Affiliation: Harvard University
- Biology of gastrointestinal stromal tumors: KIT mutations and beyondAnette Duensing
Department of Pathology, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
Cancer Invest 22:106-16. 2004..This review focuses on the biological and molecular genetic principles of GISTs, and particularly the role of mutant KIT as a therapeutic target...
- Mechanisms of oncogenic KIT signal transduction in primary gastrointestinal stromal tumors (GISTs)Anette Duensing
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
Oncogene 23:3999-4006. 2004....
- Protein Kinase C theta (PKCtheta) expression and constitutive activation in gastrointestinal stromal tumors (GISTs)Anette Duensing
Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Cancer Res 64:5127-31. 2004..PKCtheta is strongly activated in most GISTs and hence may serve, along with KIT/PDGFRA, as a novel therapeutic target...
- KIT-negative gastrointestinal stromal tumors: proof of concept and therapeutic implicationsFabiola Medeiros
Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
Am J Surg Pathol 28:889-94. 2004..Notably, some KIT-negative GISTs contain imatinib-sensitive KIT or PDGFRA mutations; therefore, patients with KIT-negative GISTs should not, a priori, be denied imatinib therapy...
- 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...
- Familial gastrointestinal stromal tumor syndrome: phenotypic and molecular features in a kindredFrederick P Li
Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
J Clin Oncol 23:2735-43. 2005..A tumor from the proband was analyzed to compare features with sporadic GISTs...
- 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....
- 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....
- 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...
- PDGFRA activating mutations in gastrointestinal stromal tumorsMichael C Heinrich
Department of Medicine, Department of Pathology, Oregon Health and Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA
Science 299:708-10. 2003..Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs...
- Viral carcinogenesis and genomic instabilityKarl Munger
The Channing Laboratory, Brigham and Women s Hospital, 181 Longwood Avenue, Boston, MA 02115, USA
EXS . 2006..Viruses that encode such activities can contribute to initiation as well as progression of human cancers...
- Mechanisms of resistance to small molecule kinase inhibition in the treatment of solid tumorsBrian P Rubin
Department of Anatomic Pathology, University of Washington Medical Center, Seattle, WA 98195, USA
Lab Invest 86:981-6. 2006..This paper focuses on what is known about mechanisms of resistance in the treatment of solid tumors by small molecule kinase inhibitors...
- Histone H2AX is a mediator of gastrointestinal stromal tumor cell apoptosis following treatment with imatinib mesylateYing Liu
Molecular Virology Program, University of Pittsburgh Cancer Institute, Pennsylvania 15213, USA
Cancer Res 67:2685-92. 2007..Our results underscore the importance of H2AX as a human tumor suppressor protein, provide mechanistic insights into imatinib-induced tumor cell apoptosis and establish H2AX as a novel target in cancer therapy...