David Gutmann

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. pmc Novel BRAF Alteration in a Sporadic Pilocytic Astrocytoma
    Sonika Dahiya
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    Case Report Med 2012:418672. 2012
  2. pmc F11R is a novel monocyte prognostic biomarker for malignant glioma
    Winnie W Pong
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, United States of America
    PLoS ONE 8:e77571. 2013
  3. pmc Somatic neurofibromatosis type 1 (NF1) inactivation characterizes NF1-associated pilocytic astrocytoma
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Genome Res 23:431-9. 2013
  4. pmc Optimizing biologically targeted clinical trials for neurofibromatosis
    David H Gutmann
    Washington University School of Medicine, Department of Neurology and Washington University Neurofibromatosis Center, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Expert Opin Investig Drugs 22:443-62. 2013
  5. pmc Neurofibromatosis type 1: modeling CNS dysfunction
    David H Gutmann
    Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 32:14087-93. 2012
  6. pmc Identification of transcriptional regulatory networks specific to pilocytic astrocytoma
    Hrishikesh Deshmukh
    Department of Pathology and Immunology, Washington University School of Medicine, 660, S, Euclid Ave, St, Louis, MO 63110, USA
    BMC Med Genomics 4:57. 2011
  7. ncbi request reprint Mouse Models of Human Cancers Consortium Workshop on Nervous System Tumors
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 66:10-3. 2006
  8. pmc Harnessing preclinical mouse models to inform human clinical cancer trials
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 116:847-52. 2006
  9. ncbi request reprint Gliomas presenting after age 10 in individuals with neurofibromatosis type 1 (NF1)
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 59:759-61. 2002
  10. ncbi request reprint Neurofibromin in the brain
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, and The Neurofibromatosis Program, St Louis Children s Hospital, MO 63110, USA
    J Child Neurol 17:592-601; discussion 602-4, 646-51. 2002

Research Grants

Collaborators

Detail Information

Publications102 found, 100 shown here

  1. pmc Novel BRAF Alteration in a Sporadic Pilocytic Astrocytoma
    Sonika Dahiya
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    Case Report Med 2012:418672. 2012
    ....
  2. pmc F11R is a novel monocyte prognostic biomarker for malignant glioma
    Winnie W Pong
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, United States of America
    PLoS ONE 8:e77571. 2013
    ..In this study, we leveraged multiple RNA analysis platforms to identify new monocyte markers relevant to GBM patient outcome...
  3. pmc Somatic neurofibromatosis type 1 (NF1) inactivation characterizes NF1-associated pilocytic astrocytoma
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Genome Res 23:431-9. 2013
    ..Importantly, we identified no additional recurrent pathogenic somatic mutations, supporting a model in which neuroglial progenitor cell NF1 loss is likely sufficient for PA formation in cooperation with a proper stromal environment...
  4. pmc Optimizing biologically targeted clinical trials for neurofibromatosis
    David H Gutmann
    Washington University School of Medicine, Department of Neurology and Washington University Neurofibromatosis Center, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Expert Opin Investig Drugs 22:443-62. 2013
    ..In this review, the authors discuss how the establishment of the Neurofibromatosis Clinical Trials Consortium (NFCTC) has positively impacted on the design and execution of treatment studies for individuals with NF1 and NF2...
  5. pmc Neurofibromatosis type 1: modeling CNS dysfunction
    David H Gutmann
    Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 32:14087-93. 2012
    ....
  6. pmc Identification of transcriptional regulatory networks specific to pilocytic astrocytoma
    Hrishikesh Deshmukh
    Department of Pathology and Immunology, Washington University School of Medicine, 660, S, Euclid Ave, St, Louis, MO 63110, USA
    BMC Med Genomics 4:57. 2011
    ....
  7. ncbi request reprint Mouse Models of Human Cancers Consortium Workshop on Nervous System Tumors
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 66:10-3. 2006
    ....
  8. pmc Harnessing preclinical mouse models to inform human clinical cancer trials
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 116:847-52. 2006
    ....
  9. ncbi request reprint Gliomas presenting after age 10 in individuals with neurofibromatosis type 1 (NF1)
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 59:759-61. 2002
    ..They also summarize the clinical data on 17 adolescents or adults with NF1 and symptomatic gliomas. The findings suggest that individuals with NF1 are at increased risk of developing gliomas throughout their lives...
  10. ncbi request reprint Neurofibromin in the brain
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, and The Neurofibromatosis Program, St Louis Children s Hospital, MO 63110, USA
    J Child Neurol 17:592-601; discussion 602-4, 646-51. 2002
    ..With continued advances in our basic understanding of NF1 function, future targeted therapies for neurofibromatosis 1-associated central nervous system abnormalities can be developed...
  11. ncbi request reprint Molecular analysis of astrocytomas presenting after age 10 in individuals with NF1
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 61:1397-400. 2003
    ..Although brain tumors are less common in teenagers and adults with NF1, recent studies have suggested that patients with NF1 are at a significantly increased risk of developing astrocytomas...
  12. ncbi request reprint Mlh1 deficiency accelerates myeloid leukemogenesis in neurofibromatosis 1 (Nf1) heterozygous mice
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Oncogene 22:4581-5. 2003
    ..These results suggest that MMR deficiency can accelerate myeloid leukemogenesis in Nf1+/- mice, presumably by inactivating Nf1 gene expression...
