Research Topics
| Stefan DuensingSummaryAffiliation: Harvard University Country: USA Publications
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Publications
The human papillomavirus type 16 E6 and E7 oncoproteins independently induce numerical and structural chromosome instabilityStefan Duensing
Department of Pathology and Harvard Center for Cancer Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 62:7075-82. 2002..Our results therefore suggest that HPV oncoproteins are a source for both numerical and structural chromosome instability during HPV-associated carcinogenesis...- Centrosomes, genomic instability, and cervical carcinogenesisStefan Duensing
Harvard Medical School, Department of Pathology, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
Crit Rev Eukaryot Gene Expr 13:9-23. 2003..Taken together, these findings support the general model in which chromosomal instability arises as a direct consequence of oncogenic insults and can develop at early stages of tumor progression... - Human papillomavirus type 16 E7 oncoprotein can induce abnormal centrosome duplication through a mechanism independent of inactivation of retinoblastoma protein family membersStefan Duensing
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
J Virol 77:12331-5. 2003..These results demonstrate that the molecular mechanism whereby HPV-16 E7 induces centrosome duplication errors is independent of its ability to inactivate pRB, p107, and p130 or to interact with the S4 proteasome subunit... - Excessive centrosome abnormalities without ongoing numerical chromosome instability in a Burkitt's lymphomaStefan Duensing
Department of Pathology, Harvard Medical School, Armenise 537, 200 Longwood Avenue, Boston, MA 02115, USA
Mol Cancer 2:30. 2003..Moreover, our results suggest a model in which additional cellular alterations may be required to promote centrosome-related mitotic defects in tumor cells... - Daughter centriole elongation is controlled by proteolysisNina Korzeniewski
Cancer Virology Program, University of Pittsburgh Cancer Institute, Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
Mol Biol Cell 21:3942-51. 2010..They also highlight the complexity of daughter centriole length control and provide a framework for future studies to dissect the molecular details of this process... - Analysis of centrosome overduplication in correlation to cell division errors in high-risk human papillomavirus (HPV)-associated anal neoplasmsAnette Duensing
Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
Virology 372:157-64. 2008.... - The helix-loop-helix protein ID1 localizes to centrosomes and rapidly induces abnormal centrosome numbersJens Hasskarl
Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Oncogene 23:1930-8. 2004..Hence, ID1 may contribute to oncogenesis not only by inhibiting transcriptional activity of basic helix-loop-helix transcription factors and abrogate differentiation but also by subverting centrosome duplication... - Abrogation of the retinoblastoma tumor suppressor checkpoint during keratinocyte immortalization is not sufficient for induction of centrosome-mediated genomic instabilitySiribang-On Piboonniyom
Department of Oral Medicine and Diagnostic Sciences, Harvard School of Dental Medicine, Boston, Massachusetts 02115, USA
Cancer Res 63:476-83. 2003..These results demonstrate that disruption of the p16INK4A/pRB checkpoint of epithelial cell immortalization does not necessarily lead to centrosome-associated genomic instability... - Centrosome abnormalities and genomic instability induced by human papillomavirus oncoproteinsStefan Duensing
Department of Pathology, Harvard Center for Cancer Biology, Harvard Medical School, Armenise Research Building, D2-537, 200 Longwood Avenue, Boston, MA 02115, USA
Prog Cell Cycle Res 5:383-91. 2003.... - Cep76, a centrosomal protein that specifically restrains centriole reduplicationWilliam Y Tsang
Department of Pathology, NYU School of Medicine and Cancer Institute, Smilow Research Building, New York, NY 10016, USA
Dev Cell 16:649-60. 2009..Our findings also point to mechanistic differences between normal duplication and aberrant centriole amplification, as well as distinctions between diverse modes of amplification... - A role of the mitotic spindle checkpoint in the cellular response to DNA replication stressAnette Duensing
Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA
J Cell Biochem 99:759-69. 2006..These findings imply that the mitotic spindle checkpoint may act in concert with DNA damage and cell-cycle checkpoints as an early anti-tumor barrier and provide a possible explanation for its frequent relaxation in human cancer... - Human papillomaviruses and centrosome duplication errors: modeling the origins of genomic instabilityStefan Duensing
