CHARLES GEORGE EBERHART

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Arsenic trioxide inhibits Hedgehog, Notch and stem cell properties in glioblastoma neurospheres
    Dacheng Ding
    Departments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Acta Neuropathol Commun 2:31. 2014
  2. pmc LIN28A facilitates the transformation of human neural stem cells and promotes glioblastoma tumorigenesis through a pro-invasive genetic program
    Xing gang Mao
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 4:1050-64. 2013
  3. pmc Effects of Zeng Sheng Ping/ACAPHA on malignant brain tumor growth and Notch signaling
    Kah Jing Lim
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Ave, Ross Building 558, Baltimore, MD 21205, USA
    Anticancer Res 32:2689-96. 2012
  4. ncbi request reprint Three down and one to go: modeling medulloblastoma subgroups
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 21:137-8. 2012
  5. pmc c-MYC expression sensitizes medulloblastoma cells to radio- and chemotherapy and has no impact on response in medulloblastoma patients
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 11:74. 2011
  6. pmc Anti-proliferative activity of the quassinoid NBT-272 in childhood medulloblastoma cells
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 7:19. 2007
  7. pmc Regulation of sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 and their epigenetic status in medulloblastoma and astrocytoma
    Mehdi H Shahi
    Brain Tumor Biology Unit CIFA, University of Navarra School of Sciences, Pamplona, Spain
    BMC Cancer 10:614. 2010
  8. pmc Identification of astrocytoma associated genes including cell surface markers
    Kathy Boon
    Department of Neurosurgery, Mason F, Lord Bldg, Center Tower, 5th Floor, 5200 Eastern Avenue, Baltimore MD 21224, USA
    BMC Cancer 4:39. 2004
  9. pmc RNA interference-mediated c-MYC inhibition prevents cell growth and decreases sensitivity to radio- and chemotherapy in childhood medulloblastoma cells
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 9:10. 2009
  10. ncbi request reprint Comparative genomic hybridization detects an increased number of chromosomal alterations in large cell/anaplastic medulloblastomas
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Brain Pathol 12:36-44. 2002

Research Grants

  1. Myc Signaling in Medulloblastomas
    Charles Eberhart; Fiscal Year: 2006
  2. Notch signaling in brain tumors
    Charles Eberhart; Fiscal Year: 2007
  3. Notch signaling in brain tumors
    Charles Eberhart; Fiscal Year: 2009
  4. Notch signaling in brain tumors
    CHARLES GEORGE EBERHART; Fiscal Year: 2010

Detail Information

Publications74

  1. pmc Arsenic trioxide inhibits Hedgehog, Notch and stem cell properties in glioblastoma neurospheres
    Dacheng Ding
    Departments of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Acta Neuropathol Commun 2:31. 2014
    ..Since arsenic trioxide has been shown to inhibit both Notch and Hedgehog in some solid tumors, we examined its effects on these pathways and on stem cell phenotype in glioblastoma...
  2. pmc LIN28A facilitates the transformation of human neural stem cells and promotes glioblastoma tumorigenesis through a pro-invasive genetic program
    Xing gang Mao
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Oncotarget 4:1050-64. 2013
    ..Taken together, these data suggest a role for LIN28A in high grade gliomas and illustrate an HMGA2-associated, pro-invasive program that can be activated in GBM by LIN28A-mediated suppression of let-7 microRNAs. ..
  3. pmc Effects of Zeng Sheng Ping/ACAPHA on malignant brain tumor growth and Notch signaling
    Kah Jing Lim
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Ave, Ross Building 558, Baltimore, MD 21205, USA
    Anticancer Res 32:2689-96. 2012
    ..It has been shown to inhibit Notch2 expression in a murine lung cancer model, leading us to investigate its therapeutic potential in Notch-dependent brain tumors...
  4. ncbi request reprint Three down and one to go: modeling medulloblastoma subgroups
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 21:137-8. 2012
    ..These tumors have a cellular origin, microscopic appearance, and molecular profile distinct from those of three other major subgroups. Thus, the models fill a significant clinical need...
