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1. Gallia GL, Rand V, Siu IM, Eberhart CG, James CD, Marie SK, Oba-Shinjo SM, Carlotti CG, Caballero OL, Simpson AJ, Brock MV, Massion PP, Carson BS Sr, Riggins GJ: PIK3CA gene mutations in pediatric and adult glioblastoma multiforme. Mol Cancer Res; 2006 Oct;4(10):709-14
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  • [Title] PIK3CA gene mutations in pediatric and adult glioblastoma multiforme.
  • Recently, a large-scale mutational analysis of eight PI3K and eight PI3K-like genes revealed somatic mutations in PIK3CA, which encodes the p110alpha catalytic subunit of class IA PI3K, in several types of cancer, including glioblastoma multiforme.
  • Given this disparity and to address the relation of patient age to mutation frequency, we examined 10 exons of PIK3CA in 73 glioblastoma samples by PCR amplification followed by direct DNA sequencing.
  • Of the primary tumors, PIK3CA mutations were identified in 21% and 17% of pediatric and adult samples, respectively.
  • [MeSH-major] Genetic Predisposition to Disease. Glioblastoma / genetics. Mutation. Phosphatidylinositol 3-Kinases / genetics

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  • (PMID = 17050665.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
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2. Chi AS, Sorensen AG, Jain RK, Batchelor TT: Angiogenesis as a therapeutic target in malignant gliomas. Oncologist; 2009 Jun;14(6):621-36
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  • Currently, adult glioblastoma (GBM) patients have poor outcomes with conventional cytotoxic treatments.
  • Because GBMs are highly angiogenic tumors, inhibitors that target tumor vasculature are considered promising therapeutic agents in these patients.
  • [MeSH-minor] Animals. Cell Movement / drug effects. Clinical Trials as Topic. Drug Resistance, Neoplasm. Edema / drug therapy. Endothelial Cells / drug effects. Humans. Protein Kinase Inhibitors / therapeutic use. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19487335.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 175
  • [Other-IDs] NLM/ NIHMS765709; NLM/ PMC4790121
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3. Paugh BS, Qu C, Jones C, Liu Z, Adamowicz-Brice M, Zhang J, Bax DA, Coyle B, Barrow J, Hargrave D, Lowe J, Gajjar A, Zhao W, Broniscer A, Ellison DW, Grundy RG, Baker SJ: Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. J Clin Oncol; 2010 Jun 20;28(18):3061-8
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  • [Title] Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease.
  • PURPOSE: To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).
  • Results were compared with publicly available data from adult tumors.
  • RESULTS: Significant differences in copy number alterations distinguish childhood and adult glioblastoma.
  • No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma.
  • Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively).
  • CONCLUSION: Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings in adult tumors cannot be simply extrapolated to younger patients.

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  • (PMID = 20479398.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / R01 CA135554; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC2903336
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4. Bax DA, Gaspar N, Little SE, Marshall L, Perryman L, Regairaz M, Viana-Pereira M, Vuononvirta R, Sharp SY, Reis-Filho JS, Stávale JN, Al-Sarraj S, Reis RM, Vassal G, Pearson AD, Hargrave D, Ellison DW, Workman P, Jones C: EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines. Clin Cancer Res; 2009 Sep 15;15(18):5753-61
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  • [Title] EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines.
  • PURPOSE: The epidermal growth factor receptor (EGFR) is amplified and overexpressed in adult glioblastoma, with response to targeted inhibition dependent on the underlying biology of the disease.
  • We have sought to clarify the role of EGFR in pediatric high-grade glioma (HGG).
  • Pediatric glioblastoma cells transduced with wild-type or deletion mutant EGFRvIII were not rendered more sensitive to erlotinib despite expressing wild-type PTEN.
  • Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Erlotinib Hydrochloride. Humans. Prognosis. Quinazolines / pharmacology. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Cells, Cultured

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  • [ErratumIn] Clin Cancer Res. 2009 Nov 15;15(22):7110
  • (PMID = 19737945.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C1178/A10294; United Kingdom / Cancer Research UK / / C309/A2187; United Kingdom / Cancer Research UK / / C309/A8274
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0 / epidermal growth factor receptor VIII; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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5. McKean-Cowdin R, Barnholtz-Sloan J, Inskip PD, Ruder AM, Butler M, Rajaraman P, Razavi P, Patoka J, Wiencke JK, Bondy ML, Wrensch M: Associations between polymorphisms in DNA repair genes and glioblastoma. Cancer Epidemiol Biomarkers Prev; 2009 Apr;18(4):1118-26
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  • [Title] Associations between polymorphisms in DNA repair genes and glioblastoma.
  • A pooled analysis was conducted to examine the association between select variants in DNA repair genes and glioblastoma multiforme, the most common and deadliest form of adult brain tumors.
  • Genetic data for approximately 1,000 glioblastoma multiforme cases and 2,000 controls were combined from four centers in the United States that have conducted case-control studies on adult glioblastoma multiforme, including the National Cancer Institute, the National Institute for Occupational Safety and Health, the University of Texas M. D.
  • The C allele of the PARP1 rs1136410 variant was associated with a 20% reduction in risk for glioblastoma multiforme (odds ratio(CT or CC), 0.80; 95% confidence interval, 0.67-0.95).
  • A 44% increase in risk for glioblastoma multiforme was found for individuals homozygous for the G allele of the PRKDC rs7003908 variant (odds ratio(GG), 1.44; 95% confidence interval, 1.13-1.84); there was a statistically significant trend (P = 0.009) with increasing number of G alleles.
  • Few studies have reported on the associations between variants in DNA repair genes and brain tumors, and few specifically have examined their impact on glioblastoma multiforme.
  • Our results suggest that common variation in DNA repair genes may be associated with risk for glioblastoma multiforme.

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  • (PMID = 19318434.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA070917; United States / NCI NIH HHS / CA / R01 CA052689-18; United States / NCI NIH HHS / CA / R01 CA052689-19; United States / NCI NIH HHS / CA / CA097257-080001; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / CA052689-19; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA070917; United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689; United States / NCI NIH HHS / CA / P50 CA097257-080001; United States / NCI NIH HHS / CA / R01 CA070917-09; United States / NCI NIH HHS / CA / CA052689-18; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS96659; NLM/ PMC2667563
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6. Pediatric and adult glioblastoma have different gene expression profiles. Nat Clin Pract Neurol; 2009 Mar;5(3):122-3

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  • [Title] Pediatric and adult glioblastoma have different gene expression profiles.

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  • [CommentOn] Neuro Oncol. 2009 Jun;11(3):274-80 [18981259.001]
  • (PMID = 20387321.001).
  • [ISSN] 1745-8358
  • [Journal-full-title] Nature clinical practice. Neurology
  • [ISO-abbreviation] Nat Clin Pract Neurol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
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7. Umesh S, Tandon A, Santosh V, Anandh B, Sampath S, Chandramouli BA, Sastry Kolluri VR: Clinical and immunohistochemical prognostic factors in adult glioblastoma patients. Clin Neuropathol; 2009 Sep-Oct;28(5):362-72
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  • [Title] Clinical and immunohistochemical prognostic factors in adult glioblastoma patients.
  • OBJECTIVE: Glioblastomas are the commonest and the most malignant of all adult brain tumors, characterized by genetic instability, intratumoral histopathological variability, and unpredictable clinical behavior.
  • The utility of tumor markers that reflect their underlying biology is becoming increasingly important with respect to patient prognostication and their potential role as molecular targets of therapy is being recognized.
  • MATERIALS AND METHODS: We evaluated 54 cases of adult supratentorial glioblastomas operated over a span of 1 year, with respect to clinical features such as age, Karnofsky performance score (KPS), extent of resection, adjuvant therapy, and immunohistochemical expression of p53, EGFR (Epidermal Growth Factor Receptor) and PTEN (Phosphatase and Tensin homolog).
  • CONCLUSIONS: Our study shows that EGFR and p53 overexpression along with loss of PTEN expression are important adjuncts to clinical variables in prognosticating glioblastoma patients.
  • [MeSH-major] Glioblastoma / diagnosis. Supratentorial Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. PTEN Phosphohydrolase / metabolism. Prognosis. Receptor, Epidermal Growth Factor / metabolism. Severity of Illness Index. Treatment Outcome. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 19788052.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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8. Kleinschmidt-DeMasters BK, Meltesen L, McGavran L, Lillehei KO: Characterization of glioblastomas in young adults. Brain Pathol; 2006 Oct;16(4):273-86
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  • Most adult glioblastoma multiformes (GBMs) present in patients 45-70 years old; tumors occurring at the extremes of the adult age spectrum are uncommon, and seldom studied.
  • We hypothesized that young-adult GBMs would differ from elderly-adult and from pediatric GBMs.
  • Twenty-eight (74%) of our 38 young-adult GBM patients had primary de novo tumors, two of which occurred in patients with cancer syndromes.
  • GBMs in young adults are a more inhomogeneous tumor group than GBMs occurring in older adult patients and show features that overlap with both pediatric and adult GBMs.
  • [MeSH-major] Brain Neoplasms / mortality. Brain Neoplasms / pathology. Glioblastoma / mortality. Glioblastoma / pathology
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Ki-67 Antigen / metabolism. Male. Mitotic Index. Neoplasms, Radiation-Induced. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / pathology. Prognosis. Receptor, Epidermal Growth Factor / metabolism. Survival Analysis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17107596.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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9. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells in pediatric brain tumors.
  • Central nervous system (CNS) tumors remain the leading cause of death among pediatric neoplasms.
  • Although standard therapies cure many pediatric CNS tumors, the long-term cognitive and physical consequences of these therapies are devastating.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


10. Tunici P, Yu JS: Pituitary adenoma stem cells. Methods Mol Biol; 2009;568:195-201
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  • The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers.
  • Reports have been published on the identification of tumor cells with stem cells characteristics in different types of tumors (acute myelogenic leukemia, breast cancer, prostate cancer, bone sarcomas, liver cancer, and melanomas).
  • We and other groups have previously reported the isolation of cancer stem cells from adult glioblastoma multiforme.
  • In vivo they give a tumor that recapitulates the characteristics of the tumor in the patient.
  • More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas.
  • The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100.
  • In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.

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  • (PMID = 19582428.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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11. Potter NE, Phipps K, Harkness W, Hayward R, Thompson D, Jacques TS, Harding B, Thomas DG, Rees J, Darling JL, Warr TJ: Astrocytoma derived short-term cell cultures retain molecular signatures characteristic of the tumour in situ. Exp Cell Res; 2009 Oct 1;315(16):2835-46
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  • [Title] Astrocytoma derived short-term cell cultures retain molecular signatures characteristic of the tumour in situ.
  • We have characterised gene expression changes induced by short-term culture in astrocytoma in order to determine whether derived short-term cell cultures are representative of the tumour in situ.
  • We have used the Affymetrix GeneChip U133A to generate gene expression profiles of 6 paediatric pilocytic astrocytoma (PA) biopsies and derived short-term cell cultures and 3 adult glioblastoma multiforme (GBM) biopsies and derived short-term cultures.
  • This gene cohort can distinguish PA and GBM tumours, regardless of the sample source, suggesting that astrocytoma derived short-term cultures do retain key aspects of the global tumour expression profile and are representative of the tumour in situ.
  • Furthermore, these genes are involved in pathways and functions characteristic of adult GBM including VEGF signalling, hypoxia and TP53 signalling.
  • [MeSH-major] Astrocytoma. Biomarkers, Tumor / metabolism. Brain Neoplasms. Tumor Cells, Cultured / metabolism
  • [MeSH-minor] Adult. Animals. Child. Cluster Analysis. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Signal Transduction / physiology

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  • (PMID = 19523942.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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12. Pistollato F, Abbadi S, Rampazzo E, Viola G, Della Puppa A, Cavallini L, Panchision DM, Te Kronnie G, Basso G: Glioblastoma-derived cells exhibit differential responses to glycolysis inhibition under hypoxia. J Clin Oncol; 2009 May 20;27(15_suppl):e13031

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  • [Title] Glioblastoma-derived cells exhibit differential responses to glycolysis inhibition under hypoxia.
  • : e13031 It has been suggested that oxygen tension is a crucial component of the brain tumor niche, as hypoxia positively correlates with tumor aggressiveness and over-activity of hypoxia inducible factor-1α (HIF-1α) reinforces tumor progression.
  • Here we investigate the effects mediated by in vitro glycolysis inhibition by using 2-deoxyglucose (2-DG) in glioblastoma (GBM) derived cells maintained under two different oxygen tensions, a lowered oxygen tension (2%) versus a higher non-physiological (20%).
  • Our results show that adult GBM displaying a highly immature phenotype manifested the highest resistance to glucose deprivation.
  • Also, hypoxia inhibits the mitochondria-controlled apoptosis induced by 2-DG, by conferring cell resistance through progressive activation of pro-survival NF-kB and induction of tumor cell autophagy.
  • These results indicate differences in tumor cells behavior that may be predictive of cell response to therapy aiming to limit glucose uptake or glucose metabolism.

