Evidence map›Paper›PMID 25412851›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2015

Next-generation sequencing of acute myeloid leukemia identifies the significance of TP53, U2AF1, ASXL1, and TET2 mutations.

Robert S Ohgami, Lisa Ma, Jason D Merker, Jason R Gotlib, Iris Schrijver, James L Zehnder, Daniel A Arber

Abstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

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  13. The Prognostic Value of TP53 Mutations in Adult Acute Myeloid Leukemia: A Meta-Analysis.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2023
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  19. Outcomes in Patients with Poor-Risk Cytogenetics with or without TP53 Mutations Treated with Venetoclax and Azacitidine.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
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  20. Article

15 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

7 authors at 2 institutions in 1 country.

Robert S OhgamiDepartment of Pathology, Stanford University Medical Center, Stanford, CA, USA.
Lisa MaDepartment of Pathology, Stanford University Medical Center, Stanford, CA, USA.
Jason D MerkerDepartment of Pathology, Stanford University Medical Center, Stanford, CA, USA.
Jason R GotlibDivision of Hematology, Department of Medicine, Stanford University Medical Center, Stanford, CA, USA.
Iris SchrijverDepartment of Pathology, Stanford University Medical Center, Stanford, CA, USA.
James L Zehnder1] Department of Pathology, Stanford University Medical Center, Stanford, CA, USA [2] Division of Hematology, Department of Medicine, Stanford University Medical Center, Stanford, CA, USA.
Daniel A ArberDepartment of Pathology, Stanford University Medical Center, Stanford, CA, USA.
Stanford Medicine · USStanford University · US

Funding

TUMOR SPECIFIC CYTOTOXIC T-LYMPHOCYTES IN BONE MARROW TRANSPLANTATIONP01CA049605 · NCI · STANFORD UNIVERSITY · PI David B. Miklos · 1989 to 2026
$73.3M
NCI NIH HHS P01 CA049605
6 · The paper itself

Abstract

We assessed the frequency and clinicopathologic significance of 19 genes currently identified as significantly mutated in myeloid neoplasms, RUNX1, ASXL1, TET2, CEBPA, IDH1, IDH2, DNMT3A, FLT3, NPM1, TP53, NRAS, EZH2, CBL, U2AF1, SF3B1, SRSF2, JAK2, CSF3R, and SETBP1, across 93 cases of acute myeloid leukemia (AML) using capture target enrichment and next-generation sequencing. Of these cases, 79% showed at least one nonsynonymous mutation, and cases of AML with recurrent genetic abnormalities showed a lower frequency of mutations versus AML with myelodysplasia-related changes (P<0.001). Mutational analysis further demonstrated that TP53 mutations are associated with complex karyotype AML, whereas ASXL1 and U2AF1 mutations are associated with AML with myelodysplasia-related changes. Furthermore, U2AF1 mutations were specifically associated with trilineage morphologic dysplasia. Univariate analysis demonstrated that U2AF1 and TP53 mutations are associated with absence of clinical remission, poor overall survival (OS), and poor disease-free survival (DFS; P<0.0001), whereas TET2 and ASXL1 mutations are associated with poor OS (P<0.03). In multivariate analysis, U2AF1 and TP53 mutations retained independent prognostic significance in OS and DFS, respectively. Our results demonstrate unique relationships between mutations in AML, clinicopathologic prognosis, subtype categorization, and morphologic dysplasia.

Indexed as

AdolescentAdultAgedBiomarkers, TumorChildDioxygenasesDisease-Free SurvivalDNA-Binding ProteinsDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansKaplan-Meier EstimateLeukemia, Myeloid, AcuteMaleMiddle AgedASXL1 protein, humanBiomarkers, TumorDioxygenasesDNA-Binding ProteinsNPM1 protein, humanNuclear ProteinsNucleophosminProto-Oncogene ProteinsRepressor ProteinsRibonucleoproteinsSplicing Factor U2AFTET2 protein, humanTP53 protein, humanTumor Suppressor Protein p53U2AF1 protein, human

Identifiers

PMID25412851
PMCPMC5436901
OpenAlexW2082365047

What OpenQuestion holds

Textmetadata
LicenceTDM
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.