17 Biotechnology Law Report 51 (Number 1, January-February 1998)

{BLR 2611} Apoptosis-

LXR Biotechnology-

SARPs.

MORE PROTEINS THAT ARE INVOLVED IN APOPTOSIS— LXR Scientists Discover Family of Secreted Products

RICHMOND, CAL. 12/8/97 - Scientists at LXR Biotechnology, Inc. havediscovered a new family ofproteins involved in programmed cell death (apoptosis) andhave cloned several of the corresponding genes. One of the proteins appears toencourage apoptosis and another to inhibit it. Patents have been applied for.

Unlike most of the previously recognized proteins involved in apoptosis, whichare intracellular products, the newly discovered proteins are secreted. Thus, theyhave been named "secreted apoptosis-related proteins" (SARPs). Another unusualfeature of the proteins is their apparent tissue specificity.

Programmed cell death is necessary for the normal development of an

organism (and the reason we do not have tails). However, it can be triggeredinappropriately, as after a myocardial infarction or stroke, leading to extensivedamage. Alternatively, it can be triggered deliberately to destroy undesirable tissuesuch as cancer. Indeed, much of the current research in oncology is directed atinducing apoptosis in malignant cells.

The paper describing SARPs was published in today's issue of the Proceedingsof the National Academy ofSciences of the United States ofAmerica.

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{BLR 2612} B. burgdorferi-

Lyme Disease-

TIGR.

Genome of Borrelia burgdorferi Published— TIGR Completes Sequencing of Lyme Disease Agent

ROCKVILLE, MD. 12/10/97-

Scientists at The Institute for GenomicResearch (TIGR) announced today in an article in Nature that they have completedthe sequencing of the genome of Borrelia burgdorferi, the spirochete that causes

Lyme disease. The genome proved to consist of a linear chromosome of 910,725basepairs and 19 linear and circular plasmids. The entire sequence can be obtainedfrom TIGR's Microbial Database at www.tigr.org

Lyme disease, which is spread principally by Ixodes ticks, initially produces arash and flu-like symptoms. Neurologic complications and arthritis appear in abouthalf of untreated patients. The organism may persist for years in the body despite a

strong immune response, and although it is sensitive to several antibiotics in vitro,

17 Biotechnology Law Report 52 (Number 1, January-February 1998)

there is some question about its response in vivo. A vaccine for this relativelyrecently recognized disease is in clinical trials.

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{BLR 2613} Epstein-Barr Virus-

Lupus Erythematosus.

OKLAHOMA SCIENTISTS PRESENT EVIDENCE THAT EBVIS INVOLVED IN LUPUS ERYTHEMATOSUS— Common Infection Might Trigger Autoimmune Disease

OKLAHOMA CITY, OK. 12/15/97-

A team of researchers from theOklahoma Medical Research Foundation today published evidence that the Epstein-Barr virus plays a significant role in the autoimmune disease, lupus erythematosus.

The EBV, a member of the herpesvirus family, is best known as a cause ofinfectious mononucleosis. Less appreciated is its ability to establish chronicinfections in approximately three quarters of the population without causingsymptoms and its association with nasopharyngeal carcinoma and African Burkitt'slymphoma.

Lupus produces a variety of injuries to organs such as the kidneys, lungs, andheart. The diversity of clinical manifestations can make it difficult to diagnose.Common laboratory findings are antibodies against DNA, the spliceosome, and othercellular constituents.

The Oklahoma researchers, led by John Harley, M.D., Ph.D., and JudithJames, M.D., Ph.D., found that a peptide important in the immunologie response tothe spliceosome and which induces a lupus-like disease in animals is nearly identicalin amino acid sequence to a segment of the EBV nuclear antigen-1. When the EBVsequence is injected into animals, they developed a lupus-like condition. Furtherevidence for the role of EBV in lupus was provided by the finding of anti-EBVantibodies in virtually all patients with lupus versus 70% of age- and sex-matchedcontrol subjects.

The article describing this work, which, if confirmed, might lead to more specificand more effective therapy for the sometimes disabling disease, was published intoday's issue of the Journal ofClinical Investigation.

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