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New Data From Satraplatin Phase 3 Trial In Second-Line Castrate-Refractory Prostate Cancer Presented At 2009 ASCO Annual Meeting
GPC Biotech AG (FRANKFURT: GPC) (XETRA: GPC) announced that data from the double- blind, randomized satraplatin Phase 3 trial, the SPARC trial (Satraplatin and Prednisone Against Refractory Cancer), were presented at the 2009 American Society for Clinical Oncology (ASCO) Annual Meeting in Orlando, Florida. The SPARC trial evaluated satraplatin plus prednisone versus placebo plus prednisone in 950 patients with castrate-refractory prostate cancer (CRPC) who had progressed after initial chemotherapy. The data presented are retrospective analyses of the SPARC trial evaluating correlations between overall survival (OS) and pain at baseline, pain progression, and progression-free survival (PFS) at three months.
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Cephalon Submits NUVIGIL Supplemental New Drug Application For The Treatment Of Excessive Sleepiness Associated With Jet Lag Disorder
Cephalon, Inc. (Nasdaq: CEPH) announced that it has submitted a supplemental New Drug Application (sNDA) to the U.S. Food and Drug Administration (FDA) requesting approval of NUVIGIL(R) (armodafinil) Tablets [C-IV] for the indication of improved wakefulness in patients with excessive sleepiness associated with jet lag disorder resulting from eastbound travel. Jet lag disorder is an acute condition that occurs when a person"s internal body clock becomes disrupted as a result of rapid travel across several time zones. Based on U.S. Bureau of Labor Statistics findings, an estimated 70 million American travelers experience jet lag annually. Currently, there are no FDA-approved medications to improve wakefulness in travelers who experience the excessive sleepiness commonly associated with long flights.
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Discovery Of Breast Cancer Gene That's Blocked By Blood Pressure Drug
Researchers have identified a gene that is overexpressed in up to 20 percent of breast cancers and that could be blocked in the lab by a currently available blood pressure drug, according to a new study from the University of Michigan Comprehensive Cancer Center.
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Alzheimer's Comment On Research That Genes In Early Onset Are Associated With Memory, Published In Nature, 28 July 2009

Memory is a fundamental function of nerve cells in the brain, and loss of memory is a key symptom in many people with Alzheimer"s disease. In order for memory to function correctly, nerve cells must be able to communicate effectively with each other. Many important proteins in the brain ensure that this communication is maintained between healthy nerve cells by monitoring the junctions, or synapses, between cells. This is also the location of production of amyloid-beta, which accumulates as plaques in Alzheimer"s disease. The gene PSEN1 is responsible for the protein presenilin1. Faulty versions of this gene are known to be linked to early onset Alzheimer"s disease. This new study shows that presenilin1 plays an important role in the functioning of synapses between nerve cells and suggests that the faulty protein disrupts communication between cells, thus affecting memory. The work also suggests that presenilin1 is linked with amyloid-beta and production of toxic plaques in the brain during Alzheimer"s disease. Alzheimer"s Society comment: "This study shows that a gene linked with early onset Alzheimer"s plays an important role in storing memory. This is an interesting finding which could lead to new research into how we can develop drug treatments that target this area. One million people will develop dementia in the next 10 years. We must act now. We need a national plan for dementia research and a tripling of investment to see research translated into better treatments for millions of people. Dementia is not a natural part of ageing; it is caused by diseases of the brain. 15,000 people under 65 live with dementia in the UK." Professor Clive Ballard Director of Research Alzheimer"s Society Reference Presenilins are essential for regulating neurotransmitter release. Chen Zhang1,2, Bei Wu1, Vassilios Beglopoulos1, Mary Wines-Samuelson1, Dawei Zhang1, Ioannis Dragatsis3, Thomas C. Su֬dhof2 & Jie Shen. Vol 460|30 July 2009| doi:10.1038/nature08177 Alzheimer"s Society


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