  13. ncbi request reprint The diagnostic evaluation and multidisciplinary management of neurofibromatosis 1 and neurofibromatosis 2
    D H Gutmann
    Washington University, St Louis, MO 63110, USA
    JAMA 278:51-7. 1997
    ....
  14. pmc Mouse models of neurofibromatosis 1 and 2
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 S Euclid Avenue, St Louis, MO 63110, USA
    Neoplasia 4:279-90. 2002
    ..Recent progress employing novel mouse targeting strategies has begun to illuminate the roles of the NF1 and NF2 gene products in the molecular pathogenesis of NF-associated tumors...
  15. ncbi request reprint Comparative gene expression profile analysis of neurofibromatosis 1-associated and sporadic pilocytic astrocytomas
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 62:2085-91. 2002
    ..We conclude that PAs are genetically unique gliomas with gene expression profiles that resemble those of fetal astrocytes and, to a lesser extent, oligodendroglial precursors...
  16. ncbi request reprint Defects in neurofibromatosis 2 protein function can arise at multiple levels
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 7:335-45. 1998
    ..Based on these findings, we propose a model for merlin growth suppression that provides a framework for analyzing NF2 patient mutations and merlin function...
  17. ncbi request reprint Increased expression of the NF2 tumor suppressor gene product, merlin, impairs cell motility, adhesionand spreading
    D H Gutmann
    The Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 8:267-75. 1999
    ..These data indicate that merlin may function to maintain normal cytoskeletal organization, and suggest that merlin's influence on cell growth depends on specific cytoskeletal rearrangements...
  18. ncbi request reprint Neurofibromatosis 2 tumor suppressor protein, merlin, forms two functionally important intramolecular associations
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, USA
    J Neurosci Res 58:706-16. 1999
    ..Lastly, we identify NF2 patient mutations that dramatically reduce each of these interactions in vitro. Based on these findings, we propose a model for merlin folding critical to its ability to function as a tumor suppressor protein...
  19. ncbi request reprint Expression of the tuberous sclerosis complex gene products, hamartin and tuberin, in central nervous system tissues
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 S Euclid Avenue, St Louis, MO 63110, USA
    Acta Neuropathol 99:223-30. 2000
    ..Unlike tuberin, loss of hamartin expression was not observed in sporadic astrocytomas. These results suggest that tuberin and hamartin may differentially contribute to the CNS pathology in TSC...
  20. ncbi request reprint Mouse models of human cancer consortium symposium on nervous system tumors
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 63:3001-4. 2003
    ..In this review, we discuss the current status of mouse modeling of human nervous system cancers with a specific focus on unresolved scientific questions pertaining to the molecular genetics and cellular biology of these tumors...
  21. ncbi request reprint Loss of DAL-1, a protein 4.1-related tumor suppressor, is an important early event in the pathogenesis of meningiomas
    D H Gutmann
    Departments of Neurology and Neuropathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 9:1495-500. 2000
    ....
  22. ncbi request reprint Loss of neurofibromatosis 1 (NF1) gene expression in NF1-associated pilocytic astrocytomas
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Neuropathol Appl Neurobiol 26:361-7. 2000
    ..These results demonstrate that, in contrast to sporadic astrocytomas, loss of NF1 expression is an important primary genetic event in the pathogenesis of NF1-associated pilocytic astrocytomas...
  23. ncbi request reprint The neurofibromatoses: when less is more
    D H Gutmann
    Department of Neurology, Center for the Study of Nervous System Injury and Neurofibromatosis Program, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 10:747-55. 2001
    ..Significant progress in our understanding of the genetics and biology of NF1 and NF2 has elucidated the roles of these genes in tumor initiation and progression...
  24. ncbi request reprint The NF2 interactor, hepatocyte growth factor-regulated tyrosine kinase substrate (HRS), associates with merlin in the "open" conformation and suppresses cell growth and motility
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 10:825-34. 2001
    ..These results suggest the possibility that merlin and HRS may regulate cell growth in schwannoma cells through interacting pathways...
  25. ncbi request reprint Mouse glioma gene expression profiling identifies novel human glioma-associated genes
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 51:393-405. 2002
    ..The use of this transgenic mouse model to identify novel genetic changes that might underlie the pathogenesis of human high-grade astrocytomas provides a unique opportunity to discover future targets for brain tumor therapy...
  26. ncbi request reprint Functional analysis of neurofibromatosis 2 (NF2) missense mutations
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 10:1519-29. 2001
    ..These results suggest that the key functional domains of merlin lie within the highly conserved FERM domain and the unique C-terminus of the protein...
  27. ncbi request reprint Heterozygosity for the neurofibromatosis 1 (NF1) tumor suppressor results in abnormalities in cell attachment, spreading and motility in astrocytes
    D H Gutmann
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 10:3009-16. 2001
    ..These results support the emerging notion that tumor suppressor gene heterozygosity results in abnormalities in cell function that may contribute to the pathogenesis of non-tumor phenotypes in NF1...
