Paul Mischel

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc mTOR signaling in glioblastoma: lessons learned from bench to bedside
    David Akhavan
    The David Geffen UCLA School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095 1732, USA
    Neuro Oncol 12:882-9. 2010
  2. pmc HOT Models in Flux: Mitochondrial Glucose Oxidation Fuels Glioblastoma Growth
    Paul S Mischel
    Departments of Pathology and Laboratory Medicine and Molecular and Medical Pharmacology, The David Geffen UCLA School of Medicine, Los Angeles, CA 90095, USA
    Cell Metab 15:789-90. 2012
  3. pmc Review: molecular pathology in adult high-grade gliomas: from molecular diagnostics to target therapies
    K Masui
    Department of Pathology and Laboratory Medicine, David Geffen University of California at Los Angeles School of Medicine, Los Angeles, California, USA
    Neuropathol Appl Neurobiol 38:271-91. 2012
  4. pmc Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutations
    Franziska Niehr
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles UCLA, USA
    J Transl Med 9:76. 2011
  5. pmc Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032
    Jonas N Søndergaard
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles, Los Angeles, CA, USA
    J Transl Med 8:39. 2010
  6. pmc Gene connectivity, function, and sequence conservation: predictions from modular yeast co-expression networks
    Marc R J Carlson
    Gonda Goldschmied Neuroscience and Genetics Research Center, Department of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095 7088, USA
    BMC Genomics 7:40. 2006
  7. ncbi request reprint Molecular analysis of glioblastoma: pathway profiling and its implications for patient therapy
    Paul S Mischel
    Department of Pathology, University of California Los Angeles, Los Angeles, California 90095, USA
    Cancer Biol Ther 2:242-7. 2003
  8. ncbi request reprint Identification of molecular subtypes of glioblastoma by gene expression profiling
    Paul S Mischel
    Department of Pathology, UCLA School of Medicine, Los Angeles, CA 90095, USA
    Oncogene 22:2361-73. 2003
  9. pmc Nerve growth factor signals via preexisting TrkA receptor oligomers
    Paul S Mischel
    Department of Pathology and Laboratory Medicine, UCLA School of Medicine, University of California, Los Angeles, California 90095 1732 USA
    Biophys J 83:968-76. 2002
  10. ncbi request reprint DNA-microarray analysis of brain cancer: molecular classification for therapy
    Paul S Mischel
    Department of Pathology and Laboratory Medicine, the Henry E Singleton Brain Cancer Research Program at the David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
    Nat Rev Neurosci 5:782-92. 2004

Detail Information

Publications58

  1. pmc mTOR signaling in glioblastoma: lessons learned from bench to bedside
    David Akhavan
    The David Geffen UCLA School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095 1732, USA
    Neuro Oncol 12:882-9. 2010
    ..This review highlights laboratory and clinical evidence of mTOR's role in glioblastoma. Mechanisms of escape from mTOR inhibition are also discussed, as well as future clinical strategies of mTOR inhibition...
  2. pmc HOT Models in Flux: Mitochondrial Glucose Oxidation Fuels Glioblastoma Growth
    Paul S Mischel
    Departments of Pathology and Laboratory Medicine and Molecular and Medical Pharmacology, The David Geffen UCLA School of Medicine, Los Angeles, CA 90095, USA
    Cell Metab 15:789-90. 2012
    ..In this issue of Cell Metabolism, Marin-Valencia et al. (2012) demonstrate that glioblastoma, an aggressive and, in culture, highly glycolytic cancer, primarily uses glucose oxidation to meet energetic and biosynthetic demands in vivo...
  3. pmc Review: molecular pathology in adult high-grade gliomas: from molecular diagnostics to target therapies
    K Masui
    Department of Pathology and Laboratory Medicine, David Geffen University of California at Los Angeles School of Medicine, Los Angeles, California, USA
    Neuropathol Appl Neurobiol 38:271-91. 2012
    ..Furthermore, we describe how these advances, especially in epidermal growth factor receptor/PI3K/mTOR signalling pathway, affect our approaches towards targeted therapy, raising new challenges and identifying new leads...
  4. pmc Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutations
    Franziska Niehr
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles UCLA, USA
    J Transl Med 9:76. 2011
    ..A molecular linkage between the MAPK and the LKB1-AMPK energy sensor pathways suggests that combined MAPK oncogene inhibition and metabolic modulation of AMPK would be more effective than either manipulation alone in melanoma cell lines...