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  • (PMID = 27962877.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Salmaggi A, Riva M, Silvani A, Merli R, Tomei G, Lorusso L, Russo A, Marchioni E, Imbesi F, Lombardia Neuro-oncology Group: A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy. Neurol Sci; 2005 Oct;26(4):227-34
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  • [Title] A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy.
  • The objective was to set the basis for a prospective, multicentre data collection on newly diagnosed adult glioblastoma patients diagnosed in Lombardia by means of a common database used by neurological and neurosurgical units of various hospitals, providing epidemiological, therapy and follow-up data.
  • All adult patients with a newly diagnosed glioblastoma in 9 Lombardia hospitals from 31 March 2003 to 31 March 2004 were followed prospectively by a form elaborated by the Lombardia Neuro-oncology Group.
  • One hundred and thirty-four newly diagnosed glioblastoma patients were enrolled during the first year of the study.
  • In 71 patients, the tumour involved 1 brain lobe at diagnosis.
  • Data in newly diagnosed glioblastoma patients in Lombardia are in line with other case series reported in other populations.
  • [MeSH-major] Brain Neoplasms / physiopathology. Glioblastoma / physiopathology
  • [MeSH-minor] Adult. Brain / pathology. Cohort Studies. Databases, Factual. Disease Progression. Female. Geography. Humans. Italy. Male. Middle Aged. Prospective Studies. Seizures / etiology. Survival Analysis

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  • (PMID = 16193249.001).
  • [ISSN] 1590-1874
  • [Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
  • [ISO-abbreviation] Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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14. Loh KC, Willert J, Meltzer H, Roberts W, Kerlin B, Kadota R, Levy M, White G, Geddis A, Schiff D, Martin L, Yu A, Kung F, Spear MA: Temozolomide and radiation for aggressive pediatric central nervous system malignancies. J Pediatr Hematol Oncol; 2005 May;27(5):254-8
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  • [Title] Temozolomide and radiation for aggressive pediatric central nervous system malignancies.
  • This study describes the outcomes of children treated with combinations of temozolomide and radiation therapy for various aggressive central nervous system malignancies.
  • Toxicities observed included low-grade neutropenia, thrombocytopenia, and lymphopenia.
  • The combination of temozolomide and radiotherapy appears to be well tolerated in a variety of treatment schemas for aggressive pediatric central nervous system malignancies.
  • This information is of particular use in designing future studies, given the recent positive results in a randomized study examining the use of temozolomide concomitant with radiation in the treatment of adult glioblastoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use

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  • (PMID = 15891559.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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15. Tang J, Shao W, Dorak MT, Li Y, Miike R, Lobashevsky E, Wiencke JK, Wrensch M, Kaslow RA, Cobbs CS: Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):2040-4
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  • [Title] Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme.
  • We examined the relationships of human leukocyte antigen (HLA) and related polymorphisms to glioblastoma multiforme in adult Caucasians (non-Hispanic Whites) from the San Francisco Bay area.
  • For 155 glioblastoma multiforme patients and 157 control subjects closely matched by ethnicity, age, and gender, PCR-based techniques resolved alleles at HLA-A, -B, -C, and -DRB1 loci along with short tandem repeat polymorphisms of MICA exon 5 and TNFb.
  • By multivariable logistic regression, B*13 and the B*07-Cw*07 haplotype were positively associated with glioblastoma multiforme (P=0.01 and <0.001, respectively), whereas Cw*01 was the only variant showing a negative association (P=0.05).
  • Among glioblastoma multiforme patients, progression to death after diagnosis was slower in those with A*32 (relative hazard, 0.45; P<0.01) and faster in those with B*55 (relative hazard, 2.27; P<0.01).
  • Thus, both the occurrence and the prognosis of glioblastoma multiforme could be associated with specific but different HLA genotypes.
  • B*07 and the B*07-Cw*07 haplotype are much more common in Caucasians than other ethnic groups in the U.S., which may partially explain the higher incidence of glioblastoma multiforme in Caucasians.
  • [MeSH-major] Biomarkers, Tumor / genetics. Glioblastoma / genetics. HLA Antigens / genetics
  • [MeSH-minor] Adult. Case-Control Studies. Female. Genetic Variation. Genotype. Humans. Male. Microsatellite Repeats. Polymerase Chain Reaction. Polymorphism, Genetic. Prognosis. San Francisco

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  • (PMID = 16103458.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA097247; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / CA52689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HLA Antigens
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16. Mendonça R, Lima LG, Fernandes LN, Ferreira NP, De Napoli G: [Primary connus medullaris glioblastoma: case report]. Arq Neuropsiquiatr; 2005 Jun;63(2B):539-42
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  • [Title] [Primary connus medullaris glioblastoma: case report].
  • [Transliterated title] Glioblastoma primário de cone medula: relato de caso.
  • Glioblastomas are the most common type of brain tumors; astrocytic in their origin, they are anaplastic tumors, and are located mainly in the cerebral hemispheres.
  • Primary growth in the conus medullaris is very rare, and the assessment and prognosis of this kind of tumor are distinct and unique.
  • We present here the case of a 39 years-old man with an intramedullary tumor of the spinal cord, with an histo pathological diagnosis of glioblastoma, along with some therapeutic considerations.
  • [MeSH-major] Glioblastoma / diagnosis. Spinal Cord Neoplasms / diagnosis
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 16059615.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
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17. Jimenez Caballero PE, Mollejo Villanueva M, Marsal Alonso C: [Gliomatosis cerebri: evolution to glioblastoma multiforme]. Neurologia; 2007 Jul-Aug;22(6):395-8
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  • [Title] [Gliomatosis cerebri: evolution to glioblastoma multiforme].
  • [Transliterated title] Gliomatosis cerebri: evolución a glioblastoma multiforme.
  • The brain magnetic resonance imaging showed hyperintense lesions in T2 suggestive of gliomatosis cerebri, this being confirmed with the brain biopsy.
  • Several months later, he suffered rapid clinical deterioration, observing the development of a glioblastoma multiforme over the lesion.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplasms, Multiple Primary / pathology. Neoplasms, Neuroepithelial / pathology
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 17610168.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 25
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18. Tramacere F, Gianicolo E, Serinelli M, Bambace S, De Luca M, Castagna R, Francavilla MC, Leone A, Monastero S, Fucilli F, Pili G, Distante A, Portaluri M: [Multivariate analysis of prognostic factors and survival in patients with "glioblastoma multiforme"]. Clin Ter; 2008 Jul-Aug;159(4):233-8
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  • [Title] [Multivariate analysis of prognostic factors and survival in patients with "glioblastoma multiforme"].
  • [Transliterated title] Multivariate analysis of prognostic factors and survival inpatients with "glioblastoma multiforme".
  • PURPOSE: The aim of this study was to evaluate the survival of patients with "glioblastoma multiforme", to analyse the prognostic factors influencing the survival rate and to review recent results in the literature.
  • Among the factors under investigation we ascertained that sex, chemotherapy, conformal treatment, surgery, and the choice of the irradiation area (whole brain or only the involved field) did not influence the survival in a statistically significant manner.
  • [MeSH-major] Brain Neoplasms / mortality. Glioblastoma / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Antineoplastic Agents, Alkylating / therapeutic use. Combined Modality Therapy. Cranial Irradiation. Craniotomy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Humans. Italy / epidemiology. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models. Radiotherapy Dosage. Radiotherapy, Conformal. Retrospective Studies. Survival Analysis. Young Adult

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  • (PMID = 18776979.001).
  • [ISSN] 1972-6007
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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19. Chaddad Neto F, Lopes A, Alberto Filho M, Catanoce A, Joaquim AF, Oliveira Ed: Tectal glioblastoma. Arq Neuropsiquiatr; 2007 Dec;65(4A):996-9
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  • [Title] Tectal glioblastoma.
  • Brain stem gliomas are a heterogeneous group of neoplasms arising mostly in paediatric patients.
  • Tectal plate gliomas represent a particular type of brain stem tumours usually with a benign, indolent clinical course, presenting with signs of raised intracranial hypertension due to supra-tentorialhydrocephalous caused by aqueductal stenosis.
  • Seldom high-grade lesions arise in this location with tremendous therapeutic implications.
  • We present the case of a glioblastoma of the tectal plate in a 22 years-old woman operated upon by a supracerebellar-infratentorial approach.
  • [MeSH-major] Brain Neoplasms. Glioblastoma. Tectum Mesencephali
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging

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  • (PMID = 18094862.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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20. Hur H, Jung S, Jung TY, Kim IY: Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc; 2008 Apr;43(4):194-7

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  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • Primary cerebellar glioblastoma multiforme (GBM) is a rare tumor in adults that accounts for just 1% of all cases of GBM.
  • After operation, glioblastoma was histologically confirmed.

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  • (PMID = 19096643.001).
  • [ISSN] 2005-3711
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2588262
  • [Keywords] NOTNLM ; Cerebellum / Differential diagnosis / Glioblastoma multiforme / Pathogenesis
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21. Mattos JP, Marenco HA, Campos JM, Faria AV, Queiroz LS, Borges G, Oliveira Ed: Cerebellar glioblastoma multiforme in an adult. Arq Neuropsiquiatr; 2006 Mar;64(1):132-5
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  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • Cerebellar glioblastoma multiforme (GBM) is a rare tumor.
  • In conjunction, we present a literature review including particular issues, clinical data, advances in imaging studies, pathological characteristics, treatment options and the behavior of such malignant tumor.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellum / pathology. Glioblastoma / pathology

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  • (PMID = 16622570.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 16
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22. Hernández-Reyna R, Medellín-Sánchez R, Cerda-Flores RM, Calderón-Garcidueñas AL: [Survival pronostic factors in Mexican patients with multiforme glioblastoma]. Rev Med Inst Mex Seguro Soc; 2010 Mar-Apr;48(2):121-6
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  • [Title] [Survival pronostic factors in Mexican patients with multiforme glioblastoma].
  • [Transliterated title] Factores pronósticos de supervivencia en pacientes mexicanos con glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms / mortality. Brain Neoplasms / surgery. Glioblastoma / mortality. Glioblastoma / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cross-Sectional Studies. Female. Humans. Male. Mexico. Middle Aged. Prognosis. Retrospective Studies. Survival Rate. Young Adult

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  • (PMID = 20929613.001).
  • [ISSN] 0443-5117
  • [Journal-full-title] Revista médica del Instituto Mexicano del Seguro Social
  • [ISO-abbreviation] Rev Med Inst Mex Seguro Soc
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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23. Brandes AA, Tosoni A, Franceschi E, Reni M, Gatta G, Vecht C: Glioblastoma in adults. Crit Rev Oncol Hematol; 2008 Aug;67(2):139-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma in adults.
  • Glioblastoma (GBM) is the most malignant among astrocytic tumours and is associated with a poor prognosis.
  • Surgery aimed to complete resection should be the first therapeutic modality in the management of glioblastoma.
  • [MeSH-major] Glioblastoma / therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. Humans. Neoplasm Staging

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  • (PMID = 18394916.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Number-of-references] 98
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24. Seif FE, Azar S, Barake M, Sawaya R: Hypercalcemia in glioblastoma multiforme. Neuro Endocrinol Lett; 2006 Aug;27(4):547-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypercalcemia in glioblastoma multiforme.
  • We report a case of a previously healthy man presenting with glioblastoma multiforme .
  • This is the first reported case of hypercalcemia associated with glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms / complications. Glioblastoma / complications. Hypercalcemia / etiology
  • [MeSH-minor] Adult. Calcitriol / blood. Calcium / blood. Humans. Male. Parathyroid Glands / physiology

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  • (PMID = 16892004.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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25. Ances BM, Danish SF, Kolson DL, Judy KD, Liebeskind DS: Cerebral gumma mimicking glioblastoma multiforme. Neurocrit Care; 2005;2(3):300-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebral gumma mimicking glioblastoma multiforme.
  • This article reports an unusual case of a syphilitic gumma with a clinical and radiographical presentation initially suggestive of glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radiography. Glioblastoma / pathology. Glioblastoma / radiography. Neurosyphilis / pathology. Neurosyphilis / radiography
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male

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  • (PMID = 16159080.001).
  • [ISSN] 1541-6933
  • [Journal-full-title] Neurocritical care
  • [ISO-abbreviation] Neurocrit Care
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. Baldi I, Huchet A, Bauchet L, Loiseau H: [Epidemiology of glioblastoma]. Neurochirurgie; 2010 Dec;56(6):433-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Epidemiology of glioblastoma].
  • An increasing incidence of glioblastoma has been observed over the last 30 years.
  • Moreover, the aging of the population and the increasing occurrence of glioblastoma beyond 60 years of age are additional explanations.
  • In Gironde (France), where a specialized registry has been established, the annual incidence of glioblastoma is 4.96/100,000.
  • Ethnicity, age, sex, hereditary syndromes, some constitutive polymorphisms, and brain irradiation are the established risk factors Allergies or asthma, certain viral infections, autoimmune diseases, nonsteroidal anti-inflammatory drug intake, substitutive hormonal therapy, and dietary antioxidant intake are the established protective factors.
  • Future studies combining constitutive polymorphisms and exposure assessment are likely to provide consistent and important data that will improve our knowledge in the epidemiology of glioblastoma.
  • [MeSH-major] Brain Neoplasms / epidemiology. Glioblastoma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged. Risk Factors. Young Adult

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20869733.001).
  • [ISSN] 1773-0619
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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27. Al-Barbarawi MM, Qudsieh SM, Ghazzawi MA, Smith SF: Glioblastoma multiforme of the cerebellum. Neurosciences (Riyadh); 2009 Jan;14(1):84-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma multiforme of the cerebellum.
  • Glioblastoma multiforme (GBM) is a highly malignant glial tumor seen commonly in the cerebral hemispheres, but rarely encountered in the cerebellum.
  • It may occur at any age, but is seen more often in adult age groups.

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  • (PMID = 21048582.001).
  • [ISSN] 1319-6138
  • [Journal-full-title] Neurosciences (Riyadh, Saudi Arabia)
  • [ISO-abbreviation] Neurosciences (Riyadh)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
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28. Kartashev AV, Vinogradov VM: [Postoperative chemoradiotherapy for cerebral glioblastoma]. Vopr Onkol; 2008;54(4):471-4
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  • [Title] [Postoperative chemoradiotherapy for cerebral glioblastoma].
  • We developed a new method of accelerated chemoimmunoradiotherapy for cerebral glioblastoma and evaluated the immediate effects.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Immunotherapy / methods. Interleukin-2 / therapeutic use
  • [MeSH-minor] Adult. Aged. Carmustine / administration & dosage. Chemotherapy, Adjuvant. Dose Fractionation. Drug Administration Schedule. Female. Humans. Lomustine / administration & dosage. Male. Middle Aged. Postoperative Period. Radiotherapy, Adjuvant. Recombinant Proteins / therapeutic use. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 18942402.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Clinical Trial; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / Recombinant Proteins; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; U68WG3173Y / Carmustine
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29. Demir MK, Hakan T, Akinci O, Berkman Z: Primary cerebellar glioblastoma multiforme. Diagn Interv Radiol; 2005 Jun;11(2):83-6
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  • [Title] Primary cerebellar glioblastoma multiforme.
  • Primary glioblastoma multiforme of cerebellar hemispheres in adults is a rare condition.
  • Most of them result from dedifferentiation of astrocytoma to glioblastoma.
  • [MeSH-major] Cerebellar Neoplasms / radiography. Glioblastoma / radiography
  • [MeSH-minor] Adolescent. Adult. Diagnosis, Differential. Female. Headache / etiology. Humans. Magnetic Resonance Imaging. Male. Nausea / etiology. Neurologic Examination. Vomiting / etiology

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  • (PMID = 15957093.001).
  • [ISSN] 1305-3825
  • [Journal-full-title] Diagnostic and interventional radiology (Ankara, Turkey)
  • [ISO-abbreviation] Diagn Interv Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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30. Chong PK, Loo AV: Visual epilepsy in glioblastoma multiforme. Med J Malaysia; 2008 Dec;63(5):406-7
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  • [Title] Visual epilepsy in glioblastoma multiforme.
  • We report a 33-year-old Chinese gentleman who presented with visual epilepsy and symptoms of raised intracranial pressure in which clinical examination revealed normal visual fields and acuity despite Magnetic Resonance Imaging (MRI) brain showing large contrast enhancing mass at the right occipital lobe.
  • Craniotomy and excision of tumour was done and the histology confirmed glioblastoma multiforme (GBM).
  • [MeSH-major] Brain Neoplasms / pathology. Epilepsies, Partial / pathology. Glioblastoma / pathology. Hallucinations / pathology. Occipital Lobe / pathology
  • [MeSH-minor] Adult. Cranial Irradiation. Craniotomy. Humans. Magnetic Resonance Imaging. Male

