A
Anette Duensing
Researcher at University of Pittsburgh
Publications - 71
Citations - 5945
Anette Duensing is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Imatinib mesylate & Centrosome. The author has an hindex of 30, co-authored 69 publications receiving 5519 citations. Previous affiliations of Anette Duensing include Brigham and Women's Hospital.
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Journal ArticleDOI
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
Michael Heinrich,Christopher L. Corless,Anette Duensing,Laura McGreevey,Chang Jie Chen,Nora E. Joseph,Samuel Singer,Diana J. Griffith,Andrea Haley,Ajia Town,George D. Demetri,Christopher D.M. Fletcher,Jonathan A. Fletcher,Jonathan A. Fletcher +13 more
TL;DR: Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression, suggesting KIT and PDGFra mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
Journal ArticleDOI
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.
Stefan Duensing,Lily Y. Lee,Anette Duensing,John R. Basile,Siribang-on Piboonniyom,Sonia L. Gonzalez,Christopher P. Crum,Karl Münger +7 more
TL;DR: It is shown that aberrant mitotic spindle pole formation caused by abnormal centrosome numbers represents an important mechanism in accounting for numeric chromosomal alterations in HPV-associated carcinogenesis.
Journal ArticleDOI
Mechanisms of oncogenic KIT signal transduction in primary gastrointestinal stromal tumors (GISTs)
Anette Duensing,Anette Duensing,Fabiola Medeiros,Bryna McConarty,Nora E. Joseph,Dipak Panigrahy,Samuel Singer,Christopher D.M. Fletcher,George D. Demetri,Jonathan A. Fletcher,Jonathan A. Fletcher +10 more
TL;DR: In this article, the authors evaluated KIT downstream signaling profiles in 15 primary GISTs with mutations in KIT exons 9, 11, 13, and 17, and in two human GIST cell lines.
Journal ArticleDOI
ERCC1-XPF Endonuclease Facilitates DNA Double-Strand Break Repair
Anwaar Ahmad,Andria Rasile Robinson,Anette Duensing,Ellen van Drunen,H. Berna Beverloo,David Weisberg,Paul Hasty,Jan H.J. Hoeijmakers,Laura J. Niedernhofer +8 more
TL;DR: Data support the conclusion that, as in yeast, ERCC1-XPF facilitates DSB repair via an end-joining mechanism that is Ku86 independent, and in vitro repair of DSBs with 3′ overhangs led to large deletions in the absence of ERCC 1- XPF.
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KIT oncogenic signaling mechanisms in imatinib-resistant gastrointestinal stromal tumor: PI3-kinase/AKT is a crucial survival pathway
TL;DR: It is concluded that GIST secondary KIT mutations can be associated with KIT hyperactivation and imatinib resistance, and targeting critical downstream signaling proteins, such as PI3-K, is a promising therapeutic strategy inImatinib-resistant GISTs.