  5. pmc c-MYC expression sensitizes medulloblastoma cells to radio- and chemotherapy and has no impact on response in medulloblastoma patients
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 11:74. 2011
    ..To study whether and how c-MYC expression determines response to radio- and chemotherapy in childhood medulloblastoma (MB)...
  6. pmc Anti-proliferative activity of the quassinoid NBT-272 in childhood medulloblastoma cells
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 7:19. 2007
    ..In neuroblastoma--an embryonal tumor with biological similarities to MB--the quassinoid NBT-272 has been demonstrated to inhibit cellular proliferation and to down-regulate c-MYC protein expression...
  7. pmc Regulation of sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 and their epigenetic status in medulloblastoma and astrocytoma
    Mehdi H Shahi
    Brain Tumor Biology Unit CIFA, University of Navarra School of Sciences, Pamplona, Spain
    BMC Cancer 10:614. 2010
    ..2 and PAX6 in medulloblastoma and astrocytic tumors...
  8. pmc Identification of astrocytoma associated genes including cell surface markers
    Kathy Boon
    Department of Neurosurgery, Mason F, Lord Bldg, Center Tower, 5th Floor, 5200 Eastern Avenue, Baltimore MD 21224, USA
    BMC Cancer 4:39. 2004
    ..SAGE tag counts can be easily added to public expression databases and quickly disseminated to research efforts worldwide...
  9. pmc RNA interference-mediated c-MYC inhibition prevents cell growth and decreases sensitivity to radio- and chemotherapy in childhood medulloblastoma cells
    Andre O Von Bueren
    Neuro Oncology Program, University Children s Hospital, Zurich, Switzerland
    BMC Cancer 9:10. 2009
    ..Deregulation of c-MYC is evident in numerous human cancers. In MB, over-expression of c-MYC has been shown to cause anaplasia and correlate with unfavorable prognosis...
  10. ncbi request reprint Comparative genomic hybridization detects an increased number of chromosomal alterations in large cell/anaplastic medulloblastomas
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Brain Pathol 12:36-44. 2002
    ..8/case) compared to non-anaplastic ones (3.3/case). These findings support an association between myc oncogene amplification, 17p loss, and large cell/anaplastic histology...
  11. ncbi request reprint Even cancers want commitment: lineage identity and medulloblastoma formation
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cancer Cell 14:105-7. 2008
    ..These data suggest that some stem cell-derived tumors must commit to a specific lineage in order to grow...
  12. ncbi request reprint In search of the medulloblast: neural stem cells and embryonal brain tumors
    Charles G Eberhart
    Division of Neuropathology, Department of Pathology, Ross Building 558, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Neurosurg Clin N Am 18:59-69, viii-ix. 2007
    ..In support of this concept, inhibition of a third pathway important in stem cells, Notch, seems to deplete the stem-like tumor fraction and block formation of xenografts...
  13. ncbi request reprint Brief report: S6 ribosomal protein phosphorylation in autistic frontal cortex and cerebellum: a tissue array analysis
    Charles G Eberhart
    Johns Hopkins University, Baltimore, MD, USA
    J Autism Dev Disord 36:1131-5. 2006
    ..However, no consistent alterations in S6 phosphorylation were detected in autistic tissues compared to controls in the brain regions analyzed...
  14. ncbi request reprint Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasia
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Neuropathol Exp Neurol 63:441-9. 2004
    ..The association we describe between c-myc expression, tumor anaplasia, and worse clinical outcomes provides further evidence for the importance of this oncogene in medulloblastoma pathobiology...
  15. pmc Molecular diagnostics in embryonal brain tumors
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Brain Pathol 21:96-104. 2011
    ..41-42, which appears to define a unique PNET subtype associated with prominent true rosettes, young age and very poor outcomes...
  16. ncbi request reprint Histopathologic grading of medulloblastomas: a Pediatric Oncology Group study
    Charles G Eberhart
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Cancer 94:552-60. 2002
    ....
  17. pmc Expression of stabilized beta-catenin in differentiated neurons of transgenic mice does not result in tumor formation
    John E Kratz
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    BMC Cancer 2:33. 2002
    ..To determine whether increased Wnt signaling in the adult CNS is sufficient to induce tumor formation, we created transgenic mice expressing either wild-type or activated beta-catenin in the brain...