  5. pmc Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032
    Jonas N Søndergaard
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles, Los Angeles, CA, USA
    J Transl Med 8:39. 2010
    ..In conclusion, BRAFV600E mutant melanoma cell lines displayed a range of sensitivities to PLX4032 and metabolic imaging using PET probes can be used to assess sensitivity...
  6. pmc Gene connectivity, function, and sequence conservation: predictions from modular yeast co-expression networks
    Marc R J Carlson
    Gonda Goldschmied Neuroscience and Genetics Research Center, Department of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095 7088, USA
    BMC Genomics 7:40. 2006
    ..Highly connected hub proteins, largely responsible for maintaining network connectivity, have been found to be much more likely to be essential for yeast survival...
  7. ncbi request reprint Molecular analysis of glioblastoma: pathway profiling and its implications for patient therapy
    Paul S Mischel
    Department of Pathology, University of California Los Angeles, Los Angeles, California 90095, USA
    Cancer Biol Ther 2:242-7. 2003
    ..Identifying biologically relevant molecular subsets of glioblastoma and detecting pathway profiles that can be used to guide patient therapy are likely to result in significant improvement in the survival of glioblastoma patients...
  8. ncbi request reprint Identification of molecular subtypes of glioblastoma by gene expression profiling
    Paul S Mischel
    Department of Pathology, UCLA School of Medicine, Los Angeles, CA 90095, USA
    Oncogene 22:2361-73. 2003
    ..These results define distinct molecular subtypes of GBMs that may be important in disease stratification, and in the discovery and assessment of GBM treatment strategies...
  9. pmc Nerve growth factor signals via preexisting TrkA receptor oligomers
    Paul S Mischel
    Department of Pathology and Laboratory Medicine, UCLA School of Medicine, University of California, Los Angeles, California 90095 1732 USA
    Biophys J 83:968-76. 2002
    ..These results indicate that in Xenopus oocytes, NGF activates signaling via pre-formed TrkA receptor oligomers...
  10. ncbi request reprint DNA-microarray analysis of brain cancer: molecular classification for therapy
    Paul S Mischel
    Department of Pathology and Laboratory Medicine, the Henry E Singleton Brain Cancer Research Program at the David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
    Nat Rev Neurosci 5:782-92. 2004
    ..Here, we review the progress made so far in using DNA microarrays to optimize brain cancer therapy...
  11. ncbi request reprint Using molecular information to guide brain tumor therapy
    Paul S Mischel
    Pathology and Laboratory Medicine, David Geffen UCLA School of Medicine, Los Angeles, CA 90095 1732, USA
    Nat Clin Pract Neurol 2:232-3. 2006
  12. pmc The extracellular domain of p75NTR is necessary to inhibit neurotrophin-3 signaling through TrkA
    P S Mischel
    Departments of Pathology and Laboratory Medicine, UCLA, Los Angeles, California 90095 1732, USA
    J Biol Chem 276:11294-301. 2001
    ..Our results suggest that the interaction of these two receptors on the cell surface mediated the inhibition of NT-3-activated signaling through TrkA...
  13. pmc Fyn and SRC are effectors of oncogenic epidermal growth factor receptor signaling in glioblastoma patients
    Kan V Lu
    Department of Pathology and Laboratory Medicine, University of California Los Angeles David Geffen School of Medicine, USA
    Cancer Res 69:6889-98. 2009
    ..These results establish a mechanism linking EGFR signaling with Fyn and Src activation to promote tumor progression and invasion in vivo and provide rationale for combined anti-EGFR and anti-SFK targeted therapies...
  14. pmc Molecular properties of CD133+ glioblastoma stem cells derived from treatment-refractory recurrent brain tumors
    Qinghai Liu
    Department of Medicine, Division of Hematology Oncology, David Geffen School of Medicine, University of California Los Angeles, Factor Building, Rm 13 260, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
    J Neurooncol 94:1-19. 2009
    ..Identifying intrinsic and extrinsic cues, which promote CD133+ GBM cell self-renewal and PCD to support ongoing tumor regeneration may highlight novel therapeutic strategies to greatly diminish the recurrence rate of GBM...
  15. ncbi request reprint Gene expression profiling identifies molecular subtypes of gliomas
    Ruty Shai
    Department of Human Genetics, Henry E Singleton Brain Tumor Program, UCLA School of Medicine, Los Angeles, CA 90095, USA
    Oncogene 22:4918-23. 2003
    ..These results further define molecular subsets of gliomas which may potentially be used for patient stratification, and suggest potential targets for treatment...
