Contents
13 September 2016
Vol 9, Issue 445
Vol 9, Issue 445
Contents
Research Articles
- CHK1 as a therapeutic target to bypass chemoresistance in AML
AML patients have new hope for overcoming resistance to therapy by inhibiting the DNA checkpoint kinase CHK1.
- Targeting the kinase activities of ATR and ATM exhibits antitumoral activity in mouse models of MLL-rearranged AML
Chemotherapy-resistant acute myeloid leukemia may respond to inhibition of ATR or ATM.
Research Resource
- Chemical proteomic map of dimethyl fumarate–sensitive cysteines in primary human T cells
Chemical proteomics analysis suggests the mechanism of action of a drug used to treat autoimmune diseases.
Podcast
- Science Signaling Podcast for 13 September 2016: DMF and the immune system
Covalent modification of a kinase by the immunosuppressive drug DMF inhibits T cell activation.
Editors' Choice
- More roles for mitochondria in the immune response
Macrophages remodel complexes in the electron transport chain of mitochondria to mediate appropriate immune responses to bacteria.
- Hypoxia limits IgG-producing B cells
Naturally occurring variations in oxygen availability in germinal centers regulate antibody class switching in B cells.
- Long noncoding RNA tells myeloid cells how long to live
A long noncoding RNA poises a proapoptotic gene for expression in myeloid cells.
- How bacteria induce animal metamorphosis
Structurally complex bacterial signals and MAPK signaling in tubeworms are involved in interspecies control of metamorphosis.
- New connections: New hope for AML patients
New mechanistic insights into the development and therapeutic resistance of acute myeloid leukemia should help identify patients most likely to benefit from treatment.
- Papers of note in Science Translational Medicine
This week’s articles describe new treatments to overcome drug resistance in chronic myeloid leukemia and to prevent stress-induced cell death in various lysosomal storage diseases.
- Papers of note in Science
This week’s articles highlight how tissue of origin affects the response of cancer cells to targeted therapies, the transmission of contractile forces in collectively migrating cells, the proteins of the inhibitory postsynaptic membrane, and a bioengineered system for following the timing and magnitude of signaling events in vivo.
About The Cover
Online Cover This week features a pair of research articles that identify the DNA replication stress response and in particular the kinases CHK1 and ATR as therapeutic targets for treating acute myeloid leukemia (AML). David et al. identified CHK1 as an independent prognostic indicator, marker for patient stratification, and target for therapeutic intervention. Morgado-Palacin et al. used a mouse model of a particularly aggressive form of AML to show that inhibition of either ATR or the kinase ATM exhibited antitumoral activity, reducing the growth of established cancer and prolonging the animals' health and survival, even when used as monotherapies. Thus, dependence on the DNA replication stress response enables therapeutic targeting in AML. [Image: Lightspring/shutterstock]
