hiPSC-derived bone marrow milieu identifies a clinically actionable driver of niche-mediated treatment resistance in leukaemia 2
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Spred1 deficit promotes treatment resistance and transformation of chronic phase CML. Spred1 deficit promotes treatment resistance and transformation of chronic phase CML
Total RNA was extracted from Lin-Sca-1+c-Kit+ (LSK) cells sorted from the BM of Spred1HSCΔ/ΔSCLtTA/BCR-ABL (HSC KO) and Spred1HSCwt/wtSCLtTA/BCR-ABL (HSC wt) (n=5 mice per group, both group given 7 do
NIAID Data Ecosystem50
Identifying non-genetic determinants of malignant clonal fitness at single cell resolution [retransplant scRNAseq]
All cancers emerge following a period of clonal selection and subsequent clonal expansion. Whilst the evolutionary principles imparted by genetic intra-tumour heterogeneity (ITH) are becoming increasi
NIAID Data Ecosystem40
EBF1 nuclear repositioning instructs chromatin refolding to promote therapy resistance in T leukemic cells.[DND41_HiC]
Purpose: To investigate the mechanisms of 3D genome organization in drug-resistant T-ALL Methods: We used multiple epigenomics, chromatin conformation, and transcriptomic assays to study the mechanism
NIAID Data Ecosystem30
EBF1 nuclear repositioning instructs chromatin refolding to promote therapy resistance in T leukemic cells.[Granta_ATACseq]
Purpose: To investigate the mechanisms of 3D genome organization in drug-resistant T-ALL Methods: We used multiple epigenomics, chromatin conformation, and transcriptomic assays to study the mechanism
NIAID Data Ecosystem50
CITE-Seq profiling of CLL under ibrutinib treatment reveals transcriptional evolution of leukemic and immune cells.
Ibrutinib, an irreversible Bruton Tyrosine Kinase (BTK) inhibitor, has revolutionized Chronic Lymphocytic Leukemia (CLL) treatment, but resistances to ibrutinib have emerged in relation or not to BTK
NIAID Data Ecosystem40
