Evidence map›Paper›PMID 27174585›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2016

Targeted next-generation sequencing identifies a subset of idiopathic hypereosinophilic syndrome with features similar to chronic eosinophilic leukemia, not otherwise specified.

Sa A Wang, Wayne Tam, Albert G Tsai, Daniel A Arber, Robert P Hasserjian, Julia T Geyer, Tracy I George, David R Czuchlewski, Kathryn Foucar, Heesun J Rogers and 9 more

Open access · bronzeAbstract readComparative StudyMulticenter Study
PubMed Publisher
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
13.5field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
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  20. Myeloid/lymphoid neoplasms with FLT3 rearrangement.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
    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

19 authors at 9 institutions in 1 country.

Sa A WangDepartment of Hematopathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Wayne TamDepartment of Pathology, Weill Cornell Medical College, New York, NY, USA.
Albert G TsaiDepartment of Pathology, Stanford University, Stanford, CA, USA.
Daniel A ArberDepartment of Pathology, Stanford University, Stanford, CA, USA.
Robert P HasserjianDepartment of Pathology, Massachusetts General Hospital, Boston, MA, USA.
Julia T GeyerDepartment of Pathology, Weill Cornell Medical College, New York, NY, USA.
Tracy I GeorgeDepartment of Pathology, University of New Mexico, Albuquerque, NM, USA.
David R CzuchlewskiDepartment of Pathology, University of New Mexico, Albuquerque, NM, USA.
Kathryn FoucarDepartment of Pathology, University of New Mexico, Albuquerque, NM, USA.
Heesun J RogersDepartment of Laboratory Medicine, Cleveland Clinic, Cleveland, OH, USA.
Eric D HsiDepartment of Laboratory Medicine, Cleveland Clinic, Cleveland, OH, USA.
B Bryan ReaDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Adam BaggDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Paola Dal CinDepartment of Pathology, Brigham and Women Hospital, Boston, MA, USA.
Chong ZhaoDepartment of Hematopathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Todd W KelleyDepartment of Pathology, University of Utah, Salt Lake City, UT, USA.
Srdan VerstovsekDepartment of Leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Carlos Bueso-RamosDepartment of Hematopathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Attilio OraziDepartment of Pathology, Weill Cornell Medical College, New York, NY, USA.
The University of Texas MD Anderson Cancer Center · USCornell University · USUniversity of New Mexico · USCleveland Clinic · USStanford University · USUniversity of Pennsylvania · USBrigham and Women's Hospital · USMassachusetts General Hospital · USUniversity of Utah · US

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

The distinction between chronic eosinophilic leukemia, not otherwise specified and idiopathic hypereosinophilic syndrome largely relies on clonality assessment. Prior to the advent of next-generation sequencing, clonality was usually determined by cytogenetic analysis. We applied targeted next-generation sequencing panels designed for myeloid neoplasms to bone marrow specimens from a cohort of idiopathic hypereosinophilic syndrome patients (n=51), and assessed the significance of mutations in conjunction with clinicopathological features. The findings were further compared with those of 17 chronic eosinophilic leukemia, not otherwise specified patients defined by their abnormal cytogenetics and/or increased blasts. Mutations were detected in 14/51 idiopathic hypereosinophilic syndrome patients (idiopathic hypereosinophilic syndrome/next-generation sequencing-positive) (28%), involving single gene in 7 and ≥2 in 7 patients. The more frequently mutated genes included ASXL1 (43%), TET2 (36%), EZH2 (29%), SETBP1 (22%), CBL (14%), and NOTCH1 (14%). Idiopathic hypereosinophilic syndrome/next-generation sequencing-positive patients showed a number of clinical features and bone marrow findings resembling chronic eosinophilic leukemia, not otherwise specified. Chronic eosinophilic leukemia, not otherwise specified patients showed a disease-specific survival of 14.4 months, markedly inferior to idiopathic hypereosinophilic syndrome/next-generation sequencing-negative (P<0.001), but not significantly different from idiopathic hypereosinophilic syndrome/next-generation sequencing-positive (P=0.117). These data suggest that targeted next-generation sequencing helps to establish clonality in a subset of patients with hypereosinophilia that would otherwise be classified as idiopathic hypereosinophilic syndrome. In conjunction with other diagnostic features, mutation data can be used to establish a diagnosis of chronic eosinophilic leukemia, not otherwise specified in patients presenting with hypereosinophilia.

Indexed as

High-Throughput Nucleotide SequencingMutationAdolescentAdultAgedAged, 80 and overBiopsyBone Marrow ExaminationDiagnosis, DifferentialDNA Mutational AnalysisFemaleGenetic MarkersGenetic Predisposition to DiseaseHumansHypereosinophilic SyndromeIn Situ Hybridization, FluorescenceGenetic Markers

Identifiers

PMID27174585
OpenAlexW2354069820

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.