about
Substrate-driven gene expression in Roseburia inulinivorans: importance of inducible enzymes in the utilization of inulin and starch.Chronic lymphocytic leukemia cells induce defective LFA-1-directed T-cell motility by altering Rho GTPase signaling that is reversible with lenalidomide.Trisomy 12 chronic lymphocytic leukemia cells exhibit upregulation of integrin signaling that is modulated by NOTCH1 mutations.Increased angiogenic sprouting in poor prognosis FL is associated with elevated numbers of CD163+ macrophages within the immediate sprouting microenvironment.Effects of alternative dietary substrates on competition between human colonic bacteria in an anaerobic fermentor system.T cells from CLL patients exhibit features of T-cell exhaustion but retain capacity for cytokine production.Follicular lymphoma cells induce changes in T-cell gene expression and function: potential impact on survival and risk of transformation.E(mu)-TCL1 mice represent a model for immunotherapeutic reversal of chronic lymphocytic leukemia-induced T-cell dysfunctionPeripheral blood T cells in acute myeloid leukemia (AML) patients at diagnosis have abnormal phenotype and genotype and form defective immune synapses with AML blasts.Follicular lymphoma cells induce T-cell immunologic synapse dysfunction that can be repaired with lenalidomide: implications for the tumor microenvironment and immunotherapyActivated pancreatic stellate cells sequester CD8+ T cells to reduce their infiltration of the juxtatumoral compartment of pancreatic ductal adenocarcinoma.Chronic lymphocytic leukemia: an update on biology and treatment.Immune dysfunction in chronic lymphocytic leukemia: the role for immunotherapy.How does lenalidomide target the chronic lymphocytic leukemia microenvironment?Tumor microenvironment (TME)-driven immune suppression in B cell malignancy.Activity of lenalidomide in mantle cell lymphoma can be explained by NK cell-mediated cytotoxicity.Identifying CLL antigens for future combinational therapy.Psoriasin (S100A7) associates with integrin β6 subunit and is required for αvβ6-dependent carcinoma cell invasion.Extracellular vesicles released by CD40/IL-4-stimulated CLL cells confer altered functional properties to CD4+ T cells.Cord blood natural killer cells exhibit impaired lytic immunological synapse formation that is reversed with IL-2 exvivo expansion.Nurse-like cells impact on disease progression in chronic lymphocytic leukemia.Generation of a poor prognostic chronic lymphocytic leukemia-like disease model: PKCα subversion induces up-regulation of PKCβII expression in B lymphocytes.Long-term repair of T-cell synapse activity in a phase II trial of chemoimmunotherapy followed by lenalidomide consolidation in previously untreated chronic lymphocytic leukemia (CLL).Exosomes and CAFs: partners in crime.Phenotype and immune function of lymph node and peripheral blood CLL cells are linked to transendothelial migration.miR-181c-BRK1 axis plays a key role in actin cytoskeleton-dependent T cell function.HS1-Associated Protein X-1 Regulates Carcinoma Cell Migration and Invasion via Clathrin-Mediated Endocytosis of Integrin αvβ6Vaccine therapy and chronic lymphocytic leukaemiaThe kiss of death in FLThe 3 Rs in CLL immune dysfunctionSubclonal heterogeneity in chronic lymphocytic leukaemia: revealing the importance of the lymphoid tumour microenvironmentCombination targeted therapy in chronic lymphocytic leukaemia - can pre-clinical studies translate to the clinic?Combination lenalidomide-rituximab immunotherapy activates anti-tumour immunity and induces tumour cell death by complementary mechanisms of action in follicular lymphoma
P50
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P50
description
researcher, ORCID id # 0000-0002-0452-0420
@en
wetenschapper
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name
Alan G Ramsay
@ast
Alan G Ramsay
@en
Alan G Ramsay
@es
Alan G Ramsay
@nl
type
label
Alan G Ramsay
@ast
Alan G Ramsay
@en
Alan G Ramsay
@es
Alan G Ramsay
@nl
prefLabel
Alan G Ramsay
@ast
Alan G Ramsay
@en
Alan G Ramsay
@es
Alan G Ramsay
@nl
P106
P1153
24462154000
P21
P31
P496
0000-0002-0452-0420