Omar Ibrahim Abdel-Wahab

In chronically stimulated human T cells, suppressed oxidative metabolism and nucleotide loss accompany MAP2K4 activation. Inhibiting MAP2K4 (with the MKK4/7 inhibitor BSJ-04-122) restored tumor-cell killing in vitro.

The paper uses multi-omics approaches to study post-translational changes in macrophages during activation, identifying endosomal mRNA transport as a target of inflammation.

This study identifies somatic DDX41 mutations as gain-of-function alleles that drive aberrant splicing, particularly of SEPTIN7, contributing to MDS/AML pathogenesis.

This study identifies splicing dysregulation in SF-mutated cancers and demonstrates that antisense oligonucleotides can correct aberrant splicing and restore tumor suppressor function.

This paper identifies a U1-U3 snRNA-snoRNA interaction that links SF3B1 mutations to chromatin-state changes and genome instability, with therapeutic potential through antisense oligonucleotides.

This study identifies mRNA glycation by methylglyoxal as a metabolic stress sensor, showing impaired translation and beta-cell dysfunction, which is mitigated by metformin.

This study uses spatial transcriptomics and single-cell analysis to reveal how MDS bone marrow microenvironments are altered, showing TGFβ dysregulation in malignant cells and immune escape mechanisms.

The paper identifies a genetic variant that protects against clonal hematopoiesis by regulating RNA-binding protein MSI2 in hematopoietic stem cells.

The paper quantifies viral mimicry in genomes across species and shows how repetitive elements maintain pathogen-like features under selection.

The paper identifies clonal inflammatory microglia as a cause of neurodegeneration in LCH and ECD, showing their association with neuronal loss and suggesting CSF1R inhibitors as a therapeutic option.

The paper identifies microglia-specific somatic clones with pathogenic variants in Alzheimer's Disease patients that drive neuro-inflammation through the MAPK pathway.

This study shows that RBM10 loss causes aberrant splicing of cytoskeletal and ECM genes, leading to RAC1 activation and metastatic fitness in thyroid cancer.

This study develops chemical probes to target splicing factors in T cells, showing state-dependent loss of ITK via SF3B1 and demonstrating covalent ligandability of splicing regulators.

This study presents a paired tumor:normal sequencing dataset for hematologic malignancies, showing improved identification of somatic variants and their clinical relevance.

The paper identifies two mitotic kinesins aberrantly spliced due to RBM39 degradation by ArSulfs, linking this splicing change to antiproliferative effects.

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