Evidence map›Paper›PMID 24749672›Full record

ReviewExpert opinion on investigational drugs2014

Investigational FMS-like tyrosine kinase 3 inhibitors in treatment of acute myeloid leukemia.

Naveen Pemmaraju, Hagop Kantarjian, Michael Andreeff, Jorge Cortes, Farhad Ravandi

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on investigational drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. New drugs for acute myeloid leukemia inspired by genomics and when to use them.Hematology. American Society of Hematology. Education Program · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Frontline treatment of acute myeloid leukemia in adults.Critical reviews in oncology/hematology · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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

5 authors at 1 institution in 1 country.

Naveen PemmarajuMD Anderson Cancer Center, Department of Leukemia , 1515 Holcombe Blvd Houston, TX 77030 , USA fravandi@mdanderson.org.
Hagop Kantarjian
Michael Andreeff
Jorge Cortes
Farhad Ravandi
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

introductionOutcomes for the majority of patients with acute myeloid leukemia (AML) remain poor. Over the past decade, significant progress has been made in the understanding of the cytogenetic and molecular determinants of AML pathogenesis. One such advance is the identification of recurring mutations in the FMS-like tyrosine kinase 3 gene (FLT3). Currently, this marker, which appears in approximately one-third of all AML patients, not only signifies a poorer prognosis but also identifies an important target for therapy. FLT3 inhibitors have now undergone clinical evaluation in Phase I, II and III clinical trials, as both single agents and in combination with chemotherapeutics. Unfortunately, to date, none of the FLT3 inhibitors have gained FDA approval for the treatment of patients with AML. Yet, several promising FLT3 inhibitors are being evaluated in all phases of drug development. AREAS COVERED: This review aims to highlight the agents furthest along in their development. It also focuses on those FLT3 inhibitors that are being evaluated in combination with other anti-leukemia agents. EXPERT OPINION: The authors believe that the field of research for FLT3 inhibitors remains promising, despite the historically poor prognosis of this subgroup of patients with AML. The most promising areas of research will likely be the elucidation of the mechanisms of resistance to FLT3 inhibitors, and development of potent FLT3 inhibitors alone or in combination with hypomethylating agents, cytotoxic chemotherapy or with other targeted agents.

Indexed as

AnimalsAntineoplastic AgentsBenzimidazolesBenzothiazolesDrug Resistance, Neoplasmfms-Like Tyrosine Kinase 3HumansImidazolesLeukemia, Myeloid, AcuteNiacinamidePhenylurea CompoundsPiperidinesProtein Kinase InhibitorsPyridazinesSorafenibStaurosporineAntineoplastic AgentsBenzimidazolesBenzothiazolescrenolanibfms-Like Tyrosine Kinase 3ImidazolesmidostaurinNiacinamidePhenylurea CompoundsPiperidinesponatinibProtein Kinase InhibitorsPyridazinesquizartinibSorafenibStaurosporinecrenolanibFMS-like tyrosine kinase 3 geneFMS-like tyrosine kinase 3 gene inhibitorquizartinibsorafenib

Identifiers

PMID24749672
PMCPMC4109297
OpenAlexW1997387466

What OpenQuestion holds

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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.