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1. Benesch M, Windelberg M, Sauseng W, Witt V, Fleischhack G, Lackner H, Gadner H, Bode U, Urban C: Compassionate use of bevacizumab (Avastin) in children and young adults with refractory or recurrent solid tumors. Ann Oncol; 2008 Apr;19(4):807-13
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  • PATIENTS AND METHODS: Fifteen patients (male: n = 8; female: n = 7; median age, 14.6 years) received bevacizumab for recurrent or progressive solid tumors (carcinoma: n = 3; neuroblastoma: n = 2; astrocytoma grade III: n = 2; rhabdomyosarcoma: n = 2; nephroblastoma: n = 2; benign vascular tumors: n = 2; synovial sarcoma: n = 1; and malignant hemangiopericytoma: n = 1) on a compassionate basis.
  • Radiographic objective responses (partial responses) were observed in two patients with astrocytoma grade III and in one patient each with neuroblastoma and pleomorphic rhabdomyosarcoma, respectively.

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  • (PMID = 18056650.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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2. Tsuji K, Nakasu S, Tsuji A, Fukami T, Nozaki K: [Postoperative regression of desmoplastic infantile astrocytoma]. No Shinkei Geka; 2008 Nov;36(11):1035-9
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  • [Title] [Postoperative regression of desmoplastic infantile astrocytoma].
  • Desmoplastic infantile astrocytoma/ganglioglioma (DIA/DIG) is a rare tumor that is usually located superficially with a large cystic component.
  • In rare cases, postoperative regression of the residual tumor has been reported.
  • A 3-month-old boy presented with increasing head circumference and developmental delay.
  • A CT scan showed a large cystic tumor in his left parieto-occipital lobe.
  • The histopathological examination revealed an astrocytic tumor with marked desmoplasia.
  • In the central portion of the tumor, anaplastic features, such as necrosis, mitosis, and high nucleus-cytoplasmic ratio, were noticed.
  • Six months later when he was admitted for the second-stage surgery, MRI showed regression of the tumor.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery
  • [MeSH-minor] Gliosis. Humans. Infant. Male. Neoplasm Regression, Spontaneous

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  • (PMID = 19048924.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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3. Vordermark D, Kölbl O, Ruprecht K, Vince GH, Bratengeier K, Flentje M: Hypofractionated stereotactic re-irradiation: treatment option in recurrent malignant glioma. BMC Cancer; 2005;5:55
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  • [Title] Hypofractionated stereotactic re-irradiation: treatment option in recurrent malignant glioma.
  • BACKGROUND: Hypofractionated stereotactic radiotherapy (HFSRT) is one salvage treatment option in previously irradiated patients with recurrent malignant glioma.
  • METHODS: Between 1997 and 2003, 19 patients with recurrent malignant glioma (14 glioblastoma on most recent histology, 5 anaplastic astrocytoma) were treated with HFSRT.
  • RESULTS: The median overall survival (OS) was 9.3 (1.9-77.6+) months from the time of HFSRT, 15.4 months for grade III and 7.9 months for grade IV tumors (p = 0.029, log-rank test).
  • Median time to tumor progression after HFSRT on imaging was 4.9 months (1.3 to 37.3) months.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Disease Progression. Dose-Response Relationship, Radiation. Glioblastoma / pathology. Glioblastoma / surgery. Humans. Neoplasm Recurrence, Local. Nimustine / pharmacology. Prognosis. Recurrence. Stereotaxic Techniques. Teniposide / pharmacology. Time Factors. Treatment Outcome

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  • (PMID = 15924621.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0S726V972K / Nimustine; 957E6438QA / Teniposide
  • [Other-IDs] NLM/ PMC1156875
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4. Finlay JL, Dhall G, Boyett JM, Dunkel IJ, Gardner SL, Goldman S, Yates AJ, Rosenblum MK, Stanley P, Zimmerman RA, Wallace D, Pollack IF, Packer RJ, Children's Cancer Group: Myeloablative chemotherapy with autologous bone marrow rescue in children and adolescents with recurrent malignant astrocytoma: outcome compared with conventional chemotherapy: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2008 Dec;51(6):806-11
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  • [Title] Myeloablative chemotherapy with autologous bone marrow rescue in children and adolescents with recurrent malignant astrocytoma: outcome compared with conventional chemotherapy: a report from the Children's Oncology Group.
  • PURPOSE: Children and adolescents with malignant astrocytomas recurring after initial treatment have a dismal prognosis, with only rare patients surviving 1-year beyond recurrence.
  • METHODS: Twenty-seven children and adolescents with malignant astrocytomas [17 glioblastoma multiforme and 10 anaplastic astrocytoma (AA)] following initial tumor progression, received myeloablative chemotherapy followed by autologous marrow rescue with one of three thiotepa and etoposide-based chemotherapy regimens, administered alone (n = 11) or combined with carmustine (n = 5) or carboplatin (n = 11).
  • Time to progression and death following myeloablative chemotherapy for these patients was compared non-randomly with outcome of a contemporaneously treated cohort of similar patients who received only conventional chemotherapy following initial tumor progression.
  • Of 56 children with recurrent malignant astrocytoma who received conventional chemotherapy following initial progression, no patient survives.
  • CONCLUSIONS: Myeloablative chemotherapy with autologous marrow rescue can produce durable remissions in children and young adults with recurrent malignant gliomas, in the setting of minimal residual tumor burden achieved surgically.

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  • (PMID = 18802947.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA013539; United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / CA013539-30; United States / NCI NIH HHS / CA / U10 CA013539-30; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA021765-259003; United States / NCI NIH HHS / CA / P30 CA021765-259003; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA 21765
  • [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 / Myeloablative Agonists; 6PLQ3CP4P3 / Etoposide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U68WG3173Y / Carmustine
  • [Other-IDs] NLM/ NIHMS65899; NLM/ PMC2844080
  • [Investigator] Bleyer A; Khayat A; Sather H; Krailo M; Buckley J; Stram D; Sposto R; Hutchinson R; Matthay K; Gaynon P; Geyer JR; Shurin S; Reaman G; Ortega J; Ruymann F; Weiner M; Blatt J; Lukens J; Wolff L; Neglia J; Lange B; Steinherz P; Breitfeld P; O'Brien R; Cohen H; Fryer C; Wells R; Finklestein J; Feig S; Tannous R; Odom L; Gilchrist G; Barnard D; Wiley J; Ettinger L; Hetherington M; Coccia P; Norris D; Nachman J; Raney B; Baker D; Sanders J; Rausen A; Cairo M
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5. McGirt MJ, Mukherjee D, Chaichana KL, Than KD, Weingart JD, Quinones-Hinojosa A: Association of surgically acquired motor and language deficits on overall survival after resection of glioblastoma multiforme. Neurosurgery; 2009 Sep;65(3):463-9; discussion 469-70
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  • OBJECTIVE: Balancing the benefits of extensive tumor resection with the consequence of potential postoperative deficits remains a challenge in malignant astrocytoma surgery.


