Molecular targets for emerging anti-tumor therapies for neurofibromatosis type 1.
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R. Gibbs | M. Tainsky | J. Kraniak | J. Reiners | R. Mattingly | R. Borch | J. Dilworth | Jonathan W. Wojtkowiak
[1] W. R. Bishop,et al. Thematic review series: Lipid Posttranslational Modifications. Farnesyl transferase inhibitors Published, JLR Papers in Press, November 8, 2005. , 2006, Journal of Lipid Research.
[2] M. Tainsky,et al. The Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Kinase Inhibitor PD184352 (CI-1040) Selectively Induces Apoptosis in Malignant Schwannoma Cell Lines , 2006, Journal of Pharmacology and Experimental Therapeutics.
[3] Huan Yang,et al. Targeting the phosphatidylinositol-3 kinase/Akt pathway for the treatment of cancer. , 2005, Current opinion in investigational drugs.
[4] Alcino J. Silva,et al. The HMG-CoA Reductase Inhibitor Lovastatin Reverses the Learning and Attention Deficits in a Mouse Model of Neurofibromatosis Type 1 , 2005, Current Biology.
[5] G. Fritz. HMG-CoA reductase inhibitors (statins) as anticancer drugs (review). , 2005, International journal of oncology.
[6] R. Deschenes,et al. DHHC9 and GCP16 Constitute a Human Protein Fatty Acyltransferase with Specificity for H- and N-Ras* , 2005, Journal of Biological Chemistry.
[7] J. Schellens,et al. Development of farnesyl transferase inhibitors: a review. , 2005, The oncologist.
[8] W. Grizzle,et al. Activation of the neuregulin-1/ErbB signaling pathway promotes the proliferation of neoplastic Schwann cells in human malignant peripheral nerve sheath tumors , 2005, Oncogene.
[9] J. Hancock,et al. Individual Palmitoyl Residues Serve Distinct Roles in H-Ras Trafficking, Microlocalization, and Signaling , 2005, Molecular and Cellular Biology.
[10] C. Johannessen,et al. The NF1 tumor suppressor critically regulates TSC2 and mTOR. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[11] L. Kluwe,et al. Malignant peripheral nerve sheath tumors (MPNST) in neurofibromatosis type 1 (NF1): diagnostic findings on magnetic resonance images and mutation analysis of the NF1 gene. , 2005, Anticancer research.
[12] M. Marra,et al. Isoprenylation of intracellular proteins as a new target for the therapy of human neoplasms: preclinical and clinical implications. , 2005, Current drug targets.
[13] S. Sebti. Protein farnesylation: implications for normal physiology, malignant transformation, and cancer therapy. , 2005, Cancer cell.
[14] D. Gutmann,et al. Neurofibromatosis 1: from lab bench to clinic. , 2005, Pediatric neurology.
[15] R. Lothe,et al. Expression Patterns of Cell Cycle Components in Sporadic and Neurofibromatosis Type 1-Related Malignant Peripheral Nerve Sheath Tumors , 2005, Journal of neuropathology and experimental neurology.
[16] S. Carroll,et al. Tumor Suppressor Mutations and Growth Factor Signaling in the Pathogenesis of NF1-Associated Peripheral Nerve Sheath Tumors: II. The Role of Dysregulated Growth Factor Signaling , 2005, Journal of neuropathology and experimental neurology.
[17] J. Declue,et al. Role for the epidermal growth factor receptor in neurofibromatosis-related peripheral nerve tumorigenesis. , 2005, Cancer cell.
[18] N. Hynes,et al. Amplification and differential expression of members of theerbB-gene family in human glioblastoma , 2005, Journal of Neuro-Oncology.
[19] D. Gutmann,et al. Glioma formation in neurofibromatosis 1 reflects preferential activation of K-RAS in astrocytes. , 2005, Cancer research.
[20] P. Casey,et al. Crystallographic analysis of CaaX prenyltransferases complexed with substrates defines rules of protein substrate selectivity. , 2004, Journal of molecular biology.