  18. pmc Medulloblastoma in mice lacking p53 and PARP: all roads lead to Gli
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Am J Pathol 162:7-10. 2003
  19. ncbi request reprint Medulloblastomas with systemic metastases: evaluation of tumor histopathology and clinical behavior in 23 patients
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Pediatr Hematol Oncol 25:198-203. 2003
    ..To review the clinical behavior and histopathologic features of medulloblastomas that metastasize outside the central nervous systems (CNS)...
  20. pmc Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus
    Charles G Eberhart
    Department of Pathology, Johns Hopkins University School of Medicine, Ross Bldg 558, 720 Rutland Ave, Baltimore, MD 21205, USA
    BMC Cancer 5:19. 2005
    ..We correlated p53 protein expression with pathological subtype and clinical outcome in 75 embryonal brain tumors. The presence of JC virus, which results in p53 protein accumulation, was also examined...
  21. ncbi request reprint Anaplasia and grading in medulloblastomas
    Charles G Eberhart
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Brain Pathol 13:376-85. 2003
    ..Correlation of these histological changes with the accumulation of genetic events suggests a model for the histological and molecular progression of medulloblastoma...
  22. pmc Cooperation between the Hic1 and Ptch1 tumor suppressors in medulloblastoma
    Kimberly J Briggs
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Genes Dev 22:770-85. 2008
    ....
  23. pmc hTERT gene amplification and increased mRNA expression in central nervous system embryonal tumors
    Xing Fan
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Am J Pathol 162:1763-9. 2003
    ..Our data indicate that hTERT gene amplification is relatively common in embryonal brain tumors, and that increased expression of hTERT mRNA may be associated with biologically aggressive tumor behavior...
  24. ncbi request reprint Notch1 and notch2 have opposite effects on embryonal brain tumor growth
    Xing Fan
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Res 64:7787-93. 2004
    ..Our data indicate that Notch1 and Notch2 can have opposite effects on the growth of a single tumor type, and show that Notch2 can be overexpressed after gene amplification in human tumors...
  25. ncbi request reprint Medulloblastoma growth inhibition by hedgehog pathway blockade
    David M Berman
    Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Science 297:1559-61. 2002
    ....
  26. pmc Coexpression of neuronatin splice forms promotes medulloblastoma growth
    I Mei Siu
    Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231 USA
    Neuro Oncol 10:716-24. 2008
    ..Our findings suggest that the frequently observed overexpression of both NNAT splice forms in MB enhances growth in this cancer...
  27. pmc DNER, an epigenetically modulated gene, regulates glioblastoma-derived neurosphere cell differentiation and tumor propagation
    Peng Sun
    Department of Neurology, The Johns Hopkins University School of Medicine and The Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, USA
    Stem Cells 27:1473-86. 2009
    ..Our findings are the first to implicate noncanonical Notch signaling in the regulation of neoplastic stem-like cells and suggest novel neoplastic stem cell targeting treatment strategies for GBM and potentially other solid malignancies...
  28. ncbi request reprint Genomic amplification of orthodenticle homologue 2 in medulloblastomas
    Kathy Boon
    Departments of Neurosurgery and Pathology, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, Baltimore, MD 21224, USA
    Cancer Res 65:703-7. 2005
    ..OTX2 functions to specify the fate of neuroectoderm in various regions of the developing brain. This developmental role is consistent with the evidence suggesting that OTX2 is a medulloblastoma oncogene...
  29. ncbi request reprint Notch pathway inhibition depletes stem-like cells and blocks engraftment in embryonal brain tumors
    Xing Fan
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Cancer Res 66:7445-52. 2006
    ..Stem-like cells in brain tumors thus seem to be selectively vulnerable to agents inhibiting the Notch pathway...
  30. ncbi request reprint The neurobiology of autism
    Carlos A Pardo
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287 USA
    Brain Pathol 17:434-47. 2007
    ..We also discuss evidence implicating oxidative stress, neuroglial activation and neuroimmunity in autism...