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  • (PMID = 19803301.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
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31. Stark AM, Maslehaty H, Hugo HH, Mahvash M, Mehdorn HM: Glioblastoma of the cerebellum and brainstem. J Clin Neurosci; 2010 Oct;17(10):1248-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma of the cerebellum and brainstem.
  • Glioblastoma multiforme (GB) is the most common and most malignant primary intracranial tumor.
  • Of the 577 patients who underwent surgery for newly diagnosed GB (World Health Organization grade IV) between January 1991 and March 2008 at our department, seven had infratentorial GB (iGB) (incidence 1.2%).
  • Because of its rarity and the non-specific radiological features of iGB, it can easily be misdiagnosed as a brain metastasis, ependymoma or even as a benign lesion such as vestibular schwannoma or meningioma.
  • Postoperative adjuvant therapy similar to that for supratentorial glioblastoma is indicated.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Stem / pathology. Cerebellum / pathology. Glioblastoma / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Retrospective Studies. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20619657.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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32. Michelakis ED, Sutendra G, Dromparis P, Webster L, Haromy A, Niven E, Maguire C, Gammer TL, Mackey JR, Fulton D, Abdulkarim B, McMurtry MS, Petruk KC: Metabolic modulation of glioblastoma with dichloroacetate. Sci Transl Med; 2010 May 12;2(31):31ra34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolic modulation of glioblastoma with dichloroacetate.
  • Solid tumors, including the aggressive primary brain cancer glioblastoma multiforme, develop resistance to cell death, in part as a result of a switch from mitochondrial oxidative phosphorylation to cytoplasmic glycolysis.
  • We tested whether the small-molecule and orphan drug dichloroacetate (DCA) can reverse this cancer-specific metabolic and mitochondrial remodeling in glioblastoma.
  • In a separate experiment with five patients who had glioblastoma, we prospectively secured baseline and serial tumor tissue, developed patient-specific cell lines of glioblastoma and putative glioblastoma stem cells (CD133(+), nestin(+) cells), and treated each patient with oral DCA for up to 15 months.
  • Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastoma.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Dichloroacetic Acid / therapeutic use. Glioblastoma / drug therapy. Glioblastoma / metabolism
  • [MeSH-minor] Adult. Apoptosis / drug effects. Cell Line, Tumor. Female. Humans. In Vitro Techniques. Male. Membrane Potential, Mitochondrial / drug effects. Middle Aged. Mitochondria / drug effects. Mitochondria / metabolism. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Neovascularization, Pathologic / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Reactive Oxygen Species / metabolism

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  • (PMID = 20463368.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 9LSH52S3LQ / Dichloroacetic Acid; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.2 / pyruvate dehydrogenase (acetyl-transferring) kinase
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33. Krex D, Klink B, Hartmann C, von Deimling A, Pietsch T, Simon M, Sabel M, Steinbach JP, Heese O, Reifenberger G, Weller M, Schackert G, German Glioma Network: Long-term survival with glioblastoma multiforme. Brain; 2007 Oct;130(Pt 10):2596-606
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival with glioblastoma multiforme.
  • The median survival of glioblastoma patients is approximately 12 months.
  • To identify specific parameters that might be associated with this phenomenon, we performed a detailed clinical and molecular analysis of 55 primary glioblastoma long-term survivors recruited at the six clinical centres of the German Glioma Network and one associated centre.
  • Comparison of these data with results from an independent series of 141 consecutive unselected glioblastoma patients registered in the German Glioma Network revealed significantly more frequent MGMT hypermethylation in the long-term survivor group.
  • Taken together, our findings underline the association of glioblastoma long-term survival with prognostically favourable clinical factors, in particular young age and good initial performance score, as well as MGMT promoter hypermethylation.
  • [MeSH-major] Brain Neoplasms / diagnosis. Glioblastoma / diagnosis
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. DNA, Neoplasm / genetics. Female. Genes, erbB-1. Humans. Karnofsky Performance Status. Loss of Heterozygosity. Male. Middle Aged. Polymorphism, Single-Stranded Conformational. Prognosis. Risk Factors. Survivors. Tumor Suppressor Proteins / genetics

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  • (PMID = 17785346.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Number-of-references] 105
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34. Hassler M, Seidl S, Fazeny-Doerner B, Preusser M, Hainfellner J, Rössler K, Prayer D, Marosi C: Diversity of cytogenetic and pathohistologic profiles in glioblastoma. Cancer Genet Cytogenet; 2006 Apr 1;166(1):46-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diversity of cytogenetic and pathohistologic profiles in glioblastoma.
  • We present a small series of patients with primary glioblastoma multiforme (GBM), and combine individual genetic data with pathohistologic characteristics and clinical outcome.
  • By classical banding methods, 15/18 patients showed at least one aberration characteristic for primary glioblastoma (+7 in 7/18, deletions of 9p in 10/18 and -10 or deletions from 10q in 8/18 patients).
  • [MeSH-major] Brain Neoplasms / genetics. Genetic Variation. Glioblastoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Cycle Proteins / genetics. Chromosome Aberrations. DNA Methylation. Epigenesis, Genetic. Female. Fibroblast Growth Factor 2 / genetics. Gene Silencing. Homeodomain Proteins / genetics. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neovascularization, Pathologic. O(6)-Methylguanine-DNA Methyltransferase / genetics. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Prognosis. Promoter Regions, Genetic. Survival Rate. Tumor Suppressor Proteins / genetics. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 16616111.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Homeodomain Proteins; 0 / ING4 protein, human; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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35. Glas M, Hundsberger T, Stuplich M, Wiewrodt D, Kurzwelly D, Nguyen-Huu B, Rasch K, Herrlinger U: Nimustine (ACNU) plus teniposide (VM26) in recurrent glioblastoma. Oncology; 2009;76(3):184-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nimustine (ACNU) plus teniposide (VM26) in recurrent glioblastoma.
  • BACKGROUND: In a previous trial (NOA-01), the combination of nimustine and teniposide showed efficacy in previously untreated glioblastoma (GBM).
  • Grade 4 hematotoxicity was observed in 12 of 35 patients (34%) and in 14 of 83 evaluable chemotherapy courses (17%).
  • The data support the efficacy of the nimustine-teniposide chemotherapy, but the rate of high-grade hematotoxicity is increased.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Nimustine / administration & dosage. Teniposide / administration & dosage
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Retrospective Studies

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19218824.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0S726V972K / Nimustine; 957E6438QA / Teniposide
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36. Koul D: PTEN signaling pathways in glioblastoma. Cancer Biol Ther; 2008 Sep;7(9):1321-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PTEN signaling pathways in glioblastoma.
  • Malignant gliomas are the most common primary brain tumor in adults, but the prognosis for patients with these tumors remains poor despite advances in diagnosis and standard therapies such as surgery, radiation therapy, and chemotherapy.
  • Recent insights into the biology of gliomas include the finding that tyrosine kinase receptors and signal transduction pathways play a role in tumor initiation and maintenance.
  • Deregulation of phosphatidylinositol 3-kinase (PI3K) signaling pathways resulting from genetic alterations in the PTEN tumor suppressor gene on 10q23 at the level of LOH, mutation and methylation have been identified in at least 60% of glioblastoma.
  • Loss of PTEN function by mutation or LOH correlates with poor survival in anaplastic astrocytoma and glioblastoma, suggesting that PTEN plays a role in patient outcome.
  • Interestingly, amplification of Epidermal growth factor receptor (EGFR) in the background of heterozygous PTEN knockout mice develop invasive glioma very similar to human glioblastoma, demonstrating the importance of PTEN in glioma progression and providing a model system to evaluate the efficacy of targeting PTEN in glioblastoma.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. PTEN Phosphohydrolase / genetics. Signal Transduction / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Adult. Humans


37. Amini A, Schmidt RH, Salzman KL, Chin SS, Couldwell WT: Glioblastoma multiforme of the pineal region. J Neurooncol; 2006 Sep;79(3):307-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma multiforme of the pineal region.
  • Glioblastoma multiforme (GBMs) tumors are exceedingly rare tumors in the pineal region.
  • Pineal region GBM seems to be a very aggressive tumor with a high rate of leptomeningeal and ependymal metastatic disease.
  • Glioblastoma should be considered in the differential diagnosis of the pineal region tumors, especially when evidence of leptomeningeal or ependymal metastatic disease is present.
  • [MeSH-major] Brain / pathology. Glioblastoma / pathology. Pinealoma / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Headache / etiology. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Nausea / etiology. Tomography, X-Ray Computed. Vision Disorders / etiology. Vomiting / etiology

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  • (PMID = 16645719.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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38. Preusser M, Gelpi E, Matej R, Marosi C, Dieckmann K, Rössler K, Budka H, Hainfellner JA: No prognostic impact of survivin expression in glioblastoma. Acta Neuropathol; 2005 May;109(5):534-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] No prognostic impact of survivin expression in glioblastoma.
  • In the present study we investigated the immunohistochemical expression of survivin and its prognostic impact in a large glioblastoma series comprising 104 consecutive adult patients undergoing a first operation for glioblastoma.
  • Survivin was expressed in all glioblastoma samples, and was prominent in a fraction of nuclei of tumor cells and vascular cells.
  • In summary, in glioblastoma, survivin is expressed predominantly in proliferating tumor cell nuclei.
  • [MeSH-major] Apoptosis / physiology. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Glioblastoma / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Blotting, Western / methods. Cell Nucleus / metabolism. DNA Topoisomerases, Type II / metabolism. Female. Fluorescent Antibody Technique / methods. Humans. Inhibitor of Apoptosis Proteins. Ki-67 Antigen / metabolism. Male. Microscopy, Confocal. Middle Aged. Models, Biological. Prognosis. Retrospective Studies. Statistics as Topic

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  • (PMID = 15843906.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II
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39. Hashiguchi A, Morioka M, Ichimura H, Mimata C, Kuratsu J: Glioblastoma with an intratumoral feeding-artery aneurysm. Clin Neurol Neurosurg; 2007 Apr;109(3):302-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma with an intratumoral feeding-artery aneurysm.
  • We report a patient with recurrent glioblastoma, in whom serial magnetic resonance angiography (MRA) demonstrated gradual enlargement of an artery feeding the tumor and the development of an intratumoral aneurysm that led to intratumoral hemorrhage.
  • This is a rare case of glioblastoma in which the association of an intratumoral feeding-artery aneurysm, whose rupture led to intratumoral bleeding, was documented by serial MRA imaging and follow-up.
  • [MeSH-major] Brain Neoplasms / diagnosis. Cerebral Arteries / pathology. Cerebral Arteries / radiography. Glioblastoma / blood supply. Glioblastoma / diagnosis. Intracranial Aneurysm / pathology. Intracranial Aneurysm / radiography
  • [MeSH-minor] Adult. Aneurysm, Ruptured / radiography. Aneurysm, Ruptured / surgery. Female. Frontal Lobe / blood supply. Frontal Lobe / pathology. Frontal Lobe / surgery. Humans. Magnetic Resonance Angiography. Magnetic Resonance Imaging. Neoplasm Recurrence, Local. Neurosurgical Procedures. Tomography, X-Ray Computed

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  • (PMID = 17222964.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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40. Bähr O, Herrlinger U, Weller M, Steinbach JP: Very late relapses in glioblastoma long-term survivors. J Neurol; 2009 Oct;256(10):1756-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Very late relapses in glioblastoma long-term survivors.
  • Long-term survival of patients with histologically confirmed glioblastoma is a rare event with figures in the range of 2-3% for 5-year survival (Scott et al. in Ann Neurol 46:183-188, 1999; McLendon and Halperin in Cancer 98:1745-1748, 2003; Krex et al. in Brain 130:2596-2606, 2007).
  • We here report on the extended follow-up (mean, 139.4 months) of a cohort of glioblastoma long-term survivors.
  • [MeSH-major] Brain Neoplasms / epidemiology. Glioblastoma / epidemiology. Neoplasm Recurrence, Local / epidemiology
  • [MeSH-minor] Adult. Cohort Studies. Female. Follow-Up Studies. Humans. Male. Middle Aged. Survivors. Time Factors

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  • [Cites] Brain. 2007 Oct;130(Pt 10):2596-606 [17785346.001]
  • [Cites] Cancer. 2003 Oct 15;98(8):1745-8 [14534892.001]
  • [Cites] J Neurooncol. 1998 Jan;36(1):61-4 [9525826.001]
  • [Cites] Ann Neurol. 1999 Aug;46(2):183-8 [10443883.001]
  • [Cites] Neurology. 2006 Jan 24;66(2):239-42 [16434662.001]
  • (PMID = 19434438.001).
  • [ISSN] 1432-1459
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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41. Fischer U, Leidinger P, Keller A, Folarin A, Ketter R, Graf N, Lenhof HP, Meese E: Amplicons on chromosome 12q13-21 in glioblastoma recurrences. Int J Cancer; 2010 Jun 1;126(11):2594-602
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplicons on chromosome 12q13-21 in glioblastoma recurrences.
  • Here, we investigated the fate of amplified regions in several independent cases of recurrent glioblastoma and the possible association of 12q13-21 amplifications and survival.
  • We analyzed 12q13-21 amplicon numbers and sizes in glioblastoma and their recurrences by array-CGH.
  • The majority of the 12q13-21 amplicons found in the original tumor are lost in the subsequent recurrence.
  • Understanding genetic changes including gene amplifications in the development of tumor recurrences will contribute to rational therapeutic strategies for an improved patient survival.
  • We recognized a significant longer survival time in glioblastoma patients that lack amplifications of either CDK4, CYP27B1, XRCC6BP1 (KUB3), or MDM2.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Comparative Genomic Hybridization / methods. Gene Amplification / genetics. Glioblastoma / genetics
  • [MeSH-minor] Adult. Aged. Biopsy. Chromosome Mapping. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Survivors

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  • (PMID = 19839052.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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42. Shibahara J, Fukayama M: Secondary glioblastoma with advanced neuronal immunophenotype. Virchows Arch; 2005 Sep;447(3):665-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary glioblastoma with advanced neuronal immunophenotype.
  • We describe an unusual progression of astrocytoma into secondary glioblastoma exhibiting advanced neuronal immunophenotype.
  • A tumor of the left frontal lobe of a 35-year-old man was diagnosed as astrocytoma.
  • The tumor was treated by partial removal with postoperative chemoradiotherapy, followed by extensive removal of the residual regrowing tumor 5 month later.
  • A secondary tumor was discovered and partially resected 8 years later, but the patient died 11 months following the operation due to extensive tumor progression showing subarachnoidal and intraventricular dissemination.
  • The secondary tumor was small cell-predominant, highly proliferative tumor with an extremely high MIB-1 labeling index (80%).
  • Unexpectedly, most of the tumor cells were positive for neuronal markers (synaptophysin and NeuN), but not for glial fibrillary acidic protein (GFAP).
  • Retrospective examination of the original tumor revealed not only diffuse GFAP expression, but also neuronal marker expressions in small numbers of tumor cells that were hard to discriminate from the other cells on hematoxylin-eosin (HE) stain.
  • This way of malignant progression of astrocytoma was quite unusual.
  • Although the secondary tumor was classified as glioblastoma according to World Health Organization (WHO) classification (2000), it might be categorized into new variants of malignant glioneuronal tumors proposed recently.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Fatal Outcome. Humans. Immunohistochemistry. Immunophenotyping. Male

