Evidence map›Paper›PMID 20733134›Full record

Trial reportJournal of clinical oncology : official journal of the American Society of Clinical Oncology2010

Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3.

Thomas Fischer, Richard M Stone, Daniel J Deangelo, Ilene Galinsky, Elihu Estey, Carlo Lanza, Edward Fox, Gerhard Ehninger, Eric J Feldman, Gary J Schiller and 7 more

Open access · bronzeAbstract readClinical Trial, Phase IIRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 262 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
262citing papers in PubMed, 5 pooled it
14.2field-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

262 citing papers in PubMed, 5 syntheses or guidelines pooled it, 501 citations in OpenAlex.

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  10. FDA Approval Summary: Gilteritinib for Relapsed or Refractory Acute Myeloid Leukemia with aClinical cancer research : an official journal of the American Association for Cancer Research · 2021
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  17. Gemtuzumab Ozogamicin Reduces Relapse Risk in FLT3/ITD Acute Myeloid Leukemia: A Report from the Children's Oncology Group.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
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202 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

17 authors at 1 institution in 1 country.

Thomas FischerDana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA.
Richard M Stone
Daniel J Deangelo
Ilene Galinsky
Elihu Estey
Carlo Lanza
Edward Fox
Gerhard Ehninger
Eric J Feldman
Gary J Schiller
Virginia M Klimek
Stephen D Nimer
D Gary Gilliland
Catherine Dutreix
Alice Huntsman-Labed
Jodi Virkus
Francis J Giles
The University of Texas MD Anderson Cancer Center · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
NCI NIH HHS P01 CA066996
6 · The paper itself

Abstract

purposeMutations leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blasts of 30% of patients with acute myeloid leukemia (AML). Midostaurin (PKC412; N-benzoylstaurosporin) is a multitargeted tyrosine kinase inhibitor, with demonstrated activity in patients with AML/myelodysplastic syndrome (MDS) with FLT3 mutations. PATIENTS AND

methodsNinety-five patients with AML or MDS with either wild-type (n = 60) or mutated (n = 35) FLT3 were randomly assigned to receive oral midostaurin at 50 or 100 mg twice daily. The drug was discontinued in the absence of response at 2 months, disease progression, or unacceptable toxicity. Response was defined as complete response, partial response (PR), hematologic improvement, or reduction in peripheral blood or bone marrow blasts by ≥ 50% (BR).

resultsThe rate of BR for the population in whom efficacy could be assessed (n = 92) was 71% in patients with FLT3-mutant and 42% in patients with FLT3 wild-type. One PR occurred in a patient with FLT3-mutant receiving the 100-mg dose regimen. Both doses were well-tolerated; there were no differences in toxicity or response rate according to the dose of midostaurin.

conclusionThese results suggest that midostaurin has hematologic activity in both patients with FLT3-mutant and wild-type. The degree of clinical activity observed supports additional studies that combine midostaurin and other agents such as chemotherapy especially in FLT3-mutant AML.

Indexed as

Administration, OralAgedAntineoplastic AgentsFemalefms-Like Tyrosine Kinase 3HumansLeukemia, Myeloid, AcuteMaleMutationMyelodysplastic SyndromesReceptor Protein-Tyrosine KinasesStaurosporineTreatment OutcomeAntineoplastic Agentsfms-Like Tyrosine Kinase 3midostaurinReceptor Protein-Tyrosine KinasesStaurosporine

Identifiers

PMID20733134
PMCPMC4135183
OpenAlexW2154625299

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.