Evidence map›Paper›PMID 39921715›Full record

ArticleAnnals of hematology2025

Prognostic impact of TET2 mutations in patients with acute myeloid leukemia: HM-SCREEN-Japan 01 and 02 study.

Satoshi Iyama, SungGi Chi, Masashi Idogawa, Takayuki Ikezoe, Kentaro Fukushima, Yoshikazu Utsu, Junya Kanda, Goichi Yoshimoto, Takahiro Kobayashi, Naoko Hosono and 15 more

Abstract readMulticenter Study
In one paragraph

Article in Annals of hematology, 2025. 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. Review
  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

25 authors.

Satoshi IyamaDepartment of Hematology, Sapporo Medical University School of Medicine, South-1, West-16, Chuo- ku, Sapporo, 060-8543, Hokkaido, Japan. iyama@sapmed.ac.jp.ORCID http://orcid.org/0000-0002-6328-494X
SungGi ChiDepartment of Hematology, National Cancer Center Hospital East, Kashiwa, Japan.
Masashi IdogawaDepartment of Medical Genome Sciences, Cancer Research Institute, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID http://orcid.org/0000-0002-8507-1726
Takayuki IkezoeDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Kentaro FukushimaDepartment of Hematology and Oncology, Osaka University, Suita, Japan.
Yoshikazu UtsuDepartment of Hematology and Oncology, Japanese Red Cross Narita Hospital, Narita, Japan.ORCID http://orcid.org/0000-0002-3836-3216
Junya KandaDepartment of Hematology, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0002-6704-3633
Goichi YoshimotoDepartment of Hematology, Saga Prefectural Kouseikan Hospital, Saga, Japan.
Takahiro KobayashiDepartment of Hematology, Nephrology, and Rheumatology, Akita University Graduate School of Medicine, Akita, Japan.
Naoko HosonoDepartment of Hematology and Oncology, University of Fukui Hospital, Fukui, Japan.
Takahiro YamauchiDepartment of Hematology and Oncology, University of Fukui Hospital, Fukui, Japan.
Takeshi KondoBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Yukinori NakamuraThird Department of Internal Medicine, Yamaguchi University Hospital, Ube, Japan.ORCID http://orcid.org/0000-0001-5498-3370
Kensuke KojimaDepartment of Hematology, Kochi Medical School Hospital, Nankoku, Japan.
Chikashi YoshidaDepartment of Hematology, NHO Mito Medical Center, Ibaraki, Japan.
Akihiko GotohDepartment of Hematology, Tokyo Medical University Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8608-4393
Kazuhito YamamotoDepartment Hematology and Cell Therapy, Aichi Cancer Center, Nagoya, Japan.ORCID http://orcid.org/0000-0002-8588-8955
Junya KurodaDivision of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kenji IshitsukaDepartment of Hematology and Rheumatology, Kagoshima University, Kagoshima, Japan.
Emiko SakaidaDepartment of Hematology, Chiba University Hospital, Chiba, Japan.
Hiroto HoriguchiDepartment of Hematology, Sapporo Medical University School of Medicine, South-1, West-16, Chuo- ku, Sapporo, 060-8543, Hokkaido, Japan.ORCID http://orcid.org/0000-0001-6811-3042
Kohichi TakadaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID http://orcid.org/0000-0002-1393-9442
Hirofumi OhnishiDepartment of Public Health, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masayoshi KobuneDepartment of Hematology, Sapporo Medical University School of Medicine, South-1, West-16, Chuo- ku, Sapporo, 060-8543, Hokkaido, Japan.ORCID http://orcid.org/0000-0003-3828-8444
Yosuke MinamiDepartment of Hematology, National Cancer Center Hospital East, Kashiwa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ten-eleven translocation-2 (TET2) gene mutations are observed in 12-20% of adult patients with acute myeloid leukemia (AML). The prognostic impact of TET2 mutations in patients with AML and myelodysplastic syndromes has been reported in several studies; however, their results remain controversial. Therefore, we aimed to analyze the prevalence and significance of TET2 mutations in patients with AML. Data were obtained from 331 patients with AML according to the Hematologic Malignancies-SCREEN-Japan 01 and 02 studies, which were prospective multicenter genomic profiling analyses. We found a distinct type of TET2 mutations, with a particularly detrimental prognosis in the patients. Thirty-five patients with TET2 'significant' mutations were identified (26 with frameshift mutations and nine with nonsense mutations). The proportion of patients with TET2 mutations was 31.7% (10.6% and 21.1% in the TET2 significant and non-significant mutation groups). The TET2 significant mutation group had a shorter OS than the TET2 non-significant mutation or wild-type TET2 group (median: 15.9 vs. 35.0 vs. 25.9 months). Regarding the response to chemotherapy according to TET2 status, the complete response (CR) or CR with incomplete count recovery rate was 37.1% in the TET2 significant mutation group and 46.6% in the non-significant mutation or wild-type group. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) improved patient prognosis in the TET2 non-significant mutation or wild-type TET2 group; however, allo-HSCT did not affect prognosis in the TET2 significant mutation group. This study indicates that certain TET2 mutations in patients with AML may have detrimental effects.

Indexed as

DioxygenasesDNA-Binding ProteinsLeukemia, Myeloid, AcuteMutationProto-Oncogene ProteinsAdolescentAdultAgedAged, 80 and overFemaleHematopoietic Stem Cell TransplantationHumansJapanMaleMiddle AgedPrognosisDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTET2 protein, human

Identifiers

PMID39921715
PMCPMC11868205

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