Evidence map›Paper›PMID 41126738›Full record

ArticleHaematologica2026

Age-specific mutation profiles and their prognostic implications in pediatric

Kota Shoji, Kenichi Yoshida, Shinju Iyoda, Moe Ishikawa, Miu Tanaka, Michidai Nobe, Nijika Saito, Yuto Shino, Yasuhito Nannya, Genki Yamato and 23 more

Abstract read
In one paragraph

Article in Haematologica, 2026. 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. Review
  2. 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

33 authors.

Kota ShojiHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Division of Cancer Evolution, National Cancer Center Research Institute, Tokyo.
Shinju IyodaHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Moe IshikawaHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Miu TanakaHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Michidai NobeHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Nijika SaitoHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Yuto ShinoHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Yasuhito NannyaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Division of Hematopoietic Disease Control, Institute of Medical Science, The University of Tokyo, Tokyo.
Genki YamatoDepartment of Pediatrics, Gunma University Graduate School of Medicine, Maebashi.
Shinichi TsujimotoDepartment of Pediatrics, Yokohama City University Hospital, Yokohama.
Norio ShibaDepartment of Pediatrics, Yokohama City University Hospital, Yokohama.
Yasuhide HayashiGunma Children's Medical Center, Shibukawa.
Yusuke ShiozawaLaboratory of Molecular Analysis, Nippon Medical School, Tokyo.
Yuichi ShiraishiDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo.
Kenichi ChibaDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo.
Ai OkadaDivision of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo.
Hiroko TanakaDepartment of Integrated Analytics, MD Data Science Center, Institute of Integrated Research, Institute of Science Tokyo, Tokyo.
Satoru MiyanoDepartment of Integrated Analytics, MD Data Science Center, Institute of Integrated Research, Institute of Science Tokyo, Tokyo.
Yuhki KogaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka.
Hiroaki GotoDivision of Hematology/Oncology, Kanagawa Children's Medical Center, Yokohama.
Kiminori TeruiDepartment of Pediatrics, Hirosaki University Graduate School of Medicine, Hirosaki.
Etsuro ItoDepartment of Pediatrics, Hirosaki University Graduate School of Medicine, Hirosaki.
Nobutaka KiyokawaDepartment of Pediatric Hematology and Oncology Research, National Research Institute for Child Health and Development, Tokyo.
Daisuke TomizawaDivision of Leukemia and Lymphoma, Children's Cancer Center, National Center for Child Health and Development, Tokyo.
Takashi TagaDepartment of Pediatrics, Shiga University of Medical Science, Otsu.
Hiroshi MoritakeDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki.
Akio TawaDepartment of Pediatrics, Higashiosaka Aramoto Heiwa Clinic, Higashiosaka.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto.
Momoko NishikoriHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto.
Souichi AdachiHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Shiga General Hospital, Moriyama.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University, Kyoto, Japan; Department of Innovative Medicine, Faculty of Medicine, Kindai University, Osaka.
Hidemasa MatsuoHuman Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya. matsuo@kuhp.kyoto-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Driver mutations in KMT2A-rearranged (KMT2A-r) have been identified in acute myeloid leukemia (AML); however, age-related differences in their frequency and prognostic factors remain unclear. In this study, we report age-specific mutation profiles and outcomes in pediatric patients with KMT2A-r AML. In 239 cases of KMT2A-r AML, infants (<1 year, N= 59) showed a significantly higher event-free survival (EFS) and overall survival (OS) compared with children (≥1 year, N=180). Conversely, in 538 cases of non-KMT2A-r AML, infants exhibited a significantly lower EFS and OS than children. KMT2A::MLLT4 was only detected in children with KMT2A-r AML and was associated with a poor prognosis. In KMT2A-r AML, mutations in signaling pathway genes, such as KRAS, were frequently detected in infants and children. However, the frequency of non-signaling pathway mutations was significantly higher in children. Moreover, non-signaling pathway mutations had no significant effect on the prognosis in infants and children, whereas KRAS mutations were associated with poor prognosis in both groups. Multivariate analysis identified older age, a high white blood cell count, KMT2A::MLLT4, and KRAS mutations as independent adverse prognostic factors for both EFS and OS. These age-specific mutation profiles suggest distinct disease mechanisms across age groups and may help to refine risk stratification and treatment strategies for pediatric KMT2A-r AML.

Indexed as

Gene RearrangementHistone-Lysine N-MethyltransferaseLeukemia, Myeloid, AcuteMutationMyeloid-Lymphoid Leukemia ProteinAdolescentAge FactorsBiomarkers, TumorChildChild, PreschoolFemaleHumansInfantMalePrognosisBiomarkers, TumorHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia Protein

Identifiers

PMID41126738
PMCPMC13040199

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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.