6. Hata N, Yoshimoto K, Yokoyama N, Mizoguchi M, Shono T, Guan Y, Tahira T, Kukita Y, Higasa K, Nagata S, Iwaki T, Sasaki T, Hayashi K: Allelic losses of chromosome 10 in glioma tissues detected by quantitative single-strand conformation polymorphism analysis. Clin Chem; 2006 Mar;52(3):370-8
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  • BACKGROUND: Detection of loss of heterozygosity (LOH) in clinical tissue samples is frequently difficult because samples are usually contaminated with noncancerous cells or because tumor cells in single tissues have genetic heterogeneity, and the precision of available techniques is insufficient for reliable analysis in such materials.
  • Anaplastic astrocytomas exhibited both 10p and 10q LOH, whereas diffuse astrocytomas frequently (63% of the cases) exhibited loss of 10p alone.
  • CONCLUSIONS: The present method is effective for precise mapping of LOH region in surgically obtained tumor tissues and could be applicable to the genetic diagnosis of cancers other than gliomas.
  • [MeSH-minor] Alleles. Astrocytoma / genetics. Humans. Polymorphism, Single Nucleotide


7. Uro-Coste E, Ssi-Yan-Kai G, Guilbeau-Frugier C, Boetto S, Bertozzi AI, Sevely A, Lolmede K, Delisle MB: Desmoplastic infantile astrocytoma with benign histological phenotype and multiple intracranial localizations at presentation. J Neurooncol; 2010 May;98(1):143-9
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  • [Title] Desmoplastic infantile astrocytoma with benign histological phenotype and multiple intracranial localizations at presentation.
  • Desmoplastic infantile astrocytoma (DIA) and desmoplastic infantile ganglioglioma (DIG) are rare intracranial tumors that mostly occur in the first 2 years of life and involve superficial cerebral cortex.
  • We report an original observation of a desmoplastic infantile astrocytoma in a 5-year-old boy with multiple localizations on initial presentation, including the unusual subtentorial region.
  • Magnetic resonance imaging showed a temporal tumor with prepontine and interpeduncular extension, and two other distinct localizations in cisterna magna and left cerebellar hemisphere.
  • The surgical samples, corresponding exclusively to subtentorial lesions, were devoid of anaplastic features; the temporal lesion was untouched because of the interpeduncular extension.
  • When the tumor is large, multilobular involvement is common, but multiple location of DIG is, on the contrary, very rare.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology


8. Deorah S, Lynch CF, Sibenaller ZA, Ryken TC: Trends in brain cancer incidence and survival in the United States: Surveillance, Epidemiology, and End Results Program, 1973 to 2001. Neurosurg Focus; 2006;20(4):E1
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  • Rising trends were noticed for glioblastoma multiforme (GBM), oligodendroglioma, anaplastic astrocytoma, medulloblastoma, and mixed glioma, and falling trends were observed for astrocytoma not otherwise specified and malignant glioma.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioblastoma / epidemiology. Glioma / epidemiology. Medulloblastoma / epidemiology. Oligodendroglioma / epidemiology. Population Surveillance

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  • (PMID = 16709014.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Shinoura N, Takahashi M, Yamada R: Delineation of brain tumor margins using intraoperative sononavigation: implications for tumor resection. J Clin Ultrasound; 2006 May;34(4):177-83
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  • [Title] Delineation of brain tumor margins using intraoperative sononavigation: implications for tumor resection.
  • PURPOSE: Sonography has been employed for real-time intraoperative delineation of tumor boundaries during resection of brain tumors.
  • However, the variably hyperechoic appearance of brain edema or gliosis surrounding the brain may interfere with accurate depiction of tumor margins.
  • The goal of the present study was to use sononavigation, which provides coregistration between real-time sonograms and MRI scans, to assess the accuracy of sonographic determination of tumor margins.
  • METHODS: Sononavigation was performed on 12 brain tumors (7 metastatic brain tumors, 2 meningiomas, 1 anaplastic oligodendroglioma, 1 anaplastic pilocytic astrocytoma, and 1 anaplastic astrocytoma).
  • Sonograms of tumor margins were categorized into 1 of 3 types: in type 1, the tumor margin was clearly visualized and corresponded to the margin of the enhanced lesion on MR scan in all areas; in type 2, the tumor margin was clearly seen in some areas but was obscure in others due to hyperechoic edema; and in type 3, the tumor margin was indistinguishable from surrounding tissues in all areas.
  • RESULTS: Three metastatic brain tumors and 1 meningioma were categorized as type 1.
  • Three metastatic brain tumors, 1 meningioma, and 1 anaplastic oligodendroglioma were categorized as type 2.
  • The anaplastic pilocytic astrocytoma, 1 metastatic brain tumor (which consisted mainly of necrotic tissue), and the anaplastic astrocytoma were categorized as type 3.
  • These data assist in determining whether the sonographic appearance of tumor margins is accurate and whether to rely on information from either sonography (type 1) or the sononavigation system when resecting tumor types 1, 2, and 3.
  • CONCLUSIONS: Sononavigation can help categorize the sonographic tumor margins into 3 different patterns, and this categorization can assist in determining which imaging modalities are needed to better delineate the tumor margins for subsequent resection.

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  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 16615048.001).
  • [ISSN] 0091-2751
  • [Journal-full-title] Journal of clinical ultrasound : JCU
  • [ISO-abbreviation] J Clin Ultrasound
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
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10. Zhang Y, Zhang N, Dai B, Liu M, Sawaya R, Xie K, Huang S: FoxM1B transcriptionally regulates vascular endothelial growth factor expression and promotes the angiogenesis and growth of glioma cells. Cancer Res; 2008 Nov 1;68(21):8733-42
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  • We previously found that FoxM1B is overexpressed in human glioblastomas and that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of highly angiogenic glioblastoma in nude mice.
  • Our findings provide both clinical and mechanistic evidence that FoxM1 contributes to glioma progression by enhancing VEGF gene transcription and thus tumor angiogenesis.

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  • (PMID = 18974115.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA116528-03; United States / NCI NIH HHS / CA / CA116528-03; United States / NCI NIH HHS / CA / R01-CA-116528; United States / NCI NIH HHS / CA / R01 CA116528; United States / NCI NIH HHS / CA / R01 CA116528-02; United States / NCI NIH HHS / CA / CA116528-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ NIHMS67455; NLM/ PMC2597644
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11. Jin M, Komohara Y, Shichijo S, Yamanaka R, Nikawa J, Itoh K, Yamada A: Erythropoietin-producing hepatocyte B6 variant-derived peptides with the ability to induce glioma-reactive cytotoxic T lymphocytes in human leukocyte antigen-A2+ glioma patients. Cancer Sci; 2008 Aug;99(8):1656-62
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  • In the present study, we examined the expression of the EphB6 variant (EphB6v) in a panel of brain tumor cell lines and glioblastoma tissues and we found that EphB6v was preferentially expressed in malignant brain tumors, such as glioblastomas and anaplastic astrocytomas.
  • [MeSH-minor] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Case-Control Studies. Cell Line, Tumor. Gene Expression. Glioblastoma / metabolism. HLA-A Antigens. HLA-A2 Antigen. Hepatocytes. Humans

