Evidence map›Paper›PMID 38349460›Full record

ArticleClinical and experimental medicine2024

TET2 mutations contribute to adverse prognosis in acute myeloid leukemia (AML): results from a comprehensive analysis of 502 AML cases and the Beat AML public database.

Xin'an Pan, Yingjun Chang, Guorui Ruan, Songhai Zhou, Hao Jiang, Qian Jiang, Xiaojun Huang, Xiao-Su Zhao

Open access · hybridAbstract readLetter
In one paragraph

Article in Clinical and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Haematologica · 2025
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  12. Review
  13. The role of TET2 in solid tumors and its therapeutic potential: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    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

8 authors at 2 institutions in 1 country.

Xin'an PanPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Yingjun ChangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Guorui RuanPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Songhai ZhouPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Hao JiangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Qian JiangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Xiaojun HuangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China.
Xiao-Su ZhaoPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Hematopoietic Stem Cell Transplantation, No. 11 Xizhimen South Street, Beijing, 100044, China. zhaoxiaosu1977@126.com.
Peking University People's Hospital · CNPeking University · CN

Funding

National Key Research and Development Program of China Stem Cell and Translational Research 2021YFC2500300the Beijing Municipal Science and Technology Commission Z221100007422008the Major Program of the National Natural Science Foundation of China 82293630 and 82293633
6 · The paper itself

Abstract

Despite the high incidence of tet methylcytosine dioxygenase 2 (TET2) mutations in acute myeloid leukemia (AML), the prognostic implications of these mutations in three AML risk groups based on the 2022 ELN AML risk classification are still unclear. A total of 502 consecutive de novo AML patients who had next-generation sequencing data available between March 2011 and July 2021 at the Peking University Institute of Hematology were enrolled in this study. Univariate and multivariate Cox regression analyses were performed to explore the prognostic impact of TET2 mutations in the above cohort and the Beat AML cohort. Of the 502 total AML patients, 76 (15.1%) carried TET2 mutations. Multivariate analysis revealed TET2 mutations as independent risk factor for overall survival (OS) in both the total AML cohort (OR = 1.649, p = 0.009) and in the 2022 ELN intermediate-risk cohort (HR = 1.967, p = 0.05). Analysis of RNA-seq data from the Beat AML study revealed 1042 differentially expressed genes (DEGs) between the TET2-mutant and TET2 wild-type groups. The results of enrichment analysis indicated the DEGs to be notably enriched in categories related to the PI3K-Akt signaling pathway. Collectively, our findings indicate that mutations in TET2 are prognostically disadvantageous in AML patients. Assessment of TET2 mutational status contributes to the stratification of intermediate-risk AML patients. Multiple genes and pathways of potential therapeutic relevance may be differentially modulated by TET2 mutations in AML.

Indexed as

DioxygenasesLeukemia, Myeloid, AcuteDNA-Binding ProteinsHumansMultivariate AnalysisMutationPhosphatidylinositol 3-KinasesPrognosisDioxygenasesDNA-Binding ProteinsPhosphatidylinositol 3-KinasesTET2 protein, humanAcute myeloid leukemiaAML Beat databaseBioinformatics analysisPrognosisRNA sequencingTET2 mutations

Identifiers

PMID38349460
PMCPMC10864580
OpenAlexW4391787068

What OpenQuestion holds

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LicenceCC BY
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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.