Evidence map›Paper›PMID 27006386›Full record

Trial reportBlood2016

Risk stratification of chromosomal abnormalities in chronic myelogenous leukemia in the era of tyrosine kinase inhibitor therapy.

Wei Wang, Jorge E Cortes, Guilin Tang, Joseph D Khoury, Sa Wang, Carlos E Bueso-Ramos, Joseph A DiGiuseppe, Zi Chen, Hagop M Kantarjian, L Jeffrey Medeiros and 1 more

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
15.2field-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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 190 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Wei WangDepartment of Hematopathology and.
Jorge E CortesDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX; and.
Guilin TangDepartment of Hematopathology and.
Joseph D KhouryDepartment of Hematopathology and.
Sa WangDepartment of Hematopathology and.
Carlos E Bueso-RamosDepartment of Hematopathology and.
Joseph A DiGiuseppeDepartment of Pathology, Hartford Hospital, Hartford, CT.
Zi ChenDepartment of Hematopathology and.
Hagop M KantarjianDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX; and.
L Jeffrey MedeirosDepartment of Hematopathology and.
Shimin HuDepartment of Hematopathology and.
The University of Texas MD Anderson Cancer Center · USHartford Financial Services (United States)

Funding

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

Abstract

Clonal cytogenetic evolution with additional chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associated with decreased response to tyrosine kinase inhibitor (TKI) therapy and adverse survival. Although ACAs are considered as a sign of disease progression and have been used as one of the criteria for accelerated phase, the differential prognostic impact of individual ACAs in CML is unknown, and a classification system to reflect such prognostic impact is lacking. In this study, we aimed to address these questions using a large cohort of CML patients treated in the era of TKIs. We focused on cases with single chromosomal changes at the time of ACA emergence and stratified the 6 most common ACAs into 2 groups: group 1 with a relatively good prognosis including trisomy 8, -Y, and an extra copy of Philadelphia chromosome; and group 2 with a relatively poor prognosis including i(17)(q10), -7/del7q, and 3q26.2 rearrangements. Patients in group 1 showed much better treatment response and survival than patients in group 2. When compared with cases with no ACAs, ACAs in group 2 conferred a worse survival irrelevant to the emergence phase and time. In contrast, ACAs in group 1 had no adverse impact on survival when they emerged from chronic phase or at the time of CML diagnosis. The concurrent presence of 2 or more ACAs conferred an inferior survival and can be categorized into the poor prognostic group.

Indexed as

Chromosome AberrationsAdultAgedAged, 80 and overChromosomes, HumanDisease-Free SurvivalFemaleHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMiddle AgedProtein Kinase InhibitorsRisk AssessmentSurvival RateProtein Kinase Inhibitors

Identifiers

PMID27006386
PMCPMC4915795
OpenAlexW2321560918

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.