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Genomes and Genes | Jeffrey A KnaufSummaryAffiliation: University of Cincinnati Country: USA Publications
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Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiationJeffrey A Knauf
Division of Endocrinology and Department of Pathology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0547, USA
Cancer Res 65:4238-45. 2005..This closely recapitulates the phenotype of BRAF-positive PTCs in humans and supports a key role for this oncogene in its pathogenesis...- RET/PTC-induced dedifferentiation of thyroid cells is mediated through Y1062 signaling through SHC-RAS-MAP kinaseJeffrey A Knauf
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
Oncogene 22:4406-12. 2003..This suggests that inhibition of this pathway may promote redifferentiation in poorly differentiated thyroid carcinomas with constitutive activation of either Ras or RET/PTC... - Acute expression of RET/PTC induces isozyme-specific activation and subsequent downregulation of PKCepsilon in PCCL3 thyroid cellsJeffrey A Knauf
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Mail Location 0547, Cincinnati, OH 45267, USA
Oncogene 22:6830-8. 2003.... - BRAF mediates RET/PTC-induced mitogen-activated protein kinase activation in thyroid cells: functional support for requirement of the RET/PTC-RAS-BRAF pathway in papillary thyroid carcinogenesisNorisato Mitsutake
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Ohio 45267-0547, USA
Endocrinology 147:1014-9. 2006..These data indicate that BRAF is required for RET/PTC-induced MAPK activation in thyroid cells and support the notion that BRAF inactivation may be an attractive target for PTCs... - Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancerRaffaele Ciampi
Department of Pathology and Laboratory Medicine and Division of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0529, USA
J Clin Invest 115:94-101. 2005.... - Conditional activation of RET/PTC3 and BRAFV600E in thyroid cells is associated with gene expression profiles that predict a preferential role of BRAF in extracellular matrix remodelingCleo Mesa
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, OH 45267, USA
Cancer Res 66:6521-9. 2006..The preferential induction of MMPs by BRAF could explain in part the more invasive behavior of thyroid cancers with BRAF mutations... - Low prevalence of BRAF mutations in radiation-induced thyroid tumors in contrast to sporadic papillary carcinomasMarina N Nikiforova
Department of Pathology and Laboratory Medicine, University of Cincinnati, 231 Albert Sabin Way, P O Box 670529, Cincinnati, OH 45267 0529, USA
Cancer Lett 209:1-6. 2004..These results demonstrate a significant difference in the molecular genetic profile of sporadic and radiation-induced thyroid tumors... - BRAF kinase activation via chromosomal rearrangement in radiation-induced and sporadic thyroid cancerRaffaele Ciampi
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0529, USA
Cell Cycle 4:547-8. 2005.... - Conditional BRAFV600E expression induces DNA synthesis, apoptosis, dedifferentiation, and chromosomal instability in thyroid PCCL3 cellsNorisato Mitsutake
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0547, USA
Cancer Res 65:2465-73. 2005..However, in contrast to RET/PTC, BRAF(V600E) may facilitate the acquisition of secondary genetic events through induction of genomic instability, which may account for its aggressive properties... - BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomasMarina N Nikiforova
Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA
J Clin Endocrinol Metab 88:5399-404. 2003..They are associated with distinct phenotypical and biological properties of papillary carcinomas and may participate in progression to poorly differentiated and anaplastic carcinomas... - Isozyme-specific abnormalities of PKC in thyroid cancer: evidence for post-transcriptional changes in PKC epsilonJeffrey A Knauf
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
J Clin Endocrinol Metab 87:2150-9. 2002..These data indicate that post-transcriptional changes in PKCepsilon are highly prevalent in thyroid tumors and may play a significant role in their development... - Inhibitors of Raf kinase activity block growth of thyroid cancer cells with RET/PTC or BRAF mutations in vitro and in vivoBin Ouyang
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0547, USA
Clin Cancer Res 12:1785-93. 2006.... - Microsomal prostaglandin E2 synthase-1 is induced by conditional expression of RET/PTC in thyroid PCCL3 cells through the activation of the MEK-ERK pathwayEfisio Puxeddu
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
J Biol Chem 278:52131-8. 2003..As enzymes involved in prostanoid biosynthesis can be targeted with pharmacological inhibitors, these findings may have therapeutic implications... - Conditional expression of RET/PTC induces a weak oncogenic drive in thyroid PCCL3 cells and inhibits thyrotropin action at multiple levelsJianwei Wang
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Ohio 45267-0547, USA
Mol Endocrinol 17:1425-36. 2003.... - High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinomaEdna T Kimura
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
Cancer Res 63:1454-7. 2003..Because these signaling proteins function along the same pathway in thyroid cells, this represents a unique paradigm of human tumorigenesis through mutation of three signaling effectors lying in tandem... - Oncogenic RAS induces accelerated transition through G2/M and promotes defects in the G2 DNA damage and mitotic spindle checkpointsJeffrey A Knauf
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, OH 45267, USA
J Biol Chem 281:3800-9. 2006..We propose that oncogenic RAS activation may predispose cells to genomic instability through both MAPK-dependent and independent pathways that affect critical checkpoints in G(2)/M... - RET/PTC-induced cell growth is mediated in part by epidermal growth factor receptor (EGFR) activation: evidence for molecular and functional interactions between RET and EGFRMichelle Croyle
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
Cancer Res 68:4183-91. 2008..These data indicate that EGFR contributes to RET kinase activation, signaling, and growth stimulation and may therefore be an attractive therapeutic target in RET-induced neoplasms... - The RET kinase inhibitor NVP-AST487 blocks growth and calcitonin gene expression through distinct mechanisms in medullary thyroid cancer cellsNagako Akeno Stuart
Division of Endocrinology and Metabolism, University of Cincinnati, Cincinnati, Ohio, USA
Cancer Res 67:6956-64. 2007..The role of traditional tumor biomarkers may need to be reassessed as targeted therapies designed against oncoproteins with key roles in pathogenesis are implemented... - Mechanisms of aneuploidy in thyroid cancer cell lines and tissues: evidence for mitotic checkpoint dysfunction without mutations in BUB1 and BUBR1Bin Ouyang
Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0547, USA
Clin Endocrinol (Oxf) 56:341-50. 2002..Moreover, mutations of BUB1 or BUBR1 are infrequent in follicular neoplasms, and do not account for aneuploidy in thyroid cancer... - BRAFV600E mutation is associated with preferential sensitivity to mitogen-activated protein kinase kinase inhibition in thyroid cancer cell linesRebecca Leboeuf
Department of Medicine and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
J Clin Endocrinol Metab 93:2194-201. 2008..Although the signal output common to these oncoproteins is ERK, a recent report showed that only BRAF mutations consistently predicted responsiveness to MAPK kinase (MEK) inhibitors...