  28. ncbi request reprint Recent advances in neurofibromatosis type 1
    Deepa Arun
    Department of Neurology, Washington University School of Medicine and St Louis Children s Hospital, St Louis, Missouri, USA
    Curr Opin Neurol 17:101-5. 2004
    ..The purpose of this review is to highlight recent advances in defining the molecular etiology of nervous system tumors and learning disabilities...
  29. ncbi request reprint Glioma formation in neurofibromatosis 1 reflects preferential activation of K-RAS in astrocytes
    Biplab Dasgupta
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cancer Res 65:236-45. 2005
    ....
  30. ncbi request reprint Developmental origin of subependymal giant cell astrocytoma in tuberous sclerosis complex
    Kevin C Ess
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 64:1446-9. 2005
    ..These results suggest that both tubers and SEGAs result from related defects in progenitor cell differentiation during brain development...
  31. ncbi request reprint Cerebrospinal fluid proteomic analysis reveals dysregulation of methionine aminopeptidase-2 expression in human and mouse neurofibromatosis 1-associated glioma
    Biplab Dasgupta
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 65:9843-50. 2005
    ..These observations suggest that MetAP2 is regulated by neurofibromin, and that MetAP2 inhibitors could be potentially employed to treat NF1-associated tumor proliferation...
  32. ncbi request reprint Proteomic analysis reveals hyperactivation of the mammalian target of rapamycin pathway in neurofibromatosis 1-associated human and mouse brain tumors
    Biplab Dasgupta
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, USA
    Cancer Res 65:2755-60. 2005
    ..These results suggest that mTOR pathway inhibition may represent a logical and tractable biologically based therapy for brain tumors in NF1...
  33. ncbi request reprint Optic nerve glioma in mice requires astrocyte Nf1 gene inactivation and Nf1 brain heterozygosity
    M Livia Bajenaru
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 63:8573-7. 2003
    ..This mouse model demonstrates that Nf1+/- cells contribute to the pathogenesis of gliomas in NF1 and provides a tool for the preclinical evaluation of potential therapeutic interventions for these tumors...
  34. ncbi request reprint Identification of a third Protein 4.1 tumor suppressor, Protein 4.1R, in meningioma pathogenesis
    Victoria A Robb
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurobiol Dis 13:191-202. 2003
    ..1B interactors including CD44 and betaII-spectrin. Collectively, these results suggest that Protein 4.1R functions as an important tumor suppressor in the molecular pathogenesis of meningioma...
  35. pmc Abnormal glutamate homeostasis and impaired synaptic plasticity and learning in a mouse model of tuberous sclerosis complex
    Ling Hui Zeng
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurobiol Dis 28:184-96. 2007
    ..These results suggest that abnormal glutamate homeostasis predisposes to excitotoxic cell death, impaired synaptic plasticity and learning deficits in Tsc1 GFAP CKO mice...
  36. pmc The natural history and treatment of epilepsy in a murine model of tuberous sclerosis
    Ebru Erbayat-Altay
    Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, U S A
    Epilepsia 48:1470-6. 2007
    ..Here, we characterize the natural history of the epilepsy in Tsc1(GFAP)CKO mice in more detail and report acute effects of treatment with standard antiepileptic drugs on seizures in these mice...
  37. pmc Microarray analyses reveal regional astrocyte heterogeneity with implications for neurofibromatosis type 1 (NF1)-regulated glial proliferation
    Tu Hsueh Yeh
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Glia 57:1239-49. 2009
    ..These findings provide molecular evidence for CNS astroglial cell heterogeneity, and suggest that differences in tumor suppressor gene expression might contribute to the regional localization of human brain tumors...
  38. pmc Astrocyte-specific inactivation of the neurofibromatosis 1 gene (NF1) is insufficient for astrocytoma formation
    Michaela Livia Bajenaru
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Mol Cell Biol 22:5100-13. 2002
    ..Collectively, our results suggest that loss of neurofibromin is not sufficient for astrocytoma formation in mice and that other genetic or environmental factors might influence NF1-associated glioma tumorigenesis...
  39. ncbi request reprint Heterozygosity for the tuberous sclerosis complex (TSC) gene products results in increased astrocyte numbers and decreased p27-Kip1 expression in TSC2+/- cells
    Erik J Uhlmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Oncogene 21:4050-9. 2002
    ..Collectively, these results suggest Tsc heterozygosity may provide a non-cell-autonomous growth advantage for astrocytes that may involve p27-Kip1 expression...
  40. ncbi request reprint Impaired glial glutamate transport in a mouse tuberous sclerosis epilepsy model
    Michael Wong
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    Ann Neurol 54:251-6. 2003
    ..These findings suggest that Tsc1 inactivation in astrocytes causes dysfunctional glutamate homeostasis, leading to seizure development in TSC...
  41. ncbi request reprint Neurofibromatosis 1
    Timothy M Lynch
    Department of Neurology, Washington University School of Medicine, Neurofibromatosis Program, St Louis Children s Hospital, St Louis, MO, USA
    Neurol Clin 20:841-65. 2002
    ..The NF1 tumor suppressor gene encodes a large protein (neurofibromin) that functions primarily as a RAS negative regulator, suggesting that targeted therapy for NF1 might derive from inhibition of the RAS signaling pathway...