  31. pmc Hypoxia increases the expression of stem-cell markers and promotes clonogenicity in glioblastoma neurospheres
    Eli E Bar
    Johns Hopkins University School of Medicine, Department of Pathology, Baltimore, MD 21287, USA
    Am J Pathol 177:1491-502. 2010
    ....
  32. ncbi request reprint Frequent gains at chromosome 7q34 involving BRAF in pilocytic astrocytoma
    Eli E Bar
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neuropathol Exp Neurol 67:878-87. 2008
    ..These data indicate that focal gains at chromosome 7q34 and increased BRAF-MEK-ERK signaling are common findings in sporadic pilocytic astrocytomas...
  33. doi request reprint Iris cross-sectional area decreases with pupil dilation and its dynamic behavior is a risk factor in angle closure
    Harry A Quigley
    Wilmer Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Glaucoma 18:173-9. 2009
    ..To estimate the change in iris cross-sectional (CS) area with pupil dilation using anterior segment optical coherence tomography comparing eyes with angle closure (AC) to open angle glaucoma (OAG)...
  34. ncbi request reprint Epilepsy and temporal lobe injury after skull base proton beam therapy
    Ricardo Horacio Roda
    Department of Neurology, Room 5050, Outpatient Center, Johns Hopkins University School of Medicine, 601 North Caroline Street, Baltimore, Maryland 21287, USA
    J Clin Neurosci 16:1220-1. 2009
    ..We present three patients who developed temporal lobe injury and epilepsy after proton beam therapy to the skull base. This particular form of treatment-related toxicity should be considered when treating skull base tumors...
  35. doi request reprint Ultrasound features of orbital granular cell tumor
    Bernadete Ayres
    Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, MD 21287, USA
    Ophthal Plast Reconstr Surg 25:320-2. 2009
    ..The echographic characteristics correlated well with the morphologic surgical findings and the histologic architecture. This is the first report describing the echographic characteristics of orbital granular cell tumor...
  36. pmc Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model
    Jason T Yustein
    Departments of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 107:3534-9. 2010
    ..Furthermore, the expression of Jagged2 in P493-6 tumors often overlapped with regions of hypoxia. These observations suggest that Notch signaling downstream of Myc enables cells to adapt in the tumor hypoxic microenvironment...
  37. ncbi request reprint Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilities
    Tong Li
    Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 27:10849-59. 2007
    ..Our findings suggest that moderate inhibition of gamma-secretase represents an attractive anti-amyloid therapy for Alzheimer's disease...
  38. ncbi request reprint Epidermal growth factor receptor and notch pathways participate in the tumor suppressor function of gamma-secretase
    Tong Li
    Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
    J Biol Chem 282:32264-73. 2007
    ....
  39. pmc Cyclopamine-mediated hedgehog pathway inhibition depletes stem-like cancer cells in glioblastoma
    Eli E Bar
    Johns Hopkins University School of Medicine, Department of Pathology, 720 Rutland Avenue, Ross Building 558, Baltimore, Maryland 21205, USA
    Stem Cells 25:2524-33. 2007
    ..Disclosure of potential conflicts of interest is found at the end of this article...
  40. ncbi request reprint Lhermitte-Duclos disease: a report of 31 cases with immunohistochemical analysis of the PTEN/AKT/mTOR pathway
    Ty W Abel
    Department of Pathology, Division of Neuropathology, Johns Hopkins University, Baltimore, Maryland 21287, USA
    J Neuropathol Exp Neurol 64:341-9. 2005
    ..These data support recommendations for genetic testing and screening for CD in patients with LDD and suggest a novel therapy for LDD through pharmacologic inhibition of mTOR...
  41. ncbi request reprint c-myc overexpression causes anaplasia in medulloblastoma
    Duncan Stearns
    Department of Neuropathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Cancer Res 66:673-81. 2006
    ..Because anaplastic changes are often observed in recurrent medulloblastoma, we propose that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms...
  42. doi request reprint Medulloblastoma stem cells
    Xing Fan
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Clin Oncol 26:2821-7. 2008
    ....
  43. pmc Hedgehog signaling promotes medulloblastoma survival via Bc/II
    Eli E Bar
    Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Ave, Ross Building 558, Baltimore, MD 21205, USA
    Am J Pathol 170:347-55. 2007
    ..These data demonstrate that BclII is an important mediator of Hh activity in medulloblastoma and suggest new strategies for combined chemotherapeutic regimens...