  16. pmc Genomic landscape of meningiomas
    Yohan Lee
    Department of Human Genetics, UCLA School of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, Calif 90095 7088, USA
    Brain Pathol 20:751-62. 2010
    ..These data offer the most complete description of the genomic landscape of meningiomas, and provide broad genomic information that may be used to further stratify meningioma patients into prognostic risk groups...
  17. ncbi request reprint Relationship between survival and edema in malignant gliomas: role of vascular endothelial growth factor and neuronal pentraxin 2
    Marc R J Carlson
    Department of Human Genetics, University of California at Los Angeles and David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, California 90095 1271, USA
    Clin Cancer Res 13:2592-8. 2007
    ..VEGF inhibition reduces edema and tumor burden in some patients with malignant glioma, whereas others show no response. The role of VEGF expression in edema production and the relationship to survival is not well understood...
  18. ncbi request reprint Robustness of gene expression profiling in glioma specimen samplings and derived cell lines
    Ruty Mehrian Shai
    Department of Human Genetics, UCLA Geffen School of Medicine, Los Angeles, CA 90095, USA
    Brain Res Mol Brain Res 136:99-103. 2005
    ..In general, the tumor cell lines vary greatly from the parental tissues and cluster more strongly with each other than the parental tissue. We select and examine the set of genes altered in expression to allow adaptation to cell culture...
  19. ncbi request reprint Distinct transcription profiles of primary and secondary glioblastoma subgroups
    Cho Lea Tso
    Department of Human Genetics, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
    Cancer Res 66:159-67. 2006
    ..These data highlight that the development of gene pathway-targeted therapies may need to be specifically tailored to each subtype of glioblastoma...
  20. ncbi request reprint Primary glioblastomas express mesenchymal stem-like properties
    Cho Lea Tso
    Department of Human Genetics, David Geffen School of Medicine, University of California at Los Angeles, Room 5506, 695 Young Drive South, Los Angeles, CA 90095, USA
    Mol Cancer Res 4:607-19. 2006
    ....
  21. doi request reprint Phase II pilot study of bevacizumab in combination with temozolomide and regional radiation therapy for up-front treatment of patients with newly diagnosed glioblastoma multiforme: interim analysis of safety and tolerability
    Albert Lai
    Department of Neurology, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095, USA
    Int J Radiat Oncol Biol Phys 71:1372-80. 2008
    ....
  22. ncbi request reprint Lymphomatosis cerebri presenting as rapidly progressive dementia
    Jonathan D Weaver
    UCLA Department of Medicine, Division of Geriatrics, Los Angeles, California, USA
    Neurologist 13:150-3. 2007
    ..Accurate and timely diagnosis provides the best hope for instituting appropriate treatment and educating the patient and family members as to prognosis based upon likely etiology in a given patient...
  23. pmc Noninvasive imaging of alphaVbeta3 function as a predictor of the antimigratory and antiproliferative effects of dasatinib
    Rebecca A Dumont
    Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095 6948, USA
    Cancer Res 69:3173-9. 2009
    ..50+/-17.68 mm(2) in controls; P=0.001). [(64)Cu]DOTA-c(RGDfK) may provide a sensitive means of monitoring tumor response to SFK inhibition in alpha(V)beta(3)-expressing cancers early in the course of therapy...
  24. pmc Stem cell associated gene expression in glioblastoma multiforme: relationship to survival and the subventricular zone
    Melanie Kappadakunnel
    University of California Los Angeles, Los Angeles, CA 90095, USA
    J Neurooncol 96:359-67. 2010
    ..More research is required to clarify the relationship between the SVZ, cancer stem cells and survival...
  25. ncbi request reprint Gene expression profiling of gliomas strongly predicts survival
    William A Freije
    Department of Human Genetics, University of California at Los Angeles, Los Angeles, California 90095, USA
    Cancer Res 64:6503-10. 2004
    ....
  26. pmc Antitumor activity of rapamycin in a Phase I trial for patients with recurrent PTEN-deficient glioblastoma
    Tim F Cloughesy
    Department of Neurology, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
    PLoS Med 5:e8. 2008
    ..Small, molecularly focused clinical studies offer the promise of the early definition of optimal biologic dose and patient population...
  27. ncbi request reprint Recurrent glioblastoma multiforme: ADC histogram analysis predicts response to bevacizumab treatment
    Whitney B Pope
    Department of Radiological Sciences, David Geffen School of Medicine at UCLA Medical Center, 10833 Le Conte Ave, BL 428 CHS, Los Angeles, CA 90095 1721, USA
    Radiology 252:182-9. 2009
    ..To determine if apparent diffusion coefficient (ADC) histogram analysis can stratify progression-free survival in patients with recurrent glioblastoma multiforme (GBM) prior to bevacizumab treatment...
