Friday, 13 June 2014

What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2014 June 13
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results
Items 1 - 3 of 3

1. Science. 2014 May 23;344(6186):807-8. doi: 10.1126/science.1255074.

Translational genomics. Targeting the host immune response to fight infection.

Baillie JK.

Author information:
Roslin Institute, University of Edinburgh, Midlothian EH25 9RG, UK, and Intensive Care Unit, Royal Infirmary of Edinburgh, Edinburgh EH16 4SA, UK. j.k.baillie@ed.ac.uk.

PMID: 24855243 [PubMed - indexed for MEDLINE]
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2. Science. 2014 May 23;344(6186):801-2. doi: 10.1126/science.1255117.

Cancer immunology. Identifying the infiltrators.

Perdiguero EG1, Geissmann F2.

Author information:
1Center for Molecular and Cellular Biology of Inflammation-CMCBI, Division of Immunology Infection & Inflammatory Diseases, King's College London, UK.
2Center for Molecular and Cellular Biology of Inflammation-CMCBI, Division of Immunology Infection & Inflammatory Diseases, King's College London, UK. frederic.geissmann@kcl.ac.uk.

Comment on

PMID: 24855239 [PubMed - indexed for MEDLINE]
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3. Science. 2014 May 23;344(6186):921-5. doi: 10.1126/science.1252510. Epub 2014 May 8.

The cellular and molecular origin of tumor-associated macrophages.

Franklin RA1, Liao W2, Sarkar A3, Kim MV1, Bivona MR3, Liu K4, Pamer EG3, Li MO5.

Author information:
1Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA.
2New York Genome Center, New York, NY 10022, USA.
3Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA.
4Department of Microbiology and Immunology, Columbia University, New York, NY 10032, USA.
5Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. lim@mskcc.org.

Comment in

Abstract

Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases, including cancer. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). TAMs express the adhesion molecule Vcam1 and proliferate upon their differentiation from inflammatory monocytes, but do not exhibit an "alternatively activated" phenotype. TAM terminal differentiation depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy.

Copyright © 2014, American Association for the Advancement of Science.

PMID: 24812208 [PubMed - indexed for MEDLINE]
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