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  • (PMID = 18754880.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; EC 2.7.1.- / EPHB6 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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12. Nagy M, Schulz-Ertner D, Bischof M, Welzel T, Hof H, Debus J, Combs SE: Long-term outcome of postoperative irradiation in patients with newly diagnosed WHO grade III anaplastic gliomas. Tumori; 2009 May-Jun;95(3):317-24
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  • [Title] Long-term outcome of postoperative irradiation in patients with newly diagnosed WHO grade III anaplastic gliomas.
  • PURPOSE: Patients with anaplastic gliomas have a more favorable overall survival than patients with glioblastomas.
  • In most analyses, WHO grade III and 1V tumors are not analyzed separately.
  • The present analysis reports outcome after postoperative radiotherapy in patients with WHO grade III gliomas.
  • PATIENTS AND METHODS: Between January 1988 and January 2007, 127 patients with WHO grade III tumors were treated with radiotherapy; the histological classification was pure astrocytoma in 104 patients, oligoastrocytoma in 12 and pure oligodendroglioma in 11 patients.
  • Median overall survival was 7 months for patients with anaplastic astrocytomas, 44 months for patients with mixed tumors, and 47 months for those with pure oligodendrogliomas.
  • CONCLUSION: Patients with WHO grade III anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas show favorable overall survival after postoperative radiotherapy compared with glioblastoma patients and should therefore be analyzed separately.
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / pathology. Astrocytoma / radiotherapy. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Oligodendroglioma / pathology. Oligodendroglioma / radiotherapy. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 19688970.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Ichimura K, Mungall AJ, Fiegler H, Pearson DM, Dunham I, Carter NP, Collins VP: Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH. Oncogene; 2006 Feb 23;25(8):1261-71
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  • [Title] Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH.
  • Deletions of chromosome 6 are a common abnormality in diverse human malignancies including astrocytic tumours, suggesting the presence of tumour suppressor genes (TSG).
  • A total of 104 adult astrocytic tumours (10 diffuse astrocytomas, 30 anaplastic astrocytomas (AA), 64 glioblastomas (GB)) were analysed using this array.
  • [MeSH-major] Astrocytoma / genetics. Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Glioblastoma / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Gene Dosage. Humans. Microsatellite Repeats. Telomere / genetics

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  • [Copyright] Oncogene (2006) 25, 1261-1271. doi:10.1038/sj.onc.1209156; published online 3 October 2005.
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  • (PMID = 16205629.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC2760128; NLM/ UKMS2686
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14. Tanaka S, Akimoto J, Kobayashi I, Oka H, Ujiie H: Individual adjuvant therapy for malignant gliomas based on O6-methylguanine-DNA methyltransferase messenger RNA quantitation by real-time reverse-transcription polymerase chain-reaction. Oncol Rep; 2008 Jul;20(1):165-71
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  • [Title] Individual adjuvant therapy for malignant gliomas based on O6-methylguanine-DNA methyltransferase messenger RNA quantitation by real-time reverse-transcription polymerase chain-reaction.
  • A new adjuvant therapy, individual adjuvant therapy (IAT), which is individualized according to the results of real-time reverse-transcription polymerase chain-reaction (RT-PCR) for O6-methylguanine-DNA methyltransferase (MGMT), was used to treat malignant gliomas.
  • Immediately after the operation, mRNA expression for drug-resistance genes was investigated in frozen samples of malignant gliomas from 55 patients (30 glioblastoma multiformes, 20 anaplastic astrocytomas and 5 anaplastic oligodendroglial tumors) by real-time quantitative RT-PCR with specific primers for MGMT.
  • The response rate was 40.9% for glioblastoma multiformes, 60.0% for anaplastic astrocytomas and 80.0% for anaplastic oligodendroglial tumors.

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  • (PMID = 18575733.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Messenger; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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15. Mikuni N, Hashimoto N: A minimally invasive transsulcal approach to the paracentral inner lesion. Minim Invasive Neurosurg; 2006 Oct;49(5):291-5
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  • METHODS: Four patients with paracentral inner lesions including anaplastic astrocytoma, cortical dysplasia, and cavernous angioma were operated on.
  • [MeSH-major] Astrocytoma / surgery. Brain Diseases / surgery. Brain Neoplasms / surgery. Hemangioma, Cavernous / surgery. Intralaminar Thalamic Nuclei / surgery. Minimally Invasive Surgical Procedures / methods. Neurosurgical Procedures / methods

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  • (PMID = 17163343.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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16. Shibui S: [Resent advances in chemotherapy for malignant brain tumors]. Gan To Kagaku Ryoho; 2005 Apr;32(4):442-7
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  • [Title] [Resent advances in chemotherapy for malignant brain tumors].
  • Most malignant brain tumors are resistant to the chemotherapeutic agents because of the existence of several mechanisms or substances such as the blood-brain barrier, genes and proteins.
  • Especially recent advances in the field of molecular biology have contributed to examination of the chemosensitivities of tumor cells.
  • Loss of chromosome 1 p and 19 q is considered to be closely related to chemosensitivity in anaplastic oligodendrogliomas.
  • This is one of the breakthroughs in the field of chemotherapy for malignant brain tumors.
  • Multi-institutional randomized controlled study by JCOG Brain Tumor Study Group is the first trial for the treatment of malignant astrocytomas under well-established quality control and quality assurance systems.
  • It can be a model of clinical trials for malignant brain tumors in Japan.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Clinical Trials, Phase II as Topic. Drug Resistance, Neoplasm. Humans. Nimustine / administration & dosage. Nitrosourea Compounds / pharmacology. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Procarbazine / administration & dosage. Quality Control. Randomized Controlled Trials as Topic

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  • (PMID = 15853207.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Nitrosourea Compounds; 0S726V972K / Nimustine; 35S93Y190K / Procarbazine; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  • [Number-of-references] 27
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17. Da Fonseca CO, Silva JT, Lins IR, Simão M, Arnobio A, Futuro D, Quirico-Santos T: Correlation of tumor topography and peritumoral edema of recurrent malignant gliomas with therapeutic response to intranasal administration of perillyl alcohol. Invest New Drugs; 2009 Dec;27(6):557-64
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  • [Title] Correlation of tumor topography and peritumoral edema of recurrent malignant gliomas with therapeutic response to intranasal administration of perillyl alcohol.
  • BACKGROUND: The aim of this study was to establish a correlation of tumor topography and peritumoral brain edema with the therapeutic response to intranasal administration of perillyl alcohol (POH) in a cohort of patients with recurrent malignant gliomas.
  • METHODS: The retrospective study reviewed clinical and neuroradiological data from patients with recurrent malignant gliomas who received intranasal daily administration of POH 440 mg.
  • The following parameters were assessed: demographic characteristics, initial symptoms, overall survival, tumor topography and tumor size, presence of midline shift and extent of peritumoral edema.
  • RESULTS: A cohort of 67 patients included 52 (78%) with glioblastoma (GBM), ten (15%) with anaplastic astrocytoma (AA) and five (7%) with anaplastic oligodendroglioma (AO).
  • Accordingly to tumor topography lobar localization was present in all (5/5) AO; eight (8/10) and 41 GBM patients whereas in the basal ganglia two AA and 11 GBM patients.
  • It was also observed a relation between the tumor size and area of peritumoral brain edema (PTBE).
  • Patients with good therapeutic response showed reduction of tumor size and PTBE area, but poor prognosis was associated with lack of response to treatment and persistence of high PTBE.
  • Patients with tumor in the basal ganglia survived significantly longer than those with lobar gliomas (log rank test, p = 0.0003).
  • (2) presence of PTBE contributes to symptoms, likely to be implicated in the morbidity and invading potential of malignant gliomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Edema / pathology. Brain Neoplasms / drug therapy. Glioma / drug therapy. Glioma / pathology. Monoterpenes / therapeutic use. Neoplasm Recurrence, Local / pathology

