Seishi Ogawa

This study identifies how RNA splicing factor mutations drive myeloid neoplasm by disrupting proteomic networks through mis-splicing, validated via single-cell transcriptomics and proteomics.

PRCGAP provides a haplotype-resolved analysis of cancer genomes, detecting variants missed by standard references and revealing new insights into structural variants and fusion events in leukemia.

This study identifies 16 AML subgroups based on chromatin accessibility profiles using ATAC-seq in 1,563 cases, revealing epigenetic heterogeneity and its clinical and therapeutic implications.

The paper shows TET2-mutant clonal hematopoiesis reduces cancer metastasis by preventing T-cell exhaustion through DNA methylation changes.

This study identifies FDXR upregulation as a prognostic marker and therapeutic target in HTLV-1-associated ATL, showing its link to disease severity and sensitivity to fluorouracil.

The paper develops scG2P to jointly capture DNA mutations and mRNA transcripts in single cells, revealing clonal architectures and phenotypes in aged esophageal tissue.

This study shows that mutations in Asxl1 and Stag2 cause dysregulation of histone modifications and chromatin structures, leading to aberrant gene upregulation and myelodysplastic syndromes.

This paper develops SMART-PTA for single-cell whole-genome and transcriptome sequencing, revealing clonal evolution in aged human esophageal tissue over 70 years.

This study identifies hyperactive PLCG1 mutations in T-cell leukemia/lymphoma that drive non-canonical signaling, enhancing cell survival and drug resistance.

This paper uses rare k-mers to identify centromere haplogroups in human populations and cancer translocations, revealing structural diversity and translocation mechanisms.

This study shows that Tax and HBZ, viral oncoproteins, alter mRNA splicing in T-cells by interacting with spliceosome components, leading to changes in cancer-related genes.

The paper investigates the prognostic significance of PKM transcripts in 25 cancers and identifies a prognostic signature in KIRC, revealing functional roles of alternatively spliced PKM transcripts.

The paper examines TP53 allelic states in MDS patients, finding that bi-allelic targeting is linked to worse outcomes, while mono-allelic targeting does not differ from wild-type patients.

The paper identifies two ccRCC subtypes based on PKM alternative splicing and proposes drug repurposing for each subtype.

The paper identifies and characterizes splicing-associated variants in cancer using a statistical framework applied to 8,976 samples across 31 cancer types, revealing 14,438 SAVs and their association with smoking and tumor suppressors.