Jeffrey A Knauf

Summary

Affiliation: University of Cincinnati
Country: USA

Publications

  1. ncbi request reprint Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation
    Jeffrey 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
  2. ncbi request reprint RET/PTC-induced dedifferentiation of thyroid cells is mediated through Y1062 signaling through SHC-RAS-MAP kinase
    Jeffrey A Knauf
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Oncogene 22:4406-12. 2003
  3. ncbi request reprint Acute expression of RET/PTC induces isozyme-specific activation and subsequent downregulation of PKCepsilon in PCCL3 thyroid cells
    Jeffrey 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
  4. ncbi request reprint 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 carcinogenesis
    Norisato Mitsutake
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Ohio 45267 0547, USA
    Endocrinology 147:1014-9. 2006
  5. pmc Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer
    Raffaele 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
  6. ncbi request reprint 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 remodeling
    Cleo 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
  7. ncbi request reprint Low prevalence of BRAF mutations in radiation-induced thyroid tumors in contrast to sporadic papillary carcinomas
    Marina 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
  8. ncbi request reprint BRAF kinase activation via chromosomal rearrangement in radiation-induced and sporadic thyroid cancer
    Raffaele Ciampi
    Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0529, USA
    Cell Cycle 4:547-8. 2005
  9. ncbi request reprint Conditional BRAFV600E expression induces DNA synthesis, apoptosis, dedifferentiation, and chromosomal instability in thyroid PCCL3 cells
    Norisato Mitsutake
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, OH 45267 0547, USA
    Cancer Res 65:2465-73. 2005
  10. ncbi request reprint BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas
    Marina N Nikiforova
    Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA
    J Clin Endocrinol Metab 88:5399-404. 2003

Collaborators

Detail Information

Publications20

  1. ncbi request reprint Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation
    Jeffrey 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...
  2. ncbi request reprint RET/PTC-induced dedifferentiation of thyroid cells is mediated through Y1062 signaling through SHC-RAS-MAP kinase
    Jeffrey 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...
  3. ncbi request reprint Acute expression of RET/PTC induces isozyme-specific activation and subsequent downregulation of PKCepsilon in PCCL3 thyroid cells
    Jeffrey 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
    ....
  4. ncbi request reprint 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 carcinogenesis
    Norisato 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...
  5. pmc Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer
    Raffaele 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
    ....
  6. ncbi request reprint 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 remodeling
    Cleo 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...
  7. ncbi request reprint Low prevalence of BRAF mutations in radiation-induced thyroid tumors in contrast to sporadic papillary carcinomas
    Marina 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...
  8. ncbi request reprint BRAF kinase activation via chromosomal rearrangement in radiation-induced and sporadic thyroid cancer
    Raffaele Ciampi
    Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0529, USA
    Cell Cycle 4:547-8. 2005
    ....
  9. ncbi request reprint Conditional BRAFV600E expression induces DNA synthesis, apoptosis, dedifferentiation, and chromosomal instability in thyroid PCCL3 cells
    Norisato 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...
  10. ncbi request reprint BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas
    Marina 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...
  11. ncbi request reprint Isozyme-specific abnormalities of PKC in thyroid cancer: evidence for post-transcriptional changes in PKC epsilon
    Jeffrey 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...
  12. ncbi request reprint Inhibitors of Raf kinase activity block growth of thyroid cancer cells with RET/PTC or BRAF mutations in vitro and in vivo
    Bin Ouyang
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0547, USA
    Clin Cancer Res 12:1785-93. 2006
    ..We postulated that compounds that inhibit a distal effector in the mitogen-activated protein kinase (MAPK) pathway would inhibit growth and tumorigenicity of human thyroid cancer cell lines with mutations of RET or BRAF...
  13. ncbi request reprint Microsomal prostaglandin E2 synthase-1 is induced by conditional expression of RET/PTC in thyroid PCCL3 cells through the activation of the MEK-ERK pathway
    Efisio 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...
  14. ncbi request reprint Conditional expression of RET/PTC induces a weak oncogenic drive in thyroid PCCL3 cells and inhibits thyrotropin action at multiple levels
    Jianwei Wang
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Ohio 45267 0547, USA
    Mol Endocrinol 17:1425-36. 2003
    ....
  15. ncbi request reprint High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma
    Edna 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...
  16. ncbi request reprint Oncogenic RAS induces accelerated transition through G2/M and promotes defects in the G2 DNA damage and mitotic spindle checkpoints
    Jeffrey 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...
  17. doi request reprint 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 EGFR
    Michelle 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...
  18. ncbi request reprint The RET kinase inhibitor NVP-AST487 blocks growth and calcitonin gene expression through distinct mechanisms in medullary thyroid cancer cells
    Nagako 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...
  19. ncbi request reprint Mechanisms of aneuploidy in thyroid cancer cell lines and tissues: evidence for mitotic checkpoint dysfunction without mutations in BUB1 and BUBR1
    Bin Ouyang
    Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 0547, USA
    Clin Endocrinol (Oxf) 56:341-50. 2002
    ..We examined the contribution of mitotic checkpoint dysfunction and mutations of BUB1 or BUBR1, components of the spindle assembly checkpoint pathway, to chromosomal instability in thyroid cancer...
  20. pmc BRAFV600E mutation is associated with preferential sensitivity to mitogen-activated protein kinase kinase inhibition in thyroid cancer cell lines
    Rebecca 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...