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  • (PMID = 19139816.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Monoterpenes; 319R5C7293 / perillyl alcohol
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18. Khan MK, Hunter GK, Vogelbaum M, Suh JH, Chao ST: Evidence-based adjuvant therapy for gliomas: current concepts and newer developments. Indian J Cancer; 2009 Apr-Jun;46(2):96-107
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  • Of the 18,820 new cases of primary central nervous system (CNS) tumors diagnosed annually in the United States, gliomas account for over 60% with 30-40% of them being glioblastoma multiforme (GBM), 10% being anaplastic astrocytoma (AA), and 10% being low grade gliomas (LGGs).
  • This is in contrast to one study from West Bengal, India, in which only 7.9% of the brain tumors were GBMs, while 46.8% were astrocytomas.
  • Of all adult primary CNS tumors, GBM is the most common and the most malignant with about 7,000 to 8,000 new cases annually in the United States.
  • Common to these approaches is the use of adjuvant radiation therapy, even as surgery alone, with or without chemotherapy, may be the mainstay for some lower grade and low-risk gliomas.
  • Specifically, the database is searched using the following keywords, with various combinations: glioma, low-grade, anaplastic, astrocytoma, oligodendroglioma, oligoastrocytoma, glioblastoma multiforme, chemotherapy, radiation, new concepts, phase III, MGMT, CDX-110 (Celldex), temozolomide, 1p/19q deletion, and bevacizumab.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Astrocytoma / therapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / therapy. Humans

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  • (PMID = 19346643.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 64
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19. Maiti AK, Ghosh K, Chatterjee U, Chakrobarti S, Chatterjee S, Basu S: Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas. Neurol India; 2008 Oct-Dec;56(4):456-62
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  • [Title] Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas.
  • AIMS: The involvement of various growth factors, growth factor receptors and proliferative markers in the molecular pathogenesis of astrocytic neoplasms are being studied extensively.
  • Since EGFR and proliferating cell nuclear antigen (PCNA) are involved in mitogenic signal transduction and cellular proliferation pathway, we have studied the correlation between the expression of EGFR and PCNA labeling index in astrocytic tumors.
  • MATERIALS AND METHODS: We investigated the immunohistochemical expression of EGFR and PCNA using the appropriate monoclonal antibodies in 40 cases of astrocytic tumors of which 21 cases were glioblastoma, eight cases were Grade III or anaplastic astrocytomas and six cases were Grade II or diffuse astrocytomas and five cases were Grade I or pilocytic astrocytomas.
  • RESULTS: Both the EGFR expression and PCNA labeling index increase with increasing grades of astrocytomas with a significantly high percentage of cells showing positive staining for both EGFR and PCNA in GBM and Grade III astrocytomas compared to Grade II astrocytomas.
  • The expression levels of both EGFR and PCNA were low in Grade I or pilocytic astrocytomas.
  • CONCLUSIONS: A significant correlation was found between EGFR overexpression and PCNA labeling index in Grade III and Grade II astrocytomas and glioblastoma.
  • These suggest that the tumor proliferation, at least in higher grades of astrocytomas is dependent in some measure on EGF and EGFR-related signaling pathways.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Receptor, Epidermal Growth Factor / metabolism


20. Walker DG, Laherty R, Tomlinson FH, Chuah T, Schmidt C: Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy. J Clin Neurosci; 2008 Feb;15(2):114-21
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  • [Title] Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy.
  • Dendritic cell vaccination has been applied to the treatment of a variety of cancers, including malignant astrocytoma.
  • We have treated 13 patients with malignant astrocytoma using dendritic cell vaccination and have shown that this treatment is safe and is likely to be effective in combination with standard adjuvant therapy.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Chemotherapy, Adjuvant / methods. Dendritic Cells / immunology. Immunotherapy, Active / methods

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  • (PMID = 18083572.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD8; 0 / Cancer Vaccines; EC 3.1.3.48 / Antigens, CD45
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21. Sarkar C, Karak AK, Nath N, Sharma MC, Mahapatra AK, Chattopadhyay P, Sinha S: Apoptosis and proliferation: correlation with p53 in astrocytic tumours. J Neurooncol; 2005 Jun;73(2):93-100
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  • [Title] Apoptosis and proliferation: correlation with p53 in astrocytic tumours.
  • We, as well as several other groups, have earlier demonstrated the association of p53 immunopositivity with increased degree of cell proliferation in astrocytic tumours.
  • Here we have studied the extent of apoptosis in 62 primary human astrocytic tumours [25 Diffuse Astrocytoma (DA), 9 Anaplastic Astrocytoma (AA) and 28 Glioblastoma multiforme (GBM)] in relation to tumour grade, proliferative status and p53 protein expression.
  • However this was not observed in p53 +ve GBM or in low grade DA either p53 positive or negative.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15981097.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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22. Yoshikawa K, Saito K, Kajiwara K, Nomura S, Ishihara H, Suzuki M: CyberKnife stereotactic radiotherapy for patients with malignant glioma. Minim Invasive Neurosurg; 2006 Apr;49(2):110-5
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  • [Title] CyberKnife stereotactic radiotherapy for patients with malignant glioma.
  • The authors report on their experience using the CyberKnife in 25 patients with malignant gliomas.
  • METHODS: Twenty-five patients with histologically proven malignant gliomas (18 glioblastoma: GB, 7 anaplastic astrocytoma: AA) were treated with the CyberKnife at Konan St. Hill Hospital between June 1998 and November 2002.
  • Patient-, tumor-, and treatment-related variables were analyzed by univariate analysis, and survival curves were generated by the Kaplan-Meier product limit.
  • CONCLUSION: This is the first report of CyberKnife stereotactic radiotherapy applied to the treatment of malignant gliomas.
  • The frameless and painless CyberKnife stereotactic radiotherapy has the potential to be as useful for treatment of malignant glioma as other radiosurgical modalities.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / pathology. Radiosurgery / instrumentation. Robotics

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  • (PMID = 16708341.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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23. El-Jawahri A, Patel D, Zhang M, Mladkova N, Chakravarti A: Biomarkers of clinical responsiveness in brain tumor patients : progress and potential. Mol Diagn Ther; 2008;12(4):199-208
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  • [Title] Biomarkers of clinical responsiveness in brain tumor patients : progress and potential.
  • Anaplastic astrocytoma and glioblastoma multiforme represent malignant astrocytomas, which are the most common type of malignant gliomas.
  • Despite research efforts in cancer therapy, the prognosis of patients with malignant gliomas remains poor.
  • Research efforts in recent years have focused on investigating the cellular, molecular, and genetic pathways involved in the progression of malignant gliomas.
  • As a result, biomarkers have emerged as diagnostic, predictive, and prognostic tools that have the potential to transform the field of brain tumor diagnostics.
  • An increased understanding of the important molecular pathways that have been implicated in the progression of malignant gliomas has led to the identification of potential diagnostic, prognostic, and predictive biomarkers, some bearing clinical implications for targeted therapy.
  • Research into the clinical relevance and applicability of such biomarkers has the potential to revolutionize our approach to the diagnosis and treatment of patients with malignant gliomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / chemistry. Glioma / chemistry

