Loss of cooperativity of secreted CD40L and increased dose-response to IL4 on CLL cell viability correlates with enhanced activation of NF-kB and STAT6

IGHV unmutated CLL B cells are more prone to spontaneous apoptosis and subject to environmental prosurvival signals than mutated CLL B cells

(2011) M Coscia et al.   LEUKEMIA

Non-malignant B cells and chronic lymphocytic leukemia cells induce a pro-survival phenotype in CD14+ cells from peripheral blood

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The functional in vitro response to CD40 ligation reflects a different clinical outcome in patients with chronic lymphocytic leukemia

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Coding RNAs with a non-coding function: Maintenance of open chromatin structure

(2011) Maïwen Caudron-Herger et al.   Nucleus

The JAK3-selective inhibitor PF-956980 reverses the resistance to cytotoxic agents induced by interleukin-4 treatment of chronic lymphocytic leukemia cells: potential for reversal of cytoprotection by the microenvironment

(2010) A. J. Steele et al.   BLOOD

Soluble CD14 is a novel monocyte-derived survival factor for chronic lymphocytic leukemia cells, which is induced by CLL cells in vitro and present at abnormally high levels in vivo

(2010) M. Seiffert et al.   BLOOD

Lenalidomide treatment promotes CD154 expression on CLL cells and enhances production of antibodies by normal B cells through a PI3-kinase-dependent pathway

(2009) R. Lapalombella et al.   BLOOD

Molecular mechanism and function of CD40/CD40L engagement in the immune system

(2009) Raul Elgueta et al.   IMMUNOLOGICAL REVIEWS

E -TCL1 mice represent a model for immunotherapeutic reversal of chronic lymphocytic leukemia-induced T-cell dysfunction

(2009) G. Gorgun et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

The NF- B subunit Rel A is associated with in vitro survival and clinical disease progression in chronic lymphocytic leukemia and represents a promising therapeutic target

(2008) S. Hewamana et al.   BLOOD

Novel Insights in Chronic Lymphocytic Leukemia: Are We Getting Closer to Understanding the Pathogenesis of the Disease?

(2008) Federico Caligaris-Cappio et al.   JOURNAL OF CLINICAL ONCOLOGY