What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Tuesday, 2012 August 28
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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 6 of 6

1.	N Engl J Med. 2012 Aug 9;367(6):e8. Images in clinical medicine. Green teeth in neonatal sepsis. Swann O, Powls A. Source Princess Royal Maternity Hospital, Glasgow, United Kingdom. livvyswann@doctors.org.uk Free Article
	PMID: 22873557 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2012 Jul 25;487(7408):482-5. doi: 10.1038/nature11286. Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy. Archin NM, Liberty AL, Kashuba AD, Choudhary SK, Kuruc JD, Crooks AM, Parker DC, Anderson EM, Kearney MF, Strain MC, Richman DD, Hudgens MG, Bosch RJ, Coffin JM, Eron JJ, Hazuda DJ, Margolis DM. Source The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. Comment in HIV: Shock and kill. [Nature. 2012] HIV: Shock and kill.Deeks SG. Nature. 2012 Jul 25; 487(7408):439-40. Epub 2012 Jul 25. Abstract Despite antiretroviral therapy, proviral latency of human immunodeficiency virus type 1 (HIV-1) remains a principal obstacle to curing the infection. Inducing the expression of latent genomes within resting CD4(+) T cells is the primary strategy to clear this reservoir. Although histone deacetylase inhibitors such as suberoylanilide hydroxamic acid (also known as vorinostat, VOR) can disrupt HIV-1 latency in vitro, the utility of this approach has never been directly proven in a translational clinical study of HIV-infected patients. Here we isolated the circulating resting CD4(+) T cells of patients in whom viraemia was fully suppressed by antiretroviral therapy, and directly studied the effect of VOR on this latent reservoir. In each of eight patients, a single dose of VOR increased both biomarkers of cellular acetylation, and simultaneously induced an increase in HIV RNA expression in resting CD4(+) cells (mean increase, 4.8-fold). This demonstrates that a molecular mechanism known to enforce HIV latency can be therapeutically targeted in humans, provides proof-of-concept for histone deacetylase inhibitors as a therapeutic class, and defines a precise approach to test novel strategies to attack and eradicate latent HIV infection directly.
	PMID: 22837004 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2012 Jul 25;487(7408):427-8. doi: 10.1038/487427a. Methods: Face up to false positives. Macarthur D. Source Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. macarthur@atgu.mgh.harvard.edu
	PMID: 22836983 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2012 Jul 23;487(7408):417. doi: 10.1038/487417a. Contest to sequence centenarians kicks off. Baker M.
	PMID: 22836978 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nature. 2012 Jul 25;487(7408):406. doi: 10.1038/487406a. Error prone. [No authors listed]
	PMID: 22836962 [PubMed - indexed for MEDLINE]
	Related citations

6.	Nature. 2012 Jul 26;487(7408):500-4. Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion. Straussman R, Morikawa T, Shee K, Barzily-Rokni M, Qian ZR, Du J, Davis A, Mongare MM, Gould J, Frederick DT, Cooper ZA, Chapman PB, Solit DB, Ribas A, Lo RS, Flaherty KT, Ogino S, Wargo JA, Golub TR. Source The Eli and Edythe L. Broad Institute, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. Abstract Drug resistance presents a challenge to the treatment of cancer patients. Many studies have focused on cell-autonomous mechanisms of drug resistance. By contrast, we proposed that the tumour micro-environment confers innate resistance to therapy. Here we developed a co-culture system to systematically assay the ability of 23 stromal cell types to influence the innate resistance of 45 cancer cell lines to 35 anticancer drugs. We found that stroma-mediated resistance is common, particularly to targeted agents. We characterized further the stroma-mediated resistance of BRAF-mutant melanoma to RAF inhibitors because most patients with this type of cancer show some degree of innate resistance. Proteomic analysis showed that stromal cell secretion of hepatocyte growth factor (HGF) resulted in activation of the HGF receptor MET, reactivation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-OH kinase (PI(3)K)-AKT signalling pathways, and immediate resistance to RAF inhibition. Immunohistochemistry experiments confirmed stromal cell expression of HGF in patients with BRAF-mutant melanoma and showed a significant correlation between HGF expression by stromal cells and innate resistance to RAF inhibitor treatment. Dual inhibition of RAF and either HGF or MET resulted in reversal of drug resistance, suggesting RAF plus HGF or MET inhibitory combination therapy as a potential therapeutic strategy for BRAF-mutant melanoma. A similar resistance mechanism was uncovered in a subset of BRAF-mutant colorectal and glioblastoma cell lines. More generally, this study indicates that the systematic dissection of interactions between tumours and their micro-environment can uncover important mechanisms underlying drug resistance.
	PMID: 22763439 [PubMed - indexed for MEDLINE]
	Related citations