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  • (PMID = 18652516.001).
  • [ISSN] 1177-1062
  • [Journal-full-title] Molecular diagnosis & therapy
  • [ISO-abbreviation] Mol Diagn Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA108633
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 71
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24. Tanaka K, Sasayama T, Kawamura A, Kondoh T, Kanomata N, Kohmura E: Isolated oculomotor nerve paresis in anaplastic astrocytoma with exophytic invasion. Neurol Med Chir (Tokyo); 2006 Apr;46(4):198-201
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  • [Title] Isolated oculomotor nerve paresis in anaplastic astrocytoma with exophytic invasion.
  • A 30-year-old man presented with a supratentorial malignant glioma manifesting as isolated progressive left oculomotor nerve paresis.
  • Computed tomography and magnetic resonance imaging showed an intra-axial tumor in the left temporal lobe, extending to the basal and prepontine cisterns, and compressing the brainstem.
  • The tumor was removed subtotally.
  • The histological diagnosis was anaplastic astrocytoma.
  • Malignant glioma with exophytic growth in the temporal lobe should be considered in the differential diagnosis of isolated oculomotor nerve paresis.
  • [MeSH-major] Astrocytoma / complications. Oculomotor Nerve Diseases / etiology. Supratentorial Neoplasms / complications. Temporal Lobe
  • [MeSH-minor] Adult. Astrocytes / pathology. Biomarkers, Tumor / analysis. Brain Stem / pathology. Cerebral Arteries / pathology. Cisterna Magna / pathology. Dominance, Cerebral / physiology. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Nerve Compression Syndromes / diagnosis. Nerve Compression Syndromes / etiology. Nerve Compression Syndromes / pathology. Nerve Compression Syndromes / surgery. Neuronavigation. Oculomotor Nerve / pathology. Oculomotor Nerve / surgery. Pons / pathology

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  • (PMID = 16636512.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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25. Chamberlain MC, Johnston S: Bevacizumab for recurrent alkylator-refractory anaplastic oligodendroglioma. Cancer; 2009 Apr 15;115(8):1734-43
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  • [Title] Bevacizumab for recurrent alkylator-refractory anaplastic oligodendroglioma.
  • BACKGROUND: A retrospective evaluation of single agent bevacizumab was carried out in adults with recurrent alkylator-refractory 1p19q codeleted anaplastic oligodendrogliomas (AO) with an objective of determining progression-free survival (PFS).
  • Bevacizumab-related toxicity included fatigue (14 patients; 4 grade 3), leukopenia (9; 1 grade 3), anemia (5; 0 grade 3), hypertension (5; 1 grade 3), deep vein thrombosis (4; 1 grade 3), and wound dehiscence (2; 1 grade 3).
  • Time to tumor progression ranged from 1 to 18 months (median, 6.75 months).
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Bevacizumab. Chromosomes, Human, Pair 1. Disease-Free Survival. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis

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  • (PMID = 19197992.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents, Alkylating; 2S9ZZM9Q9V / Bevacizumab
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26. Nano R, Capelli E, Facoetti A, Benericetti E: Immunobiological and experimental aspects of malignant astrocytoma. Anticancer Res; 2009 Jul;29(7):2461-5
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  • [Title] Immunobiological and experimental aspects of malignant astrocytoma.
  • Starting from 1992, the goal of our studies was to obtain new biological data on malignant astrocytomas to better understand the basic biology of the tumour and these are reviewed here.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology

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  • (PMID = 19596914.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-2
  • [Number-of-references] 51
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27. Pavlisa G, Rados M, Pavlisa G, Pavic L, Potocki K, Mayer D: The differences of water diffusion between brain tissue infiltrated by tumor and peritumoral vasogenic edema. Clin Imaging; 2009 Mar-Apr;33(2):96-101
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  • [Title] The differences of water diffusion between brain tissue infiltrated by tumor and peritumoral vasogenic edema.
  • The differences between peritumoral brain tissue infiltrated by tumor and vasogenic edema were prospectively evaluated by comparing the apparent diffusion coefficient (ADC) of peritumoral areas of infiltrative tumors (anaplastic astrocytomas and glioblastomas) to that of peritumoral areas of noninfiltrative tumors (metastatic carcinomas) on 54 patients.
  • Peritumoral ADCs indicated the possibility of differentiation between tumor infiltration and vasogenic edema, as well as between primary gliomas and metastases.
  • [MeSH-minor] Astrocytoma / diagnosis. Astrocytoma / pathology. Female. Glioblastoma / diagnosis. Glioblastoma / pathology. Humans. Male. Middle Aged

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  • (PMID = 19237051.001).
  • [ISSN] 1873-4499
  • [Journal-full-title] Clinical imaging
  • [ISO-abbreviation] Clin Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Vidiri A, Carapella CM, Pace A, Mirri A, Fabi A, Carosi M, Giannarelli D, Pompili A, Jandolo B, Occhipinti E, Di Giovanni S, Crecco M: Early post-operative MRI: correlation with progression-free survival and overall survival time in malignant gliomas. J Exp Clin Cancer Res; 2006 Jun;25(2):177-82
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  • [Title] Early post-operative MRI: correlation with progression-free survival and overall survival time in malignant gliomas.
  • Forty-seven patients with Glioblastoma (42) and Anaplastic Astrocytoma (5) were studied with MR 24 hrs after surgery.
  • In order to evaluate the role of early MR in defining the extent of surgical resection and its relation with the prognosis of malignant glioma patients, three categories of surgical resection were considered: gross total, sub-total and partial resection.
  • The study confirms that early-MR has to be considered an accurate technique for monitoring the extension of malignant glioma surgical resection and shows a good correlation between early-MR findings, PFS and ST.

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  • (PMID = 16918127.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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29. Gimenez M, Souza VC, Izumi C, Barbieri MR, Chammas R, Oba-Shinjo SM, Uno M, Marie SK, Rosa JC: Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin. Proteomics; 2010 Aug;10(15):2812-21
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  • [Title] Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin.
  • The aim of this study was to identify differentially expressed proteins in diffuse astrocytoma grade II, anaplastic astrocytoma grade III and glioblastoma multiforme grade IV in human tumor samples and in non-neoplastic brain tissue as control using 2-DE and MS.
  • Tumor and control brain tissue dissection was guided by histological hematoxylin/eosin tissue sections to provide more than 90% of tumor cells and astrocytes.
  • Six proteins were detected as up-regulated in higher grade astrocytomas and the most important finding was nucleophosmin (NPM) (p<0.05), whereas four proteins were down-regulated, among them raf kinase inhibitor protein (RKIP) (p<0.05).
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Phosphatidylethanolamine Binding Protein / genetics. Proteomics


30. Terasaki M, Bouffet E, Katsuki H, Fukushima S, Shigemori M: Pilot trial of the rate of response, safety, and tolerability of temozolomide and oral VP-16 in patients with recurrent or treatment-induced malignant central nervous system tumors. Surg Neurol; 2008 Jan;69(1):46-50
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  • [Title] Pilot trial of the rate of response, safety, and tolerability of temozolomide and oral VP-16 in patients with recurrent or treatment-induced malignant central nervous system tumors.
  • METHODS: Eleven patients with recurrent or treatment-induced malignant CNS tumors, including treatment-induced PNET (in 1 patient), brainstem glioma (in 3 patients; 1 with treatment-induced, 2 with recurrence), recurrent anaplastic astrocytoma (in 3 patients), and recurrent glioblastoma (in 4 patients) were evaluated in a pilot study of TMZ and oral VP-16 chemotherapy.
  • The histologic subtype of the tumor, its location, and its maximum response to chemotherapy did not have an impact on the duration of disease control.
  • CONCLUSION: This limited pilot study confirms the innocuousness and the activity of the combination of TMZ and oral VP-16 in recurrent malignant brain tumors.
  • This promising activity warrants further investigation of this combination in larger phase II or III studies.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Etoposide / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Neoplasms, Neuroepithelial / drug therapy. Neoplasms, Second Primary / drug therapy