[21] F. Tamanoi,et al. A tagging-via-substrate technology for detection and proteomics of farnesylated proteins. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[22] J. Kyriakis,et al. A Novel Role for Mixed Lineage Kinase 3 (MLK3) in B-Raf Activation and Cell proliferation , 2004, Cell cycle.
[23] E. Pérez-Nadales,et al. The Ras/Raf/ERK signalling pathway drives Schwann cell dedifferentiation , 2004, The EMBO journal.
[24] W. R. Bishop,et al. Farnesyltransferase inhibitors as anticancer agents: critical crossroads. , 2004, Current opinion in drug discovery & development.
[25] J. Sebolt-Leopold. MEK inhibitors: a therapeutic approach to targeting the Ras-MAP kinase pathway in tumors. , 2004, Current pharmaceutical design.
[26] I. M. Bell. Inhibitors of farnesyltransferase: a rational approach to cancer chemotherapy? , 2004, Journal of medicinal chemistry.
[27] D. Gutmann,et al. Recent advances in neurofibromatosis type 1 , 2004, Current opinion in neurology.
[28] D. Spandau,et al. Loss of the nf1 tumor suppressor gene decreases fas antigen expression in myeloid cells. , 2004, The American journal of pathology.
[29] A. Cox,et al. Role of TC21/R-Ras2 in enhanced migration of neurofibromin-deficient Schwann cells , 2004, Oncogene.
[30] J. Baell,et al. The Tyr-Kinase Inhibitor AG879, that Blocks the ETK-PAK1 Interaction, Suppresses the RAS-induced PAK1 Activation and Malignant Transformation , 2004, Cancer biology & therapy.
[31] David A. Williams,et al. Neurofibromin-deficient Schwann cells secrete a potent migratory stimulus for Nf1+/– mast cells , 2003 .
[32] D. Viskochil. It takes two to tango: mast cell and Schwann cell interactions in neurofibromas. , 2003, The Journal of clinical investigation.
[33] R. Mattingly,et al. Cell surface receptors activate p21-activated kinase 1 via multiple Ras and PI3-kinase-dependent pathways. , 2003, Cellular signalling.
[34] M. Pierotti,et al. p15INK4b, p14ARF, and p16INK4a inactivation in sporadic and neurofibromatosis type 1-related malignant peripheral nerve sheath tumors. , 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.
[35] W. Su,et al. Malignant peripheral nerve sheath tumor cell invasion is facilitated by Src and aberrant CD44 expression , 2003, Glia.
[36] J. Eccleston,et al. The mechanism of Ras GTPase activation by neurofibromin. , 2003, Biochemistry.
[37] R. Deschenes,et al. Identification of a Ras Palmitoyltransferase in Saccharomyces cerevisiae * , 2002, The Journal of Biological Chemistry.
[38] Linyi Chen,et al. The yeast DHHC cysteine-rich domain protein Akr1p is a palmitoyl transferase , 2002, The Journal of cell biology.
[39] R. Gibbs,et al. Potent Suppression of Proliferation of A10 Vascular Smooth Muscle Cells by Combined Treatment with Lovastatin and 3-Allylfarnesol, an Inhibitor of Protein Farnesyltransferase , 2002, Journal of Pharmacology and Experimental Therapeutics.
[40] S. Velasco-Miguel,et al. Epidermal growth factor receptor signaling pathways are associated with tumorigenesis in the Nf1:p53 mouse tumor model. , 2002, Cancer research.
[41] R. Zimmerman,et al. Plexiform neurofibromas in NF1: toward biologic-based therapy. , 2002, Neurology.
[42] D. Burns,et al. Neurofibromas in NF1: Schwann Cell Origin and Role of Tumor Environment , 2002, Science.
[43] Yinghua Zhu,et al. Neurofibromin regulates G protein–stimulated adenylyl cyclase activity , 2002, Nature Neuroscience.
