Saturday, 18 October 2008

DB: 2 new microRNA - Disease association databases

http://cmbi.bjmu.edu.cn/hmdd
http://www.mir2disease.org/

CombiMatrix hires Dr Muneesh Tewari to Scientific Advisory Board.

profiling of microRNAs in blood samples for cancer diagnosis.
http://www.globenewswire.com/newsroom/news.html?ref=rss&d=152206

Tuesday, 2 September 2008

Characterization of microRNAs in serum: a novel class of biomarkers for diagnosis of cancer and other diseases


The miRNA profile of human serum was analysed. Harsh storage conditions and RNAse A digestion which destroyed longer RNA species was shown to have little effect on miRNA levels. Sequencing showed that miRNAs made up the largest part of small polynucleotide species, with about 190 miRNAs referenced. Measured expression was seen to be similar across individuals. Analysis of diseased subjects showed large changes in the profile (NSC-lung carcinoma = 28 miRNA missing, 63 novel) compared to healthy individuals. Serum samples from patients with colorectal cancer, and diabetes showed further differentiation of miRNA profiles. The particular miRNAs elevated came contained members previously associated with the diseases mentioned.
[email], [paper]

Friday, 22 August 2008

NEWS: Rosetta/NIH HIV collaboration

Following on from work showing that latent stage exit may be influenced by microRNA signalling, Rosetta is to leverage its intellectual property holdings in a collaboration with NIH
Pharmabiz

Monday, 11 August 2008

patent: LET-7 MICRORNA AND MIMETICS THEREOF AS THERAPEUTICS FOR CANCER

Treatment of cancer using let-7 or mimics. Treatment of cancer by replacing downregulated microRNAs. Using miRNAs to identify and enrich a population of cancer cells. blah blah blah.
WO/2008/095096
lab

Wednesday, 30 July 2008

MiR-9, a factor in alcohol tolerance


MiR-9 levels were shown to increase in the brain within minutes of alcohol exposure. MiR-9 was shown to target alcohol sensitive variants of the BK channel protein. This protein has been previously implicated in development of alcohol resistance, and has many variants. The development of alcohol resistance in itself is thought to be a risk factor for alcoholism.
[CTA]

Thursday, 10 July 2008

patent: Classifying patients for Bcl-2 inhibitor therapy

Abbot Laboratories
The patent covers the evaluation of patients suitable for therapy by Bcl-2 inhibitors (ABT-263, ABT-737). The patient is profiled for deletions in the region of microRNAs miR-15a, miR-16-1, and miR-34c. Flourescence in-situ hybridization (FISH) is used for analysis.
[patent:WO/2008/082643]

Thursday, 3 July 2008

patent: Monitoring organ rejection by miRNA profiles

This describes measurement of several dozen miRNAs, most identified as being similair to mouse miRNAs, in various body fluids and biopsies, using a range of techniques. It also mentions similair diagnostics in other mammals and measurement of other short RNAs.
[patent:WO/2008/079303], [lab]

Sunday, 29 June 2008

Dispatched Homolog 2 is targeted by miR-214 through a combination of three weak microRNA recognition sites.

Overexpression of dre-miR-214 during development creates a curved-embryo phenotype which can also be created by disp2 knockdown. It was shown that miR-214 targets disp2 via 3 regions that show only loose pairing, in the same way that it targets Sufu.

[lab][connotea]

Accelerated sequence divergence of conserved genomic elements in Drosophila melanogaster

Genome alignment of Drosophila spp. 28% of the variation in D. melanogaster was in non-coding regions. One of these (DMAR 3R.463388) may represent an alteration of the 3'UTR of CG13716. One altered region, DMAR 3R.1966842 folds into a simple hairpin and my represent an unannotated miRNA. miRScan scored this with 11.48, and the region was shown to be expressed.
[lab][connotea]

Thursday, 29 May 2008

MicroRNAs regulate ocular neovascularization

MicroRNA profiles under ischemia-induced neovascularization were measured, the 3 downregulated miRNAs - 31, 150, and 184 were studied further. Injection of these miRNAs reduced angiogenesis in retinal cells, injection of-31, and -150 had the same effect on choroidal cells. Reporter assays validated targets for miR-31 (Pdgfb, Hif1a), and miR-150 (Pdgfb, Vegf) - all proangiogenic. Frizzled4 was identified bioinformatically as a target of miR-184. Induced VEGF expression, blockaded in AMD treatment, suppressed miR-150 while VEGF levels were also reduced by miR-31, possibly through HIF-1alpha, a transcriptional activator of VEGF.
[lab][cta]

Cloning, characterization, and expression of microRNAs from the Asian malaria mosquito, Anopheles stephensi.

A. stephensi was profiled for microRNAs and candidates compared to those identified in A. Gambiae and Drosophila.
[cta][lab]

Expression of microRNA-146 suppresses NF-kappaB activity with reduction of metastatic potential in breast cancer cells

Constitutively active NF-kB is a functioning feature of many cancers.Mir-146a and miR-146b have been shown to downregulate 2 branches of the upstream cascade (IL-1 and Toll-like) through their repression of IRAK1 and TRAF6. In MDA-MB-231 cells ectopic expression of these miRNAs reduced phosphorylation of the inhibitor IkBa and NF-kB levels concomittantly by 70%. These cells showed a 80% and 60% loss of invasive capacity and migration respectively. siRNA-mediated inhibition of IkBa restored more than half of the NF-kB levels, indicating other pathways affected by these miRNAs to which end EGFR has also been identified as a target.

[cta][Oncogene][buck institute]

Isolation and characterization of CD146(+) multipotent mesenchymal stromal cells.

There is no good marker for mesenchymal stromal cells. A culture was selected on the basis of CD146. These were profiled for miRNA expression and a novel profile of differentiated chondrocytes was compared. Of 36 miRNAs altered a third were increased.Let-7 was the most significantly downregulated with pre-miR-204 at the top of the table.

[cte][lab][Exp. Haem.]

The MYCN oncogene is a direct target of miR-34a

Elevated MYCN, seen in about 20-30% of neuroblastoma cases, is currently the only marker of disease progression - and characterizes it's most aggressive form. 1p36 deletions have been implicated in this cancer, as in others, but no single suppressor gene from this region has been found. Of 5 microRNAs mapping to this region miR-34a had the greatest effect on neuroblastoma cells, was complementary to MCYN 3'UTR at 2 locations, and mediated a profile of neural (GPCRs) rather than cell cycle genes. In 1p36 mutants, where mir-34a expression is lower, transfection causes an 80-90% reduction in MYCN.


[connotea],[CCR]