Evidence map›Paper›PMID 40164719›Full record

ArticleLeukemia2025

Whole-genome sequencing of myeloproliferative neoplasms revealed dynamic clonal changes in the fibrotic or leukemic transformation and novel FOXP1 mutations in the fibrotic transformation.

Hiroyuki Takamori, Ying-Jung Huang, Hidehito Fukushima, Kazuaki Yokoyama, Ting-Yu Huang, Ming-Chung Kuo, Seishi Ogawa, Yasuhito Nannya, Lee-Yung Shih

Abstract read
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Article in Leukemia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

9 authors.

Hiroyuki Takamori *Division of Hematopoietic Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-0179-3335
Ying-Jung Huang *Division of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan.
Hidehito FukushimaDivision of Hematopoietic Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kazuaki YokoyamaDivision of Hematopoietic Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ting-Yu HuangDivision of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan.
Ming-Chung KuoDivision of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-7778-5374
Yasuhito NannyaDivision of Hematopoietic Disease Control, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ynanya@ims.u-tokyo.ac.jp.ORCID 0000-0002-6526-0992
Lee-Yung ShihDivision of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan. sly7012@adm.cgmh.org.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloproliferative neoplasms (MPNs) are characterized by clonal proliferation of hematopoietic stem cells, which can lead to secondary myelofibrosis or acute myeloid leukemia. We explored the changes in genomic alterations during MPN transformation using whole-genome sequencing of samples from both the chronic and fibrotic or leukemic phases of 20 patients. We identified FOXP1 mutations in 3 of 14 (21.4%) patients with secondary myelofibrosis. This novel mutation was identified in another 5 of the 35 patients (14.3%) in an independent cohort. All these 8 patients with FOXP1 mutations did not experience leukemic transformation after a median follow-up of 5.1 years. The acquisition of non-canonical MPL

Indexed as

Cell Transformation, NeoplasticClonal EvolutionLeukemia, Myeloid, AcuteMyeloproliferative DisordersPrimary MyelofibrosisAdultAgedAged, 80 and overFibrosisForkhead Transcription FactorsHumansMiddle AgedMutationRepressor ProteinsWhole Genome SequencingForkhead Transcription FactorsFOXP1 protein, humanRepressor Proteins

Identifiers

PMID40164719

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.