Research Topics
| Paul MischelSummaryAffiliation: University of California Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
HOT Models in Flux: Mitochondrial Glucose Oxidation Fuels Glioblastoma GrowthPaul 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...
Review: molecular pathology in adult high-grade gliomas: from molecular diagnostics to target therapiesK 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...- Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutationsFranziska 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... - Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032Jonas 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... - Gene connectivity, function, and sequence conservation: predictions from modular yeast co-expression networksMarc 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... 
Molecular analysis of glioblastoma: pathway profiling and its implications for patient therapyPaul 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...- Identification of molecular subtypes of glioblastoma by gene expression profilingPaul 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... - Nerve growth factor signals via preexisting TrkA receptor oligomersPaul 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... - DNA-microarray analysis of brain cancer: molecular classification for therapyPaul 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... - Using molecular information to guide brain tumor therapyPaul 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 - The extracellular domain of p75NTR is necessary to inhibit neurotrophin-3 signaling through TrkAP 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... - Fyn and SRC are effectors of oncogenic epidermal growth factor receptor signaling in glioblastoma patientsKan 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... - Molecular properties of CD133+ glioblastoma stem cells derived from treatment-refractory recurrent brain tumorsQinghai 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... - Gene expression profiling identifies molecular subtypes of gliomasRuty 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... - Genomic landscape of meningiomasYohan 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... - Primary glioblastomas express mesenchymal stem-like propertiesCho-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.... - Robustness of gene expression profiling in glioma specimen samplings and derived cell linesRuty 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... - Relationship between survival and edema in malignant gliomas: role of vascular endothelial growth factor and neuronal pentraxin 2Marc 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... - Distinct transcription profiles of primary and secondary glioblastoma subgroupsCho-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... - 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 tolerabilityAlbert 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.... - Lymphomatosis cerebri presenting as rapidly progressive dementiaJonathan 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... - Antitumor activity of rapamycin in a Phase I trial for patients with recurrent PTEN-deficient glioblastomaTim 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... - Recurrent glioblastoma multiforme: ADC histogram analysis predicts response to bevacizumab treatmentWhitney 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... - Gene expression profiling of gliomas strongly predicts survivalWilliam A Freije
Department of Human Genetics, University of California at Los Angeles, Los Angeles, California 90095, USA
Cancer Res 64:6503-10. 2004.... - Dendritic cell vaccination in glioblastoma patients induces systemic and intracranial T-cell responses modulated by the local central nervous system tumor microenvironmentLinda 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... - Stem cell associated gene expression in glioblastoma multiforme: relationship to survival and the subventricular zoneMelanie 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... - Relationship between gene expression and enhancement in glioblastoma multiforme: exploratory DNA microarray analysisWhitney 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)... - Phase II study of bevacizumab plus temozolomide during and after radiation therapy for patients with newly diagnosed glioblastoma multiformeAlbert 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... - Active matrix metalloproteinase 9 expression is associated with primary glioblastoma subtypeGheeyoung 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... - Noninvasive imaging of alphaVbeta3 function as a predictor of the antimigratory and antiproliferative effects of dasatinibRebecca 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... - Targeted molecular therapy of GBMPaul 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... - Differential induction of glioblastoma migration and growth by two forms of pleiotrophinKan 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... - Upregulation of tissue inhibitor of metalloproteinases (TIMP)-2 promotes matrix metalloproteinase (MMP)-2 activation and cell invasion in a human glioblastoma cell lineKan V Lu
Department of Pathology and Laboratory Medicine, University of California at Los Angeles, Los Angeles, CA, USA
Lab Invest 84:8-20. 2004.... - A microfluidic platform for systems pathology: multiparameter single-cell signaling measurements of clinical brain tumor specimensJing 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... - Mammalian target of rapamycin inhibition promotes response to epidermal growth factor receptor kinase inhibitors in PTEN-deficient and PTEN-intact glioblastoma cellsMaria 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... - Imaging proliferation in brain tumors with 18F-FLT PET: comparison with 18F-FDGWei 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... - EGFR signaling through an Akt-SREBP-1-dependent, rapamycin-resistant pathway sensitizes glioblastomas to antilipogenic therapyDeliang 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... - Analysis of the phosphatidylinositol 3'-kinase signaling pathway in glioblastoma patients in vivoGheeyoung 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... - Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formationEduard 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... - The AMPK agonist AICAR inhibits the growth of EGFRvIII-expressing glioblastomas by inhibiting lipogenesisDeliang 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... - p53 disruption profoundly alters the response of human glioblastoma cells to DNA topoisomerase I inhibitionYinglin 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... - Molecular determinants of the response of glioblastomas to EGFR kinase inhibitorsIngo 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..In vitro, coexpression of EGFRvIII and PTEN sensitized glioblastoma cells to erlotinib. CONCLUSIONS: Coexpression of EGFRvIII and PTEN by glioblastoma cells is associated with responsiveness to EGFR kinase inhibitors... - Neurosphere formation is an independent predictor of clinical outcome in malignant gliomaDan 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... - PTEN-mediated resistance to epidermal growth factor receptor kinase inhibitorsIngo 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... - HDJ-2 as a target for radiosensitization of glioblastoma multiforme cells by the farnesyltransferase inhibitor R115777 and the role of the p53/p21 pathwayChun-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... - Development of a real-time RT-PCR assay for detecting EGFRvIII in glioblastoma samplesKoji 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... - MR imaging correlates of survival in patients with high-grade gliomasWhitney 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..CONCLUSION: Of 15 tumor imaging features in GBM patients, only nCET, edema, and multifocality/satellites are statistically significant prognostic indicators. The survival advantage of nCET is a novel finding... - Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cellsIchiro 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... - mTOR signaling in glioblastoma: lessons learned from bench to bedsideDavid 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... - Targeted therapy for malignant glioma patients: lessons learned and the road aheadTiffany 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.... - Anti-MHC class I antibody activation of proliferation and survival signaling in murine cardiac allograftsPeter 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... - Deregulation of a STAT3-interleukin 8 signaling pathway promotes human glioblastoma cell proliferation and invasivenessNuria 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... - New roles for galectins in brain tumors--from prognostic markers to therapeutic targetsBrianna 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... - PTEN dosage is essential for neurofibroma development and malignant transformationCaroline 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... - Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in gliomaAndrew 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... - High-throughput oncogene mutation profiling in human cancerRoman 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... - Assessing the significance of chromosomal aberrations in cancer: methodology and application to gliomaRameen 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 Grants
- Trk receptor mediated apoptosis of medulloblastoma cellsPaul Mischel; Fiscal Year: 2005..Dr. Paul Mischel is a board certified neuropathologist, and has done a period of initial molecular neuroscience training with Dr...
- Glioblastoma - Molecular Analysis for Clinical TrialsPaul Mischel; Fiscal Year: 2009..abstract_text> ..