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  • (PMID = 18054615.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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31. Miyatake S, Kawabata S, Kajimoto Y, Aoki A, Yokoyama K, Yamada M, Kuroiwa T, Tsuji M, Imahori Y, Kirihata M, Sakurai Y, Masunaga S, Nagata K, Maruhashi A, Ono K: Modified boron neutron capture therapy for malignant gliomas performed using epithermal neutron and two boron compounds with different accumulation mechanisms: an efficacy study based on findings on neuroimages. J Neurosurg; 2005 Dec;103(6):1000-9
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  • [Title] Modified boron neutron capture therapy for malignant gliomas performed using epithermal neutron and two boron compounds with different accumulation mechanisms: an efficacy study based on findings on neuroimages.
  • OBJECT: To improve the effectiveness of boron neutron capture therapy (BNCT) for malignant gliomas, the authors used epithermal rather than thermal neutrons for deep penetration and two boron compounds-sodium borocaptate (BSH) and boronophenylalanine (BPA)-with different accumulation mechanisms to increase the boron level in tumors while compensating for each other's faults.
  • METHODS: Thirteen patients, 10 of whom harbored a glioblastoma multiforme (GBM), one a gliosarcoma, one an anaplastic astrocytoma, and one an anaplastic oligoastrocytoma, were treated using this modified BNCT between January 2002 and December 2003.
  • The mean tumor volume before BNCT was 42.3 cm3.
  • Regardless of the pre-BNCT tumor volume, in every patient harboring an assessable lesion, improvements on MR or CT images were recognized both at the initial assessment (range of volume reduction rate 17.4-71%, mean rate 46.4%) and at follow-up assessments (range of volume reduction rates 30.3-87.6%, mean rate 58.5%).
  • CONCLUSIONS: This modified BNCT produced a good improvement in malignant gliomas, as seen on neuroimages.
  • [MeSH-minor] Adult. Aged. Astrocytoma / radiotherapy. Boron Compounds / therapeutic use. Brain Edema / diagnosis. Brain Edema / etiology. Female. Glioblastoma / radiotherapy. Gliosarcoma / radiotherapy. Humans. Male. Middle Aged. Neutrons. Treatment Outcome

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  • (PMID = 16381186.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boron Compounds
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32. Gil-Salú JL, Nieto A, Rodríguez-Gutiérrez JF, Almarcha J: [Allelic loss at 1p/19q analysis in brain tumors of glial lineage]. Neurocirugia (Astur); 2007 Aug;18(4):285-93; discussion 293
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  • [Transliterated title] Análisis de la presencia de mutaciones por pérdida de heterocigocidad de 1p/19q en tumores cerebrales de estirpe glial.
  • RESULTS: Were included in the first part of this study 45 sample of neuroepithelial tissue supratentorial tumors: 29 glioblastoma, 1 gliosarcoma, 7 diffuse astrocytoma grade II, 1 oligoastrocytoma, 3 oligodendroglioma, 1 anaplastic oligodendroglioma, 1 xanthoastrocytoma, 1 dysembryoplastic neuroepithelial tumour and 1 pilocytic astrocytoma.
  • 80% of oligodendroglial tumors, 14% glioblastoma and 14% of diffuse astrocytoma grade II.
  • [MeSH-minor] Base Sequence. DNA, Neoplasm / analysis. Genetic Markers. Humans. Microsatellite Repeats. Molecular Sequence Data. Retrospective Studies

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  • (PMID = 17882335.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Genetic Markers
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33. Wrensch M, Rice T, Miike R, McMillan A, Lamborn KR, Aldape K, Prados MD: Diagnostic, treatment, and demographic factors influencing survival in a population-based study of adult glioma patients in the San Francisco Bay Area. Neuro Oncol; 2006 Jan;8(1):12-26
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  • Survival differences between anaplastic astrocytoma (AA) and astrocytoma were apparent from review diagnoses (median months of survival for AA, 13.0 [95% CI, 9.9-19.5], and astrocytoma, 101.3 [95% CI lower limit, 42.1; upper limit not yet reached]), but not with ICD-O-2 diagnoses reported by SEER (median months of survival for AA, 16.6 [95% CI, 12.0-20.7], and astrocytoma, not otherwise specified, 17.2 [95% CI, 10.6-71.6]).
  • This finding emphasizes the need for improvements in coding for nonglioblastoma astrocytomas to provide better population survival estimates.

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  • (PMID = 16443944.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES06717; United States / NIEHS NIH HHS / ES / R01 ES006717; United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / CA89032; United States / NIEHS NIH HHS / ES / ES04705; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / CA52689; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1871921
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34. Yang SH, Hong YK, Yoon SC, Kim BS, Lee YS, Lee TK, Lee KS, Jeun SS, Kim MC, Park CK: Radiotherapy plus concurrent and adjuvant procarbazine, lomustine, and vincristine chemotherapy for patients with malignant glioma. Oncol Rep; 2007 Jun;17(6):1359-64
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  • [Title] Radiotherapy plus concurrent and adjuvant procarbazine, lomustine, and vincristine chemotherapy for patients with malignant glioma.
  • We analyzed the clinical efficacy and toxicity of concurrent therapy as a first line modality for malignant glioma patients.
  • From 1998 to 2004, 39 patients, 22 with glioblastoma (GM), nine with anaplastic astrocytoma (AA), 7 with anaplastic oligodendroglioma (AO) and 1 with anaplastic oligodendro-astrocytoma (AOA) were enrolled in this study.
  • Grade III/IV hematological toxicity was reduced from 25.6 to 13% after reduction of the dose of CCNU (75 mg/m(2)).
  • Modified concurrent chemoradiotherapy may be a feasible option for treating malignant glioma with acceptable toxicity.

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  • (PMID = 17487391.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
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35. Marie Y, Carpentier AF, Omuro AM, Sanson M, Thillet J, Hoang-Xuan K, Delattre JY: EGFR tyrosine kinase domain mutations in human gliomas. Neurology; 2005 Apr 26;64(8):1444-5
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  • In this study, the authors tested the presence of such mutations in 95 gliomas including glioblastomas, anaplastic oligodendrogliomas, and low-grade gliomas.
  • [MeSH-minor] Astrocytoma / drug therapy. Astrocytoma / enzymology. Astrocytoma / genetics. Carcinoma / drug therapy. Carcinoma / enzymology. Carcinoma / genetics. DNA Mutational Analysis. Drug Resistance, Neoplasm / genetics. Genetic Testing. Glioblastoma / drug therapy. Glioblastoma / enzymology. Glioblastoma / genetics. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Oligodendroglioma / drug therapy. Oligodendroglioma / enzymology. Oligodendroglioma / genetics. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Protein Structure, Tertiary / genetics. Quinazolines / pharmacology. Quinazolines / therapeutic use

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  • (PMID = 15851741.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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36. Perez-Saldana MT, Vilar C, Geffner-Sclarsky D, Belenguer-Benavides A, Del Villar-Igea A, Gil-Fortuno M, Bahamonde D: [Meningoencephalomyelitis as the initial symptom of a brain tumour mimicking encephalitis due to herpes simplex virus: a case report]. Rev Neurol; 2007 Mar 16-31;44(6):348-52
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  • [Transliterated title] Meningoencefalomielitis como manifestacion inicial de un tumor cerebral que imita una encefalitis por virus del herpes simple: descripcion de un caso.
  • A tumoural aetiology is rare and they are generally malignant tumours with an ominous prognosis.
  • We report a case of meningoencephalomyelitis that initially presented as encephalitis due to herpes simplex virus (HSV) and which was finally seen to be an anaplastic oligoastrocytoma.
  • The post-mortem examination revealed a grade III oligoastrocytoma in both temporal lobes, which had extended into the adjacent subarachnoid space and the cerebral and cervical leptomeninges.
  • [MeSH-major] Astrocytoma. Brain Neoplasms. Encephalitis, Herpes Simplex / etiology. Meninges / pathology. Meningitis / etiology


