This Week In Blood: January 10, 2013

Source : American Society of Hematology

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.

Systemic delivery of a TLR7 agonist in combination with radiation primes durable anti-tumor immune responses in mouse models of lymphoma, Dovedi et al.

This week’s plenary paper offers a promising potential new immunotherapeutic modality for the treatment of lymphoma. The authors present convincing data to suggest that a toll-like receptor 7 (TLR7) agonist sensitizes tumor cells to radiotherapy. In a mouse model, this increases radiation-induced cell death and prolongs responses.

Model-based decision rules reduce the risk of molecular relapse after cessation of tyrosine kinase inhibitor therapy in chronic myeloid leukemia, Horn et al.

The success of tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia (CML) has led to early investigation of the safety of discontinuing therapy for patients with prolonged deep response to treatment. In this manuscript, Horn and colleagues present a way of predicting the safety of therapy discontinuation.

Biologic and clinical significance of somatic mutations of SF3B1 in myeloid and lymphoid neoplasms, Cazzola et al.

This manuscript, featured as this week’s Perspective, discusses how our understanding of the pathophysiology of myelodysplastic syndromes (MDS) and other hematologic malignancies has been transformed over the last year with the discovery of the prevalence and prognostic significance of mutations in genes encoding the cellular splicing machinery.

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.
 

blood® is a registered trademark of the American Society of Hematology.
 

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Articles List

  • More than One Way to Change a Base

    More than One Way to Change a Base

    It’s easier than ever these days to clone and sequence DNA. Thanks to CRISPR/Cas and related technologies, it’s even straightforward to rewrite genomic sequences in living cells and organisms. But as powerful as it is, CRISPR, et al., cannot induce genetic rewrites in a test tube—genome editing requires cellular machinery to repair the DNA breaks the methods produce. Instead, researchers interested in mutating cloned genes on plasmids must revert to a tried-and-true method, site-directed mutagenesis. First described in the 1970s—and earning its inventor a share of the Nobel Prize in Chemistry in 1993—site-directed mutagenesis uses short oligonucleotides to introduce single base changes, as well as insertions and deletions, to DNA plasmids. Researchers can use the method to swap amino acids in expressed proteins, test clinically relevant mutations and tweak promoters. But there’s more than one way to change a base, and molecular-tools vendors have commercialized multiple strategies. Here, we review some of the more popular approaches to site-directed mutagenesis.
  • What Doesn’t Kill You … Testing for Chemical Toxicity

    What Doesn’t Kill You … Testing for Chemical Toxicity

    Understanding the effects of small molecules, compounds and chemicals on cells is the very core of drug discovery, one in which the pharmaceutical industry continues to invest billions of dollars. Yet alongside the question of whether such entities have a desired effect looms that of whether they have a toxic effect on those cells—and ultimately the tissues and organisms the cells compose. This question has equal importance to those who protect our environment and assure that our food is safe to eat. Testing chemical toxicity can take many forms, from looking for simple surrogates of death, such as the inability to exclude trypan blue, to sophisticated measures of changes in a specific cell type’s physiology. Various assays look at pathways leading to cell death, membrane integrity, depletion of energy, ability to proliferate and changes in differentiation. They are accomplished using instruments ranging from a hemocytometer and light microscope; to a Coulter counter, microplate reader or flow cytometer; to a high-content analysis solution found principally in screening cores at biotech and larger pharmaceutical companies. Screens for loss of viability are often the first line of inquiry, and only after an entity is shown to cause a decrease in survival is it then subjected to more nuanced assays [1]. Here we look at the principal means by which entities are tested for their effects on viability.

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