  44. pmc NKX3.1 as a marker of prostatic origin in metastatic tumors
    Bora Gurel
    Department of Pathology, The Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA
    Am J Surg Pathol 34:1097-105. 2010
    ..1, along with other prostate-restricted markers, may prove to be a valuable adjunct to definitively determine prostatic origin in poorly differentiated metastatic carcinomas...
  45. doi request reprint Establishment of a human glioblastoma stemlike brainstem rodent tumor model
    I Mei Siu
    Departments of Neurosurgery, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA
    J Neurosurg Pediatr 6:92-7. 2010
    ..It is therefore essential to develop a reliable animal model to screen new therapeutic agents for the treatment of this type of tumor...
  46. doi request reprint Spectrum of pilomyxoid astrocytomas: intermediate pilomyxoid tumors
    Michael W Johnson
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Am J Surg Pathol 34:1783-91. 2010
    ..Further follow-up is needed to more accurately determine the prognosis of intermediate tumors...
  47. pmc Ghrelin and the growth hormone secretagogue receptor constitute a novel autocrine pathway in astrocytoma motility
    Vishwa Deep Dixit
    Laboratory of Immunology, NIA Intramural Research Program, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 281:16681-90. 2006
    ..Together, these findings suggest a novel role for the ghrelin/GHS-R axis in astrocytoma cell migration and invasiveness of cancers of central nervous system origin...
  48. ncbi request reprint Expression of p75NTR in fetal brain and medulloblastomas: evidence of a precursor cell marker and its persistence in neoplasia
    Michael Barnes
    Department of Pathology, UCSF Medical Center, San Francisco, CA, USA
    J Neurooncol 92:193-201. 2009
    ..The persistence of p75NTR in a small group of medulloblastomas raises the possibility that in such tumors, the receptor could be a potential therapeutic target...
  49. ncbi request reprint Comparison of medulloblastoma and normal neural transcriptomes identifies a restricted set of activated genes
    Kathy Boon
    Department of Pathology, Duke University Medical Center, Box 3156, Durham NC 27710, USA
    Oncogene 22:7687-94. 2003
    ..The genes highly expressed in the medulloblastoma include PRAME, a cancer-testis antigen and potential targets for immunotherapy...
  50. pmc Just say no to ATOH: how HIC1 methylation might predispose medulloblastoma to lineage addiction
    Kimberly J Briggs
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland, USA
    Cancer Res 68:8654-6. 2008
    ..Because demethylating agents can induce reexpression of silenced tumor suppressors, restoring HIC1 function may present an attractive therapeutic avenue in medulloblastoma by exploiting an apparent addiction to ATOH1...
  51. ncbi request reprint PIK3CA gene mutations in pediatric and adult glioblastoma multiforme
    Gary L Gallia
    Department of Neurosurgery, Johns Hopkins University School of Medicine, 1550 Orleans Street, CRB II, Room 257, Baltimore, MD 21231, USA
    Mol Cancer Res 4:709-14. 2006
    ..Moreover, this is the first study showing PIK3CA mutations in pediatric glioblastomas, thus providing a molecular target in this important pediatric malignancy...
  52. pmc Ligand-dependent Notch signaling is involved in tumor initiation and tumor maintenance in pancreatic cancer
    Michael E Mullendore
    Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Clin Cancer Res 15:2291-301. 2009
    ..Aberrant activation of the Notch signaling pathway is commonly observed in human pancreatic cancer, although the mechanism(s) for this activation has not been elucidated...
  53. ncbi request reprint beta2-adrenergic receptor activation and genetic polymorphisms in autism: data from dizygotic twins
    Susan L Connors
    Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, Baltimore, MD 21205, USA
    J Child Neurol 20:876-84. 2005
    ....
  54. pmc Tissue inhibitor of matrix metalloproteinase-3 levels in the extracellular matrix of lung, kidney, and eye increase with age
    Anne M Macgregor
    Department of Pathology AMM, CGE, MF, Jl, MKH and Department of Ophthalmology CGE, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Histochem Cytochem 57:207-13. 2009
    ..These findings may help to explain the late onset of the TIMP-3-associated ocular diseases Sorsby fundus dystrophy and age-related macular degeneration and suggest a similar phenomenon could be at work in other age-related conditions...
