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Acute myeloid leukemia (AML) is a genetically complex and clinically heterogeneous hematopoietic malignancy. This study employs long-read transcriptome analysis using oxford nanopore technologies sequencing on 60 primary AML bone marrow samples. This approach delivers comprehensive isoform-level resolution of splicing abnormalities and overcomes limitations of short-read sequencing. We detect extensive AML-specific splicing anomalies and identify 119,278 previously unannotated transcript isoforms. Of these, 80,294 (67.31%) contain complete open reading frames, with 9,812 (12.22%) validated using liquid chromatography-tandem mass spectrometry. Quantitative analysis in 175 RNA sequencing samples enables non-negative matrix factorization clustering, defining distinct molecular subtypes. These isoform-defined subtypes exhibit strong correlations with patient prognosis, indicating their potential as biomarkers for clinical classification. The findings highlight alternative splicing as a major contributor to AML molecular heterogeneity and provide a valuable foundation for advancing precision medicine and developing innovative therapeutic strategies targeting splicing abnormalities in AML.
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http://dx.doi.org/10.1016/j.celrep.2025.116216 | DOI Listing |
NPJ Precis Oncol
September 2025
Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Breast cancer is a highly heterogeneous disease with diverse outcomes, and intra-tumoral heterogeneity plays a significant role in both diagnosis and treatment. Despite its importance, the spatial distribution of intra-tumoral heterogeneity is not fully elucidated. Spatial transcriptomics has emerged as a promising tool to study the molecular mechanisms behind many diseases.
View Article and Find Full Text PDFSci Rep
September 2025
Institute of Biomedical Engineering, University of Toronto, Toronto, Canada.
Signal Transduct Target Ther
September 2025
State Key Laboratory of Molecular Oncology & Department of Medical Oncology & Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Small-cell lung cancer (SCLC), an aggressive neuroendocrine tumor strongly associated with exposure to tobacco carcinogens, is characterized by early dissemination and dismal prognosis with a five-year overall survival of less than 7%. High-frequency gain-of-function mutations in oncogenes are rarely reported, and intratumor heterogeneity (ITH) remains to be determined in SCLC. Here, via multiomics analyses of 314 SCLCs, we found that the ASCL1/MKI67 and ASCL1/CRIP2 clusters accounted for 74.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Molecular and Translational Medicine, University of Brescia 25123 Brescia, Italy. Electronic address:
Ribonucleotide reductase (RR) is the rate-limiting enzyme for NTPs conversion into dNTPs, playing a central role in genome replication and maintenance. It is composed by two catalytic (RRM1) and two regulatory (alternatively RRM2 and p53R2) subunits, of which RRM2's functionality depends on a diferric center in the active site and is one of the most expressed genes in many tumors, among which Rhabdomyosarcoma (RMS), a rare and aggressive pediatric tumor. Didox (3,4-dihydroxy-benzohydroxamic acid) is a highly effective RRM2 inhibitor with iron chelating properties which shows fewer in vivo side effects than classical RR inhibitors.
View Article and Find Full Text PDFCell Genom
September 2025
Institute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany. Electronic address:
Inherited genetic variants contribute to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), but it is unknown which cell types are involved in this process. We performed single-cell RNA sequencing of BE, EAC, and paired normal tissues and integrated genome-wide association data to determine cell-type-specific genetic risk and cellular processes that contribute to BE and EAC. The analysis reveals that EAC development is driven to a greater extent by local cellular processes than BE development and suggests that one cell type of BE origin (intestinal metaplasia cells) and cellular processes that control the differentiation of columnar cells are of particular relevance for EAC development.
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