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 Ecosystem90
The spleen as a sanctuary site for residual leukemic cells following ABT-199 monotherapy in ETP-ALL
Two mice in which luciferase-positive LOUCY ETP-ALL cells were xenografted were treated with either vehicle or ABT-199 (50 mg/kg) for 11 days. Afterwards, single cells suspensions were made from bone
NIAID Data Ecosystem50
Single cell RNA-seq reveals developmental plasticity with coexisting oncogenic states and immune evasion programs in ETP-ALL [PDX_ETPs_scRNA-seq]
Lineage plasticity and stemness have been invoked as the cause of therapy resistance in cancer, as these flexible states allow cancer cells to de-differentiate and alter their dependencies. We investi
NIAID Data Ecosystem30
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 Ecosystem60
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 Ecosystem40
