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Leukemia, Lymphocytic, Chronic, B-Cell
Myeloid Cell Leukemia Sequence 1 Protein
Aberrant regulation of pVHL levels by microRNA promotes the HIF/VEGF axis in CLL B cells.
Phase II trials of single-agent anti-VEGF therapy for patients with chronic lymphocytic leukemia.
Phase 2 trial of daily, oral Polyphenon E in patients with asymptomatic, Rai stage 0 to II chronic lymphocytic leukemia.
Critical signal transduction pathways in CLL.
Tris (dibenzylideneacetone) dipalladium: a small-molecule palladium complex is effective in inducing apoptosis in chronic lymphocytic leukemia B-cells.
Phase I trial of daily oral Polyphenon E in patients with asymptomatic Rai stage 0 to II chronic lymphocytic leukemia.
Circulating microvesicles in B-cell chronic lymphocytic leukemia can stimulate marrow stromal cells: implications for disease progression.
The novel receptor tyrosine kinase Axl is constitutively active in B-cell chronic lymphocytic leukemia and acts as a docking site of nonreceptor kinases: implications for therapy.
HSP90 overexpression potentiates the B-cell receptor and fibroblast growth factor receptor survival signals in chronic lymphocytic leukemia cells.
Prognostic value of miR-155 in individuals with monoclonal B-cell lymphocytosis and patients with B chronic lymphocytic leukemia.
Curcumin inhibits prosurvival pathways in chronic lymphocytic leukemia B cells and may overcome their stromal protection in combination with EGCG.
Bi-directional activation between mesenchymal stem cells and CLL B-cells: implication for CLL disease progression.
Targeted Axl Inhibition Primes Chronic Lymphocytic Leukemia B Cells to Apoptosis and Shows Synergistic/Additive Effects in Combination with BTK Inhibitors.
Chronic lymphocytic leukemia cells from ibrutinib treated patients are sensitive to Axl receptor tyrosine kinase inhibitor therapy.
Microvesicle Dynamics in B-Cell Chronic Lymphocytic Leukemia Tumor Microenvironme
Upregulation of AXL and ß-catenin in chronic lymphocytic leukemia cells cultured with bone marrow stroma cells is associated with enhanced drug resistance.
SIRT3 overexpression and epigenetic silencing of catalase regulate ROS accumulation in CLL cells activating AXL signaling axis.
Idelalisib activates AKT via increased recruitment of PI3Kd/PI3Kß to BCR signalosome while reducing PDK1 in post-therapy CLL cells.