Macrophages target tumor cells following monoclonal antibody therapy
Monoclonal antibodies directed against tumor antigens have proven effective for treating some forms of cancer. Despite the increasing use of monoclonal antibody therapy, it is not clear how these antibodies drive tumor removal. In this issue of the Journal of Clinical Investigation, Marjolein van Egmond and colleagues at the VU University Medical Center found that macrophage populations mediate tumor cell removal following monoclonal antibody treatment by actively phagocytosing tumor cells. Macrophage-dependent tumor cell removal required both the high affinity and low affinity Fc receptors. This study suggests that monoclonal antibody therapies that are optimized to enhance macrophage recruitment and activity may enhance removal of circulating tumor cells in cancer patients.
TITLE: Macrophages eliminate circulating tumor cells after monoclonal antibody therapy
AUTHOR CONTACT: Marjolein van Egmond
VU University Medical Center, Amsterdam, , NLD
Phone: +3120 4445975; Fax: ; E-mail: m.vanegmond@vumc.nl
View this article at: http://www.jci.org/articles/view/66776?key=5bbe1c588bfc574caed3
Targeting a cell cycle inhibitor promotes β cell replication
One of the factors underlying the development of type 2 diabetes is loss of β cell mass, resulting in decreased insulin production. Once lost, β cell mass cannot be restored. In contrast, infants with focal hyperinsulinism of infancy exhibit rapid expansion of the β cell mass due to a silencing of a region of chromosome 11 that includes the gene encoding the cell cycle inhibitor p57Kip2. In this issue of the Journal of Clinical Investigation, Klaus Kaestner and colleagues at the University of Pennsylvania demonstrate that silencing the gene encoding p57Kip2 in isolated adult human islets promotes β cell replication and that these new cells exhibit many properties associated with β cells. This study provides an explanation for excessive β cell expansion in children with focal hyperinsulinism and suggests that targeting the p57Kip2 pathway in adults with type 2 diabetes may improve β cell function.
TITLE: Targeting the cell cycle inhibitor p57Kip2 promotes adult human β cell replication
AUTHOR CONTACT: Klaus Kaestner
University of Pennsylvania, Perelman School of Medicine, Philadeplhia, PA, USA
Phone: 215.898.8759; Fax: 215.573.5892; E-mail: kaestner@mail.med.upenn.edu
View this article at: http://www.jci.org/articles/view/69519?key=5ed5fc651e71db738504
ALSO IN THIS ISSUE
TITLE: Tie1 deletion inhibits tumor growth and improves angiopoietin antagonist therapy
AUTHOR CONTACT: Kari Alitalo
Biomedicum Helsinki; University of Helsinki, Helsinki, , FIN
Phone: +358 9 191 25511; Fax: +358 9 191 25510; E-mail: kari.alitalo@helsinki.fi
View this article at: http://www.jci.org/articles/view/68897?key=11bf029b7b12a0a66cdd
TITLE: Nutrient sensing by the mitochondrial transcription machinery dictates oxidative phosphorylation
AUTHOR CONTACT: Marcus Cooper
UMass Medical School, Worcester, MA, USA
Phone: 5088566907; E-mail: Marcus.Cooper@umassmed.edu
View this article at: http://www.jci.org/articles/view/69413?key=e2559384b590321fe20f
TITLE: Inactivation of SAG/RBX2 E3 ubiquitin ligase suppresses KrasG12D-driven lung tumorigenesis
AUTHOR CONTACT: Yi Sun
University of Michigan, Ann Arbor,, MI, USA
Phone: 734-615-1989; Fax: 734-763-1581; E-mail:sunyi@umich.edu
View this article at: http://www.jci.org/articles/view/70297?key=82b5eebc21e48312b244
TITLE: Changes in neural network homeostasis trigger neuropsychiatric symptoms
AUTHOR CONTACT: Jochen Meier
Max Delbrück Center for Molecular Medicine, Berlin, , DEU
Phone: +49-30-94063062; E-mail: jochen.meier@mdc-berlin.de
View this article at: http://www.jci.org/articles/view/71472?key=43e592fa514460c33f19
TITLE: Thrombocytopenia-associated mutations in the ANKRD26 regulatory region induce MAPK hyperactivation
AUTHOR CONTACT: Hana Raslova
INSERM U1009, Villejuif, , FRA
Phone: 00 33 1 42 11 46 71; Fax: 00 33 1 42 11 52 40; E-mail: hraslova@igr.fr
View this article at: http://www.jci.org/articles/view/71861?key=f6c4390e624d72df05e0
TITLE: Prion disease tempo determined by host-dependent substrate reduction
AUTHOR CONTACT: Charles Mays
University of Alberta, Edmonton, AB, CAN
Phone: 780-492-9377; E-mail: cemays3@ualberta.ca
View this article at: http://www.jci.org/articles/view/72241?key=a94cf532dec1b0dc3fcf
Journal
Journal of Clinical Investigation