  42. ncbi request reprint Spatiotemporal differences in CXCL12 expression and cyclic AMP underlie the unique pattern of optic glioma growth in neurofibromatosis type 1
    Nicole M Warrington
    Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 67:8588-95. 2007
    ..Collectively, these studies provide a mechanism for the unique pattern of NF1-associated glioma growth...
  43. pmc Immunohistochemical analysis supports a role for INI1/SMARCB1 in hereditary forms of schwannomas, but not in solitary, sporadic schwannomas
    Sushama Patil
    Division of Neuropathology, Washington University School of Medicine, St Louis, MO, USA
    Brain Pathol 18:517-9. 2008
    ..These results confirm a role for INI1/SMARCB1 in multiple schwannoma syndromes and suggest that a different pathway of tumorigenesis occurs in solitary, sporadic tumors...
  44. ncbi request reprint Natural history of neurofibromatosis 1-associated optic nerve glioma in mice
    M Livia Bajenaru
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Avenue, St Louis, MO 63110, USA
    Ann Neurol 57:119-27. 2005
    ..Last, we observed neovascularization and microglial cell infiltration by 3 weeks of age before overt neoplastic transformation, suggesting that these cellular changes participate in the early stages of tumor formation...
  45. ncbi request reprint Expression profiling in tuberous sclerosis complex (TSC) knockout mouse astrocytes to characterize human TSC brain pathology
    Kevin C Ess
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Glia 46:28-40. 2004
    ....
  46. pmc Molecular characterization of human meningiomas by gene expression profiling using high-density oligonucleotide microarrays
    Mark A Watson
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110 1093, USA
    Am J Pathol 161:665-72. 2002
    ..This report represents the first gene expression profiling studies of meningiomas and identifies some initial candidate genes that may provide further insights into the genetic basis for meningioma pathogenesis...
  47. ncbi request reprint Epileptogenesis and reduced inward rectifier potassium current in tuberous sclerosis complex-1-deficient astrocytes
    Laura A Jansen
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Epilepsia 46:1871-80. 2005
    ..Here, we investigated the hypothesis that impairment of potassium uptake through astrocyte inward rectifier potassium (Kir) channels may contribute to epileptogenesis in Tsc1(GFAP)CKO mice...
  48. pmc CXCL12 alone is insufficient for gliomagenesis in Nf1 mutant mice
    Tao Sun
    Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neuroimmunol 224:108-13. 2010
    ..Forced CXCL12 expression induced glioma at a low frequency. Further, treatment of Nf1 OPG mice with AMD3100, a CXCR4 antagonist, did not attenuate glioma growth. Thus, it appears, CXCL12 alone cannot promote gliomagenesis in NF1 mice...
  49. ncbi request reprint Differential involvement of protein 4.1 family members DAL-1 and NF2 in intracranial and intraspinal ependymomas
    Pratima K Singh
    Department of Pathology, Washington University School of Medicine, St Louis, Missouri 63110 10963, USA
    Mod Pathol 15:526-31. 2002
    ....
  50. ncbi request reprint Astrocyte-specific expression of CDK4 is not sufficient for tumor formation, but cooperates with p53 heterozygosity to provide a growth advantage for astrocytes in vivo
    Zhi Yong Huang
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, MO 63110, USA
    Oncogene 21:1325-34. 2002
    ..These results support the hypothesis that cdk4 overexpression alone is not sufficient for astrocytoma formation, but can provide a cooperative growth advantage in concert with genetic alterations in the p53 pathway...
  51. pmc Detection and measurement of neurofibromatosis-1 mouse optic glioma in vivo
    Debasish Banerjee
    Department of Radiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuroimage 35:1434-7. 2007
    ..In all cases, OPG presence or absence was correctly identified. In addition, the OPG size and shape were accurately measured in vivo, facilitating the use of this model for preclinical drug studies...
  52. ncbi request reprint Neurofibromatosis-1 (Nf1) heterozygous brain microglia elaborate paracrine factors that promote Nf1-deficient astrocyte and glioma growth
    Girish C Daginakatte
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 16:1098-112. 2007
    ....
  53. ncbi request reprint Astrocyte-specific TSC1 conditional knockout mice exhibit abnormal neuronal organization and seizures
    Erik J Uhlmann
    Department of Neurology, Washington University School of Medicine, St Louis Children s Hospital, St Louis, MO 63110, USA
    Ann Neurol 52:285-96. 2002
    ..Collectively, our results demonstrate that astrocyte-specific disruption of Tsc1 in mice provides a context-dependent growth advantage for astrocytes that results in abnormalities in neuronal organization and epilepsy...
  54. doi request reprint Preclinical cancer therapy in a mouse model of neurofibromatosis-1 optic glioma
    Balazs Hegedus
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cancer Res 68:1520-8. 2008
    ..Collectively, these findings suggest that this Nf1 optic glioma model may be a potential preclinical benchmark for identifying novel therapies that have a high likelihood of success in human clinical trials...
  55. doi request reprint Neurofibromatosis-1 regulates neuronal and glial cell differentiation from neuroglial progenitors in vivo by both cAMP- and Ras-dependent mechanisms
    Balazs Hegedus
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Stem Cell 1:443-57. 2007
    ..Together, these findings demonstrate that neurofibromin is required for normal glial and neuronal development involving separable Ras-dependent and cAMP-dependent mechanisms...