  28. ncbi request reprint Dendritic cell vaccination in glioblastoma patients induces systemic and intracranial T-cell responses modulated by the local central nervous system tumor microenvironment
    Linda M Liau
    Division of Neurosurgery, Department of Surgery, The Brain Research Institute, David Geffen School of Medicine at University of California at Los Angeles, University of California Los Angeles, Los Angeles, California 90095, USA
    Clin Cancer Res 11:5515-25. 2005
    ..As a next step in vaccine development, a phase I clinical trial was established to evaluate this strategy for its feasibility, safety, and induction of systemic and intracranial T-cell responses in patients with glioblastoma multiforme...
  29. ncbi request reprint Active matrix metalloproteinase 9 expression is associated with primary glioblastoma subtype
    Gheeyoung Choe
    Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, California 90095 1732, USA
    Clin Cancer Res 8:2894-901. 2002
    ..Because EGFR signaling promotes MMP-9 expression and activation in other cancer cell types, we analyzed whether MMP-9 was associated with primary GBM subtype...
  30. pmc Relationship between gene expression and enhancement in glioblastoma multiforme: exploratory DNA microarray analysis
    Whitney B Pope
    Department of Radiological Sciences, David Geffen School of Medicine at University of California Los Angeles UCLA Medical Center, 10833 Le Conte Ave, BL 428 CHS, Los Angeles, CA 90095 1721, USA
    Radiology 249:268-77. 2008
    ..To determine the difference in gene expression between completely versus incompletely enhancing glioblastoma multiforme (GBM)...
  31. pmc Phase II study of bevacizumab plus temozolomide during and after radiation therapy for patients with newly diagnosed glioblastoma multiforme
    Albert Lai
    David Geffen School of Medicine at UCLA, Reed Neurological Research Center, Los Angeles, CA 90095, USA
    J Clin Oncol 29:142-8. 2011
    ..The objectives were to determine the efficacy of this treatment combination and the associated toxicity...
  32. ncbi request reprint Targeted molecular therapy of GBM
    Paul S Mischel
    Department of Pathology and Laboratory Medicine, The David Geffen UCLA School of Medicine, Los Angeles, Calif 90095 1732, USA
    Brain Pathol 13:52-61. 2003
    ..These new approaches are likely to revolutionize the treatment of GBM patients. They will also present new challenges and opportunities for neuropathology...
  33. ncbi request reprint Differential induction of glioblastoma migration and growth by two forms of pleiotrophin
    Kan V Lu
    Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
    J Biol Chem 280:26953-64. 2005
    ..These results indicate that the PTN18-PTPRZ1 and the PTN15-ALK signaling pathways represent potentially important therapeutic targets for glioblastoma invasion and growth...
  34. pmc A microfluidic platform for systems pathology: multiparameter single-cell signaling measurements of clinical brain tumor specimens
    Jing Sun
    Crump Institute for Molecular Imaging, University of California at Los Angeles, Los Angeles, California 90095, USA
    Cancer Res 70:6128-38. 2010
    ..Together with bioinformatic analysis, the MIC platform represents a robust, enabling in vitro molecular diagnostic technology for systems pathology analysis and personalized medicine...
  35. ncbi request reprint Upregulation of tissue inhibitor of metalloproteinases (TIMP)-2 promotes matrix metalloproteinase (MMP)-2 activation and cell invasion in a human glioblastoma cell line
    Kan V Lu
    Department of Pathology and Laboratory Medicine, University of California at Los Angeles, Los Angeles, CA, USA
    Lab Invest 84:8-20. 2004
    ....
  36. ncbi request reprint Mammalian target of rapamycin inhibition promotes response to epidermal growth factor receptor kinase inhibitors in PTEN-deficient and PTEN-intact glioblastoma cells
    Maria Y Wang
    Department of Pathology and Laboratory Medicine, Henry E Singleton Brain Tumor Program, Howard Hughes Medical Institute, David Geffen School of Medicine, University of California at Los Angeles, CA 90095 1732, USA
    Cancer Res 66:7864-9. 2006
    ..These studies provide strong rationale for combined mTOR/EGFR kinase inhibitor therapy in glioblastoma patients, particularly those with PTEN-deficient tumors...
