Evidence map›Paper›PMID 26371140›Full record

ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2015

Tyrosine Kinase Inhibitor-Associated Cardiovascular Toxicity in Chronic Myeloid Leukemia.

Javid J Moslehi, Michael Deininger

Abstract readReview
In one paragraph

Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed
26.8field-weighted citation impact, top 1% 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

226 citing papers in PubMed, 435 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Article
  10. Observational
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

166 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Javid J MoslehiJavid J. Moslehi, Vanderbilt-Ingram Cancer Center and Vanderbilt University School of Medicine, Nashville, TN; and Michael Deininger, University of Utah Huntsman Cancer Institute, Salt Lake City, UT.
Michael DeiningerJavid J. Moslehi, Vanderbilt-Ingram Cancer Center and Vanderbilt University School of Medicine, Nashville, TN; and Michael Deininger, University of Utah Huntsman Cancer Institute, Salt Lake City, UT. michael.deininger@hci.utah.edu.
Vanderbilt University · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
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
Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
NCI NIH HHS P01 CA049639NCI NIH HHS P01CA049639NCI NIH HHS P30 CA042014NCI NIH HHS P30CA042014NCI NIH HHS R01 CA178397NCI NIH HHS R01CA178397-01A1NHLBI NIH HHS K08HL09703
6 · The paper itself

Abstract

For most patients with chronic myeloid leukemia, tyrosine kinase inhibitors (TKIs) have turned a fatal disease into a manageable chronic condition. Imatinib, the first BCR-ABL1 TKI granted regulatory approval, has been surpassed in terms of molecular responses by the second-generation TKIs nilotinib, dasatinib, and bosutinib. Recently, ponatinib was approved as the only TKI with activity against the T315I mutation. Although all TKIs are associated with nonhematologic adverse events (AEs), experience with imatinib suggested that toxicities are typically manageable and apparent early during drug development. Recent reports of cardiovascular AEs with nilotinib and particularly ponatinib and of pulmonary arterial hypertension with dasatinib have raised concerns about long-term sequelae of drugs that may be administered for decades. Here, we review what is currently known about the cardiovascular toxicities of BCR-ABL1 TKIs, discuss potential mechanisms underlying cardiovascular AEs, and elucidate discrepancies between the reporting of such AEs between oncology and cardiovascular trials. Whenever possible, we provide practical recommendations, but we concede that cause-directed interventions will require better mechanistic understanding. We suggest that chronic myeloid leukemia heralds a fundamental shift in oncology toward effective but mostly noncurative long-term therapies. Realizing the full potential of these treatments will require a proactive rational approach to minimize long-term cardiovascular and cardiometabolic toxicities.

Indexed as

Aniline CompoundsAntineoplastic AgentsCardiovascular SystemClinical Trials as TopicDasatinibFusion Proteins, bcr-ablHumansHypertensionImatinib MesylateImidazolesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMolecular Targeted TherapyNitrilesProtein Kinase InhibitorsPyridazinesPyrimidinesAniline CompoundsAntineoplastic AgentsbosutinibDasatinibFusion Proteins, bcr-ablImatinib MesylateImidazolesnilotinibNitrilesponatinibProtein Kinase InhibitorsPyridazinesPyrimidinesQuinolines

Identifiers

PMID26371140
PMCPMC4658454
OpenAlexW1939978733

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.