  55. ncbi request reprint Prevention of experimental cerebral vasospasm by intracranial delivery of a nitric oxide donor from a controlled-release polymer: toxicity and efficacy studies in rabbits and rats
    Patrik Gabikian
    Department of Neurological Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Stroke 33:2681-6. 2002
    ..We investigated the toxicity and efficacy of a locally delivered NO donor from a controlled-release polymer in preventing experimental cerebral vasospasm in rats and rabbits, respectively...
  56. ncbi request reprint Notch3 gene amplification in ovarian cancer
    Joon T Park
    Department of Gynecology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Res 66:6312-8. 2006
    ..These results indicate that Notch3 is required for proliferation and survival of Notch3-amplified tumors and inactivation of Notch3 can be a potential therapeutic approach for ovarian carcinomas...
  57. ncbi request reprint Rhabdoid meningioma: cytopathologic findings in cerebrospinal fluid
    Anil V Parwani
    Department of Pathology, The Johns Hopkins Hospital, Baltimore, Maryland 21287, USA
    Diagn Cytopathol 29:297-9. 2003
    ....
  58. ncbi request reprint Epigenetic silencing of multiple genes in primary CNS lymphoma
    Linda C Chu
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Int J Cancer 119:2487-91. 2006
    ..Our study provides insight into the epigenetic alterations in PCNSL and provides potential biomarkers of disease...
  59. pmc Ocular MECP2 protein expression in patients with and without Rett syndrome
    Deepali Jain
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Pediatr Neurol 43:35-40. 2010
    ..The findings suggest that the normally limited expression of MECP2 in visual pathway neurons may underlie the intact vision observed in Rett syndrome...
  60. doi request reprint Intraorbital meningiomas: a pathologic review using current World Health Organization criteria
    Deepali Jain
    Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Arch Pathol Lab Med 134:766-70. 2010
    ..Meningiomas represent approximately 4% of all intraorbital tumors and can arise from the optic nerve or extend into the orbit from adjacent structures...
  61. ncbi request reprint The application of surgical cordectomy in the management of an intramedullary-extramedullary atypical meningioma: case report and literature review
    Shaan M Raza
    Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, MD, 21287, USA
    J Spinal Disord Tech 18:449-54. 2005
    ..The presentation of an intramedullary atypical World Health Organization grade II meningioma is rare. The authors report a case of a transformed intramedullary-extramedullary atypical meningioma treated with cordectomy...
  62. ncbi request reprint Presenilin couples the paired phosphorylation of beta-catenin independent of axin: implications for beta-catenin activation in tumorigenesis
    David E Kang
    Department of Neurosciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Cell 110:751-62. 2002
    ..These findings highlight an aspect of beta-catenin regulation outside of the canonical Wnt-regulated pathway and a function of presenilin separate from intramembrane proteolysis...
  63. ncbi request reprint Functional and molecular interactions between the HGF/c-Met pathway and c-Myc in large-cell medulloblastoma
    Yunqing Li
    Department of Neurology, University of Virginia, Charlottesville, VA 22908, USA
    Lab Invest 88:98-111. 2008
    ..The findings provide a potential explanation for the high frequency of c-Myc overexpression in medulloblastoma and suggest a cooperative role for c-Met and c-Myc in large-cell anaplastic medulloblastoma formation...
  64. pmc Abnormal expression of REST/NRSF and Myc in neural stem/progenitor cells causes cerebellar tumors by blocking neuronal differentiation
    Xiaohua Su
    Department of Molecular Genetics, University of Texas M D Anderson Cancer Center, 1515 Holcombe Boulevard, Mail 1006, Room S13 8136C, Houston, TX 77030, USA
    Mol Cell Biol 26:1666-78. 2006
    ..Furthermore, these results suggest that such a mechanism plays a role in the formation of human medulloblastoma...
