Associated Papers
Persistent postremission clonal hematopoiesis shapes the relapse trajectories of acute myeloid leukemia.
Chow RD et al.
Blood Advances, 2025
39938015 (PubMed )
Supplement: BLOODA_ADV-2024-015149-mmc2.xlsx › S2
Early drivers of clonal hematopoiesis shape the evolutionary trajectories of de novo acute myeloid leukemia.
Chow RD et al.
Medrxiv : the Preprint Server for Health Sciences, 2024
39252918 (PubMed )
Supplement: media-1.xlsx › S1
UBTF tandem duplications in pediatric myelodysplastic syndrome and acute myeloid leukemia: implications for clinical screening and diagnosis.
Barajas JM et al.
Haematologica, 2024
38426285 (PubMed )
Supplement: 2023_284683_BARAJAS_SUPPL.pdf
UBTF Tandem Duplications in Pediatric MDS and AML: Implications for Clinical Screening and Diagnosis.
Barajas JM et al.
Medrxiv : the Preprint Server for Health Sciences, 2023
38014207 (PubMed )
Supplement: media-5.xlsx › Sheet1
Response of high-risk MDS to azacitidine and lenalidomide is impacted by baseline and acquired mutations in a cluster of three inositide-specific genes.
Follo MY et al.
Leukemia, 2019
The genomic landscape of pediatric myelodysplastic syndromes.
Schwartz JR et al.
Nature Communications, 2017
29146900 (PubMed )
Supplement: 41467_2017_1590_MOESM15_ESM.xlsx › Sup._T12_-_Validation_primers
Structure-energy-based predictions and network modelling of RASopathy and cancer missense mutations.
Kiel C et al.
Molecular Systems Biology, 2014
24803665 (PubMed )
Supplement: MSB-10-5-727-s13.xls › energies
Activating CBL mutations are associated with a distinct MDS/MPN phenotype.
Schwaab J et al.
Annals of Hematology, 2012
Select a paper to view details