O. Abdel-Wahab

The paper shows SF3B1 splicing modulators impair DNA damage response in cohesin-mutant MDS/AML, leading to increased sensitivity to PARP inhibitors and chemotherapy.

This study shows that SRSF2 mutations disrupt mitochondrial mRNA splicing, impair complex I function, and increase mitophagy through a PINK1 splicing mechanism, identifying mitophagy as a therapeutic target in MDS and AML.

This study identifies ferroptosis as a mechanism by which imetelstat induces therapeutic effects in AML, showing that targeting fatty acid metabolism enhances its efficacy.

This study develops a proteomic strategy to identify chemical probes that perturb protein complexes in human cells by analyzing electrophilic compounds' effects on protein interactions.

This study introduces GoT-Splice, a multi-omics method to analyze splicing aberrations in human hematopoietic cells, revealing cell-type specific effects of SF3B1 mutations in clonal outgrowths.

This paper develops GoT-ChA to link genotypes to chromatin accessibility in single cells, revealing JAK2V617F mutation-induced epigenetic changes in hematopoietic differentiation.

This study uses single-cell multi-omics to show DNMT3A R882 mutations cause hypomethylation and alter progenitor cell fates in clonal hematopoiesis.

The paper identifies sex-biased ZRSR2 mutations in BPDCN that impair pDC activation and apoptosis, linking X chromosome mutations to male-predominant leukemia.

This study introduces GoT, a high-throughput method linking single-cell genotypes and transcriptomes, revealing that somatic mutations' transcriptional effects depend on cell identity.

This paper generates a mouse model with a conditional knock-in of the U2af1(S34F) mutation to study its role in hematopoiesis and leukemia, finding that it requires additional mutations for leukemogenesis.