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  • [Cites] Neurosurgery. 2004 Dec;55(6):1377-91: discussion 1391-2 [15574220.001]
  • [Cites] Clin Neuropathol. 1994 Jan-Feb;13(1):1-11 [7518371.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Nov;60(11):1099-104 [11706939.001]
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  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Acta Neurochir (Wien). 1994;126(2-4):84-92 [8042560.001]
  • [Cites] Nat Rev Neurosci. 2001 Apr;2(4):287-93 [11283751.001]
  • [Cites] Am J Pathol. 1991 Jul;139(1):67-79 [1713022.001]
  • (PMID = 15968544.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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43. Kroonen J, Nguyen-Khac MT, Deprez M, Rogister B, Robe P: [Glioblastoma, an example of translational research?]. Rev Med Liege; 2008 May-Jun;63(5-6):251-6
ORBi (University of Liege). Free full Text at ORBi .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Glioblastoma, an example of translational research?].
  • Among patients which develop glioblastoma multiform (GBM), recurrence is the rule despite continuous progress in surgery, radiotherapy and chemotherapy.
  • In the adult, GBM is the most frequent and most aggressive tumour of the Central Nervous System.
  • It is thus very attractive to speculate on a possible relationship between these GBM stem cells and the neural stem cells which are persisting in the neurogenic zones of the adult brain.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology

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  • (PMID = 18669189.001).
  • [ISSN] 0370-629X
  • [Journal-full-title] Revue médicale de Liège
  • [ISO-abbreviation] Rev Med Liege
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Belgium
  • [Number-of-references] 27
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44. Schmidt F, Fischer J, Herrlinger U, Dietz K, Dichgans J, Weller M: PCV chemotherapy for recurrent glioblastoma. Neurology; 2006 Feb 28;66(4):587-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PCV chemotherapy for recurrent glioblastoma.
  • The authors administered procarbazine, 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU, lomustine), and vincristine (PCV) to 86 patients with recurrent glioblastoma.
  • World Health Organization grade III/IV hematologic toxicity was common (25.6%), but nonhematologic toxicity was mild.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Aged. Disease Progression. Disease-Free Survival. Female. Humans. Lomustine / administration & dosage. Male. Middle Aged. Procarbazine / administration & dosage. Recurrence. Time Factors. Vincristine / administration & dosage

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  • (PMID = 16505319.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; PCV protocol
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45. Birbilis TA, Matis GK, Eleftheriadis SG, Theodoropoulou EN, Sivridis E: Spinal metastasis of glioblastoma multiforme: an uncommon suspect? Spine (Phila Pa 1976); 2010 Apr 1;35(7):E264-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spinal metastasis of glioblastoma multiforme: an uncommon suspect?
  • OBJECTIVE: To report a case and review the literature on glioblastoma multiforme (GBM) with drop-like metastasis to the spine.
  • SUMMARY OF BACKGROUND DATA: GBM constitutes the most common adult malignant brain tumor with poor prognosis.
  • CONCLUSION: Spinal metastases should be commonly suspected in patients with a history of intracranial GBM who complain about symptoms not explained by the primary lesion.Glioblastoma multiforme (GBM) was first described by Rudolph Virchow in 1863 and represents the most common and most malignant tumor of the cerebral hemispheres, usually arising between the ages of 40 and 60 years.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / secondary. Pineal Gland / pathology. Spinal Neoplasms / secondary

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  • (PMID = 20195200.001).
  • [ISSN] 1528-1159
  • [Journal-full-title] Spine
  • [ISO-abbreviation] Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. Quick A, Patel D, Hadziahmetovic M, Chakravarti A, Mehta M: Current therapeutic paradigms in glioblastoma. Rev Recent Clin Trials; 2010 Jan;5(1):14-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current therapeutic paradigms in glioblastoma.
  • Glioblastoma (GBM), a WHO grade IV malignant glioma, is the most common and lethal adult primary brain tumor.
  • The expression of specific molecular biomarkers, especially O-6-methylguanine methyltransferase (MGMT) status, may determine the response of the tumor to treatment, and helps in identifying the magnitude of benefit from this regimen.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery
  • [MeSH-minor] Adult. Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Chemotherapy, Adjuvant. Clinical Trials as Topic. DNA Modification Methylases / analysis. DNA Repair Enzymes / analysis. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Humans. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Radiotherapy, Adjuvant. Receptor, Epidermal Growth Factor / antagonists & inhibitors. TOR Serine-Threonine Kinases. Tumor Suppressor Proteins / analysis

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  • (PMID = 20205684.001).
  • [ISSN] 1876-1038
  • [Journal-full-title] Reviews on recent clinical trials
  • [ISO-abbreviation] Rev Recent Clin Trials
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1RC2CA148190-01; United States / NCI NIH HHS / CA / 7R01CA108633-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Intracellular Signaling Peptides and Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 6.5.1.- / DNA Repair Enzymes
  • [Number-of-references] 117
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47. Martini M, Pallini R, Luongo G, Cenci T, Lucantoni C, Larocca LM: Prognostic relevance of SOCS3 hypermethylation in patients with glioblastoma multiforme. Int J Cancer; 2008 Dec 15;123(12):2955-60
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic relevance of SOCS3 hypermethylation in patients with glioblastoma multiforme.
  • Alterations in the signal transduction pathways are key mechanisms in the pathogenesis of de novo glioblastoma multiforme (GBM), which are also involved in the resistance to chemo- and radiotherapy.
  • Our data suggest that methylation of SOCS3 may be involved in the pathogenesis of GBM and in the resistance of this neoplasm to conventional treatment.
  • [MeSH-major] DNA Methylation. Glioblastoma / metabolism. Suppressor of Cytokine Signaling Proteins / metabolism
  • [MeSH-minor] Adult. Aged. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Promoter Regions, Genetic. RNA, Messenger / metabolism. Tumor Suppressor Proteins / metabolism

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18770864.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / SOCS1 protein, human; 0 / SOCS2 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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48. Biswas T, Okunieff P, Schell MC, Smudzin T, Pilcher WH, Bakos RS, Vates GE, Walter KA, Wensel A, Korones DN, Milano MT: Stereotactic radiosurgery for glioblastoma: retrospective analysis. Radiat Oncol; 2009;4:11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stereotactic radiosurgery for glioblastoma: retrospective analysis.
  • PURPOSE: This retrospective study was done to better understand the conditions for which stereotactic radiosurgery (SRS) for glioblastoma may be efficacious.
  • METHODS: Between 2000 and 2007, 33 patients with a pathological diagnosis of glioblastoma received SRS with the Novalis Shaped Beam Radiosurgery system.
  • Eighteen patients (54%) underwent salvage SRS for recurrence while 15 (45%) patients received upfront SRS following standard fractionated RT for newly diagnosed glioblastoma.
  • RESULTS: There were no RTOG grade >2 acute side effects.
  • CONCLUSION: SRS is well tolerated in the treatment of glioblastoma.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery. Radiosurgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Retrospective Studies. Salvage Therapy / methods. Treatment Outcome

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  • (PMID = 19292912.001).
  • [ISSN] 1748-717X
  • [Journal-full-title] Radiation oncology (London, England)
  • [ISO-abbreviation] Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2662864
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49. Stockhammer F, Misch M, Koch A, Czabanka M, Plotkin M, Blechschmidt C, Tuettenberg J, Vajkoczy P: Continuous low-dose temozolomide and celecoxib in recurrent glioblastoma. J Neurooncol; 2010 Dec;100(3):407-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Continuous low-dose temozolomide and celecoxib in recurrent glioblastoma.
  • Even after gross tumor resection and combined radiochemotherapy, glioblastomas recur within a few months.
  • Previously, low-dose metronomic temozolomide in combination with cyclo-oxigenase 2 inhibitors has had a beneficial effect as first-line treatment for glioblastoma.
  • From June 2007 to April 2009, 28 patients with recurrent glioblastoma received continuous low-dose temozolomide of 10 mg/m(2) twice daily and 200 mg celecoxib.
  • Before therapy the recurrent tumor was resected in 19 of 28 patients.
  • Tumor progression was defined by the Macdonald criteria on MRI every 8-12 weeks or by clinical deterioration.
  • Except for a lymphopenia in one patient, there was no grade 3 or 4 toxicity.
  • A high FET uptake correlated with tumor control after 6 months under therapy (P = 0.041, t-test).
  • Low-dose continuous temozolomide in combination with celecoxib seems to have activity in recurrent glioblastoma without relevant toxicity.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols. Celecoxib. DNA Modification Methylases / genetics. DNA Modification Methylases / metabolism. DNA Repair Enzymes / genetics. DNA Repair Enzymes / metabolism. Disease-Free Survival. Female. Fluorine Radioisotopes. Follow-Up Studies. Humans. Male. Methylation / drug effects. Middle Aged. Positron-Emission Tomography / methods. Retrospective Studies. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. Tyrosine / analogs & derivatives

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  • (PMID = 20446016.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cyclooxygenase 2 Inhibitors; 0 / Fluorine Radioisotopes; 0 / O-(3-fluoropropyl)tyrosine; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tumor Suppressor Proteins; 42HK56048U / Tyrosine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; JCX84Q7J1L / Celecoxib
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50. Arslan M, Karadeniz AN, Aksu G, Güveli M, Fayda M, Doğan AK, Akyüz F: Postoperative hypofractionated radiotherapy in glioblastoma multiforme. J BUON; 2006 Jan-Mar;11(1):39-42
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  • [Title] Postoperative hypofractionated radiotherapy in glioblastoma multiforme.
  • PURPOSE: To evaluate the safety and efficacy of hypofractionated radiotherapy (HRT) in glioblastoma multiforme (GM) patients in terms of overall and progression-free survival.
  • PATIENTS AND METHODS: Adult patients with GM were prospectively treated with HRT after total, subtotal or partial tumor excision.
  • HRT was applied 3 days a week with a tumor dose of 3.33 Gy per fraction.
  • The tumor was multifocal in one (5%) case.
  • The types of operations used were total tumor excision 10(50%) cases, subtotal excision 5 (25%) cases and partial excision 5 (25%) cases.
  • Acute toxicity was minimal and only one HRT patient had late toxicity (brain necrosis).
  • [MeSH-major] Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Radiotherapy, Conformal / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose Fractionation. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / radiotherapy. Pilot Projects. Postoperative Period. Prognosis. Prospective Studies. Radiotherapy Planning, Computer-Assisted. Survival Rate

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  • (PMID = 17318950.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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51. Haynik DM, Roma AA, Prayson RA: HER-2/neu expression in glioblastoma multiforme. Appl Immunohistochem Mol Morphol; 2007 Mar;15(1):56-8
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  • [Title] HER-2/neu expression in glioblastoma multiforme.
  • Although information is limited, one study suggested that 15% of glioblastoma multiforme (GBM) express HER-2/neu by immunohistochemistry (IHC); gene amplification by fluorescence in situ hybridization (FISH) was not investigated.
  • Initial surgery involved tumor debulking or subtotal resection in 34 patients.
  • At follow-up (range 1.0 to 49.5 mo, mean 10.5 mo), 40 patients died with tumor and 4 patients were lost to follow-up.

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  • (PMID = 17536308.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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52. Kaneshiro D, Kobayashi T, Chao ST, Suh J, Prayson RA: Chromosome 1p and 19q deletions in glioblastoma multiforme. Appl Immunohistochem Mol Morphol; 2009 Dec;17(6):512-6
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  • [Title] Chromosome 1p and 19q deletions in glioblastoma multiforme.
  • In glioblastoma multiforme (GBM), the impact on prognosis of these alterations in GBM is unclear.

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  • (PMID = 19602970.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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53. Weiler M, Hartmann C, Wiewrodt D, Herrlinger U, Gorlia T, Bähr O, Meyermann R, Bamberg M, Tatagiba M, von Deimling A, Weller M, Wick W: Chemoradiotherapy of newly diagnosed glioblastoma with intensified temozolomide. Int J Radiat Oncol Biol Phys; 2010 Jul 1;77(3):670-6
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  • [Title] Chemoradiotherapy of newly diagnosed glioblastoma with intensified temozolomide.
  • PURPOSE: To evaluate the toxicity and efficacy of chemoradiotherapy with temozolomide (TMZ) administered in an intensified 1-week on/1-week off schedule plus indomethacin in patients with newly diagnosed glioblastoma.
  • PATIENTS AND METHODS: A total of 41 adult patients (median Karnofsky performance status, 90%; median age, 56 years) were treated with preirradiation TMZ at 150 mg/m(2) (1 week on/1 week off), involved-field radiotherapy combined with concomitant low-dose TMZ (50 mg/m(2)), maintenance TMZ starting at 150 mg/m(2) using a 1-week on/1-week off schedule, plus maintenance indomethacin (25 mg twice daily).
  • Grade 4 hematologic toxicity was observed in 15 patients (36.6%).
  • Treatment-related nonhematologic Grade 4-5 toxicity was reported for 2 patients (4.9%).
  • The presence of O(6)-methylguanine-DNA methyltransferase (MGMT) gene promoter methylation in the tumor tissue was associated with significantly superior progression-free survival.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adult. Aged. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Combined Modality Therapy / methods. Confidence Intervals. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Germany. Humans. Indomethacin / administration & dosage. Karnofsky Performance Status. Male. Middle Aged. Prospective Studies. Survival Rate. Tumor Suppressor Proteins / genetics

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  • [Copyright] (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19836157.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; XXE1CET956 / Indomethacin
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54. Hottinger AF, Yoon H, DeAngelis LM, Abrey LE: Neurological outcome of long-term glioblastoma survivors. J Neurooncol; 2009 Dec;95(3):301-305
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurological outcome of long-term glioblastoma survivors.
  • Extended survival of 3 or more years is rare in patients with glioblastoma (GBM) but is becoming more common.
  • Twenty-seven had tumor progression a median of 29.2 months after diagnosis (range: 1.2-167 months); 18 had multiple relapses.
  • [MeSH-major] Brain Neoplasms / mortality. Cognition Disorders / mortality. Glioblastoma / mortality. Quality of Life. Survivors / statistics & numerical data
  • [MeSH-minor] Adolescent. Adult. Aged. Databases, Factual. Follow-Up Studies. Humans. Karnofsky Performance Status. Middle Aged. Neoplasm Recurrence, Local / mortality. Retrospective Studies. Survival Analysis. Young Adult

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  • (PMID = 19557499.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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55. Ang C, Guiot MC, Ramanakumar AV, Roberge D, Kavan P: Clinical significance of molecular biomarkers in glioblastoma. Can J Neurol Sci; 2010 Sep;37(5):625-30
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  • [Title] Clinical significance of molecular biomarkers in glioblastoma.
  • AIM: To review the impact of molecular biomarkers on response to therapy and survival in patients with primary glioblastoma (GBM).
  • [MeSH-major] Biomarkers / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Glioblastoma / diagnosis. Glioblastoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / therapeutic use. DNA Methylation / drug effects. DNA Methylation / genetics. DNA Modification Methylases / genetics. DNA Modification Methylases / metabolism. DNA Repair Enzymes / genetics. DNA Repair Enzymes / metabolism. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Regression Analysis. Retrospective Studies. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism. Young Adult

