Evidence map›Paper›PMID 38987297›Full record

ArticleScientific reports2024

Initiating-clone analysis in patients with acute myeloid leukemia secondary to essential thrombocythemia.

Yoko Ushijima, Seara Naruse, Yuichi Ishikawa, Naomi Kawashima, Masashi Sanada, Marie Nakashima, Jeong Hui Kim, Seitaro Terakura, Rika Kihara, Koichi Watamoto and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. bioRxiv : the preprint server for biology · 2025
    Article
  3. Review
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

14 authors.

Yoko Ushijima *Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.ORCID 0000-0002-2897-2843
Seara Naruse *Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.
Yuichi IshikawaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan. yishikaw@med.nagoya-u.ac.jp.ORCID 0000-0001-6024-6617
Naomi KawashimaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.ORCID 0000-0002-9914-739X
Masashi SanadaClinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Marie NakashimaDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.
Jeong Hui KimDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.
Seitaro TerakuraDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan.ORCID 0000-0002-1194-8046
Rika KiharaDepartment of Hematology and Oncology, Konan Kosei Hospital, Konan, Japan.
Koichi WatamotoDepartment of Hematology, Komaki City Hospital, Komaki, Japan.
Takahiro NishiyamaDivision of Hematology, Ichinomiya Municipal Hospital, Ichinomiya, Japan.
Kunio KitamuraDivision of Hematology, Ichinomiya Municipal Hospital, Ichinomiya, Japan.
Tadashi MatsushitaDepartment of Transfusion Medicine, Nagoya University Hospital, Nagoya, Japan.ORCID 0000-0002-3646-3125
Hitoshi KiyoiDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Tsurumai-Cho 65, Showa-Ku, Nagoya, 466-8550, Japan. kiyoi@med.nagoya-u.ac.jp.ORCID 0000-0001-6382-9498

Funding

Japan Agency for Medical Research and Development, AMED 19cm0106562h0001Japan Society for the Promotion of Science 19K08835Japan Society for the Promotion of Science 23H02933
6 · The paper itself

Abstract

Most of essential thrombocythemia (ET) patients have the clone harboring a mutation in one of the JAK2, CALR, or MPL gene, and these clones generally acquire additional mutations at transformation to acute myeloid leukemia (AML). However, the proliferation of triple-negative clones has sometimes been observed at AML transformation. To clarify the clonal evolution of ET to AML, we analyzed paired samples at ET and AML transformation in eight patients. We identified that JAK2-unmutated AML clones proliferated at AML transformation in three patients in whom the JAK2-mutated clone was dominant at ET. In two patients, TET2-mutated, but not JAK2-mutated, clones might be common initiating clones for ET and transformed AML. In a patient with JAK2-mutated ET, SMARCC2, UBR4, and ZNF143, but not JAK2, -mutated clones proliferated at AML transformation. Precise analysis using single-cell sorted CD34

Indexed as

Janus Kinase 2Leukemia, Myeloid, AcuteMutationThrombocythemia, EssentialAdultAgedAged, 80 and overCell Transformation, NeoplasticClonal EvolutionDioxygenasesDNA-Binding ProteinsFemaleHumansMaleMiddle AgedDioxygenasesDNA-Binding ProteinsJAK2 protein, humanJanus Kinase 2TET2 protein, human

Identifiers

PMID38987297
PMCPMC11237009

What OpenQuestion holds

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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.