  56. pmc Neurofibromin regulates somatic growth through the hypothalamic-pituitary axis
    Balazs Hegedus
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 17:2956-66. 2008
    ..Collectively, these data demonstrate a critical role for neurofibromin in hypothalamic-pituitary axis function and provide further insights into the short stature and GH deficits seen in children with NF1...
  57. ncbi request reprint Cancer stem cells and brain tumors: uprooting the bad seeds
    Da Yong Lee
    Washington University School of Medicine, Department of Neurology, St Louis, MO 63110, USA
    Expert Rev Anticancer Ther 7:1581-90. 2007
    ..While these seminal studies clearly highlight the central role of stem cells in brain tumors, they also evoke important questions regarding the importance of these unique cells to tumor initiation, maintenance and treatment...
  58. pmc Using neurofibromatosis-1 to better understand and treat pediatric low-grade glioma
    David H Gutmann
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Child Neurol 23:1186-94. 2008
    ..In addition, genetically engineered mouse low-grade glioma models have recently been used in preclinical therapeutic studies to evaluate the efficacy of particular biologically based therapies and to define outcome measures...
  59. doi request reprint Gliomas in patients with neurofibromatosis type 1
    Anne C Albers
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Avenue, Campus Box 8111, St Louis, MO 63110, USA
    Expert Rev Neurother 9:535-9. 2009
    ..Adults, in contrast, are more likely to develop higher grade gliomas, which are treated in a similar fashion as their sporadic counterparts...
  60. pmc Optic nerve dysfunction in a mouse model of neurofibromatosis-1 optic glioma
    Balazs Hegedus
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neuropathol Exp Neurol 68:542-51. 2009
    ....
  61. ncbi request reprint RAS pathway activation and an oncogenic RAS mutation in sporadic pilocytic astrocytoma
    Mukesh K Sharma
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 65:1335-6. 2005
  62. ncbi request reprint Insights into meningioangiomatosis with and without meningioma: a clinicopathologic and genetic series of 24 cases with review of the literature
    Arie Perry
    Division of Neuropathology, Washington University, St Louis, MO 63110 1093, USA
    Brain Pathol 15:55-65. 2005
    ..In contrast, most perivascular spindled cells of pure MA are genetically and immunohistochemically similar to non-neoplastic meningothelial cells, consistent with current histogenetic theories...
  63. ncbi request reprint Loss of tumor suppressor in lung cancer-1 (TSLC1) expression in meningioma correlates with increased malignancy grade and reduced patient survival
    Ezequiel I Surace
    partment of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neuropathol Exp Neurol 63:1015-27. 2004
    ..Moreover, TSLC1 loss was associated with decreased patient survival, within the overall group, and in the atypical meningiomas. Collectively, these results suggest that TSLC1 plays an important role in meningioma pathogenesis...
  64. ncbi request reprint Molecular pathogenesis of meningiomas
    Arie Perry
    Division of Neuropathology, Washington University School of Medicine, St Louis, MO 63110 1093, USA
    J Neurooncol 70:183-202. 2004
    ....
  65. ncbi request reprint Loss of tuberous sclerosis complex 1 (Tsc1) expression results in increased Rheb/S6K pathway signaling important for astrocyte cell size regulation
    Erik J Uhlmann
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Glia 47:180-8. 2004
    ..Collectively, these observations suggest that TSC inactivation in astrocytes results in defective cell size regulation associated with dysregulated Rheb/mTOR/S6K pathway activity...
  66. ncbi request reprint Alterations of protein 4.1 family members in ependymomas: a study of 84 cases
    Veena Rajaram
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110 1093, USA
    Mod Pathol 18:991-7. 2005
    ..009). We conclude that alterations of Protein 4.1 family members are common in ependymal tumors and that specific alterations are associated with distinct clinicopathologic subsets...
  67. ncbi request reprint Gene expression profiling reveals unique molecular subtypes of Neurofibromatosis Type I-associated and sporadic malignant peripheral nerve sheath tumors
    Mark A Watson
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA
    Brain Pathol 14:297-303. 2004
    ..We conclude that distinct molecular classes of MPNST exist and that the ability to stratify these tumors based on unique and biologically relevant gene expression profiles may be important for future targeted therapeutics...
  68. pmc Defective cAMP generation underlies the sensitivity of CNS neurons to neurofibromatosis-1 heterozygosity
    Jacquelyn A Brown
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 30:5579-89. 2010
    ....
  69. ncbi request reprint The neurofibromatosis 1 gene product neurofibromin regulates pituitary adenylate cyclase-activating polypeptide-mediated signaling in astrocytes
    Biplab Dasgupta
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 23:8949-54. 2003
    ..These results demonstrate that neurofibromin positively influences cAMP generation and activation of cAMP growth regulatory targets in astrocytes and expands the role of the NF1 gene in astrocyte growth regulation...
  70. ncbi request reprint Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma
    Eriks A Lusis
    Division of Neuropathology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 65:7121-6. 2005
    ....
  71. ncbi request reprint Meningothelial hyperplasia: a detailed clinicopathologic, immunohistochemical and genetic study of 11 cases
    Arie Perry
    Division of Neuropathology, Washington University School of Medicine, Campus Box 8118, 660 South Euclid Ave, St Louis, MO 63110, USA
    Brain Pathol 15:109-15. 2005
    ..It may be preneoplastic in some, though further studies are needed to test this hypothesis...