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  • (PMID = 21059509.001).
  • [ISSN] 0317-1671
  • [Journal-full-title] The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
  • [ISO-abbreviation] Can J Neurol Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers; 0 / Neoplasm Proteins; 0 / P16 protein, human; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.5.1.- / DNA Repair Enzymes
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56. Pistollato F, Abbadi S, Rampazzo E, Viola G, Della Puppa A, Cavallini L, Frasson C, Persano L, Panchision DM, Basso G: Hypoxia and succinate antagonize 2-deoxyglucose effects on glioblastoma. Biochem Pharmacol; 2010 Nov 15;80(10):1517-27
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  • [Title] Hypoxia and succinate antagonize 2-deoxyglucose effects on glioblastoma.
  • Glioblastoma multiforme (GBM) are highly proliferative brain tumors characterized by a hypoxic microenvironment which controls GBM stem cell maintenance.
  • Tumor hypoxia promotes also elevated glycolytic rate; thus, limiting glucose metabolism is a potential approach to inhibit tumor growth.
  • By adding succinate these effects are reverted, as succinate stabilizes HIF-1α and increases GBM stem cell fraction particularly under hypoxia, thus preserving the tumor stem cell niche.
  • 2-DG inhibits anaerobic glycolysis altering GBM cell phenotype by forcing tumor cells into mitochondrial metabolism and by inducing differentiation.
  • [MeSH-major] Brain. Deoxyglucose / pharmacology. Glioblastoma. Succinic Acid / metabolism
  • [MeSH-minor] Adult. Apoptosis / drug effects. Blotting, Western. Cell Adhesion / drug effects. Cell Culture Techniques. Cell Differentiation / drug effects. Cell Hypoxia / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Child. Glutathione / metabolism. Glycolysis. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. Membrane Potential, Mitochondrial / drug effects. Oxygen / pharmacology. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Succinate Dehydrogenase / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20705058.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Reactive Oxygen Species; 9G2MP84A8W / Deoxyglucose; AB6MNQ6J6L / Succinic Acid; EC 1.3.99.1 / Succinate Dehydrogenase; GAN16C9B8O / Glutathione; S88TT14065 / Oxygen
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57. Gaspar N, Sharp SY, Eccles SA, Gowan S, Popov S, Jones C, Pearson A, Vassal G, Workman P: Mechanistic evaluation of the novel HSP90 inhibitor NVP-AUY922 in adult and pediatric glioblastoma. Mol Cancer Ther; 2010 May;9(5):1219-33
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  • [Title] Mechanistic evaluation of the novel HSP90 inhibitor NVP-AUY922 in adult and pediatric glioblastoma.
  • The dismal prognosis of glioblastoma (GB) indicates the urgent need for new therapies for these tumors.
  • Here, we explored the mechanistic potential of the potent synthetic diarylisoxazole amide resorcinol HSP90 inhibitor, NVP-AUY922, in adult and pediatric GB.
  • In vitro antiproliferative potency (nanomolar range) was seen in both adult and pediatric human GB cell lines with different molecular pathologies.
  • A cytostatic effect was observed in all GB lines; more apoptosis was observed at lower concentrations in the SF188 pediatric GB line and at 144 hours in the slower growing KNS42 pediatric GB line, as compared with the adult GB lines U87MG and SF268.
  • NVP-AUY922 antitumor activity with objective tumor regression resulted from antiproliferative, proapoptotic, and antiangiogenic effects, the latter shown by decreased microvessel density and HIF1alpha levels.
  • Our results have established a mechanistic proof of concept for the potential of novel synthetic HSP90 inhibitors in adult and pediatric GB, alone or in combination with phosphoinositide 3-kinase/mammalian target of rapamycin and mitogen-activated protein/ERK kinase inhibitors.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Isoxazoles / pharmacology. Isoxazoles / therapeutic use. Resorcinols / pharmacology. Resorcinols / therapeutic use
  • [MeSH-minor] Adult. Animals. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Child. Dose-Response Relationship, Drug. Female. Humans. Maximum Tolerated Dose. Mice. Mice, Nude. Treatment Outcome. Xenograft Model Antitumor Assays


58. Bryant NL, Suarez-Cuervo C, Gillespie GY, Markert JM, Nabors LB, Meleth S, Lopez RD, Lamb LS Jr: Characterization and immunotherapeutic potential of gammadelta T-cells in patients with glioblastoma. Neuro Oncol; 2009 Aug;11(4):357-67
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  • [Title] Characterization and immunotherapeutic potential of gammadelta T-cells in patients with glioblastoma.
  • Classical immunotherapeutic approaches to glioblastoma multiforme (GBM) have shown mixed results, and therapies focused on innate lymphocyte activity against GBM have not been rigorously evaluated.
  • We examined peripheral blood lymphocyte phenotype, gammadelta T-cell number, mitogenic response, and cytotoxicity against GBM cell lines and primary tumor explants from GBM patients at selected time points prior to and during GBM therapy.
  • Perivascular T-cell accumulation was noted in paraffin sections, but no organized T-cell invasion of the tumor parenchyma was seen.
  • Taken together, these data suggest that gammadelta T-cell depletion and impaired function occur prior to or concurrent with the growth of the tumor.

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  • (PMID = 19211933.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50 CA 097247-06A1; United States / NINDS NIH HHS / NS / R21 NS057431-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptors, Antigen, T-Cell, gamma-delta
  • [Other-IDs] NLM/ PMC2743216
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59. Vredenburgh JJ, Desjardins A, Herndon JE 2nd, Marcello J, Reardon DA, Quinn JA, Rich JN, Sathornsumetee S, Gururangan S, Sampson J, Wagner M, Bailey L, Bigner DD, Friedman AH, Friedman HS: Bevacizumab plus irinotecan in recurrent glioblastoma multiforme. J Clin Oncol; 2007 Oct 20;25(30):4722-9
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  • [Title] Bevacizumab plus irinotecan in recurrent glioblastoma multiforme.
  • PURPOSE: The prognosis for patients with recurrent glioblastoma multiforme is poor, with a median survival of 3 to 6 months.
  • After this regimen was deemed safe and effective, the irinotecan schedule was changed to an accepted brain tumor regimen of four doses in 6 weeks, in anticipation of a phase III randomized trial of irinotecan versus irinotecan and bevacizumab.
  • One patient developed a CNS hemorrhage, which occurred in his 10th cycle.
  • CONCLUSION: Bevacizumab and irinotecan is an effective treatment for recurrent glioblastoma multiforme and has moderate toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • [CommentIn] Nat Clin Pract Oncol. 2008 Apr;5(4):186-7 [18285760.001]
  • [CommentIn] J Clin Oncol. 2007 Oct 20;25(30):4705-6 [17947716.001]
  • [CommentIn] J Clin Oncol. 2008 Nov 10;26(32):5304-5; author reply 5305 [18854564.001]
  • [CommentIn] Nat Clin Pract Neurol. 2008 May;4(5):242-3 [18212790.001]
  • [CommentIn] J Clin Oncol. 2008 Feb 20;26(6):1012-3; author reply 1013 [18281677.001]
  • (PMID = 17947719.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 4 R37 CA11898; United States / NCI NIH HHS / CA / 5 P50 CA108786; United States / NINDS NIH HHS / NS / 5 P50 NS20023
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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60. Martinez R, Rohde V, Schackert G: Different molecular patterns in glioblastoma multiforme subtypes upon recurrence. J Neurooncol; 2010 Feb;96(3):321-9
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  • [Title] Different molecular patterns in glioblastoma multiforme subtypes upon recurrence.
  • One of the hallmarks of glioblastoma is its inherent tendency to recur.
  • In all tumor samples, we have analyzed p53 and PTEN status by sequencing analysis, EGFR amplification by semiquantitative PCR and a wide-genome fingerprinting was performed by microsatellite analysis.
  • Upon recurrence, we have detected two molecular patterns of tumor progression: GBM initially showing either type 1 or type 2 profiles conserved them at the time of relapse.
  • Taken together, our results strongly suggest that recurrences of GBM may display two distinct pattern of accumulation of molecular alterations depending on the profile of the original tumor.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Glioblastoma / genetics. Mutation / genetics. PTEN Phosphohydrolase / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. DNA Mutational Analysis. Female. Humans. Male. Middle Aged

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  • (PMID = 19644652.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2811648
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61. Parsons DW, Jones S, Zhang X, Lin JC, Leary RJ, Angenendt P, Mankoo P, Carter H, Siu IM, Gallia GL, Olivi A, McLendon R, Rasheed BA, Keir S, Nikolskaya T, Nikolsky Y, Busam DA, Tekleab H, Diaz LA Jr, Hartigan J, Smith DR, Strausberg RL, Marie SK, Shinjo SM, Yan H, Riggins GJ, Bigner DD, Karchin R, Papadopoulos N, Parmigiani G, Vogelstein B, Velculescu VE, Kinzler KW: An integrated genomic analysis of human glioblastoma multiforme. Science; 2008 Sep 26;321(5897):1807-12
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  • [Title] An integrated genomic analysis of human glioblastoma multiforme.
  • Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer.
  • To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples.
  • These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.

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  • (PMID = 18772396.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA043460-27; United States / NCI NIH HHS / CA / CA57345; United States / NCI NIH HHS / CA / R37 CA043460; United States / NCI NIH HHS / CA / R37 CA043460-27; United States / NINDS NIH HHS / NS / NS052507; United States / NCI NIH HHS / CA / CA121113; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R37 CA057345-13; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / R37 CA057345-18; United States / NCI NIH HHS / CA / CA09547; United States / NCI NIH HHS / CA / R01 CA121113; United States / NCI NIH HHS / CA / R01 CA140316; United States / NCI NIH HHS / CA / CA108786; United States / NCI NIH HHS / CA / CA43460; United States / NCI NIH HHS / CA / CA062924-160017; United States / NCI NIH HHS / CA / R01 CA121113-04; United States / NCI NIH HHS / CA / CA057345-13; United States / NCI NIH HHS / CA / P50 CA062924-160017; United States / NCI NIH HHS / CA / CA057345-17; United States / NCI NIH HHS / CA / CA11898; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA057345-18; United States / NCI NIH HHS / CA / R37 CA057345-17; United States / NCI NIH HHS / CA / R37 CA057345; United States / NINDS NIH HHS / NS / 5P50-NS-20023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
  • [Other-IDs] NLM/ NIHMS105586; NLM/ PMC2820389
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62. Luetjens G, Mirzayan MJ, Brandis A, Krauss JK: Exophytic giant cell glioblastoma of the medulla oblongata. J Neurosurg; 2009 Mar;110(3):589-93
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  • [Title] Exophytic giant cell glioblastoma of the medulla oblongata.
  • Giant cell glioblastoma is a rare variant within the spectrum of glioblastoma multiforme (GBM) tumors.
  • A giant cell glioblastoma may be associated with a better prognosis than the common type of GBM after combined treatment involving tumor resection and radiochemotherapy.
  • A giant cell glioblastoma may occur at various sites in the brain and spinal cord.
  • To the authors' knowledge, this type of tumor has not been previously reported as arising as an exophytic tumor from the medulla oblongata.
  • The authors report on a 40-year-old man who presented with a large tumor located in the caudal fourth ventricle.
  • The tumor was removed completely and the patient underwent percutaneous radiotherapy with 60 Gy and concomitant chemotherapy with temozolomide.
  • Histopathological examination of the tumor revealed the typical features of a giant cell glioblastoma.
  • At the 2-year follow-up the patient was doing well and showed no signs of tumor recurrence.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Medulla Oblongata
  • [MeSH-minor] Adult. Combined Modality Therapy. Humans. Male

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  • (PMID = 19061354.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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63. Mulholland PJ, Fiegler H, Mazzanti C, Gorman P, Sasieni P, Adams J, Jones TA, Babbage JW, Vatcheva R, Ichimura K, East P, Poullikas C, Collins VP, Carter NP, Tomlinson IP, Sheer D: Genomic profiling identifies discrete deletions associated with translocations in glioblastoma multiforme. Cell Cycle; 2006 Apr;5(7):783-91
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  • [Title] Genomic profiling identifies discrete deletions associated with translocations in glioblastoma multiforme.
  • Glioblastoma multiforme is the most common tumor arising in the central nervous system.
  • In this study, we identify copy number changes in a series of glioblastoma multiforme tumors and cell lines by applying high-resolution microarray comparative genomic hybridization.
  • [MeSH-major] Chromosome Deletion. Gene Expression Profiling. Genome, Human / genetics. Glioblastoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Cytogenetics. Female. Gene Dosage / genetics. Gene Expression. Genomics. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nucleic Acid Hybridization

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  • (PMID = 16582634.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A3585; United Kingdom / Cancer Research UK / / A6618
  • [Publication-type] Journal Article
  • [Publication-country] United States
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64. Roma AA, Prayson RA: Fascin expression in 90 patients with glioblastoma multiforme. Ann Diagn Pathol; 2005 Dec;9(6):307-11
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  • [Title] Fascin expression in 90 patients with glioblastoma multiforme.
  • Fascin immunohistochemical analysis was performed in 90 glioblastoma multiforme, including 53 males and 37 females (mean age, 58.3 years).
  • Nineteen tumors showed more than 75% positive staining tumor cells, 14 tumors had more than 50% to 75% staining, 23 tumors had more than 25% to 50% staining, 26 tumors had more than 5% to 25% staining, and 8 tumors had less than 5% staining.
  • In comparison, 9 of 11 low-grade astrocytomas had 50% or less staining for fascin.
  • Higher grade tumors generally expressed a greater degree of fascin staining.
  • There was no obvious correlation with the extent of staining and survival among glioblastoma multiforme.
  • Fascin may play a role in tumor cell infiltration.
  • [MeSH-major] Brain Neoplasms / metabolism. Carrier Proteins / metabolism. Glioblastoma / metabolism. Microfilament Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytoma / metabolism. Astrocytoma / pathology. Child. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis

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  • (PMID = 16308158.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Microfilament Proteins; 146808-54-0 / fascin
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65. Wei KC, Huang CY, Chen PY, Feng LY, Wu TW, Chen SM, Tsai HC, Lu YJ, Tsang NM, Tseng CK, Pai PC, Shin JW: Evaluation of the prognostic value of CD44 in glioblastoma multiforme. Anticancer Res; 2010 Jan;30(1):253-9
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  • [Title] Evaluation of the prognostic value of CD44 in glioblastoma multiforme.
  • BACKGROUND/AIM: Glioblastoma and astrocytoma are the most common brain tumors affecting adults 45-60 years of age.
  • The poor prognosis for glioblastoma patients results from recurrence after treatment.
  • PATIENTS AND METHODS: Microarray analyses of clinical specimens from glioblastoma patients were used to identify potential tumor markers.
  • In particular, expression of the CD44 antigen was elevated in more severe tumor types, and higher in tumor cores than in peripheral regions.
  • [MeSH-major] Antigens, CD44 / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics
  • [MeSH-minor] Adult. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 20150644.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / CD44 protein, human
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66. Ricci-Vitiani L, Pallini R, Larocca LM, Lombardi DG, Signore M, Pierconti F, Petrucci G, Montano N, Maira G, De Maria R: Mesenchymal differentiation of glioblastoma stem cells. Cell Death Differ; 2008 Sep;15(9):1491-8
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesenchymal differentiation of glioblastoma stem cells.
  • Glioblastoma multiforme is a severe form of cancer most likely arising from the transformation of stem or progenitor cells resident in the brain.
  • Although the tumorigenic population in glioblastoma is defined as composed by cancer stem cells (CSCs), the cellular target of the transformation hit remains to be identified.
  • Subcutaneous injection of CSCs or single CSC clones from two of seven patients produced tumor xenografts containing osteo-chondrogenic areas in the context of glioblastoma-like tumor lesions.
  • Interestingly, mesenchymal differentiation of the tumor xenografts was associated with reduction of both growth rate and mitotic index.
  • The discovery of such biological properties might provide considerable information to the development of new therapeutic strategies aimed at forcing glioblastoma stem cell differentiation.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Mesoderm / cytology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Adult. Aged. Animals. Cell Differentiation. Clone Cells. Female. Humans. Male. Mice. Mice, SCID. Middle Aged. Neurons / cytology. Xenograft Model Antitumor Assays

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  • (PMID = 18497759.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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67. Shih HA, Betensky RA, Dorfman MV, Louis DN, Loeffler JS, Batchelor TT: Genetic analyses for predictors of radiation response in glioblastoma. Int J Radiat Oncol Biol Phys; 2005 Nov 1;63(3):704-10
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  • [Title] Genetic analyses for predictors of radiation response in glioblastoma.
  • PURPOSE: Radiotherapy (RT) for patients with glioblastoma improves survival and is recommended for nearly all patients with this diagnosis.
  • Prior studies have suggested that underlying genetic alterations in the tumor may account for some of this treatment-related heterogeneity.
  • It has been previously reported that epidermal growth factor receptor (EGFR) gene amplification and TP53 mutation correlate with the response to RT in patients with glioblastoma.
  • METHODS AND MATERIALS: We sought to identify molecular markers that could predict the response to RT, progression-free survival after RT, and overall survival among 75 glioblastoma patients treated with RT at a single institution.
  • However, in accordance with recent observations that the prognostic effects of genetic alterations in glioblastoma may depend on patient age, we observed age-dependent prognostic effects of TP53 and CDKN2A/p16 alterations in our patient population.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / radiotherapy. Glioblastoma / genetics. Glioblastoma / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 19 / genetics. Disease-Free Survival. Female. Gene Amplification. Gene Deletion. Genes, p16. Genes, p53 / genetics. Genetic Markers. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 15978739.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA57683
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Neoplasm Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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68. Deb P, Sharma MC, Mahapatra AK, Agarwal D, Sarkar C: Glioblastoma multiforme with long term survival. Neurol India; 2005 Sep;53(3):329-32
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  • [Title] Glioblastoma multiforme with long term survival.
  • Glioblastoma multiforme (GBM) Patients generally have a dismal prognosis, with median survival of 10-12 months.
  • [MeSH-major] Glioblastoma / physiopathology
  • [MeSH-minor] Adolescent. Adult. Brain Neoplasms / mortality. Brain Neoplasms / pathology. Brain Neoplasms / physiopathology. Child. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Survivors


69. Shirai K, Suzuki Y, Oka K, Noda SE, Katoh H, Suzuki Y, Itoh J, Itoh H, Ishiuchi S, Sakurai H, Hasegawa M, Nakano T: Nuclear survivin expression predicts poorer prognosis in glioblastoma. J Neurooncol; 2009 Feb;91(3):353-8
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  • [Title] Nuclear survivin expression predicts poorer prognosis in glioblastoma.
  • However, the prognostic value of survivin expression in patients with glioblastoma is still controversial.
  • Therefore, in this study the role of survivin as a predictor for survival was investigated in patients with glioblastoma.
  • Tissue specimens were obtained from 66 patients with glioblastoma treated with radiotherapy.
  • Nuclear survivin expression may be a useful biomarker for predicting prognosis in patients with glioblastoma.
  • [MeSH-major] Glioblastoma / metabolism. Glioblastoma / mortality. Microtubule-Associated Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Gene Expression Regulation, Neoplastic / physiology. Gene Expression Regulation, Neoplastic / radiation effects. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Radiotherapy / methods. Time Factors

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  • (PMID = 18953492.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins
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70. Kumar R, Kamdar D, Madden L, Hills C, Crooks D, O'Brien D, Greenman J: Th1/Th2 cytokine imbalance in meningioma, anaplastic astrocytoma and glioblastoma multiforme patients. Oncol Rep; 2006 Jun;15(6):1513-6
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  • [Title] Th1/Th2 cytokine imbalance in meningioma, anaplastic astrocytoma and glioblastoma multiforme patients.
  • Serum samples from 61 newly diagnosed patients with brain tumours and 50 age- and sex-matched non-tumour controls were analysed by ELISA for circulating levels of interleukin-12 (IL-12p70 and p40) and interleukin-10 (IL-10); pivotal Th1 and Th2 cytokines, respectively.
  • Patients were divided into various groups depending on their histological diagnosis: meningioma (n=11), anaplastic astrocytoma (n=4) and glioblastoma multiforme (GBM; n=46).
  • Significant reduction in serum IL-12 was seen in all groups as compared with the controls: meningioma, p=0.03; anaplastic astrocytoma, p<0.001; and GBM, p<0.001.
  • Conversely, serum IL-10 was significantly increased in anaplastic astrocytoma, p=0.02, and GBM, p=0.03.
  • This study shows that patients with advanced primary intracranial malignancies have decreased circulating IL-12 and increased circulating IL-10, demonstrating that brain tumours have a major systemic effect on the immune system.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-10 / blood. Interleukin-12 / blood. Meningioma / immunology. Th1 Cells / immunology. Th2 Cells / immunology
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. Humans. Male. Middle Aged


71. Herrlinger U, Rieger J, Steinbach JP, Nägele T, Dichgans J, Weller M: UKT-04 trial of continuous metronomic low-dose chemotherapy with methotrexate and cyclophosphamide for recurrent glioblastoma. J Neurooncol; 2005 Feb;71(3):295-9
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  • [Title] UKT-04 trial of continuous metronomic low-dose chemotherapy with methotrexate and cyclophosphamide for recurrent glioblastoma.
  • Glioblastoma is a highly angiogenic tumor with a dismal prognosis.
  • We explored the efficacy of 100 mg CPM daily and 5 mg MTX twice weekly in relapsed glioblastoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Breast Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Cyclophosphamide / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Humans. Male. Methotrexate / administration & dosage. Middle Aged

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  • (PMID = 15735920.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate
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72. Tunca B, Bekar A, Cecener G, Egeli U, Vatan O, Tolunay S, Kocaeli H, Aksoy K: Impact of novel PTEN mutations in Turkish patients with glioblastoma multiforme. J Neurooncol; 2007 May;82(3):263-9
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  • [Title] Impact of novel PTEN mutations in Turkish patients with glioblastoma multiforme.
  • Glioblastoma multiforme (GBM) represents the most common and aggressive type of primary neoplasms of the central nervous system.
  • The PTEN (phosphatase, tensin homologue, deleted on chromosome TEN; MIM # 601728) tumor suppressor gene has an essential biological role in the formation of glioblastomas.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Mutation. PTEN Phosphohydrolase / genetics
  • [MeSH-minor] Adult. Aged. Base Sequence. Female. Humans. Male. Middle Aged. Polymorphism, Single-Stranded Conformational. Turkey

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  • (PMID = 17151929.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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73. Iacob G, Dinca EB: Current data and strategy in glioblastoma multiforme. J Med Life; 2009 Oct-Dec;2(4):386-93
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  • [Title] Current data and strategy in glioblastoma multiforme.
  • Glioblastoma multiforme (GBM) or astrocytoma grade IV on WHO classification is the most aggressive and the most frequent of all primary brain tumors.
  • Glioblastoma is multiforme, resistant to therapeutic interventions illustrating the heterogeneity exhibited by this tumor in its every aspect, including clinical presentation, pathology, genetic signature.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Chromosome Mapping. Diagnosis, Differential. Gene Amplification. Humans. Middle Aged. Mutation. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. Prognosis. Receptor, Epidermal Growth Factor / genetics. Survival Analysis. Young Adult

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  • (PMID = 20108752.001).
  • [ISSN] 1844-122X
  • [Journal-full-title] Journal of medicine and life
  • [ISO-abbreviation] J Med Life
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 45
  • [Other-IDs] NLM/ PMC3019011
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74. Yamamoto T, Nakai K, Kageji T, Kumada H, Endo K, Matsuda M, Shibata Y, Matsumura A: Boron neutron capture therapy for newly diagnosed glioblastoma. Radiother Oncol; 2009 Apr;91(1):80-4
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  • [Title] Boron neutron capture therapy for newly diagnosed glioblastoma.
  • PURPOSE: The efficacy, safety, and dose distribution of neutron capture therapy (NCT) were evaluated in 15 patients with newly diagnosed glioblastoma.
  • The median overall survival and the time to tumor progression (TTP) for all patients were 25.7 and 11.9 M, respectively.
  • Three protocol-1 patients and one protocol-2 patient suffered transient orbital swelling accompanied by double vision (Grade 2); one of the three protocol-1 patients suffered post-epileptic brain swelling (Grade 4) requiring surgical intervention.
  • CONCLUSION: It is suggested that NCT is effective for survival of newly diagnosed glioblastoma with acceptable adverse effects.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Male. Middle Aged. Radiotherapy Dosage. Survival Rate. Treatment Outcome

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  • (PMID = 19285355.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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75. Nieder C, Grosu AL, Astner S, Molls M: Treatment of unresectable glioblastoma multiforme. Anticancer Res; 2005 Nov-Dec;25(6C):4605-10
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  • [Title] Treatment of unresectable glioblastoma multiforme.
  • Uncertainty exists about the adequate treatment of adult patients with unresectable, primary, biopsy-proven glioblastoma multiforme (GBM), because the different options for this group of patients have not been evaluated in randomized clinical trials to date.
  • With different radiochemotherapy approaches, the median survival was approximately 5 months in recursive partitioning analysis (RPA) class VI, but 8-14 months in classes IV and V Thus, careful patient selection is necessary to avoid overtreatment in prognostically unfavorable groups with unresectable GBM.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Glioblastoma / radiotherapy

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  • (PMID = 16334150.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 34
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76. Taha M, Ahmad A, Wharton S, Jellinek D: Extra-cranial metastasis of glioblastoma multiforme presenting as acute parotitis. Br J Neurosurg; 2005 Aug;19(4):348-51
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  • [Title] Extra-cranial metastasis of glioblastoma multiforme presenting as acute parotitis.
  • We present an unusual case of extracranial metastasis of glioblastoma multiforme (GBM) to the parotid gland and cervical lymph nodes.
  • This case illustrates how GBM behaves in an aggressive manner even outside the CNS.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / secondary. Parotid Neoplasms / secondary. Parotitis / etiology
  • [MeSH-minor] Acute Disease. Adult. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed

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  • (PMID = 16455543.001).
  • [ISSN] 0268-8697
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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77. Schwartzbaum JA, Xiao Y, Liu Y, Tsavachidis S, Berger MS, Bondy ML, Chang JS, Chang SM, Decker PA, Ding B, Hepworth SJ, Houlston RS, Hosking FJ, Jenkins RB, Kosel ML, McCoy LS, McKinney PA, Muir K, Patoka JS, Prados M, Rice T, Robertson LB, Schoemaker MJ, Shete S, Swerdlow AJ, Wiemels JL, Wiencke JK, Yang P, Wrensch MR: Inherited variation in immune genes and pathways and glioblastoma risk. Carcinogenesis; 2010 Oct;31(10):1770-7
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  • [Title] Inherited variation in immune genes and pathways and glioblastoma risk.
  • To determine whether inherited variations in immune function single-nucleotide polymorphisms (SNPs), genes or pathways affect glioblastoma risk, we analyzed data from recent genome-wide association studies in conjunction with predefined immune function genes and pathways.
  • Gene and pathway analyses were conducted on two independent data sets using 6629 SNPs in 911 genes on 17 immune pathways from 525 glioblastoma cases and 602 controls from the University of California, San Francisco (UCSF) and a subset of 6029 SNPs in 893 genes from 531 cases and 1782 controls from MD Anderson (MDA).
  • Although three correlated epidermal growth factor receptor (EGFR) SNPs were consistently associated with glioblastoma in all four data sets (Mantel-Haenzel P values = 1 × 10⁻⁵ to 4 × 10⁻³), independent replication is required as genome-wide significance was not attained.
  • In gene-level analyses, eight immune function genes were significantly (minP < 0.05) associated with glioblastoma; the IL-2RA (CD25) cytokine gene had the smallest minP values in both UCSF (minP = 0.01) and MDA (minP = 0.001) data sets.
  • The IL-2RA receptor is found on the surface of regulatory T cells potentially contributing to immunosuppression characteristic of the glioblastoma microenvironment.
  • In pathway correlation analyses, cytokine signaling and adhesion-extravasation-migration pathways showed similar associations with glioblastoma risk in both MDA and UCSF data sets.
  • Our findings represent the first systematic description of immune genes and pathways that characterize glioblastoma risk.