37. Kaderali Z, Lamberti-Pasculli M, Rutka JT: The changing epidemiology of paediatric brain tumours: a review from the Hospital for Sick Children. Childs Nerv Syst; 2009 Jul;25(7):787-93
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  • METHODS: We classified 1,866 surgical pathology cases of brain tumours in children under the age of 19 according to the World Health Organization 2007 consensus and analysed them by gender, histological tumour type, age distribution and decade.
  • The main histological tumour types were low-grade (I/II) astrocytomas (26.4%), medulloblastoma (10.6%), anaplastic astrocytoma/glioblastoma multiforme (7.1%) and ependymoma (7.0%).
  • Over three decades, an increasing proportion of certain tumour types, including pilocytic astrocytoma, atypical teratoma/rhabdoid tumours and neuronal/mixed neuronal-glial tumours was seen.
  • [MeSH-minor] Age Factors. Astrocytoma / epidemiology. Astrocytoma / pathology. Canada / epidemiology. Child. Ependymoma / epidemiology. Ependymoma / pathology. Glioblastoma / epidemiology. Glioblastoma / pathology. Humans. Medulloblastoma / epidemiology. Medulloblastoma / pathology. Neoplasm Staging. Neoplasms, Complex and Mixed / epidemiology. Neoplasms, Complex and Mixed / pathology. Neoplasms, Nerve Tissue / epidemiology. Neoplasms, Nerve Tissue / pathology. Rhabdoid Tumor / epidemiology. Rhabdoid Tumor / pathology. Risk Factors. Sex Factors. Teratoma / epidemiology. Teratoma / pathology. Time Factors

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  • (PMID = 19082611.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 30
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38. Kim JH, Choi C, Benveniste EN, Kwon D: TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells. Biochem Biophys Res Commun; 2008 Dec 5;377(1):195-9
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  • [Title] TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells.
  • Matrix metalloproteinase-9 (MMP-9) is an important angiogenic and prognostic factor in malignant tumors.
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as the death ligand, which induces preferential apoptosis of transformed tumor cells.
  • We demonstrated that TRAIL induces MMP-9 expression in human astrocytoma cells, which is preceded by activation of extracellular signal-regulated protein kinase (ERK).
  • These findings indicate that TRAIL treatment in human astrocytoma cells leads to the activation of NF-kappaB and subsequent expression of MMP-9, which are dependent on ERK activation.
  • Collectively, these results suggest that TRAIL has alternative biological functions in addition to its role in inducing apoptosis in human malignant astrocytoma cells.
  • [MeSH-major] Astrocytoma / enzymology. Extracellular Signal-Regulated MAP Kinases / metabolism. Matrix Metalloproteinase 9 / biosynthesis. TNF-Related Apoptosis-Inducing Ligand / physiology
  • [MeSH-minor] Butadienes / pharmacology. Cell Line, Tumor. Enzyme Activation. Humans. NF-kappa B / metabolism. Nitriles / pharmacology. Protein Kinase Inhibitors

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  • (PMID = 18834856.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / NF-kappa B; 0 / Nitriles; 0 / Protein Kinase Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / U 0126; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
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39. Levin VA, Ictech S, Hess KR: Impact of phase II trials with progression-free survival as end-points on survival-based phase III studies in patients with anaplastic gliomas. BMC Cancer; 2007;7:106
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  • [Title] Impact of phase II trials with progression-free survival as end-points on survival-based phase III studies in patients with anaplastic gliomas.
  • BACKGROUND: To assess progression-free survival (PFS) as the appropriate end-point for phase II trials for anaplastic gliomas (AGs) and to determine the impact of PFS on survival-based phase III trials.
  • CONCLUSION: Based on PFS rates at 6, 9, and 12 months for AG patients, a differential of 1.5 to 2 years is the norm and could invalidate overall survival as an end-point for phase III studies in patients with AG.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Oligodendroglioma / drug therapy. Oligodendroglioma / mortality

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  • (PMID = 17587447.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC1919386
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40. Galloway M: CD34 expression in glioblastoma and giant cell glioblastoma. Clin Neuropathol; 2010 Mar-Apr;29(2):89-93
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  • OBJECTIVE: This study aimed to determine whether CD34 is expressed in glioblastomas and giant cell glioblastomas, as this information may be of value when attempting to differentiate between giant cell glioblastomas and other relevant differential diagnoses such as pleomorphic xanthoastrocytomas with anaplastic features and anaplastic gangliogliomas.
  • CD34 staining in isolation is unlikely to be of assistance in differentiating between giant cell glioblastoma and pleomorphic xanthoastrocytomas with anaplastic features or anaplastic gangliogliomas.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology
  • [MeSH-minor] Astrocytoma / pathology. Diagnosis, Differential. Ganglioglioma / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Humans

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  • (PMID = 20175958.001).
  • [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 / Antigens, CD34; 0 / Biomarkers, Tumor
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41. Kirby S, Gertler SZ, Mason W, Watling C, Forsyth P, Aniagolu J, Stagg R, Wright M, Powers J, Eisenhauer EA: Phase 2 study of T138067-sodium in patients with malignant glioma: Trial of the National Cancer Institute of Canada Clinical Trials Group. Neuro Oncol; 2005 Apr;7(2):183-8
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  • [Title] Phase 2 study of T138067-sodium in patients with malignant glioma: Trial of the National Cancer Institute of Canada Clinical Trials Group.
  • We studied the activity of T138067-sodium in patients with malignant gliomas.
  • Patients with recurrent anaplastic astrocytoma or glioblastoma multiforme were treated intravenously with 330 mg/m(2) of T138067-sodium weekly.
  • There were two patients with anaplastic astrocytoma and 16 with glioblastoma multiforme.
  • Our results suggest that given in this dose and schedule T138067-sodium does not have activity in this population of anaplastic astrocytoma and glioblastoma multiforme.

