Research Topics
Genomes and Genes | CHARLES GEORGE EBERHARTSummaryAffiliation: Johns Hopkins University Country: USA Publications
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Publications
Effects of Zeng Sheng Ping/ACAPHA on malignant brain tumor growth and Notch signalingKah 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...- Three down and one to go: modeling medulloblastoma subgroupsCharles 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... 
c-MYC expression sensitizes medulloblastoma cells to radio- and chemotherapy and has no impact on response in medulloblastoma patientsAndre 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)...
Anti-proliferative activity of the quassinoid NBT-272 in childhood medulloblastoma cellsAndre 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...- Regulation of sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 and their epigenetic status in medulloblastoma and astrocytomaMehdi 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... - Identification of astrocytoma associated genes including cell surface markersKathy 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... - RNA interference-mediated c-MYC inhibition prevents cell growth and decreases sensitivity to radio- and chemotherapy in childhood medulloblastoma cellsAndre 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... - Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasiaCharles 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... - Brief report: S6 ribosomal protein phosphorylation in autistic frontal cortex and cerebellum: a tissue array analysisCharles 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... - Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virusCharles 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... - Comparative genomic hybridization detects an increased number of chromosomal alterations in large cell/anaplastic medulloblastomasCharles 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... - Anaplasia and grading in medulloblastomasCharles 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... - In search of the medulloblast: neural stem cells and embryonal brain tumorsCharles 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... - Medulloblastomas with systemic metastases: evaluation of tumor histopathology and clinical behavior in 23 patientsCharles 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)... - Medulloblastoma in mice lacking p53 and PARP: all roads lead to GliCharles G Eberhart
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Am J Pathol 162:7-10. 2003 - Expression of stabilized beta-catenin in differentiated neurons of transgenic mice does not result in tumor formationJohn 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... 
Molecular diagnostics in embryonal brain tumorsCharles 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...- Even cancers want commitment: lineage identity and medulloblastoma formationCharles 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... - Histopathologic grading of medulloblastomas: a Pediatric Oncology Group studyCharles G Eberhart
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Cancer 94:552-60. 2002.... - Cooperation between the Hic1 and Ptch1 tumor suppressors in medulloblastomaKimberly J Briggs
The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
Genes Dev 22:770-85. 2008.... - hTERT gene amplification and increased mRNA expression in central nervous system embryonal tumorsXing 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... - Notch1 and notch2 have opposite effects on embryonal brain tumor growthXing 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... - Medulloblastoma growth inhibition by hedgehog pathway blockadeDavid M Berman
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Science 297:1559-61. 2002.... - Coexpression of neuronatin splice forms promotes medulloblastoma growthI 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... - Notch pathway inhibition depletes stem-like cells and blocks engraftment in embryonal brain tumorsXing 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... - DNER, an epigenetically modulated gene, regulates glioblastoma-derived neurosphere cell differentiation and tumor propagationPeng 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... - Genomic amplification of orthodenticle homologue 2 in medulloblastomasKathy 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... - Epidermal growth factor receptor and notch pathways participate in the tumor suppressor function of gamma-secretaseTong Li
Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205, USA
J Biol Chem 282:32264-73. 2007.... - Cyclopamine-mediated hedgehog pathway inhibition depletes stem-like cancer cells in glioblastomaEli 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... - The neurobiology of autismCarlos 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... - Frequent gains at chromosome 7q34 involving BRAF in pilocytic astrocytomaEli 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... - Medulloblastoma stem cellsXing Fan
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
J Clin Oncol 26:2821-7. 2008.... - Lhermitte-Duclos disease: a report of 31 cases with immunohistochemical analysis of the PTEN/AKT/mTOR pathwayTy 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... - Hedgehog signaling promotes medulloblastoma survival via Bc/IIEli 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... - Moderate reduction of gamma-secretase attenuates amyloid burden and limits mechanism-based liabilitiesTong 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... - Ultrasound features of orbital granular cell tumorBernadete 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... - Epilepsy and temporal lobe injury after skull base proton beam therapyRicardo 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... - c-myc overexpression causes anaplasia in medulloblastomaDuncan 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... - Induction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell modelJason 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... - Iris cross-sectional area decreases with pupil dilation and its dynamic behavior is a risk factor in angle closureHarry 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)... - Hypoxia increases the expression of stem-cell markers and promotes clonogenicity in glioblastoma neurospheresEli E Bar