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  • (PMID = 20668009.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108961; United States / NCI NIH HHS / CA / 5R01 CA119215; United States / NCI NIH HHS / CA / R25 CA112355; United Kingdom / Cancer Research UK / / C1298/A8362; United States / NCI NIH HHS / CA / R25 CA 112355; United States / NCI NIH HHS / CA / 5R01 CA070917; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA070917; United States / NCI NIH HHS / CA / R01CA122163; United States / NCI NIH HHS / CA / P30 CA015083; United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01 CA119215; United States / NCI NIH HHS / CA / R01CA52689; United States / NCI NIH HHS / CA / P30 CA15083; United States / NCI NIH HHS / CA / R01 CA122163; United Kingdom / Wellcome Trust / / ; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Other-IDs] NLM/ PMC2950934
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78. Yu JM, Jun ES, Jung JS, Suh SY, Han JY, Kim JY, Kim KW, Jung JS: Role of Wnt5a in the proliferation of human glioblastoma cells. Cancer Lett; 2007 Nov 18;257(2):172-81
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  • [Title] Role of Wnt5a in the proliferation of human glioblastoma cells.
  • Wnt5a operates as either a tumor suppressor or a tumor stimulator, according to tumor type.
  • The functions of Wnt5a in human glioblastoma (GBM) have yet to be determined.
  • The results of immunohistochemical analyses have revealed that Wnt5a expression was higher in human GBM than in normal brain tissue and low-grade astrocytoma.
  • In order to assess the role of Wnt5a on proliferation in human glioblastoma cells, we employed U87MG and GBM-05, a newly established GBM cell line.
  • GBM-05 cells formed infiltrating brain tumors after being intracerebrally transplanted into nude mice, and xenotransplanted GBM-05 cells were observed to differentiate into neuronal and astrocyte lineages.
  • Wnt5a expression in the xenotransplanted tumors was higher than that detected in the surrounding brain tissues.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Proliferation. Glioblastoma / pathology. Proto-Oncogene Proteins / physiology. Wnt Proteins / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Blotting, Western. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / analysis. Humans. Immunohistochemistry. Intermediate Filament Proteins / analysis. Karyotyping. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Nerve Tissue Proteins / analysis. Nestin. Transfection. Transplantation, Heterologous

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  • (PMID = 17709179.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Proto-Oncogene Proteins; 0 / WNT5A protein, human; 0 / Wnt Proteins
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79. Rosati A, Marconi S, Pollo B, Tomassini A, Lovato L, Maderna E, Maier K, Schwartz A, Rizzuto N, Padovani A, Bonetti B: Epilepsy in glioblastoma multiforme: correlation with glutamine synthetase levels. J Neurooncol; 2009 Jul;93(3):319-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epilepsy in glioblastoma multiforme: correlation with glutamine synthetase levels.
  • PURPOSE: The hypothesis addressed by this study is that a glutamine synthetase (GS) deficiency in neoplastic astrocytes is a possible molecular basis associated with seizure generation in glioblastoma multiforme (GBM).
  • [MeSH-major] Brain Neoplasms / enzymology. Epilepsy / enzymology. Epilepsy / etiology. Glioblastoma / complications. Glioblastoma / enzymology. Glutamate-Ammonia Ligase / metabolism
  • [MeSH-minor] Adult. Aged. Blotting, Western. Female. Humans. Male. Middle Aged

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  • (PMID = 19183851.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.1.2 / Glutamate-Ammonia Ligase
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80. Secer HI, Dinc C, Anik I, Duz B, Gonul E: Glioblastoma multiforme of the lateral ventricle: report of nine cases. Br J Neurosurg; 2008 Jun;22(3):398-401
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  • [Title] Glioblastoma multiforme of the lateral ventricle: report of nine cases.
  • Glioblastoma multiforme is the most common lethal primary central nervous system (CNS) tumour in adults and they are rarely seen as primary intraventricular tumours.
  • We present nine cases with lateral ventricle glioblastoma multiforme treated in our department.
  • [MeSH-major] Cerebral Ventricle Neoplasms / surgery. Glioblastoma / surgery. Lateral Ventricles / surgery
  • [MeSH-minor] Adult. Aged. Female. Humans. Karnofsky Performance Status. Male. Middle Aged. Treatment Outcome

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  • (PMID = 18568728.001).
  • [ISSN] 0268-8697
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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81. Bohman LE, Gallardo J, Hankinson TC, Waziri AE, Mandigo CE, McKhann GM 2nd, Sisti MB, Canoll P, Bruce JN: The survival impact of postoperative infection in patients with glioblastoma multiforme. Neurosurgery; 2009 May;64(5):828-34; discussion 834-5
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  • [Title] The survival impact of postoperative infection in patients with glioblastoma multiforme.
  • METHODS: A single-center operative experience accumulated over 10 years was examined to evaluate whether postoperative infections conferred a survival advantage in patients with glioblastoma multiforme.
  • CONCLUSION: In this single-center study, postoperative infection did not confer any survival advantage in patients with glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms / mortality. Glioblastoma / mortality. Neurosurgical Procedures / adverse effects. Postoperative Complications / mortality
  • [MeSH-minor] Adult. Aged. Bacterial Infections / classification. Bacterial Infections / etiology. Bacterial Infections / mortality. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Retrospective Studies. Statistics, Nonparametric

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  • (PMID = 19404146.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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82. Kawabata S, Miyatake S, Kuroiwa T, Yokoyama K, Doi A, Iida K, Miyata S, Nonoguchi N, Michiue H, Takahashi M, Inomata T, Imahori Y, Kirihata M, Sakurai Y, Maruhashi A, Kumada H, Ono K: Boron neutron capture therapy for newly diagnosed glioblastoma. J Radiat Res; 2009 Jan;50(1):51-60
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  • [Title] Boron neutron capture therapy for newly diagnosed glioblastoma.
  • We evaluate the clinical results of a form of tumor selective particle radiation known as boron neutron capture therapy (BNCT) for newly-diagnosed glioblastoma (NDGB) patients, especially in combination with X-ray treatment (XRT).
  • The first 10 were treated with only BNCT (protocol 1), and the last 11 were treated with BNCT followed by XRT of 20 to 30 Gy (protocol 2) to reduce the possibility of local tumor recurrence.
  • No chemotherapy was applied until tumor progression was observed.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 18957828.001).
  • [ISSN] 0449-3060
  • [Journal-full-title] Journal of radiation research
  • [ISO-abbreviation] J. Radiat. Res.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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83. Aoyanagi E, Sasai K, Nodagashira M, Wang L, Nishihara H, Ihara H, Ikeda Y, Tanaka S: Clinicopathologic application of lectin histochemistry: bisecting GlcNAc in glioblastoma. Appl Immunohistochem Mol Morphol; 2010 Dec;18(6):518-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic application of lectin histochemistry: bisecting GlcNAc in glioblastoma.
  • Thus, discovering aberrant glycosylation patterns that serve as markers for brain tumor progression and metastasis represents an attractive strategy to improve clinicopathologic diagnosis and to provide aids to the development of novel therapies.
  • To identify glioblastoma (GBM) cells expressing glycoproteins that contain high levels of the bisecting N-acetylglucosamine (GlcNAc) structures, lectin histochemistry was carried out using erythroagglutinating phytohemagglutinin.
  • Although GBM frequently expressed the bisecting GlcNAc, the lectin reactivity varied among tumor regions within individual specimens.
  • Since detailed histopathologic analysis revealed that oligosaccharides with bisecting GlcNAc structures were preferably expressed in tumor regions with low KI67 immunopositivity, immunodetection of the bisecting GlcNAc could be useful to indicate less proliferative regions in human GBM.

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  • (PMID = 20661133.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins; 0 / Membrane Glycoproteins; 0 / Phytohemagglutinins; 0 / erythroagglutinating phytohemagglutinin; EC 2.4.1.- / N-Acetylglucosaminyltransferases; V956696549 / Acetylglucosamine
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84. Chan TA, Weingart JD, Parisi M, Hughes MA, Olivi A, Borzillary S, Alahakone D, Detorie NA, Wharam MD, Kleinberg L: Treatment of recurrent glioblastoma multiforme with GliaSite brachytherapy. Int J Radiat Oncol Biol Phys; 2005 Jul 15;62(4):1133-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of recurrent glioblastoma multiforme with GliaSite brachytherapy.
  • PURPOSE: In this study, we assess the efficacy of GliaSite brachytherapy in the treatment of patients with recurrent glioblastoma multiforme (GBM).
  • METHODS AND MATERIALS: Between 1999 and 2004, 24 patients with recurrent glioblastoma multiforme were treated with the GliaSite Radiation Therapy System (RTS).
  • CONCLUSIONS: GliaSite radiotherapy confers a prolongation of survival in patients with recurrent glioblastoma multiforme compared to historical controls with recurrent GBM.
  • [MeSH-major] Brachytherapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Adult. Aged. Benzenesulfonates / therapeutic use. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / therapeutic use. Male. Middle Aged. Radiotherapy Dosage. Reoperation. Survival Rate

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  • (PMID = 15990019.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Iodine Radioisotopes; 0 / iotrex
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85. Silvani A, Gaviani P, Lamperti EA, Eoli M, Falcone C, Dimeco F, Milanesi IM, Erbetta A, Boiardi A, Fariselli L, Salmaggi A: Cisplatinum and BCNU chemotherapy in primary glioblastoma patients. J Neurooncol; 2009 Aug;94(1):57-62
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

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  • [Title] Cisplatinum and BCNU chemotherapy in primary glioblastoma patients.
  • BACKGROUND: The prognosis of patients with glioblastoma is very poor with a mean survival of 10-12 months.
  • However, these have been shown to improve survival only marginally in glioblastoma multiforme (GBM) patients.
  • METHODS: A retrospective analysis on 160 adult patients (> or =16 years) treated for histologically confirmed GBM between 2003 and 2005 at our Institution was performed.
  • The primary toxicities were: neutropenia (grade 3-4: 23%), thrombocytopenia (grade 3-4: 18.5%), and nausea and vomiting (13%).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carmustine / therapeutic use. Cisplatin / therapeutic use. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Treatment Outcome. Young Adult

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  • (PMID = 19212704.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
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86. Showalter TN, Andrel J, Andrews DW, Curran WJ Jr, Daskalakis C, Werner-Wasik M: Multifocal glioblastoma multiforme: prognostic factors and patterns of progression. Int J Radiat Oncol Biol Phys; 2007 Nov 1;69(3):820-4
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  • [Title] Multifocal glioblastoma multiforme: prognostic factors and patterns of progression.
  • PURPOSE: To assess the progression patterns in patients with multifocal glioblastoma multiforme who had undergone whole brain radiotherapy (WBRT), the historical standard, versus three-dimensional conformal radiotherapy, and to identify predictive treatment and pretreatment factors.
  • METHODS AND MATERIALS: The records of 50 patients with multifocal glioblastoma multiforme treated with RT were reviewed.
  • On the basis of the progression pattern, we do not recommend WBRT as a mandatory component of the treatment of multifocal glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Cranial Irradiation / methods. Disease Progression. Humans. Middle Aged. Prognosis. Proportional Hazards Models. Radiotherapy, Conformal. Retrospective Studies. Survival Analysis

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  • [CommentIn] Int J Radiat Oncol Biol Phys. 2007 Nov 15;69(4):1335; author reply 1335 [17967325.001]
  • (PMID = 17499453.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Saidi A, Javerzat S, Bellahcène A, De Vos J, Bello L, Castronovo V, Deprez M, Loiseau H, Bikfalvi A, Hagedorn M: Experimental anti-angiogenesis causes upregulation of genes associated with poor survival in glioblastoma. Int J Cancer; 2008 May 15;122(10):2187-98
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  • [Title] Experimental anti-angiogenesis causes upregulation of genes associated with poor survival in glioblastoma.
  • Exploring gene regulation in tumor cells during anti-angiogenesis might help to comprehend the molecular basis of response to treatment.
  • In glioblastoma patients, these genes showed coregulation and their expression differed significantly from low-grade glioma.
  • Elafin-positive tumor cells were only found in glioblastoma, where they were clustered around necrotic areas.
  • Our results indicate that anti-angiogenesis in experimental glioma drives expression of critical genes which relate to disease aggressiveness in glioblastoma patients.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / blood supply. Glioblastoma / mortality. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Adipokines. Adult. Astrocytoma / blood supply. Astrocytoma / metabolism. Astrocytoma / mortality. Brain / metabolism. Brain / pathology. Brain Neoplasms / blood supply. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Cell Proliferation. Elafin / metabolism. Female. Gene Expression Profiling. Glycoproteins / metabolism. Humans. Immunoenzyme Techniques. Lectins. Male. Middle Aged. Neovascularization, Pathologic. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Up-Regulation

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • [CommentIn] Int J Cancer. 2009 Mar 15;124(6):1492-4 [19089918.001]
  • (PMID = 18092325.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adipokines; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Elafin; 0 / Glycoproteins; 0 / Lectins; 0 / PI3 protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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88. Parsa AT, Wachhorst S, Lamborn KR, Prados MD, McDermott MW, Berger MS, Chang SM: Prognostic significance of intracranial dissemination of glioblastoma multiforme in adults. J Neurosurg; 2005 Apr;102(4):622-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of intracranial dissemination of glioblastoma multiforme in adults.
  • OBJECT: The clinical outcome and treatment of adult patients with disseminated intracranial glioblastoma multiforme (GBM) is unclear.
  • The objective in the present study was to assess the prognostic significance of disseminated intracranial GBM in adults at presentation and at the time of tumor progression.
  • Patients with dissemination at first tumor progression (52 patients) overall had a shorter PPS than those in a control group with local progression, after adjusting for age, Kamofsky Performance Scale score, and time from tumor diagnosis to its progression (311 patients).
  • When analyzed according to tumor dissemination type, PPS was significantly shorter in patients with Type II (33 patients, p < 0.01) and Type III spread (11 patients, p < 0.01) but not in those with Type I spread (eight patients, p = 0.18).
  • CONCLUSIONS: Apparently, the presence of intracranial tumor dissemination on initial diagnosis does not in itself preclude aggressive treatment if a patient is otherwise well.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplasm Staging
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 15871503.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA13525; United States / NCI NIH HHS / CA / CA82103; United States / NINDS NIH HHS / NS / NS42927
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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89. Ali K, Lu Y, Das U, Sharma RK, Wiebe S, Meguro K, Sadanand V, Fourney DR, Vitali A, Kelly M, May T, Gomez J, Pellerin E: Biomolecular diagnosis of human glioblastoma multiforme using Synchrotron mid-infrared spectromicroscopy. Int J Mol Med; 2010 Jul;26(1):11-6
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  • [Title] Biomolecular diagnosis of human glioblastoma multiforme using Synchrotron mid-infrared spectromicroscopy.
  • Glioblastoma multiforme (GBM) is one of the most malignant human tumors, with a uniformly poor outcome.
  • One obstacle in curing malignant brain tumors is the limitation of conventional light microscopy in detecting microscopic residual tumor in biopsy samples from the perimeter of the surgically resected tumor.
  • We further refined the identification of GBM tumor tissue at the sub-cellular level, utilising the technique of Synchrotron, sourced mid-infrared (mid-IR) spectromicroscopy.
  • Paired, thin (5 microm) cryosections of snap-frozen human GBM tumor samples removed at elective surgery were mounted on glass slides (hematoxylin and eosin-stained tissue section) and calcium fluoride (CaF2) windows (unstained tissue section for transmission spectromicroscopy), respectively.
  • Concordance of tumor bearing areas identified in the stained section with the unstained IR tissue section was confirmed by the pathologist of the study.
  • Compared with molecular signatures obtained from normal control brain tissue, unique spectroscopic patterns were detected in GBM tumor samples from 6 patients.
  • False color images of 5 clusters obtained by HCA identified dominant clusters corresponding to tumor tissue.
  • Corroboration of these findings in a larger number of GBM may allow for more precise identification of these and other types of brain tumors.
  • [MeSH-major] Brain Neoplasms / diagnosis. Glioblastoma / diagnosis. Spectrophotometry, Infrared / methods. Synchrotrons
  • [MeSH-minor] Adult. Aged. Calcium Fluoride / chemistry. Child. Cluster Analysis. Cryoultramicrotomy / methods. Female. Histocytochemistry / methods. Humans. Lipids / analysis. Lipids / chemistry. Male. Middle Aged. Proteins / analysis. Proteins / chemistry

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  • (PMID = 20514416.001).
  • [ISSN] 1791-244X
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Lipids; 0 / Proteins; O3B55K4YKI / Calcium Fluoride
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90. Sarissky M, Lavicka J, Kocanová S, Sulla I, Mirossay A, Miskovsky P, Gajdos M, Mojzis J, Mirossay L: Diazepam enhances hypericin-induced photocytotoxicity and apoptosis in human glioblastoma cells. Neoplasma; 2005;52(4):352-9
Hazardous Substances Data Bank. DIAZEPAM .