  72. ncbi request reprint Role of the Rap1 GTPase in astrocyte growth regulation
    Anthony J Apicelli
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Glia 42:225-34. 2003
    ..Collectively, these results argue that the tumor suppressor properties of tuberin are unlikely to be related to Rap1 inactivation and that Rap1 inhibits mitogenic Ras pathway signaling in astrocytes...
  73. pmc Rapamycin prevents epilepsy in a mouse model of tuberous sclerosis complex
    Ling Hui Zeng
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 63:444-53. 2008
    ..Here, we tested whether rapamycin could prevent or reverse epilepsy, as well as other cellular and molecular brain abnormalities in Tsc1(GFAP)CKO mice...
  74. ncbi request reprint Neurofibromatosis 1: closing the GAP between mice and men
    Biplab Dasgupta
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Curr Opin Genet Dev 13:20-7. 2003
    ..Lastly, Nf1 knockout mouse studies have also demonstrated important roles for cooperating genetic changes that accelerate tumorigenesis as well as modifier genes that impact on cancer susceptibility...
  75. doi request reprint The neurofibromatosis type 1 tumor suppressor controls cell growth by regulating signal transducer and activator of transcription-3 activity in vitro and in vivo
    Sutapa Banerjee
    Department of Neurology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 70:1356-66. 2010
    ....
  76. ncbi request reprint Functional analysis of the relationship between the neurofibromatosis 2 tumor suppressor and its binding partner, hepatocyte growth factor-regulated tyrosine kinase substrate
    Chun Xiao Sun
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 11:3167-78. 2002
    ..These results suggest that merlin growth suppression requires HRS expression and that the binding of merlin to HRS may facilitate its ability to function as a tumor suppressor...
  77. ncbi request reprint Effect of merlin phosphorylation on neurofibromatosis 2 (NF2) gene function
    Ezequiel I Surace
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 S Euclid Avenue, St Louis, MO 63110, USA
    Oncogene 23:580-7. 2004
    ....
  78. pmc The neurofibromatosis 2 protein, merlin, regulates glial cell growth in an ErbB2- and Src-dependent manner
    S Sean Houshmandi
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Mol Cell Biol 29:1472-86. 2009
    ..Lastly, we show that merlin competes with Src for direct binding to ErbB2 and present a novel molecular mechanism for merlin regulation of ErbB2-dependent Src signaling and growth control...
  79. ncbi request reprint Increased c-Jun-NH2-kinase signaling in neurofibromatosis-1 heterozygous microglia drives microglia activation and promotes optic glioma proliferation
    Girish C Daginakatte
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 68:10358-66. 2008
    ....
  80. ncbi request reprint Neurofibromatosis type 1 - a model for nervous system tumour formation?
    Joshua B Rubin
    Department of Pediatrics, Washington University School of Medicine and St Louis Children s Hospital, St Louis, Missouri 63110, USA
    Nat Rev Cancer 5:557-64. 2005
    ....
  81. ncbi request reprint Meningioma: an update
    Eriks Lusis
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Curr Opin Neurol 17:687-92. 2004
    ..Recent clinical and molecular research has shed new light on the biology of meningiomas--a common but understudied CNS neoplasm. This review will focus on recent advances and their significance for future research and treatment...
  82. ncbi request reprint Protein 4.1 tumor suppressors: getting a FERM grip on growth regulation
    Chun Xiao Sun
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Cell Sci 115:3991-4000. 2002
    ..On the basis of insights derived from studying the NF2 tumor suppressor, we propose a model for merlin growth regulation in which CD44 links growth signals from plasma membrane to the nucleus by interacting with ERM proteins and merlin...
  83. pmc Interpreting mammalian target of rapamycin and cell growth inhibition in a genetically engineered mouse model of Nf1-deficient astrocytes
    Sutapa Banerjee
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Mol Cancer Ther 10:279-91. 2011
    ..These new findings argue for the identification of more accurate biomarkers for rapamycin treatment response and provide reference preclinical data for comparing human rapamycin levels with target effects in the brain...
  84. ncbi request reprint Expression and function of somatostatin receptors in peripheral nerve sheath tumors
    Christian Mawrin
    Department of Neuropathology, Otto von Guericke University, Magdeburg, Germany
    J Neuropathol Exp Neurol 64:1080-8. 2005
    ..Furthermore, our findings suggest a potential clinical role for somatostatin receptor agonists in tumor imaging and/or treatment of schwannomas and MPNSTs...
  85. ncbi request reprint Neurofibromatosis 2 (NF2) tumor suppressor schwannomin and its interacting protein HRS regulate STAT signaling
    Daniel R Scoles
    Cedars Sinai Medical Center, School of Medicine, University of California at Los Angeles, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA
    Hum Mol Genet 11:3179-89. 2002
    ..These data are consistent with the hypothesis that schwannomin requires HRS interaction to be fully functionally active and to inhibit STAT activation...
  86. ncbi request reprint Neurofibromatosis 2
    Michael E Baser
    Curr Opin Neurol 16:27-33. 2003
    ..Recent clinical and molecular research on neurofibromatosis 2 (NF2) is reviewed, and the implications for clinical practice and research are discussed...
