On The Spot e-News

Volume 3, Issue 5 | May 2008

In this issue:

Signature is Moving!

Signature Genomic Laboratories announced that it will be relocating its headquarters and laboratory to a new building in north Spokane, Wash. June 2nd. The new headquarters provides the wet-laboratory and administrative space necessary to accomodate Signature’s rapid growth.

Designed by Matthew Collins at Spokane architecture firm Nystrom Olson Collins and constructed by Doric, Inc., the 18,500-square-foot building features 9,000 square feet of wet lab space, compared to 5,000 square feet of wet lab space in its current location.

"Since we moved into our current location 18 months ago, Signature has doubled in size, and with the increasing diagnostic use of our oligonucleotide microarray and our expanding Genoglyphix service, we anticipate even more growth in the next few years," said Lisa G. Shaffer, Ph.D., President and CEO of Signature. "Our new headquarters allow us to continue to offer the excellent service our clients have come to expect."

During the move, laboratory operations will run concurrently in the new building and in Signature’s current location in the SIRTI Technology Center in downtown Spokane. Signature’s new location is 2820 N. Astor St. Spokane WA 99207.

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Signature Signs Long-Term Supply Agreement with Agilent Technologies for Oligo Microarrays

Signature and Agilent Technologies, Inc., announced they have signed a long-term supply agreement in which Agilent will supply custom oligonucleotide microarrays based on the Signature-designed SignatureChip Oligo Solution™ (SignatureChipOS™) to Signature and its customers.

The SignatureChipOS is designed for the detection of chromosome abnormalities in individuals with mental retardation/developmental delay, autism and congenital anomalies. The 105,000-feature, 60-mer microarray covers over 150 syndromes, the subtelomeric and pericentromeric regions, and more than 500 genes in important developmental pathways.

"We are committed to giving our customers the best services and technology available, and this agreement reflects this focus," said Lisa G. Shaffer, Ph.D., President and CEO of Signature. "Oligo arrays have improved dramatically in the past few years and we are delighted there are now oligos that meet our high standards. This supply agreement also allows our Genoglyphix® customers the opportunity to use high-quality oligo arrays for research applications in their laboratories."

"We’re very pleased about this agreement, which is the latest example of how the marketplace is recognizing the value of our highly flexible, high-quality oligo synthesis capability," said Yvonne Linney, Ph.D., Agilent Vice President and General Manager, Genomics. "We’re delighted to work with Signature Genomic Laboratories which specializes in microarray technology and is an innovative leader in microarray testing."

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Signature Reports Characterization of Previously Unrecognized 3q29 Microduplications

Microscopic deletions of chromosome 3q29 have been described recently in individuals with mental retardation and highly variable clinical features. All individuals reported to date have the same-sized deletion. Because this region of chromosome 3 is thought to be caused by recombination between flanking segments of highly repetitive DNA sequences, duplications of 3q29 should occur with the same frequency as deletions. However, with the exception of one three-generation family, no individuals with microduplications of 3q29 have been reported. Researchers at Signature Genomic Laboratories recently characterized 19 individuals with 3q29 microduplications and suggest that duplication alone may not account for the clinical features in those individuals.

In the study, published in the journal Molecular Cytogenetics, researchers identified 19 individuals with microduplications of 3q29 in almost 20,000 individuals with unexplained mental retardation and congenital anomalies referred to the laboratory for microarray testing. The clinical features of the individuals varied widely, with mental retardation the only feature common to all patients. Surprisingly, only five individuals had reciprocal duplications that were the same size and location as the 3q29 microdeletion; the remaining 14 duplications flank, span, or partially overlap the common deletion region. This suggests other factors besides the segmental duplications that cause the common-sized 3q29 deletions play a role in rearrangements of this region. Because some of the duplications were inherited from a clinically normal parent, the clinical significance of these duplications is unclear and may require an as-yet unidentified genetic modifier for medical problems to occur.

"Although further studies are required to determine what role, if any, these duplications play in the patients" clinical features, microarray analysis was essential for identifying this novel chromosome abnormality. Their highly variable clinical features—and the lack of similar patients reported in the literature—would have prevented their identification without this technology," said Dr. Blake C. Ballif, Ph.D., Director of Product Development and Research at Signature and lead author of the study. "These cases are an excellent example of how microarray technology can provide answers that traditional methods cannot."

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