  37. ncbi request reprint Imaging proliferation in brain tumors with 18F-FLT PET: comparison with 18F-FDG
    Wei Chen
    Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA
    J Nucl Med 46:945-52. 2005
    ..We characterized (18)F-FLT PET of brain gliomas and compared (18)F-FLT with (18)F-FDG PET in side-by-side studies of the same patients...
  38. ncbi request reprint Analysis of the phosphatidylinositol 3'-kinase signaling pathway in glioblastoma patients in vivo
    Gheeyoung Choe
    Departments of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
    Cancer Res 63:2742-6. 2003
    ..These results provide the first dissection of the PI3K pathway in glioblastoma in vivo and suggest an approach to stratifying patients for targeted kinase inhibitor therapy...
  39. ncbi request reprint p53 disruption profoundly alters the response of human glioblastoma cells to DNA topoisomerase I inhibition
    Yinglin Wang
    Department of Pathology and Laboratory Medicine, UCLA School of Medicine, 13 317 Center for the Health Science, Los Angeles, CA 90095 1732, USA
    Oncogene 23:1283-90. 2004
    ..These results indicate that p53 disruption has a dramatic effect on how glioblastoma cells process topoisomerase I inhibitor-mediated DNA damage...
  40. pmc Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formation
    Eduard H Panosyan
    Department of Pediatrics, University of California Los Angeles UCLA, Los Angeles, California 90095, USA
    Pediatr Blood Cancer 55:644-51. 2010
    ..Renewable neurosphere formation has clinical predictive value in adult malignant gliomas, yet its prognostic role for pediatric brain tumors is unknown...
  41. pmc The AMPK agonist AICAR inhibits the growth of EGFRvIII-expressing glioblastomas by inhibiting lipogenesis
    Deliang Guo
    Department of Pathology and Laboratory Medicine, The David Geffen UCLA School of Medicine, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 106:12932-7. 2009
    ..These results suggest a mechanism by which AICAR inhibits the proliferation of EGFRvIII expressing glioblastomas and point toward a potential therapeutic strategy for targeting EGFR-activated cancers...
  42. pmc EGFR signaling through an Akt-SREBP-1-dependent, rapamycin-resistant pathway sensitizes glioblastomas to antilipogenic therapy
    Deliang Guo
    1Department of Pathology and Laboratory Medicine, David Geffen UCLA School of Medicine, Los Angeles, CA 90095, USA
    Sci Signal 2:ra82. 2009
    ..These results identify a previously undescribed EGFR-mediated prosurvival metabolic pathway and suggest new therapeutic approaches to treating EGFR-activated glioblastomas...
  43. ncbi request reprint Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors
    Ingo K Mellinghoff
    Department of Molecular and Medical Pharmacology and Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles 90095 1732, USA
    N Engl J Med 353:2012-24. 2005
    ..The mechanism of responsiveness of glioblastomas to these inhibitors is unknown...
  44. pmc Neurosphere formation is an independent predictor of clinical outcome in malignant glioma
    Dan R Laks
    Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
    Stem Cells 27:980-7. 2009
    ..Furthermore, this study suggests that the ability to propagate brain tumor stem cells in vitro is associated with clinical outcome...
  45. ncbi request reprint HDJ-2 as a target for radiosensitization of glioblastoma multiforme cells by the farnesyltransferase inhibitor R115777 and the role of the p53/p21 pathway
    Chun Chieh Wang
    Departments of Radiation Oncology and Pathology and Laboratory Medicine, University of California at Los Angeles School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
    Cancer Res 66:6756-62. 2006
    ..These results have clinical relevance in that they help explain the variability in responses to FTIs that occurs following radiotherapy and elucidate some of the reasons for the complexity underlying FTI-induced radiosensitization...
  46. ncbi request reprint MR imaging correlates of survival in patients with high-grade gliomas
    Whitney B Pope
    Department of Radiological Sciences, David Geffen School of Medicine at UCLA Medical Center, Los Angeles, CA 90095 1721, USA
    AJNR Am J Neuroradiol 26:2466-74. 2005
    ..The purpose of this study was to assess the validity of these results and determine whether other imaging features are useful in predicting survival...
  47. ncbi request reprint PTEN-mediated resistance to epidermal growth factor receptor kinase inhibitors
    Ingo K Mellinghoff
    Departments of Molecular and Medical Pharmacology, Neurology, and Pathology and Henry E Singleton Brain Tumor Program, David Geffen School of Medicine, University of California Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
    Clin Cancer Res 13:378-81. 2007
    ..Here, we will discuss resistance to epidermal growth factor receptor tyrosine kinase inhibitors in glioblastoma patients that is mediated by loss of the PTEN tumor-suppressor protein...
