Issue Archive

A randomized phase 3 trial conducted in France and Belgium shows that a chemoimmunotherapy consisting of fludarabine, cyclophosphamide, and alemtuzumab (FCA) causes an excess mortality and is less efficient compared with fludarabine, cyclophosphamide, and rituximab (FCR), the current standard therapy for physically fit patients with chronic lymphocytic leukemia (CLL).^1,2 

Congenital Factor XIII (FXIII) deficiency is a rare autosomal recessive inherited disease leading to severe bleeding diathesis. In this issue of Blood, Inbal and colleagues report on a safe and novel treatment of this rare disorder with recombinant FXIII (rFXIII).¹ 

Although the chimeric anti-CD20 monoclonal antibody (mAb) rituximab has revolutionized the treatment of B-cell non-Hodgkin lymphoma (NHL), still many patients relapse and an increasing number become refractory to rituximab-containing therapy. This has initiated intense research to develop more potent anti-CD20 antibodies.

In this issue of Blood, Beekman et al provide compelling evidence for the multistep evolution of acute myeloid leukemia (AML) from severe congenital neutropenia (SCN) over a 17-year period. Moreover, they found that 5 different gain-of-function mutations in the granulocyte colony-stimulating factor receptor (GCSFR) arose during this transformation, suggesting that 2 mutations behaved as drivers for clonal outgrowth, while 3 others did not.¹ 

I have always been puzzled by the ability of normal erythroid cells to produce a stoichiometric amount of α- and β-globin chains in the absence of cross-talk mechanisms that would control and normalize the relative rate of expression of the genes encoding these proteins.

In this issue of Blood, Kasthuri and colleagues have examined the role of Fcγ receptors and signaling molecules in monocytes in HIT.¹ 

The article by Chien at al in this issue of Blood uses a novel approach to assess the role of single nucleotide polymorphisms (SNPs) in acute graft-versus-host disease (GVHD). Using a genome-wide association study (GWAS) employing an Affymetrix GeneChip Genome-Wide Human 500 000 SNP array, they screened 1298 allogeneic hematopoietic stem cell transplant donors and recipients and tested whether the results from 40 previously reported candidate SNPs could be replicated. They also used a novel approach to impute data using IMPUTE software (http://nathgen.stats-ox.ac.uk/impute/impute.html) where the genotyping data were not available.¹