Evidence map›Paper›PMID 30282643›Full record

ArticleBlood advances2018

Cell-lineage level-targeted sequencing to identify acute myeloid leukemia with myelodysplasia-related changes.

Kazuaki Yokoyama, Eigo Shimizu, Nozomi Yokoyama, Sousuke Nakamura, Rika Kasajima, Miho Ogawa, Tomomi Takei, Mika Ito, Asako Kobayashi, Rui Yamaguchi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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

13 authors at 3 institutions in 3 countries.

Kazuaki YokoyamaDepartment of Hematology/Oncology, Research Hospital, Institute of Medical Science.ORCID 0000-0002-2556-3833
Eigo ShimizuLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science.ORCID 0000-0002-2486-2321
Nozomi YokoyamaDepartment of Applied Genomics, Research Hospital, Institute of Medical Science.
Sousuke NakamuraDivision of Molecular Therapy, Advanced Clinical Research Center, Institute of Medical Science, and.
Rika KasajimaDivision of Health Medical Data Science, Health Intelligence Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Miho OgawaDivision of Molecular Therapy, Advanced Clinical Research Center, Institute of Medical Science, and.
Tomomi TakeiDivision of Molecular Therapy, Advanced Clinical Research Center, Institute of Medical Science, and.
Mika ItoDivision of Molecular Therapy, Advanced Clinical Research Center, Institute of Medical Science, and.
Asako KobayashiDivision of Molecular Therapy, Advanced Clinical Research Center, Institute of Medical Science, and.
Rui YamaguchiLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science.ORCID 0000-0003-1224-227X
Seiya ImotoDivision of Health Medical Data Science, Health Intelligence Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan.ORCID 0000-0002-2989-308X
Satoru MiyanoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science.ORCID 0000-0002-1753-6616
Arinobu TojoDepartment of Hematology/Oncology, Research Hospital, Institute of Medical Science.ORCID 0000-0001-9016-1948
Advanced Medical Research Institute · USShiga University of Medical Science Hospital · JPGenomics (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a clonal myeloid neoplasm that typically arises de novo; however, some cases evolve from a preleukemic state, such as myelodysplastic syndrome (MDS). Such secondary AMLs and those with typical MDS-related clinical features are known as AMLs with myelodysplasia-related changes (AML-MRC). Because patients with AML-MRC have poor prognosis, more accurate diagnostic approaches are required. In this study, we performed targeted sequencing of 54 genes in 3 cell populations (granulocyte, blast, and T-cell fractions) using samples from 13 patients with MDS, 16 patients with clinically diagnosed AML-MRC, 4 patients with suspected AML-MRC but clinically diagnosed as AML not otherwise specified (AML-NOS), and 11 patients with de novo AML. We found that overlapping mutations, defined as those shared at least by the blast and granulocyte fractions, were significantly enriched in patients with MDS and AML-MRC, including those with suspected AML-MRC, indicating a substantial history of clonal hematopoiesis. In contrast, blast-specific nonoverlapping mutations were significantly enriched in patients with de novo AML. Furthermore, the presence of overlapping mutations, excluding

Indexed as

Genetic Predisposition to DiseaseBiomarkersBone MarrowCell LineageDiagnosis, DifferentialDisease ProgressionFemaleGene FrequencyGenetic Association StudiesGenetic VariationHumansLeukemia, Myeloid, AcuteMaleMutationMyelodysplastic SyndromesROC CurveBiomarkers

Identifiers

PMID30282643
PMCPMC6177645
OpenAlexW2895531718

What OpenQuestion holds

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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.