Johns Hopkins University School of Medicine, Department of Pathology, Baltimore, MD 21287, USA
Am J Pathol 177:1491-502. 2010.... - Expression of p75NTR in fetal brain and medulloblastomas: evidence of a precursor cell marker and its persistence in neoplasiaMichael 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... - Establishment of a human glioblastoma stemlike brainstem rodent tumor modelI 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... - NKX3.1 as a marker of prostatic origin in metastatic tumorsBora 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... - Spectrum of pilomyxoid astrocytomas: intermediate pilomyxoid tumorsMichael 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... - Comparison of medulloblastoma and normal neural transcriptomes identifies a restricted set of activated genesKathy 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... - Ghrelin and the growth hormone secretagogue receptor constitute a novel autocrine pathway in astrocytoma motilityVishwa 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... - Ligand-dependent Notch signaling is involved in tumor initiation and tumor maintenance in pancreatic cancerMichael 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... - beta2-adrenergic receptor activation and genetic polymorphisms in autism: data from dizygotic twinsSusan L Connors
Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, Baltimore, MD 21205, USA
J Child Neurol 20:876-84. 2005.... - PIK3CA gene mutations in pediatric and adult glioblastoma multiformeGary 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... - Just say no to ATOH: how HIC1 methylation might predispose medulloblastoma to lineage addictionKimberly 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... - Tissue inhibitor of matrix metalloproteinase-3 levels in the extracellular matrix of lung, kidney, and eye increase with ageAnne 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... - Ocular MECP2 protein expression in patients with and without Rett syndromeDeepali 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... - Notch3 gene amplification in ovarian cancerJoon 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... - Epigenetic silencing of multiple genes in primary CNS lymphomaLinda 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... - 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 ratsPatrik Gabikian
Department of Neurological Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Stroke 33:2681-6. 2002..2+/-6.4%; P=0.003). CONCLUSIONS: Local delivery of DETA/NO prevents vasospasm in the rabbit basilar artery. Local delivery of DETA/NO via polymers is a safe and effective strategy for preventing cerebral vasospasm after SAH in this model... - Rhabdoid meningioma: cytopathologic findings in cerebrospinal fluidAnil V Parwani
Department of Pathology, The Johns Hopkins Hospital, Baltimore, Maryland 21287, USA
Diagn Cytopathol 29:297-9. 2003.... - The application of surgical cordectomy in the management of an intramedullary-extramedullary atypical meningioma: case report and literature reviewShaan M Raza
Department of Neurosurgery, Johns Hopkins Hospital, Baltimore, MD, 21287, USA
J Spinal Disord Tech 18:449-54. 2005..CONCLUSIONS: This case highlights the viability of surgical cordectomy in the treatment of varying intramedullary processes under appropriate indications... - Intraorbital meningiomas: a pathologic review using current World Health Organization criteriaDeepali 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... - Presenilin couples the paired phosphorylation of beta-catenin independent of axin: implications for beta-catenin activation in tumorigenesisDavid 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... - Biologic risk stratification of medulloblastoma: the real time is nowPaul Graham Fisher
J Clin Oncol 22:971-4. 2004 - Expression of Notch-1 and its ligands, Delta-like-1 and Jagged-1, is critical for glioma cell survival and proliferationBenjamin 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... - Isochromosome 17q is a negative prognostic factor in poor-risk childhood medulloblastoma patientsEdward Pan
University of California San Francisco, San Francisco, California, USA
Clin Cancer Res 11:4733-40. 2005..i(17)(q10) was a significant independent negative prognostic factor. Infant medulloblastomas may be a distinct genetic subset from those of older patients... - The tumor suppressors Ink4c and p53 collaborate independently with Patched to suppress medulloblastoma formationTamar 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... - Abnormal expression of REST/NRSF and Myc in neural stem/progenitor cells causes cerebellar tumors by blocking neuronal differentiationXiaohua 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... - Genome wide copy number abnormalities in pediatric medulloblastomas as assessed by array comparative genome hybridizationKen 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... - Gain of 1q is a potential univariate negative prognostic marker for survival in medulloblastomaKen 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... - Functional and molecular interactions between the HGF/c-Met pathway and c-Myc in large-cell medulloblastomaYunqing 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... - The Smo/Smo model: hedgehog-induced medulloblastoma with 90% incidence and leptomeningeal spreadBeryl 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... - Epithelial downgrowth following Descemet's-stripping automated endothelial keratoplastyB Michael Walker
Arch Ophthalmol 126:278-80. 2008 - Ectopic recurrence of craniopharyngioma after an interhemispheric transcallosal approach: case reportJeannette M Liu
Division of Neurosurgery, The University of Texas at Galveston, Galveston, Texas, USA
Neurosurgery 50:639-44; discussion 644-5. 2002..Furthermore, it is recommended that, after primary craniopharyngioma resection, patients undergo long-term clinical and radiological follow-up monitoring for the rare development of an ectopically recurring tumor...
Research Grants
- Myc Signaling in MedulloblastomasCharles 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. ..
- Notch signaling in brain tumorsCharles 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. ..
- Notch signaling in brain tumorsCHARLES GEORGE EBERHART; Fiscal Year: 2010..In Aim IV, we will introduce activated Notch2 into cerebellar precursor cells and assess its transforming capacity. ..