Evidence map›Paper›PMID 27615555›Full record

ReviewFuture oncology (London, England)2017

Targeting acute myeloid leukemia with TP53-independent vosaroxin.

Christopher B Benton, Farhad Ravandi

Abstract readReview
In one paragraph

Review in Future oncology (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Trial
  2. Review
  3. 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

2 authors.

Christopher B BentonDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Farhad RavandiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

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

Vosaroxin is a quinolone compound that intercalates DNA and induces TP53-independent apoptosis, demonstrating activity against acute myeloid leukemia (AML) in Phase I-III trials. Here, we examine vosaroxin's mechanism of action and pharmacology, and we review its use in AML to date, focusing on details of individual clinical trials. Most recently, when combined with cytarabine in a randomized Phase III trial (VALOR), vosaroxin improved outcomes versus cytarabine alone for relapsed/refractory AML in patients older than 60 years and for patients in early relapse. We consider its continued role in the context of a multifaceted strategy against AML, including its current use in clinical trials. Prospective use will define its role in the evolving landscape of AML therapy.

Indexed as

Antineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisClinical Trials, Phase I as TopicClinical Trials, Phase II as TopicClinical Trials, Phase III as TopicHumansLeukemia, Myeloid, AcuteNaphthyridinesThiazolesTreatment OutcomeTumor Suppressor Protein p53Antineoplastic AgentsNaphthyridinesThiazolesTumor Suppressor Protein p53vosaroxinacute myeloid leukemiaantineoplastic agentsintercalating agentsprospective studiesvosaroxin

Identifiers

PMID27615555
PMCPMC5144553

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.