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| http://dx.doi.org/10.1172/JCI96202 | DOI Listing |
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Microsatellite instability at U2AF-binding polypyrimidic tract sites perturbs alternative splicing during colorectal cancer initiation.
Genome Biol
August 2024
Sorbonne Université, INSERM, Unité Mixte de Recherche Scientifique 938 and SIRIC CURAMUS, Centre de Recherche Saint-Antoine, Equipe Instabilité Des Microsatellites Et Cancer, Equipe Labellisée Par La Ligue Nationale Contre Le Cancer, 75012, Paris, France.
Article Synopsis
- Microsatellite instability (MSI), often linked to mismatch repair deficiency in colorectal cancer (CRC), leads to numerous noncoding DNA mutations, particularly affecting RNA splicing sites.
- This research shows that these noncoding mutations happen early in tumor development, even before the cancer cells become mutated in their coding regions, and are associated with altered splicing patterns in mRNA.
- The altered RNA splicing impacts cellular differentiation and promotes the initiation of MSI CRC, indicating that these noncoding changes are significant for cancer progression before traditional coding mutations occur.
Mutant U2AF1-Induced Mis-Splicing of mRNA Translation Genes Confers Resistance to Chemotherapy in Acute Myeloid Leukemia.
Cancer Res
May 2024
Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Unlabelled: Patients with primary refractory acute myeloid leukemia (AML) have a dismal long-term prognosis. Elucidating the resistance mechanisms to induction chemotherapy could help identify strategies to improve AML patient outcomes. Herein, we retrospectively analyzed the multiomics data of more than 1,500 AML cases and found that patients with spliceosome mutations had a higher risk of developing refractory disease.
View Article and Find Full Text PDFMyelodysplastic neoplasm-associated U2AF1 mutations induce host defense defects by compromising neutrophil chemotaxis.
Leukemia
October 2023
Department of Immunology and Genomic Medicine, National Jewish Health, Denver, CO, USA.
Myelodysplastic neoplasm (MDS) is a hematopoietic stem cell disorder that may evolve into acute myeloid leukemia. Fatal infection is among the most common cause of death in MDS patients, likely due to myeloid cell cytopenia and dysfunction in these patients. Mutations in genes that encode components of the spliceosome represent the most common class of somatically acquired mutations in MDS patients.
View Article and Find Full Text PDFU2AF1 mutation connects DNA damage to the alternative splicing of RAD51 in lung adenocarcinomas.
Clin Exp Pharmacol Physiol
July 2022
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, China.
The recurrent mutation (S34F) in splicing factor U2AF1 is frequently observed in lung adenocarcinoma, but its function remains largely unknown. To determine the mechanistic basis and consequences of U2AF1 mutations, we established non-small cell lung carcinoma A549 cell lines with exogenous expression of wildtype (U2AF1-WT) or mutant (U2AF1-S34F). Splicing analysis revealed that U2AF1-S34F mainly caused aberrant exon usage and affected splicing of numerous DNA damage repair genes.
View Article and Find Full Text PDFU2af1 is a haplo-essential gene required for hematopoietic cancer cell survival in mice.
J Clin Invest
November 2021
Division of Oncology, Department of Medicine and.
Somatic mutations in the spliceosome gene U2AF1 are common in patients with myelodysplastic syndromes. U2AF1 mutations that code for the most common amino acid substitutions are always heterozygous, and the retained WT allele is expressed, suggesting that mutant hematopoietic cells may require the residual WT allele to be viable. We show that hematopoiesis and RNA splicing in U2af1 heterozygous knockout mice were similar to those in control mice, but that deletion of the WT allele in U2AF1(S34F) heterozygous mutant-expressing hematopoietic cells (i.
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