leukemia Stem CellsR01CA172447 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BHATIA, RAVI · 2013 to 2023
$3.4M
NCI NIH HHS R01 CA095684NCI NIH HHS R01 CA172447
6 · The paper itself

Abstract

Treatment with tyrosine kinase inhibitors (TKIs) results in remission and prolongation of survival in most chronic myeloid leukemia (CML) patients but fails to eliminate the leukemia stem cells (LSCs) responsible for disease development and propagation. This accounts for the clinical observation that TKI discontinuation leads to rapid leukemia relapse. Most patients require continued treatment to prevent relapse, with associated risk of relapse, toxicity, teratogenic effects, financial burden, and noncompliance. Understanding LSC resistance to TKI and development of strategies to increase the proportion of CML patients achieving treatment-free remissions is a critical area of investigation in CML. In addition, LSCs are the source of TKI resistance, relapse, or disease progression, which is another major area of need in CML treatment. It is now understood that BCR-ABL kinase-independent mechanisms are responsible for retention of LSC subpopulations. It is likely that both cell-intrinsic and microenvironmental mechanisms contribute to LSC maintenance. Here, we review the current understanding of mechanisms underlying persistence of CML LSCs during TKI treatment, recently described approaches to target these cells and emerging clinical trials, and the challenges impeding more rapid progress in achieving cures for a greater number of CML patients.

Indexed as

Drug Resistance, NeoplasmFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsFusion Proteins, bcr-ablProtein Kinase Inhibitors

Identifiers

PMID29222245
PMCPMC6142563

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.