Welcome to “This Week in Blood,” a weekly snapshot of the hottest studies from each week’s issue of Blood, the official journal of the American Society of Hematology (ASH), hand-picked by Blood Editor-in-Chief Bob Löwenberg, MD, and Deputy Editor Nancy Berliner, MD. If you would like a PDF copy of any of the manuscripts highlighted below or would like to request an interview with the author, please email aslesinski@hematology.org.
SOX11 regulates PAX5 expression and blocks terminal B-cell differentiation in aggressive mantle cell lymphoma, Vegliante et al.
While the transcription factor SOX11 is a common, uniquely upregulated gene in mantle cell lymphoma (MCL), its biological role in MCL remains largely obscure. In this manuscript, authors demonstrate for the first time the oncogenic role and mechanistic effects of SOX11 in this disease. In this study Amador and colleagues analyze the genes and pathways controlled by SOX11, integrating genomic and biologic approaches and demonstrating effects on plasma cell differentiation programs. Study conclusions represent a conceptual advance in our understanding of the pathobiology of this aggressive form of malignant lymphoma.
Integrin activation by P-Rex1 is required for selectin-mediated slow leukocyte rolling and intravascular crawling, Herter et al.
The activation of integrins following leukocyte contact with the vessel wall is a central event in the inflammatory response. In this manuscript authors identify a novel and crucial role for P-Rex1, a Rac-specific guanine nucleotide exchange factor, in integrin activation, downstream signaling, and leukocyte recruitment.
Rapid activation of monocyte tissue factor by antithymocyte globulin is dependent on complement and protein disulfide isomerase, Langer et al.
Tissue factor (TF) initiates coagulation through complex formation with factor VIIa. TF is typically sequestered from the blood or exists in an inactive or encrypted form on hematopoietic cells. Although specific signaling pathways have been identified that activate TF in mouse models of thrombosis, the mechanisms responsible for controlling TF activation in human monocytes and other cell types are not yet fully understood. This manuscript establishes a novel mechanism for a link between complement activation and coagulation and identifies the most potent activator of this central initiator molecule of blood coagulation to date.
Clonal architecture of chronic myelomonocytic leukemias, Itzykson et al.
Chronic myelomonocytic leukemias (CMML) are myeloid neoplasms characterized by the accumulation of monocytes with dysplastic granulocytes in the peripheral blood, the bone marrow, and the spleen. Through an innovative approach involving cell sorting, cell culture, gene expression profiling, gene knockdown experiments, and gene mutation analysis in 28 patients, this manuscript elucidates the clonal architecture of CMML. Additionally, it reveals the stepwise and highly dynamic process of evolution of the most permissive clones, through acquisition of new genetic lesions and the competition between clones which develop in various directions, and shows how treatment may modulate this process, significantly advancing our understanding of the molecular basis of this disease.
Reporters who wish to receive a copy of any of the manuscripts highlighted above or would like to request an interview with the authors may contact Andrea Slesinski at 202-552-4927 or aslesinski@hematology.org
Blood (www.bloodjournal.org), the most cited peer-reviewed publication in the field of hematology, is available weekly in print and online. Blood is the official journal of the American Society of Hematology (ASH) (www.hematology.org), the world’s largest professional society concerned with the causes and treatment of blood disorders.
ASH’s mission is to further the understanding, diagnosis, treatment, and prevention of disorders affecting blood, bone marrow, and the immunologic, hemostatic, and vascular systems by promoting research, clinical care, education, training, and advocacy in hematology.
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