Hassan Jumaa

Correction to: Nature https://doi.org/10.1038/nature09883 Published online 18 May 2011 In the version of this article initially published, the panel “Adriamycin/BCL6+/+” in Fig. 2d represents another image of the “Control/BCL6−/−” condition. The error occurred during figure assembly and did not affect the calculation of mean values and s.d. Our own image analysis, not available at the time of publication, revealed that the panel “SFO2/Imatinib” in Supplementary Fig.

To the Editor: Chronic lymphocytic leukemia (CLL) is always preceded by monoclonal B cell lymphocytosis (MBL), characterized by the presence of circulating clonal B cells with a CLL phenotype, albeit at a lower number [1]. MBL, found in otherwise healthy individuals, is classified into two subtypes based on the number of circulating, “CLL-like” B cells [1].

Abstract A shared feature of B-cell receptors (BCRs) expressed on neoplastic B cells from patients with chronic lymphocytic leukaemia (CLL) concerns their continual activation of intracellular signalling without requiring external antigens. This autonomous signalling mechanism has previously been demonstrated to arise from BCR-BCR homotypic interactions in three distinct stereotyped CLL subsets (2, 4 and 169).