| Publications
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Associate
Professor of Clinical Pharmacy, Pharmaceutical Sciences, Pediatrics and Molecular Sciences
The fungus Candida albicans is a cause of mucosal, cutaneous, and systemic
infections, including oropharyngeal candidiasis (OPC), the most frequent
opportunistic infection among AIDS patients. Furthermore, bloodstream
infections due to Candida species are an increasingly important complication
in hospitalized patients. In the United States, candidemia is the
fourth most common nosocomial bloodstream infection, has a significant
impact on mortality rates, and is associated with excessive morbidity
and prolongation of hospital stay. The interests of Dr. David Rogers
lab revolve around three areas central to the management of infections
due to C. albicans: 1) the molecular basis for the mechanism of specific
antifungal agents; 2) molecular mechanisms of antifungal resistance;
and 3) the role of the innate immune response in the interaction between
C. albicans and the host. With the recent sequencing of the C. albicans genome, his group has made use of new technologies that have subsequently
become available to the field of Candida research. These studies have
clarified the molecular basis of azole resistance and have identified
new molecules for further study. It is their hope that newly identified
mediators of this phenotype will serve as targets for the development
of therapeutic strategies to circumvent resistance and improve the
therapeutic index of the azole antifungal agents. |
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Rogers PD, Lewis RE, Kramer RE. Extracellular calcium is not
associated with the activity of amphotericin B against Candida albicans.
J Antimicrob Chemother 2003; 51:305-312
Rogers PD, Barker KS, Herring V. Heat-induced superaggregation
of amphotericin B attenuates its ability to induce cytokine and chemokine
production in the human mono-cytic cell line THP-1. J Antimicrob Chemother 2003; 51:405-408
Barker KS, Liu T, Rogers PD. Analysis of differential gene expression in the human monocytic cell line THP-1 in response to Candida albicans. J Infectious Dis 2005; 192:901-912
Liu, TT, Lee REB, Barker KS, Lee RE, Wei L, Homayouni R, Rogers PD. Genome-wide expression profiling of the response to azole, polyene, echinocandin, and pyrimidine antifungal agents in Candida albicans. Antimicrob Agents Chemother 2005; 49:2226-2236
Lee REB, Liu TT, Barker KS, Lee RE, Rogers PD. Genome-wide expression profiling of the response to ciclopirox olamine in Candida albicans. J Antimicrob Chemother 2005; 55:655-662
Vermitsky JP, Earhart KE, Smith L, Homayouni R, Edlind TE, Rogers PD. PDR1 regulates multidrug resistance in Candida glabrata: gene disruption and genome-wide expression studies. Mol Microbiol 2006, 61:704-722
Rogers PD, Vermitski JP, Edlind TD, Hilliard GM. Proteomic analysis of experimentally induced azole resistance in Candida glabrata. J Antimicrob Chemother 2006, 58: 434-438
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