Department of Pathology, Harvard Medical School, Armenise Research Building, D2-537, 200 Longwood Avenue, Boston, Massachusetts, MA 02115, USA
Oncogene 21:6241-8. 2002..These findings suggest that HPV oncoprotein-induced chromosomal instability increases the risk for genetic changes that may ultimately facilitate carcinogenic progression... - p21(Waf1/Cip1) deficiency stimulates centriole overduplicationAnette Duensing
Department of Pathology, Molecular Virology Program, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Cell Cycle 5:2899-902. 2006.... - Centrosome-mediated chromosomal instability and steroid hormones as co factors in human papillomavirus-associated cervical carcinogenesis: small viruses help to answer big questionsAnette Duensing
Molecular Virology Program, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
Adv Exp Med Biol 617:109-17. 2008 - Dissection of human papillomavirus E6 and E7 function in transgenic mouse models of cervical carcinogenesisRebeccah R Riley
University of California San Francisco Comprehensive Cancer Center and Department of Surgery, University of California, San Francisco 94143-0808, USA
Cancer Res 63:4862-71. 2003..Centrosome copy number increases and p53 loss likely contributed to malignant growth; however, dysregulated proliferation and differentiation were required for carcinogenic progression... - Quantitative role of the human papillomavirus type 16 E5 gene during the productive stage of the viral life cycleSybil M Genther
McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine, Madison, Wisconsin 53706, USA
J Virol 77:2832-42. 2003..These data demonstrate that E5 plays a subtle role during the productive stage of the HPV16 life cycle... - Mechanisms of genomic instability in human cancer: insights from studies with human papillomavirus oncoproteinsStefan Duensing
Molecular Virology Program, University of Pittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, PA 15213, USA
Int J Cancer 109:157-62. 2004..We summarize the current state of knowledge concerning HPV-induced genomic instability and discuss its significance in the context of human carcinogenesis... - Recapitulation of the effects of the human papillomavirus type 16 E7 oncogene on mouse epithelium by somatic Rb deletion and detection of pRb-independent effects of E7 in vivoScott J Balsitis
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, 1400 University Avenue, Madison, WI 53706, USA
Mol Cell Biol 23:9094-103. 2003..These findings indicate that inactivation of the Rb pathway can largely account for E7's phenotypes at an early age, but that pRb-independent activities of E7 are detectable in vivo... - Guilt by association? p53 and the development of aneuploidy in cancerAnette Duensing
Molecular Virology Program, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA
Biochem Biophys Res Commun 331:694-700. 2005.... - The forkhead-associated domain protein Cep170 interacts with Polo-like kinase 1 and serves as a marker for mature centriolesGiulia Guarguaglini
Department of Cell Biology, Max Planck Institute for Biochemistry, D 82152, Martinsried, Germany
Mol Biol Cell 16:1095-107. 2005..We show that Cep170 labeling can be used to discriminate bona fide centriole overduplication from centriole amplification that results from aborted cell division... - Cyclin-dependent kinase inhibitor indirubin-3'-oxime selectively inhibits human papillomavirus type 16 E7-induced numerical centrosome anomaliesStefan Duensing
Molecular Virology Program, University of Pittsburgh Cancer Institute, Hillman Cancer Center, 5117 Centre Avenue, Pittsburgh, PA 15213, USA
Oncogene 23:8206-15. 2004..Our results suggest that cyclin/CDK2 activity is critically involved in abnormal centrosome duplication induced by HPV-16 E7 oncoprotein expression, but may be dispensable for normal centrosome duplication and cell cycle progression... - The human papillomavirus type 16 E7 oncoprotein activates the Fanconi anemia (FA) pathway and causes accelerated chromosomal instability in FA cellsNicole Spardy
Biochemistry and Molecular Genetics Graduate Program, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA
J Virol 81:13265-70. 2007.... - A tentative classification of centrosome abnormalities in cancerStefan Duensing
Molecular Virology Program, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15213, USA
Cell Biol Int 29:352-9. 2005..Therefore, centrosome anomalies should not per se be viewed as a universal cause of chromosomal instability, rather, they need to be assessed in the cellular context in which they occur...