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Stefan Mark Duensing, M.D.
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Associate Professor
1.8 HCCLB
5117 Centre Avenue
Pittsburgh, Pennsylvania 15213
Phone: (412) 623-7719
Fax: (412) 624-1401
E-mail: duensing@pitt.edu
Lab Phone: (412) 623-7731
Lab Website
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Research
The Duensing laboratory is interested in the molecular mechanisms of human papillomavirus (HPV)-induced carcinogenesis, specifically in the induction of genomic instability by HPV oncoproteins. The HPV-16 E7 oncoprotein has been identified as driving force for numerical chromosomal aberrations ("mitotic mutator"). We are dissecting the precise molecular mechanisms through which HPV-16 E7 causes cell division errors with a focus on centrosome duplication control. A second line of research aims to identify how the HPV-16 E7 oncoprotein induces DNA damage and possible mechanisms that thwart anti-proliferative responses associated with chronic host cell DNA damage checkpoint activation.
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Selected Publications
- Korzeniewski N, Zheng L, Cuevas, R, Parry J, Chatterjee P, Anderton B, Duensing A, Münger K, Duensing S. Cullin 1 functions as a centrosomal suppressor of centriole multiplication by regulating Polo-like kinase 4 protein levels. Cancer Res., 2009; 69:6668-6675. | Abstract
- Spardy N, Covella K, Cha E, Hoskins EE, Park JW, Lambert PF, Wells SI, Duensing A, Duensing S. The human papillomavirus type 16 E7 (HPV-16 E7) oncoprotein attenuates DNA damage checkpoint responses by increasing the proteolytic turnover of claspin. Cancer Res., 2009; 69:7022-7029. | Abstract
- Tsang WY, Spektor A, Vijayakumar S, Bista B, Li J, Sanchez I, Duensing S, Dynlacht BD. 2009. Cep76, a centrosomal protein that specifically restrains centriole reduplication. Dev. Cell 16:649-660. | Abstract
- Spardy N, Duensing A, Hoskins EE, Wells SI, Duensing S. HPV-16 E7 reveals a link between DNA replication stress, FANCD2 and alternative lengthening of telomeres (ALT)-associated PML bodies (APBs). Cancer Res. 2008; 68:9954-9963. | Abstract
- Spardy N, Duensing A, Charles D, Haines N, Nakahara T, Lambert PF, Duensing S. Human papillomavirus type 16 E7 activates the Fanconi Anemia (FA) pathway and causes accelerated chromosomal instability in FA cells. J. Virol. 2007; 81:13265-13270. | Abstract
- Duensing A, Liu Y, Perdreau SA, Kleylein-Sohn J, Nigg EA, Duensing S. Centriole overduplication through the concurrent formation of multiple daughter centrioles at single maternal templates. Oncogene 2007; 26:6280-6288. | Abstract
- Duensing A, Liu Y, Tseng M, Malumbres M, Barbacid M, Duensing S. Cyclin-dependent kinase 2 is dispensable for normal centrosome duplication but required for oncogene-induced centrosome overduplication. Oncogene 2006; 25:2943-2949. | Abstract
- Guarguaglini G, Duncan PI, Stierhof PI, Holmström T, Duensing S, Nigg EA. The forkhead-associated domain protein Cep170 interacts with Polo-like kinase 1 and serves as a marker for mature centrioles. Mol. Biol. Cell 2005; 16:1095-1107. | Abstract
- Duensing S, Münger K. Human papillomavirus type 16 E7 oncoprotein can induce abnormal centrosome duplication through a mechanism independent of inactivation of retinoblastoma protein family members. J. Virol. 2003; 77:12331-12335. | Abstract
- Duensing S, Lee LY, Duensing A, Basile J, Piboonniyom S, Gonzalez S, Crum CP, Münger K. The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle. Proc. Natl. Acad. Sci. USA 2000; 97:10002-10007. | Abstract
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