ArticleAnnals of laboratory medicine2015
Alteration of the SETBP1 gene and splicing pathway genes SF3B1, U2AF1, and SRSF2 in childhood acute myeloid leukemia.
Article in Annals of laboratory medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Comprehensive biomarker profiles in hematological malignancies: improving diagnosis, prognosis, and treatment.Biomarkers in medicine · 2025Review
- Rare Hematologic Malignancies and Pre-Leukemic Entities in Children and Adolescents Young Adults.Cancers · 2024Review
- Acute myeloid leukemia: novel mutations and their clinical implications.American journal of blood research · 2023Review
- Multi-omics reveals mitochondrial metabolism proteins susceptible for drug discovery in AML.Leukemia · 2022Article
- Review
- Somatic SETBP1 mutations in myeloid neoplasms.International journal of hematology · 2017Review
- Transcriptome Analysis of Monozygotic Twin Brothers with Childhood Primary Myelofibrosis.Genomics, proteomics & bioinformatics · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecurrent somatic SET-binding protein 1 (SETBP1) and splicing pathway gene mutations have recently been found in atypical chronic myeloid leukemia and other hematologic malignancies. These mutations have been comprehensively analyzed in adult AML, but not in childhood AML. We investigated possible alteration of the SETBP1, splicing factor 3B subunit 1 (SF3B1), U2 small nuclear RNA auxiliary factor 1 (U2AF1), and serine/arginine-rich splicing factor 2 (SRSF2) genes in childhood AML.
methodsCytogenetic and molecular analyses were performed to reveal chromosomal and genetic alterations. Sequence alterations in the SETBP1, SF3B1, U2AF1, and SRSF2 genes were examined by using direct sequencing in a cohort of 53 childhood AML patients.
resultsChildhood AML patients did not harbor any recurrent SETBP1 gene mutations, although our study did identify a synonymous mutation in one patient. None of the previously reported aberrations in the mutational hotspot of SF3B1, U2AF1, and SRSF2 were identified in any of the 53 patients.
conclusionsAlterations of the SETBP1 gene or SF3B1, U2AF1, and SRSF2 genes are not common genetic events in childhood AML, implying that the mutations are unlikely to exert a driver effect in myeloid leukemogenesis during childhood.
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