  87. pmc T-cadherin-mediated cell growth regulation involves G2 phase arrest and requires p21(CIP1/WAF1) expression
    Zhi Yong Huang
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Mol Cell Biol 23:566-78. 2003
    ..Collectively, these observations suggest a novel mechanism of growth regulation for T-cadherin involving p21(CIP1/WAF1) expression and G2 arrest...
  88. ncbi request reprint Oligodendrogliomas result from the expression of an activated mutant epidermal growth factor receptor in a RAS transgenic mouse astrocytoma model
    Hao Ding
    Samuel Lunenfeld Research Institute, Mount Sinai Hospital, USA
    Cancer Res 63:1106-13. 2003
    ....
  89. pmc Nf2 gene inactivation in arachnoidal cells is rate-limiting for meningioma development in the mouse
    Michel Kalamarides
    INSERM U434, Fondation Jean Dausset Centre d Etude du Polymorphisme Humain, 75010 Paris, France
    Genes Dev 16:1060-5. 2002
    ..This first mouse model initiated with a genetic lesion found in human meningiomas provides a powerful tool for investigating tumor progression and for the preclinical evaluation of therapeutic interventions...
  90. pmc The 4.1/ezrin/radixin/moesin domain of the DAL-1/Protein 4.1B tumour suppressor interacts with 14-3-3 proteins
    Tingxi Yu
    David and Doreen Hermelin Laboratory of Molecular Oncogenetics, Department of Neurosurgery and Hermelin Brain Tumor Center, Henry Ford Hospital, E and R Bldg Rm 3096, 2799 W Grand Blvd Detroit, MI 48202, U S A
    Biochem J 365:783-9. 2002
    ..1/ezrin/radixin/moesin domain. The identification of this novel DAL-1/Protein 4.1B-interacting protein represents the first step towards elucidating its potentially unique mechanism of action...
  91. pmc Loss of heterozygosity for the NF2 gene in retinal and optic nerve lesions of patients with neurofibromatosis 2
    Chi Chao Chan
    National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Pathol 198:14-20. 2002
    ..Merlin was not expressed in the retina, optic nerve, or iris lesions. These results suggest that inactivation of the NF2 gene is associated with the formation of a variety of retinal and optic nerve lesions in NF2 patients...
  92. pmc Gliomas in neurofibromatosis type 1: a clinicopathologic study of 100 patients
    Fausto J Rodriguez
    Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    J Neuropathol Exp Neurol 67:240-9. 2008
    ..Classic PA and LGSI are the most common, and most have favorable prognoses. By contrast, DAs are more aggressive, similar to those that arise sporadically...
  93. ncbi request reprint Large-scale molecular comparison of human schwann cells to malignant peripheral nerve sheath tumor cell lines and tissues
    Shyra J Miller
    Division of Experimental Hematology, Cincinnati Children s Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA
    Cancer Res 66:2584-91. 2006
    ....
  94. ncbi request reprint Pten loss causes hypertrophy and increased proliferation of astrocytes in vivo
    Melissa M Fraser
    Department of Developmental Neurobiology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Cancer Res 64:7773-9. 2004
    ..This study shows cell-type dependent effects of Pten loss in the adult brain, including increased astrocyte proliferation that may render astroglial cells susceptible to neoplastic transformation or malignant progression...
  95. ncbi request reprint Functional significance of S6K overexpression in meningioma progression
    Ezequiel I Surace
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 56:295-8. 2004
    ..Collectively, these results suggest that S6K is functionally important for meningioma progression and may represent a target for future meningioma therapy...
  96. ncbi request reprint Nucleophosmin mediates mammalian target of rapamycin-dependent actin cytoskeleton dynamics and proliferation in neurofibromin-deficient astrocytes
    Danielle K Sandsmark
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Cancer Res 67:4790-9. 2007
    ....
  97. pmc Merlin is a potent inhibitor of glioma growth
    Ying Ka Ingar Lau
    Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA
    Cancer Res 68:5733-42. 2008
    ..Collectively, our results show that merlin is a potent inhibitor of high-grade human glioma...
  98. ncbi request reprint Diethylstilbestrol effects and lymphomagenesis in Mlh1-deficient mice
    Omar Kabbarah
    Division of Biology and Biomedical Sciences, Washington University School of Medicine, St Louis, MO, USA
    Int J Cancer 115:666-9. 2005
    ..Comparison of DES-treated and untreated Mlh1-/- animals suggests the combination of Mlh1 deficiency and DES exposure accelerates lymphomagenesis...
  99. pmc Pathological and molecular progression of astrocytomas in a GFAP:12 V-Ha-Ras mouse astrocytoma model
    Patrick Shannon
    Department of Neuropathology, The University of Toronto, Toronto, Ontario, Canada, M5T 2S8
    Am J Pathol 167:859-67. 2005
    ..Of interest, many of these acquired alterations occur in human astrocytomas, further validating GFAP-RAS as a useful model for studying astrocytoma development and progression...
  100. ncbi request reprint Mice with GFAP-targeted loss of neurofibromin demonstrate increased axonal MET expression with aging
    Weiping Su
    Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 158th Avenue, Beaverton, OR 97006, USA
    Glia 55:723-33. 2007
    ..Collectively, these data suggest that loss of Nf1 in either astrocytes or GFAP(+) neural progenitor cells results in increased axonal MET expression, which may contribute to the CNS abnormalities in children and adults with NF1...
  101. ncbi request reprint High-grade glioma formation results from postnatal pten loss or mutant epidermal growth factor receptor expression in a transgenic mouse glioma model
    Qingxia Wei
    Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, University Health Network, Toronto, Ontario, Canada
    Cancer Res 66:7429-37. 2006
    ..This novel preclinical model of high-grade glioma will be useful in evaluating brain tumor therapies targeted to the pathways specifically dysregulated by EGFR expression or Pten loss...

Research Grants27

  1. PROTEIN 4.1 TUMOR SUPPRESSORS IN MENINGIOMA PATHOGENESIS
    David Gutmann; Fiscal Year: 2002
    ..and (3) analyzing the ability of DAL-1 to impair cell growth and motility. These studies are collectively designed to define the role of this novel family of growth regulators in meningioma tumorigenesis and progression. ..
  2. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 2003
    ..Our ability to design rational therapies for schwannomas and meningiomas is dependent on an improved understanding of the mechanisms by which loss of merlin expression and function promotes tumor formation. ..
  3. PRECLINICAL MODELS FOR HUMAN ASTROCYTOMAS
    David Gutmann; Fiscal Year: 2003
    ..abstract_text> ..
  4. PROTEIN 4.1 TUMOR SUPPRESSORS IN MENINGIOMA PATHOGENESIS
    David Gutmann; Fiscal Year: 2003
    ..and (3) analyzing the ability of DAL-1 to impair cell growth and motility. These studies are collectively designed to define the role of this novel family of growth regulators in meningioma tumorigenesis and progression. ..
  5. PRECLINICAL MODELS FOR HUMAN ASTROCYTOMAS
    David Gutmann; Fiscal Year: 2002
    ..abstract_text> ..
  6. Neurofibromatosis Foundation International Consortium
    David Gutmann; Fiscal Year: 2003
    ..abstract_text> ..
  7. PRECLINICAL MODELS FOR HUMAN ASTROCYTOMAS
    David Gutmann; Fiscal Year: 2004
    ..abstract_text> ..
  8. Identification and Preclinical Evaluation of New Brain Tumor Therapies
    David Gutmann; Fiscal Year: 2007
    ....
  9. Molecular Determinants of Neural Stem Cell Function
    David Gutmann; Fiscal Year: 2007
    ....
  10. PRECLINICAL MODELS FOR HUMAN ASTROCYTOMAS
    David Gutmann; Fiscal Year: 2002
    ..abstract_text> ..
  11. NEUROFIBROMIN AS A NEGATIVE REGULATOR FOR ASTROCYTES
    David Gutmann; Fiscal Year: 2002
    ....
  12. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 2002
    ..Our ability to design rational therapies for schwannomas and meningiomas is dependent on an improved understanding of the mechanisms by which loss of merlin expression and function promotes tumor formation. ..
  13. NEUROFIBROMIN AS A NEGATIVE REGULATOR FOR ASTROCYTES
    David Gutmann; Fiscal Year: 1999
    ....
  14. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 1999
    ....
  15. NEUROFIBROMIN AS A NEGATIVE REGULATOR FOR ASTROCYTES
    David Gutmann; Fiscal Year: 2000
    ....
  16. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 2000
    ..Our ability to design rational therapies for schwannomas and meningiomas is dependent on an improved understanding of the mechanisms by which loss of merlin expression and function promotes tumor formation. ..
  17. PRECLINICAL MODELS FOR HUMAN ASTROCYTOMAS
    David Gutmann; Fiscal Year: 2001
    ..abstract_text> ..
  18. PROTEIN 4.1 TUMOR SUPPRESSORS IN MENINGIOMA PATHOGENESIS
    David Gutmann; Fiscal Year: 2001
    ..and (3) analyzing the ability of DAL-1 to impair cell growth and motility. These studies are collectively designed to define the role of this novel family of growth regulators in meningioma tumorigenesis and progression. ..
  19. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 2000
    ..Our ability to design rational therapies for schwannomas and meningiomas is dependent on an improved understanding of the mechanisms by which loss of merlin expression and function promotes tumor formation. ..
  20. NEUROFIBROMIN AS A NEGATIVE REGULATOR FOR ASTROCYTES
    David Gutmann; Fiscal Year: 2000
    ....
  21. FUNCTIONAL ANALYSIS OF NF2 GENE MUTATIONS
    David Gutmann; Fiscal Year: 2001
    ..Our ability to design rational therapies for schwannomas and meningiomas is dependent on an improved understanding of the mechanisms by which loss of merlin expression and function promotes tumor formation. ..
  22. NEUROFIBROMIN AS A NEGATIVE REGULATOR FOR ASTROCYTES
    David Gutmann; Fiscal Year: 2001
    ....
  23. NEUROFIBROMIN REGULATION OF NEURAL STEM CELL FUNCTION IN VITRO AND IN VIVO
    David H Gutmann; Fiscal Year: 2010
    ..These studies may lead to the development of therapies that specifically target the critical growth and fate control pathways that cause brain tumors in children. ..