[44] J. R. Reeves,et al. Evaluating HER2 amplification and overexpression in breast cancer , 2001, The Journal of pathology.
[45] A. Adjei,et al. Ras signaling pathway proteins as therapeutic targets. , 2001, Current pharmaceutical design.
[46] R. Gibbs,et al. Synthesis and evaluation of GGPP geometric isomers: divergent substrate specificities of FTase and GGTase I. , 2001, Bioorganic & medicinal chemistry letters.
[47] L. Lim,et al. Signal therapy for RAS-induced cancers in combination of AG 879 and PP1, specific inhibitors for ErbB2 and Src family kinases, that block PAK activation. , 2001, Cancer journal.
[48] G. Bollag,et al. Neurofibromin GTPase-activating Protein-related Domains Restore Normal Growth in Nf1−/− Cells* , 2001, The Journal of Biological Chemistry.
[49] T. Roberts,et al. Schwann Cell Proliferative Responses to cAMP andNf1 Are Mediated by Cyclin D1 , 2001, The Journal of Neuroscience.
[50] D. Gutmann,et al. Loss of Neurofibromin Is Associated with Activation of RAS/MAPK and PI3‐K/AKT Signaling in a Neurofibromatosis 1 Astrocytoma , 2000, Journal of neuropathology and experimental neurology.
[51] L. Parada. Neurofibromatosis type 1. , 2000, Biochimica et biophysica acta.
[52] G. Benvenuto,et al. Epidermal growth factor receptor expression in neurofibromatosis type 1-related tumors and NF1 animal models. , 2000, The Journal of clinical investigation.
[53] David A. Williams,et al. Genetic and Biochemical Evidence That Haploinsufficiency of the Nf1 Tumor Suppressor Gene Modulates Melanocyte and Mast Cell Fates in Vivo , 2000, The Journal of experimental medicine.
[54] J. Downward,et al. Farnesylation of Ras is important for the interaction with phosphoinositide 3-kinase gamma. , 1999, European journal of biochemistry.
[55] T. Jacks,et al. In vitro and in vivo effects of a farnesyltransferase inhibitor on Nf1-deficient hematopoietic cells. , 1999, Blood.
[56] K. Shannon,et al. Hyperactive Ras as a therapeutic target in neurofibromatosis type 1. , 1999, American journal of medical genetics.
[57] A. Guha,et al. Neurofibromatosis type 1 peripheral nerve tumors: aberrant activation of the Ras pathway. , 1999, Surgical neurology.
[58] P. Casey,et al. Enzymology and biology of CaaX protein prenylation. , 1999, Recent progress in hormone research.
[59] J. Schlegel,et al. Expression of the ERBB2/neu and neurofibromatosis type 1 gene products in reactive and neoplastic schwann cell proliferation. , 1998, International journal of oncology.
[60] A. Wittinghofer,et al. Selective disactivation of neurofibromin GAP activity in neurofibromatosis type 1. , 1998, Human molecular genetics.
[61] J. Rutkowski,et al. A role for Pak protein kinases in Schwann cell transformation. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[62] N. Ratner,et al. Nf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferase , 1997, Molecular and cellular biology.
[63] B. Seizinger,et al. Farnesyltransferase inhibitors block the neurofibromatosis type I (NF1) malignant phenotype. , 1995, Cancer research.
[64] N. Kohl,et al. Farnesyltransferase inhibitors: Ras research yields a potential cancer therapeutic , 1994, Cell.
[65] S. Pulst,et al. Differential expression and tissue distribution of type I and type II neurofibromins during mouse fetal development. , 1994, Developmental biology.
[66] M. Boguski,et al. Neurofibromatosis type 1 gene product (neurofibromin) associates with microtubules , 1993, Somatic cell and molecular genetics.
[67] F. Collins,et al. Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients , 1992, Nature.
[68] D. Lowy,et al. Identification and characterization of the neurofibromatosis type 1 protein product. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[69] C. Marshall. The ras oncogenes , 1988, Journal of Cell Science.