  65. ncbi request reprint Biologic risk stratification of medulloblastoma: the real time is now
    Paul Graham Fisher
    J Clin Oncol 22:971-4. 2004
  66. ncbi request reprint Gain of 1q is a potential univariate negative prognostic marker for survival in medulloblastoma
    Ken C Lo
    Department of Cancer Genetics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, New York 14263, USA
    Clin Cancer Res 13:7022-8. 2007
    ..In this context, current strategies for risk assessment, which are based on clinical parameters, remain unsatisfactory...
  67. ncbi request reprint Expression of Notch-1 and its ligands, Delta-like-1 and Jagged-1, is critical for glioma cell survival and proliferation
    Benjamin W Purow
    Neuro Oncology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Cancer Res 65:2353-63. 2005
    ..Notch-1 and its ligands may present novel therapeutic targets in the treatment of glioma...
  68. ncbi request reprint Genome wide copy number abnormalities in pediatric medulloblastomas as assessed by array comparative genome hybridization
    Ken C Lo
    Department of Cancer Genetics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Brain Pathol 17:282-96. 2007
    ..Using high density oligonucleotide expression arrays, candidate genes were identified within these consistently involved regions in a subset of the tumors...
  69. ncbi request reprint Isochromosome 17q is a negative prognostic factor in poor-risk childhood medulloblastoma patients
    Edward Pan
    University of California San Francisco, San Francisco, California, USA
    Clin Cancer Res 11:4733-40. 2005
    ..We hypothesized that genetic copy number aberrations (CNA) predict prognosis and would provide improved criteria for predicting outcome...
  70. pmc The tumor suppressors Ink4c and p53 collaborate independently with Patched to suppress medulloblastoma formation
    Tamar Uziel
    Department of Tumor Cell Biology and Genetics, Memphis, Tennessee 38105, USA
    Genes Dev 19:2656-67. 2005
    ..Methylation of INK4C (CDKN2C) was observed in four of 23 human MBs, and p18(INK4C) protein expression was extinguished in 14 of 73 cases. Hence, p18(INK4C) loss may contribute to MB formation in children...
  71. doi request reprint The Smo/Smo model: hedgehog-induced medulloblastoma with 90% incidence and leptomeningeal spread
    Beryl A Hatton
    Clinical Research Division, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, Washington, USA
    Cancer Res 68:1768-76. 2008
    ..The Smo/Smo model is the first mouse medulloblastoma model to show leptomeningeal spread. The adherence to human pathology, high incidence, and early onset of tumors thus make Smo/Smo mice an efficient model for preclinical studies...
  72. doi request reprint Epithelial downgrowth following Descemet's-stripping automated endothelial keratoplasty
    B Michael Walker
    Arch Ophthalmol 126:278-80. 2008
  73. ncbi request reprint Ectopic recurrence of craniopharyngioma after an interhemispheric transcallosal approach: case report
    Jeannette M Liu
    Division of Neurosurgery, The University of Texas at Galveston, Galveston, Texas, USA
    Neurosurgery 50:639-44; discussion 644-5. 2002
    ..Ectopic recurrence of a craniopharyngioma is a rare postoperative complication. We present a case of a craniopharyngioma that ectopically recurred along the tract of a previous surgical route...

Research Grants5

  1. Myc Signaling in Medulloblastomas
    Charles Eberhart; Fiscal Year: 2006
    ..Finally, in Specific Aim 4 we propose developing a novel medulloblastoma transgenic model by overexpressing c-Myc in the cerebellum of transgenic mice. ..
  2. Notch signaling in brain tumors
    Charles Eberhart; Fiscal Year: 2007
    ..Finally, it is not known if persistent activation of Nbtch2 is sufficient to initiate the formation of medulloblastoma. In Aim IV, we will introduce activated Notch2 into cerebellar precursor cells and assess its transforming capacity. ..
  3. Notch signaling in brain tumors
    Charles Eberhart; Fiscal Year: 2009
    ..In Aim IV, we will introduce activated Notch2 into cerebellar precursor cells and assess its transforming capacity. ..
  4. Notch signaling in brain tumors
    CHARLES GEORGE EBERHART; Fiscal Year: 2010
    ..In Aim IV, we will introduce activated Notch2 into cerebellar precursor cells and assess its transforming capacity. ..