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  • (PMID = 15831236.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Sulfonamides; T4NP8G3K6Q / batabulin
  • [Other-IDs] NLM/ PMC1871890
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42. Rousselot C, Francois P, Jan M, Bergemer AM: [Report of seven cases of clear-cell meningioma and a literature review]. Ann Pathol; 2010 Apr;30(2):73-82
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  • [Transliterated title] Etude de sept cas de méningiomes à cellules claires et revue de la littérature.
  • Three patients belonged to the same family, probably affected by neurofibromatosis type 2.
  • CONCLUSION: Our study supports the fact that MCC course is less favourable than meningioma WHO grade I, even in the absence of anaplastic area, high mitotic activity, or necrosis.
  • [MeSH-major] Biomarkers, Tumor / analysis. Meningeal Neoplasms / pathology. Meningioma / pathology. Neoplasm Proteins / analysis
  • [MeSH-minor] Adult. Aged. Astrocytoma / diagnosis. Child, Preschool. Diagnostic Errors. Ependymoma / diagnosis. Female. Humans. Keratins / analysis. Ki-67 Antigen / analysis. Male. Middle Aged. Mucin-1 / analysis. Neurofibromatosis 2 / diagnosis. Neurofibromatosis 2 / genetics. Neurofibromatosis 2 / pathology. Receptors, Progesterone / analysis. Retrospective Studies. S100 Proteins / analysis. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20451062.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Mucin-1; 0 / Neoplasm Proteins; 0 / Receptors, Progesterone; 0 / S100 Proteins; 68238-35-7 / Keratins
  • [Number-of-references] 33
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43. Ellis JA, Waziri A, Balmaceda C, Canoll P, Bruce JN, Sisti MB: Rapid recurrence and malignant transformation of pilocytic astrocytoma in adult patients. J Neurooncol; 2009 Dec;95(3):377-382
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  • [Title] Rapid recurrence and malignant transformation of pilocytic astrocytoma in adult patients.
  • Pilocytic astrocytoma is a slow-growing, circumscribed glioma that most frequently occurs within the pediatric population.
  • In general, surgical resection for pilocytic astrocytoma is thought to be curative with tumor recurrence or malignant transformation being relatively rare.
  • However, there have been very few studies specifically looking at the prognosis for adult patients diagnosed with pilocytic astrocytoma.
  • To evaluate the frequency of recurrence and malignant transformation of pilocytic astrocytoma in adults, we performed a retrospective analysis of all adult patients who underwent surgical resection for this tumor at our institution over a period of 10 years.
  • A high rate of malignant transformation was observed in the patients that underwent repeat surgery with 75% (3/4) progressing to anaplastic astrocytoma on pathological examination.
  • This study provides further evidence that the clinical course of a subset of adult patients with pilocytic astrocytoma will not be benign.
  • The potential for rapid tumor recurrence and malignant transformation necessitates careful post-operative follow-up for adult patients with this tumor.
  • [MeSH-major] Astrocytoma / mortality. Astrocytoma / pathology. Brain Neoplasms / mortality. Brain Neoplasms / pathology. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / pathology

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  • (PMID = 19533024.001).
  • [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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44. Jha P, Agarwal S, Pathak P, Srivastava A, Suri V, Sharma MC, Chosdol K, Srivastava T, Gupta D, Gupta A, Suri A, Sarkar C: Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India. Cancer Genet Cytogenet; 2010 Apr 15;198(2):126-34
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  • [Title] Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India.
  • There are few reports of loss of heterozygosity (LOH) of 1p and 19q in astrocytic tumors, especially glioblastoma multiforme (GBM).
  • We evaluated 1p and 19q (either or both) heterozygosity status in 71 astrocytomas, including 6 pediatric cases: 20 diffuse astrocytomas (DA), 9 anaplastic astrocytomas (AA), and 42 GBM.
  • Thus, 1p and 19q LOH can occur in astrocytic tumors, most commonly in secondary GBMs without morphological correlation with an oligodendroglial histology.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Gene Amplification. Genes, erbB-1. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362227.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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45. Waha A, Felsberg J, Hartmann W, von dem Knesebeck A, Mikeska T, Joos S, Wolter M, Koch A, Yan PS, Endl E, Wiestler OD, Reifenberger G, Pietsch T, Waha A: Epigenetic downregulation of mitogen-activated protein kinase phosphatase MKP-2 relieves its growth suppressive activity in glioma cells. Cancer Res; 2010 Feb 15;70(4):1689-99
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  • Critical tumor suppression pathways in brain tumors have yet to be fully defined.
  • In 83 astrocytic gliomas and 5 glioma cell lines examined, hypermethylation of the MKP-2 promoter was found to occur relatively more frequently in diffuse or anaplastic astrocytomas and secondary glioblastomas relative to primary glioblastomas.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. DNA Methylation. Down-Regulation / physiology. Female. Gene Expression Regulation, Neoplastic / physiology. Gene Silencing / physiology. Genes, Tumor Suppressor / physiology. Humans. Male. Middle Aged

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  • (PMID = 20124482.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP4 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases
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46. Smith SF, Simpson JM, Sekhon LH: What progress has been made in surgical management of patients with astrocytoma and oligodendroglioma in Australia over the last two decades? J Clin Neurosci; 2005 Nov;12(8):915-20; discussion 921
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  • [Title] What progress has been made in surgical management of patients with astrocytoma and oligodendroglioma in Australia over the last two decades?
  • OBJECTIVE: To determine changes since 1977 in demographic characteristics, tumour frequencies, surgical management, morbidity and survival for 1,339 patients discharged with astrocytoma (A) and oligodendroglioma (O), which comprise the majority of primary brain cancers, recorded prospectively in northern Sydney neurosurgery databases.
  • Of 144 re-biopsies, 16% had less anaplastic pathology, 54% the same and 30% more anaplastic pathology than the first biopsy.
  • Age and histopathologic grade were predictors of survival from 1980.
  • After adjustment for age using proportional hazards regression, survival improved only for anaplastic A, with a 60% improvement for patients diagnosed in era 3, and a 50% improvement for patients diagnosed in era 4 relative to those in era 1.
  • CONCLUSIONS: Although markers of inpatient care have improved since the 1980s, age-adjusted survival has not increased except for patients with anaplastic A.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Neurosurgical Procedures / statistics & numerical data. Oligodendroglioma / surgery. Postoperative Complications

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  • (PMID = 16326271.001).
  • [ISSN] 0967-5868
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
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47. Ishihara H, Kubota H, Lindberg RL, Leppert D, Gloor SM, Errede M, Virgintino D, Fontana A, Yonekawa Y, Frei K: Endothelial cell barrier impairment induced by glioblastomas and transforming growth factor beta2 involves matrix metalloproteinases and tight junction proteins. J Neuropathol Exp Neurol; 2008 May;67(5):435-48
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  • Occludin, claudin 1, and claudin 5 were expressed in microvascular endothelial cells in nonneoplastic brain samples but were significantly reduced in anaplastic astrocytoma and glioblastoma samples.
  • [MeSH-minor] Brain / blood supply. Brain / pathology. Brain / physiopathology. Brain Edema / metabolism. Brain Edema / pathology. Brain Edema / physiopathology. Cells, Cultured. Cerebral Arteries / metabolism. Cerebral Arteries / pathology. Cerebral Arteries / physiopathology. Claudin-1. Claudin-5. Coculture Techniques. Down-Regulation / physiology. Extracellular Matrix / metabolism. Extracellular Matrix / pathology. Humans. Infant, Newborn. Membrane Proteins / metabolism. Occludin. Tumor Cells, Cultured

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  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 18431253.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLDN1 protein, human; 0 / CLDN5 protein, human; 0 / Claudin-1; 0 / Claudin-5; 0 / Membrane Proteins; 0 / OCLN protein, human; 0 / Occludin; 0 / Transforming Growth Factor beta2; EC 3.4.24.- / Matrix Metalloproteinases
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48. Chen YJ, Hakin-Smith V, Teo M, Xinarianos GE, Jellinek DA, Carroll T, McDowell D, MacFarlane MR, Boet R, Baguley BC, Braithwaite AW, Reddel RR, Royds JA: Association of mutant TP53 with alternative lengthening of telomeres and favorable prognosis in glioma. Cancer Res; 2006 Jul 1;66(13):6473-6
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  • We examined TP53 status in relation to telomere maintenance mechanism (TMM) in 108 patients with glioblastoma multiforme and two patients with anaplastic astrocytoma from New Zealand and United Kingdom.
  • Tumor samples were analyzed with respect to telomerase activity, telomere length, and ALT-associated promyelocytic leukemia nuclear bodies to determine their TMM.
  • We found an association between TP53 mutation and ALT mechanism and between wild-type TP53 and telomerase and absence of a known TMM (P < 0.0001).
  • [MeSH-major] Astrocytoma / genetics. