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Archive - Apr 2009

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April 25th

Discovery of New Targets May Aid Fight Against Dengue Fever

Using a genome-wide RNA interference screen in Drosophila cells, researchers have identified 116 genes that are potential host factors for the mosquito-borne Dengue viruses that cause Dengue fever. Such host factors aid propagation of the Denque virus, and it is suggested that inhibitors of these host factors might interfere with this propagation. Dengue fever is the most frequent insect-borne viral disease of humans, and the virus sickens 50 million to 100 million people, and kills approximately 20,000 people, each year. There are presently no specific drugs to treat this painful and sometimes fatal disease, with only palliative treatment available. This work was carried out by researchers at the Duke University Medical Center, and collaborating institutions, and published in the April 22 issue of Nature. [NIH press release] [Nature abstract]

April 24th

Domestic Cattle Genome Sequenced

An international consortium of researchers has reported the sequencing and analysis of the genome of domestic cattle. This is the first livestock mammal to have its genome sequenced and it is believed that this achievement will aid in efforts to produce better beef and dairy products and also lead to a better understanding of the human genome. The analysis indicates that the bovine genome shares approximately 80% of its genes with humans. The particular cow whose genome was sequenced was named Dominette, a Hereford. [NIH press release] [CSIRO press release] [Science article 1] [Science article 2]

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EDITOR & PUBLISHER

Michael D. O'Neill, MA (Microbiology & Immunology, Duke University)
logophile2000@yahoo.com

SCIENCE & MEDICINE ADVISORS

Alex Andrus, PhD, JD (Patent Attorney, Genentech)
Kazako Aoyagi, PhD (Senior Director, Business Development, Celerion)
Philip Askenase, MD (Professor of Medicine-Immunology, Yale School of Medicine)
Leonora Balaj, PhD (Harvard, MGH)
Ben Zane Cohen, MD (Ophthalmologist)
Patricia Dahl (CEO/Executive Director, Eye Bank for Sight Restoration, New York City)
Rachel DeRita, PhD candidate (Thomas Jefferson University, Department of Cancer Biology)
Dolores Di Vizio, MD, PhD (Cedars-Sinai Medical Center)
Erika Ebbel, PhD (CEO, Ixcela; Founder & Executive Director, Science from Scientists)
Ronald Faanes, PhD (Past Head, Immunology, Boerhinger-Ingelheim)
Bert Fisher, PhD (Principal & Founding Member, Lithochimeia, Inc.)
Richard A. Gatti, MD (Professor-in-Residence, Human Genetics, UCLA)
Michael A. Goldman, PhD (Professor & Chair, Biology, San Francisco State University)
Charles Halasz, MD (Associate Clinical Professor, Dermatology, Columbia University, New York)
Elaine Heron, PhD (Director, BioMarin Pharmaceutical; Past Chairman, Amplyx Pharmaceuticals)
Andrew Hill, PhD (Professor & Department Head, La Trobe University; President, ISEV))

April 23rd

New Drug Starves Brain Cancer Cells

In animal studies, researchers have shown that a new drug (3-BrOP) is effective at starving neuroblastoma cells and reducing tumor growth by 75%. The drug, developed by scientists at the University of Texas M.D. Anderson Center, is an inhibitor of glycolysis, the energy-producing process upon which neuroblastoma cells are highly dependent. Neuroblastoma is a childhood brain cancer, and estimates are that approximately 650 children under the age of 5 are diagnosed with this cancer each year in the United States. Long-term survival of patients with metastatic neuroblastoma is less than 40% because the tumors are often resistant to traditional chemotherapy. The new research results were reported at the 22nd annual meeting of the American Society of Pediatric Hematology/Oncology. [Press release]

April 22nd

News

This is the news page

April 21st

Gene Signature Associated with Gleevec Resistance in GIST Patients

A genetic signature associated with increased resistance to Gleevec in patients with gastrointestinal stromal tumors (GIST) has been identified by researchers at the Fox Chase Cancer Center. Efforts to affect the expression and/or activity of genes in the signature may help increase the responsiveness to Gleevec in resistant patients. Currently, approximately 80% of GIST patients are responsive to Gleevec. This work was presented at the annual AACR meeting April 18-22. [Press release]

Clues to Mechanism of Lithium Action in Bipolar Disease

New research provides insights into how lithium works in the treatment of bipolar mood disorder, and may lay the groundwork for advances in the treatment of this disease. Scientists from Cardiff University, together with colleagues, have shown that lithium inhibits the enzyme inositol monophosphatase, and this leads to the inhibition of the production of PIP3, a molecule that is important in controlling brain cell signaling. Professor Adrian Harwood of Cardiff School of Biosciences, who led the research, said "We still cannot say definitively how lithium can help stabilize bipolar disorder. However, our research does suggest a possible pathway for its operation. By better understanding lithium, we can learn about the genetics of bipolar disorder and develop more potent and selective drugs. Further, altered PIP3 signalling is linked to other disorders, including epilepsy and autism, so this well established drug could be used to treat other conditions." The research was published in Disease Models & Mechanisms. [Press release]

April 20th

DICER1 Mutations Implicated in Rare Childhood Cancer

Mutations in the microRNA processing enzyme DICER1 appear to the cause of the inherited form of a rare, aggressive childhood cancer called pleuropulmonary blastoma (PPB). "PPB is the first malignancy found to be directly associated with inherited DICER1 mutations, making the cancer an important model for understanding how mutations and loss of DICER1 function lead to cancer," says lead author D. Ashley Hill, M.D., chief of pathology at Children's National Medical Center. "Additionally, we now believe that PPB tumors arise from an unusual mechanism in which cells carrying mutations induce nearby cells to become cancerous without becoming cancerous themselves." The results of this study were presented April 19 at the annual AACR meeting. [Press release]

Possible New Avenue for Huntington Disease Treatment

Increasing the levels of a key protein (RCAN1-1L) can, in vitro, rescue cells from the toxic effects of mutant huntingtin proteins that cause Huntington disease. "Our findings allow for the possibility that controlled over-expression of RCAN1-1L might in the future be a viable avenue for therapeutic intervention in Huntington disease patients," said Kelvin J. A. Davies, professor of gerontology in the USC Davis School of Gerontology and professor of biological sciences in the USC College of Letters, Arts and Sciences, and an author of the study. The report is now available online and will be published in June 2009 in the Journal of Biological Chemistry. [Press release] [JBC article]

April 19th

Novel Drug Targeted at Cancer Stem Cells Shows Promise in Pancreatic Cancer

The combination of a novel drug (tigatuzumab) directed against pancreatic cancer stem cells, and the drug (gemcitabine) currently used for the treatment of pancreatic cancer, has shown promising results in achieving tumor remission and preventing recurrence. Tigatuzumab is a humanized antibody directed against death receptor-5, which the researchers showed is overexpressed in pancreatic cancer stem cells. In the studies, ten patient-derived tumors were implanted in laboratory mice and the effects of the combination therapy were evaluated. Treatment with gemcitabine and tigatuzumab resulted in the reduction of pancreatic cancer stem cells, caused tumor remission, and significantly increased time-to-tumor progression in fifty percent of treated cases from a median of 54 days to 103 days. These results were obtained by researchers from Johns Hopkins and colleagues, and will be presented at the annual AACR meeting April 18-22. [Press release]