Evidence map›Paper›PMID 23502220›Full record

Trial reportBlood2013

Nilotinib is associated with a reduced incidence of BCR-ABL mutations vs imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase.

Andreas Hochhaus, Giuseppe Saglio, Richard A Larson, Dong-Wook Kim, Gabriel Etienne, Gianantonio Rosti, Carmino De Souza, Mineo Kurokawa, Matt E Kalaycio, Albert Hoenekopp and 4 more

Registry-linked trialAbstract readClinical Trial, Phase IIIMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00471497 (A Phase III Multi-center, Open-label, Randomized Study of Imatinib Versus Nilotinib in Adult Patients With Newly Diagnosed Philadelphia Chromosome Positive), which is not on this map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% 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.

NCT00471497 phase3completednot on this map

A Phase III Multi-center, Open-label, Randomized Study of Imatinib Versus Nilotinib in Adult Patients With Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP)

TypeinterventionalSponsorNovartis PharmaceuticalsRan2007 to 2019Enrolled846ConditionsMyelogenous Leukemia, ChronicArmsnilotinib, imatinib
3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 12 institutions in 9 countries.

Andreas HochhausAbteilung Hämatologie/Onkologie, Universitätsklinikum Jena, Jena, Germany. andreas.hochhaus@med.uni-jena.de
Giuseppe Saglio
Richard A Larson
Dong-Wook Kim
Gabriel Etienne
Gianantonio Rosti
Carmino De Souza
Mineo Kurokawa
Matt E Kalaycio
Albert Hoenekopp
Xiaolin Fan
Yaping Shou
Hagop M Kantarjian
Timothy P Hughes
Catholic University of Korea · KRCleveland Clinic · USInstitut Bergonié · FRJena University Hospital · DENovartis (Switzerland) · CHSouth Australia Pathology · AUThe University of Texas MD Anderson Cancer Center · USUniversidade Estadual de Campinas (UNICAMP) · BRUniversity of Bologna · ITUniversity of Chicago Medical Center · USUniversity of Tokyo Hospital · JPUniversity of Turin · IT

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

In patients with chronic myeloid leukemia, BCR-ABL mutations contribute to resistance to tyrosine kinase inhibitor therapy. We examined the occurrence of treatment-emergent mutations and their impact on response in patients from the ENESTnd phase 3 trial. At the 3-year data cutoff, mutations were detected in approximately twice as many patients (21) on imatinib 400 mg once daily as on nilotinib (11 patients each on nilotinib 300 mg twice daily and nilotinib 400 mg twice daily). The majority of mutations occurred in patients with intermediate or high Sokal scores. Most mutations (14 [66.7%]) emerging during imatinib treatment were imatinib-resistant and nilotinib-sensitive. Incidence of the T315I mutation was low (found in 3, 2, and 3 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice daily, and imatinib, respectively) and mostly occurred in patients with high Sokal scores. Of the patients with emergent mutations, 1 of 11, 2 of 11, and 7 of 21 patients on nilotinib 300 mg twice daily, nilotinib 400 mg twice daily, and imatinib, respectively, progressed to accelerated phase/blast crisis (AP/BC) on treatment. Overall, nilotinib led to fewer treatment-emergent BCR-ABL mutations than imatinib and reduced rates of progression to AP/BC in patients with these mutations. (Clinicaltrials.gov NCT00471497).

Indexed as

Antineoplastic AgentsBenzamidesBlast CrisisDisease ProgressionDose-Response Relationship, DrugDown-RegulationDrug Administration ScheduleFollow-Up StudiesFusion Proteins, bcr-ablGene FrequencyHumansImatinib MesylateIncidenceLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMutationPiperazinesAntineoplastic AgentsBenzamidesFusion Proteins, bcr-ablImatinib MesylatenilotinibPiperazinesPyrimidines

Identifiers

PMID23502220
PMCPMC4915803
OpenAlexW1966006461

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.