purcc 2012 - University of the Pacific

Poster Session Abstracts
to chromosomal instability. In this research, the
interactions of the five paralogs and the two
complexes, both containing Rad51C that form
from them will be investigated. Escherichia coli
containing either human Rad51B or human
Xrcc3 were grown and the plasmids containing
the appropriate target gene were isolated. The
plasmids were treated with restriction enzymes
and the samples were run on an agarose gel to
verify that the DNA of each repair gene was the
expected size. Samples will be sequenced to
verify the cDNA is mutation free. The target
gene will be isolated and placed in a plasmid for
expression in the yeast, Pichia pastoris, more
suited for recombinant protein expression of
higher eukaryotic organisms. The plasmid will
be inserted into P. pastoris using electroporation
and the corresponding protein will be expressed.
These proteins will be used to examine protein
interaction and function. This study will increase
current understanding of Rad51C complex
formation and function in the repair of DNA
double-strand breaks.
Histological Characterization of Vitamin
D-induced Apoptosis in a Hamster Buccal
Pouch Model of Head and Neck
Squamous Cell Carcinoma
Cina Kim, Katie Ross
Faculty Mentor: Joanna Albala
Head and neck squamous cell carcinoma
(HNSCC) remains a major cause of mortality
and morbidity in the U.S. and around the world.
Vitamin D 3 (VD 3 ), in addition to its primary role
in maintaining calcium homeostasis, has been
shown to induce differentiation and suppress the
growth of squamous cell carcinomas in vitro. As
such, proteins and compounds that act in the
vitamin D pathway are potential candidates for
therapeutic intervention for treatment of
HNSCC. Previous work in the Albala lab has
demonstrated that VD 3 was chemopreventive in
cancer formation in the hamster buccal pouch
model. The hamster buccal pouch tumor model
is a well-characterized model system since the
progression from normal epithelium to
carcinoma closely resembles those changes in
humans.
Rad51 protein plays an important role in is cell
proliferation and homologous recombinational
DNA repair. Defects in the pathway may render
cells sensitive to DNA cross-linking agents and
ionizing radiation, while up-regulation of the
pathway can render cellular DNA more resistant
to damage, and strengthen cellular resistance to
radiation therapy and selective chemotherapeutic
agents. Studies have documented the elevation of
Rad51 levels in several cancer cell lines,
including immortalized cells. Previous studies in
the Albala lab have demonstrated the downregulation
of Rad51 by VD 3 in the hamster
buccal cheek pouch model. This work aims to
demonstrate a correlation between the reduction
of Rad51 protein by VD 3 in this hamster model
and the effects of 7,12-
dimethylbenz[a]anthracene (DMBA) as a
carcinogen, inducing the repair mechanism when
administered to the hamster buccal pouches.
Preliminary Proteomic Analysis of a
Vesicle-enriched Fraction from the
Protozoal Parasite Trichomonas vaginalis
Casey Ardrey
Faculty Mentors: Kirkwood Land, Lisa
Wrischnik
We have analyzed using mass spectrometry a
vesicle-enriched fraction from the human
protozoal parasite Trichomonas vaginalis.
Using the recently completed T. vaginalis
genome, we have carried out an extensive
bioinformatic analysis of this subcellular fraction
and have identified a number of interesting
targets for future biological study. We will
discuss the implications of our analysis on drug
discovery against this important human parasite.
Characterization of an
Adenosylhomocysteine Hydrolase
Enzyme in the protozoal parasite
Trichomonas vaginalis
Aaron Au, Steven An
Faculty Mentor: Kirkwood Land
Trichomonas vaginalis is the causative agent of
trichomoniasis, a common sexually-transmitted
disease in humans. Approximately 5% of cases
of trichomoniasis are resistant to treatment with
the commonly prescribed metronidazole. The
search for alternative new therapies for both
nitroimidazole susceptible and resistant cases is
imperative. Here, we have shown that 2'-deoxy-
2'-fluoroadenosine, 9-(β,Darabinofuranosyl)adenine,
9-(2-deoxy-2-fluoroβ,D-arabinofuranosyl)adenine
, and 9-(2-chloro-
2-deoxy-β,D-arabinofuranosyl)adenine inhibit T.
52