Issue Archive

The effects of aging, medical comorbidity, and systemic therapeutics interplay with the varied and distinctive capacities of neoplasms to usurp the physiological machinery regulating bone structure and function, thus determining skeletal morbidity and related mortality. In this issue of Blood, Fitter and colleagues report frequent increases in trabecular bone volume—a 2-fold increase over baseline in nearly half of patients with chronic myeloid leukemia (CML)—treated with the multi–tyrosine kinase receptor inhibitor, imatinib mesylate. Although the clinical significance of this anabolic and/or anticatabolic effect remains to be determined, these mechanistic studies offer a plausible explanation for the outcome.

In the February 1 issue of Blood, Jobe and colleagues elucidated the function of the mitochondrial permeability transition pore (MPTP), in platelet activation and demonstrated that cyclophilin D (CypD), a regulator of MPTP formation, is a critical factor in the procoagulant response to strong agonists.

IgE/antigen-FcϵRI crosslinking promotes antigen internalization and apoptosis in mouse mast cells. Dendritic cells uptake the apoptotic mast cells carrying internalized antigens, and thus can efficiently present the antigens to memory T cells.

In recent years, powerful technologies to globally examine epigenetic targets of transcription factors and directly link these to changes in gene expression have emerged. Acute leukemias are characterized by translocations leading to the production of chimeric transcription factors, which are perfect targets for such analyses.

In this issue of Blood, Pardanani and colleagues provide evidence that single nucleotide polymorphisms (SNPs) in JAK2 contribute to the phenotypic pleiotropy of chronic myeloproliferative disorders (MPDs).

In this issue of Blood, Andreas Beilhack and coworkers show that T cells can be activated to induce graft-versus-host disease (GVHD) in animals lacking certain priming sites: Peyer's patches (PPs), lymph nodes (LNs), or the spleen, or in animals treated with monoclonal antibodies preventing the access of T cells to PPs and LNs.

In this issue of Blood, Chrzanowska-Wodnicka and colleagues identify a regulatory role for Rap1B in angiogenesis. Although not absolutely required for angiogenesis, loss of Rap1B affects both proliferation and migration of endothelial cells.

The article by Carmona and colleagues in this issue of Blood demonstrates that activation of Epac1 increases integrin activity and integrin-dependent homing functions of progenitor cells and enhances their in vivo therapeutic potential.

In this issue of Blood, Chen and colleagues demonstrate that ZAP-70 enhances BCR signaling in B-CLL cells by promoting phosphorylation of the ITAMs in the Ig signaling subunit independently of its kinase activity.

For the past several decades, multiple myeloma (MM), the second most common hematologic malignancy, has been considered a fatal disease with a median survival of 5 years. However, recent advances in the understanding of the molecular pathogenesis of MM have led to new treatment strategies.

FLT3 mutations may influence prognosis in acute myeloid leukemia (AML), but the context in which they occur may be just as important.