  48. doi request reprint Development of a real-time RT-PCR assay for detecting EGFRvIII in glioblastoma samples
    Koji Yoshimoto
    Departments of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095 1732, USA
    Clin Cancer Res 14:488-93. 2008
    ..Further, frozen tissue is not routinely available, particularly for patients treated in the community. Thus, detection of EGFRvIII in formalin-fixed paraffin-embedded (FFPE) clinical samples is a major challenge...
  49. ncbi request reprint Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cells
    Ichiro Nakano
    Department of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
    J Neurosci Res 86:48-60. 2008
    ..These results demonstrate a critical role for MELK in the proliferation of brain tumors, including their stem cells, and suggest that MELK may be a compelling molecular target for treatment of high-grade brain tumors...
  50. ncbi request reprint New roles for galectins in brain tumors--from prognostic markers to therapeutic targets
    Brianna N Stillman
    Department of Pathology and Laboratory Medicine and the Jonsson Comprehensive Cancer Center, UCLA School of Medicine, Los Angeles, California 90095, USA
    Brain Pathol 15:124-32. 2005
    ..This review highlights the roles of galectins in cancer and specifically, the developing field of galectins in brain cancer...
  51. pmc Targeted therapy for malignant glioma patients: lessons learned and the road ahead
    Tiffany T Huang
    Departments of Pathology and Laboratory Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095
    Neurotherapeutics 6:500-12. 2009
    ....
  52. pmc Anti-MHC class I antibody activation of proliferation and survival signaling in murine cardiac allografts
    Peter T Jindra
    UCLA Immunogenetics Center and Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, 1000 Veteran Avenue, Los Angeles, CA 90095, USA
    J Immunol 180:2214-24. 2008
    ..These results provide the first analysis of the interrelationships between these signaling molecules in vivo that reflects our knowledge of the signaling pathway derived from in vitro experiments...
  53. pmc Deregulation of a STAT3-interleukin 8 signaling pathway promotes human glioblastoma cell proliferation and invasiveness
    Nuria de la Iglesia
    Department of Pathology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 28:5870-8. 2008
    ..These studies suggest that STAT3 activation or IL8 inhibition may have potential in patient-tailored treatment of PTEN-deficient brain tumors...
  54. pmc PTEN dosage is essential for neurofibroma development and malignant transformation
    Caroline Gregorian
    Department of Molecular and Medical Pharmacology, Institute for Molecular Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 106:19479-84. 2009
    ..Our data suggest that combined inhibition of RAS/RAF/MAPK and PTEN/PI3K/AKT pathways may be beneficial for patients with MPNST...
  55. ncbi request reprint High-throughput oncogene mutation profiling in human cancer
    Roman K Thomas
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
    Nat Genet 39:347-51. 2007
    ..These results offer a new dimension in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously and in 'real time' to guide cancer classification and rational therapeutic intervention...
  56. ncbi request reprint Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma
    Andrew T Parsa
    Department of Neurological Surgery, University of California San Francisco, 505 Parnassus Avenue, M 779, San Francisco, California 94143, USA
    Nat Med 13:84-8. 2007
    ..These data identify a previously unrecognized mechanism linking loss of the tumor suppressor PTEN with immunoresistance, mediated in part by B7-H1...
  57. pmc Assessing the significance of chromosomal aberrations in cancer: methodology and application to glioma
    Rameen Beroukhim
    Broad Institute, Massachusetts Institute of Technology and Harvard University, 7 Cambridge Center, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 104:20007-12. 2007
    ..Our results support the feasibility and utility of systematic characterization of the cancer genome...

Research Grants5

  1. Trk receptor mediated apoptosis of medulloblastoma cells
    Paul Mischel; Fiscal Year: 2005
    ..Dr. Paul Mischel is a board certified neuropathologist, and has done a period of initial molecular neuroscience training with Dr...
  2. Glioblastoma - Molecular Analysis for Clinical Trials
    Paul Mischel; Fiscal Year: 2006
    ..abstract_text> ..
  3. Glioblastoma - Molecular Analysis for Clinical Trials
    Paul Mischel; Fiscal Year: 2007
    ..abstract_text> ..
  4. Glioblastoma - Molecular Analysis for Clinical Trials
    Paul Mischel; Fiscal Year: 2009
    ..abstract_text> ..