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  • [Title] Diazepam enhances hypericin-induced photocytotoxicity and apoptosis in human glioblastoma cells.
  • Glioblastoma multiforme (GBM) is neoplasm which is resistant to all currently used treatment modalities including surgery, radiation therapy and chemotherapy.
  • For the study, we used U-87 MG and U373 MG glioma cell lines and primary cultures of GBM cells prepared from peroperatively obtained tumor specimens.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Brain Neoplasms / pathology. Diazepam / pharmacology. GABA Modulators / pharmacology. Glioblastoma / pathology. Perylene / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Drug Interactions. Female. Flow Cytometry. Humans. Male. Middle Aged. Photochemotherapy. Tumor Cells, Cultured

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  • (PMID = 16059654.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GABA Modulators; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin; Q3JTX2Q7TU / Diazepam
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91. Tchirkov A, Sapin V, Marceau G, Chautard E, Narla G, Veronese L, Friedman S, Khalil T, Vago P, Kemeny JL, Verrelle P: Increased expression of the oncogenic KLF6-SV1 transcript in human glioblastoma. Clin Chem Lab Med; 2010 Aug;48(8):1167-70
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  • [Title] Increased expression of the oncogenic KLF6-SV1 transcript in human glioblastoma.
  • BACKGROUND: Gliomas constitute the vast majority of primary central nervous system tumors in adults.
  • Glioblastoma multiforme (GBM) is the most aggressive form of these primary brain tumors.
  • METHODS: Fifty-three primary gliomas tumor samples were analyzed using quantitative real-time PCR for the total KLF6, wild-type and alternatively spliced (SV1) KLF6 mRNA.

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  • (PMID = 20545576.001).
  • [ISSN] 1437-4331
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carcinogens; 0 / KLF6 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger
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92. Reithmeier T, Graf E, Piroth T, Trippel M, Pinsker MO, Nikkhah G: BCNU for recurrent glioblastoma multiforme: efficacy, toxicity and prognostic factors. BMC Cancer; 2010;10:30
Hazardous Substances Data Bank. Carmustine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCNU for recurrent glioblastoma multiforme: efficacy, toxicity and prognostic factors.
  • BACKGROUND: The prognosis for patients with recurrent glioblastoma is still poor with a median survival between 3 and 6 months.
  • Reports about the application of carmustine (BCNU), one of the standard chemotherapeutic drugs in the treatment of newly diagnosed glioblastoma, in the recurrent situation are rare.
  • METHODS: We performed a retrospective analysis of 35 patients with recurrent or progressive glioblastoma treated with 80 mg/m2 BCNU on days 1 on 3 intravenously at our department for efficacy, toxicity and prognostic factors.
  • The influence of age, Karnofsky performance status (KPS), tumor burden, pretreatment with temozolomide (TMZ), type of surgery for initial diagnosis and number of previous relapses on outcome was analyzed in a proportional hazards regression model.
  • No influence of age, KPS, tumor burden, pre-treatment with TMZ and number of previous relapses on outcome could be demonstrated, while gross total resection prior to recurrence showed a borderline statistically significant negative impact on PFS and OS.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Carmustine / pharmacology. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis. Regression Analysis. Retrospective Studies. Treatment Outcome

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  • (PMID = 20122270.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; U68WG3173Y / Carmustine
  • [Other-IDs] NLM/ PMC2837009
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93. Kim B, Myung JK, Seo JH, Park CK, Paek SH, Kim DG, Jung HW, Park SH: The clinicopathologic values of the molecules associated with the main pathogenesis of the glioblastoma. J Neurol Sci; 2010 Jul 15;294(1-2):112-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinicopathologic values of the molecules associated with the main pathogenesis of the glioblastoma.
  • Glioblastoma (GBM) is a malignant CNS neoplasm.
  • Stratified by age, resectability and tumor size <5 cm were favorable survival factors in young (40<yrs) and old age groups (> or =40 yrs), respectively.
  • Furthermore, the patients with supratentorial tumor lived longer than the patients with infratentorial tumor (p<0.05).
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism
  • [MeSH-minor] Adult. Age Factors. Brain / metabolism. Brain / surgery. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infratentorial Neoplasms / diagnosis. Infratentorial Neoplasms / metabolism. Infratentorial Neoplasms / mortality. Infratentorial Neoplasms / pathology. Male. PTEN Phosphohydrolase / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Prognosis. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / metabolism. Supratentorial Neoplasms / diagnosis. Supratentorial Neoplasms / metabolism. Supratentorial Neoplasms / mortality. Supratentorial Neoplasms / pathology. Survival Analysis. Tumor Suppressor Protein p53 / metabolism


94. Plotkin M, Gneveckow U, Meier-Hauff K, Amthauer H, Feussner A, Denecke T, Gutberlet M, Jordan A, Felix R, Wust P: 18F-FET PET for planning of thermotherapy using magnetic nanoparticles in recurrent glioblastoma. Int J Hyperthermia; 2006 Jun;22(4):319-25
Hazardous Substances Data Bank. L-TYROSINE .

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  • [Title] 18F-FET PET for planning of thermotherapy using magnetic nanoparticles in recurrent glioblastoma.
  • MATERIALS AND METHODS: Eleven patients with glioblastoma recurrences underwent MR and FET-PET imaging for planning of the nano cancer therapy.
  • [MeSH-major] Brain Neoplasms / therapy. Glioblastoma / therapy. Hyperthermia, Induced / methods. Magnetics. Nanostructures. Neoplasm Recurrence, Local / therapy. Positron-Emission Tomography / methods. Tyrosine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Radiotherapy Planning, Computer-Assisted

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  • (PMID = 16754352.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / O-(2-fluoroethyl)tyrosine; 42HK56048U / Tyrosine
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95. Keir ST, Farland MM, Lipp ES, Friedman HS: Distress persists in long-term brain tumor survivors with glioblastoma multiforme. J Cancer Surviv; 2008 Dec;2(4):269-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distress persists in long-term brain tumor survivors with glioblastoma multiforme.
  • INTRODUCTION: Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor.
  • RESULTS: Eight-three brain tumor patients participated in this study.
  • CONCLUSIONS: This study indicates that LTS of GBM report experiencing distress at similar levels to other brain tumor patients.
  • [MeSH-major] Anxiety Disorders / epidemiology. Brain Neoplasms / psychology. Glioblastoma / psychology. Survivors
  • [MeSH-minor] Adult. Aged. Fatigue / epidemiology. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prevalence. Research Design


96. Gross MW, Altscher R, Brandtner M, Haeusser-Mischlich H, Chiricuta IC, Siegmann AD, Engenhart-Cabillic R: Open-label simultaneous radio-chemotherapy of glioblastoma multiforme with topotecan in adults. Clin Neurol Neurosurg; 2005 Apr;107(3):207-13
Hazardous Substances Data Bank. Topotecan .

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  • [Title] Open-label simultaneous radio-chemotherapy of glioblastoma multiforme with topotecan in adults.
  • BACKGROUND: Due to its radioresistance, the prognosis of glioblastoma multiforme (GBM) remains poor.
  • CTC toxicity grade 3 was observed in six patients and grade 4 toxicity in two patients (three events).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Topotecan / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Disease-Free Survival. Feasibility Studies. Female. Humans. Male. Middle Aged. Pilot Projects. Prospective Studies. Quality of Life. Survival Rate

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  • (PMID = 15823676.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7M7YKX2N15 / Topotecan
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97. Wheeler CJ, Black KL, Liu G, Mazer M, Zhang XX, Pepkowitz S, Goldfinger D, Ng H, Irvin D, Yu JS: Vaccination elicits correlated immune and clinical responses in glioblastoma multiforme patients. Cancer Res; 2008 Jul 15;68(14):5955-64
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  • [Title] Vaccination elicits correlated immune and clinical responses in glioblastoma multiforme patients.
  • Therapeutic vaccination represents an intriguing additional therapy for glioblastoma multiforme (GBM; grade 4 glioma), which has a dismal prognosis and treatment response, but only early phase I vaccine trial results have been reported.
  • Posttreatment times to tumor progression (TTP) and survival (TTS) were compared in vaccine responders and nonresponders and were correlated with immune response magnitudes.
  • This is the first report of a progressive correlation between cancer clinical outcome and T-cell responsiveness after therapeutic vaccination in humans and the first tracing of such correlation to therapeutically exploitable tumor alteration.
  • [MeSH-major] Brain Neoplasms / microbiology. Brain Neoplasms / therapy. Glioblastoma / immunology. Glioblastoma / therapy
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / metabolism. Cancer Vaccines. Dendritic Cells / immunology. Female. Humans. Immune System. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 18632651.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
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98. Pellettieri L, H-Stenstam B, Rezaei A, Giusti V, Sköld K: An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme. Acta Neurol Scand; 2008 Mar;117(3):191-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme.
  • Objectives - To explore the use of boron neutron capture therapy (BNCT) for patients with glioblastoma multiforme (GBM), recurring after surgery and conventional radiotherapy (photon radiotherapy).
  • BNCT was well tolerated and quality of life remained stable until tumor progression for all 12 patients.
  • No correlation was found between survival times and minimum tumor dose and number of radiation fields.
  • Conclusions - Boron neutron capture therapy, with the prolonged procedure for infusion, is at least as effective as other radiation therapies for recurrent GBM and is delivered in one treatment session, with low radiation dose to the healthy brain.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Adult. Aged. Body Weight. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Radiotherapy Dosage. Tomography, X-Ray Computed

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  • (PMID = 18297764.001).
  • [ISSN] 1600-0404
  • [Journal-full-title] Acta neurologica Scandinavica
  • [ISO-abbreviation] Acta Neurol. Scand.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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99. Stupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJ, Belanger K, Brandes AA, Marosi C, Bogdahn U, Curschmann J, Janzer RC, Ludwin SK, Gorlia T, Allgeier A, Lacombe D, Cairncross JG, Eisenhauer E, Mirimanoff RO, European Organisation for Research and Treatment of Cancer Brain Tumor and Radiotherapy Groups, National Cancer Institute of Canada Clinical Trials Group: Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med; 2005 Mar 10;352(10):987-96
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  • [Title] Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma.
  • BACKGROUND: Glioblastoma, the most common primary brain tumor in adults, is usually rapidly fatal.
  • The current standard of care for newly diagnosed glioblastoma is surgical resection to the extent feasible, followed by adjuvant radiotherapy.
  • METHODS: Patients with newly diagnosed, histologically confirmed glioblastoma were randomly assigned to receive radiotherapy alone (fractionated focal irradiation in daily fractions of 2 Gy given 5 days per week for 6 weeks, for a total of 60 Gy) or radiotherapy plus continuous daily temozolomide (75 mg per square meter of body-surface area per day, 7 days per week from the first to the last day of radiotherapy), followed by six cycles of adjuvant temozolomide (150 to 200 mg per square meter for 5 days during each 28-day cycle).
  • Concomitant treatment with radiotherapy plus temozolomide resulted in grade 3 or 4 hematologic toxic effects in 7 percent of patients.
  • CONCLUSIONS: The addition of temozolomide to radiotherapy for newly diagnosed glioblastoma resulted in a clinically meaningful and statistically significant survival benefit with minimal additional toxicity.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Glioblastoma / drug therapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Aged. Chemotherapy, Adjuvant. Disease Progression. Female. Humans. Male. Middle Aged. Proportional Hazards Models. Radiotherapy, Computer-Assisted / adverse effects. Survival Analysis

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  • [Copyright] Copyright 2005 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2005 Mar 10;352(10):1036-8 [15758016.001]
  • [CommentIn] N Engl J Med. 2005 Jun 2;352(22):2350-3; author reply 2350-3 [15938011.001]
  • [CommentIn] N Engl J Med. 2005 Jun 2;352(22):2350-3; author reply 2350-3 [15938012.001]
  • [CommentIn] N Engl J Med. 2005 Jun 2;352(22):2350-3; author reply 2350-3 [15938013.001]
  • (PMID = 15758009.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10CA11488-30; United States / NCI NIH HHS / CA / 5U10CA11488-31; United States / NCI NIH HHS / CA / 5U10CA11488-32; United States / NCI NIH HHS / CA / 5U10CA11488-33; United States / NCI NIH HHS / CA / 5U10CA11488-34
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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100. Reardon DA, Wen PY, Desjardins A, Batchelor TT, Vredenburgh JJ: Glioblastoma multiforme: an emerging paradigm of anti-VEGF therapy. Expert Opin Biol Ther; 2008 Apr;8(4):541-53
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  • [Title] Glioblastoma multiforme: an emerging paradigm of anti-VEGF therapy.
  • BACKGROUND: Adults with malignant glioma, especially the most common subtype, glioblastoma multiforme, have an unacceptably poor outcome with current therapies.

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  • [CommentIn] Expert Opin Biol Ther. 2008 Oct;8(10):1449-53 [18774913.001]
  • (PMID = 18352856.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108786-029003; United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / NS20023; United States / NCI NIH HHS / CA / CA108786-059003; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / NS020023-268626; United States / NINDS NIH HHS / NS / NS020023-240020; United States / NINDS NIH HHS / NS / NS020023-220020; United States / NCI NIH HHS / CA / 1-P50-CA108786-01; United States / NCI NIH HHS / CA / P50 CA108786-039003; United States / NINDS NIH HHS / NS / NS020023-250020; United States / NINDS NIH HHS / NS / P50 NS020023-210020; United States / NCI NIH HHS / CA / CA108786-049003; United States / NCI NIH HHS / CA / P50 CA108786-059003; United States / NCI NIH HHS / CA / P50 CA108786-029003; United States / NINDS NIH HHS / NS / P50 NS020023-230020; United States / NCI NIH HHS / CA / CA108786-05S19003; United States / NCI NIH HHS / CA / P50 CA108786-049003; United States / NCI NIH HHS / CA / CA11898; United States / NCI NIH HHS / CA / CA108786-039003; United States / NINDS NIH HHS / NS / P50 NS020023-240020; United States / NINDS NIH HHS / NS / P50 NS020023-268626; United States / NCI NIH HHS / CA / P50 CA108786-019003; United States / NINDS NIH HHS / NS / P50 NS020023-220020; United States / NCI NIH HHS / CA / P50 CA108786-05S19003; United States / NCI NIH HHS / CA / CA108786-019003; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / P50 NS020023-250020; United States / NCI NIH HHS / CA / R37 CA011898; United States / NINDS NIH HHS / NS / NS020023-210020; United States / NINDS NIH HHS / NS / NS020023-230020
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 139
  • [Other-IDs] NLM/ NIHMS180495; NLM/ PMC2871667
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