Vol 31, Part I - forums.sou.edu • Index page - Southern Oregon ...

ABSTRACTS – Symposia
detection of genomic aberrants. Yet, despite the ability to
pinpoint cancer phenotypes that correlate with disease and
treatment outcomes, we are not much closer to determining
how and why particular “omics” expression patterns lead
to disease. Recently, significant evidence has shown that
genomic aberrants such as copy number alterations, deletions,
and single nucleotide variants are associated with
cancers. For example, a set of deletions and gene amplifications
on Chromosome 8 are associated with differentiation
between the basal and luminal breast cancers. These cancer
types have widely different treatment outcomes and survival
prognoses, and show significantly different expression patterns
at the transcriptome and proteome level. Determining
the mechanisms by which these aberrations lead to cancers
is a key goal for both diagnosis and improved treatment.
Yet integration of knowledge across levels, from genome to
transcriptome to proteome to phenotype is extraordinarily
challenging.
We describe an effort to unify “omics” data sets from
human in mouse breast tumor models, and from TCGA
samples now being analyzed via large scale proteomic methods
within the CPTAC consortium headed by the NCI. We
show how data can be unified and analyzed within a genome
browser view to yield new insights about the relationship
between cancer genomes, proteomes, and their resultant phenotypes.
We illustrate with examples of previously unknown
genes that appear involved in specific cancer phenotypes.
79 Oncostatin M Interacts with ECM Components: Implications
for Chronic Inflammation and Tumor Metastasis,
RANDALL RYAN*, BRYAN MARTIN, LILIANA MEL-
LOR, OWEN McDOUGAL, REED JACOB, CHERYL
JORCYK, and JULIA OXFORD (Department of Biological
Sciences, Department of Chemistry and Biochemistry,
Biomolecular Research Center, Boise State University,
Boise Idaho, 83725 USA; randyryan7@hotmail.com).
Oncostatin M (OSM) is a proinflammatory cytokine that
has been reported to promote a metastatic phenotype in cancer
cells via its effects on cell migration, invasion and the EMT.
The ECM has been reported to regulate the properties and
activities of numerous cytokines and growth factors, as well as
the behavior and properties of tumor cells. In the current study,
OSM was observed to bind to ECM components, in vitro, in
a pH dependent fashion. OSM bound to ECM was observed
to be protected from cleavage by tumor associated proteases,
when compared to unbound OSM. In addition, OSM bound to
ECM was demonstrated to induce OSM signaling and target
proteins in breast carcinoma cells that could be inhibited with
an OSM neutralizing antibody. The data suggests that OSM
bound to ECM may play an important role in the acquisition
of chronic inflammation and provides additional evidence for
the role of inflammatory processes in cancer.
NIH/NCRR P20RR016454 and P20GM103408, NASA NNX10AN29A,
ACS RSG-09-276-01-CSM, and Susan G Komen KG100513.
Emerging and Re-Emerging
Infectious Diseases
Wednesday, 8:00 a.m. in DOUGLAS FIR 1 & 2
80 Toxin Production by Methicillin Resistant Strains of Staphylococcus
aureus (MRSA): The Effect of Antibiotics, DEN-
NIS L STEVENS 1,2 *, AMY E BRYANT 1,2,3 , STEPHANIE
HAMILTON 1,3 and YONGSHENG MA 1 ( 1 Department of
Veterans Affairs Medical Center, 500 West Fort Street, Boise,
Idaho 83702; 2 University of Washington School of Medicine,
1959 NE Pacific St, Seattle WA 98195; 3 University of Idaho,
Department of Life Sciences, PO Box 443051, Moscow, ID
83844-305; dlsteven@mindspring.com).
The emergence of MRSA has been associated with a
variety of new types of infections which have been associated
with the production of potent exotoxins. Specifically,
the Panton-Valentine Leukotoxins (PVL), alpha hemolysin
and staphylococcal toxic shock toxin-1 (TSST-1). Early in
the course of the MRSA epidemic it was noted that 50%
of patients with MRSA infections were being treated with
antibiotics to which the organism was resistant. This was
further associated with worse outcomes, prolonged hospitalization
and death. We hypothesized that inappropriate
antibiotics might not only delay definitive treatment but be
associated with enhanced toxin production. We first determined
the susceptibility of these strains to nafcillin, vancomycin
and linezolid and performed growth curves using
a rising gradient of antibiotics. Further, we then measured
gene expression for alpha toxin, PVL and TSST-1 at inhibitory
and sub-inhibitory concentrations of antibiotics. Nafcillin
induced markedly increased gene expression for PVL,
TSST-1 and alpha hemolysin in MRSA despite intrinsic
resistance to this agent. Further, sub-inhibitory concentrations
of nafcillin marked increased gene expression of these
toxins in methicillin susceptible strains of S. aureus (MSSA)
as well. Though linezolid also enhanced toxin gene expression,
toxin production at the protein level was curtailed. In
summary, antibiotic choices markedly affect the virulence
of S. aureus.
81 Yersinia pestis Ompx Virulence Factor and Role in Host
Cell Attachment, Internalization, and Immune Modulation,
ANNA M Kolodziejek 1 *, Scott A Minnich 1 ,
Carolyn J Hovde 1 , and Gregory A Bohach 2
( 1 School of Food Science, University of Idaho, 604 Rayburn
Street, Moscow, Idaho 83844 -2311; 2 Division of Agriculture,
Forestry and Veterinary Medicine, Box 9800, Mississippi
State University, Starkville, Mississippi 39762; akolodziejek@vandals.uidaho.edu).
Yersinia pestis is the causative agent of plague. Multiple
virulence determinants contribute to its highly efficient
transmission and pathogenicity. Representatives of a large
Enterobacteriaceae Ail/Lom family of outer membrane
proteins (Omp) are found in the genomes of all pathogenic
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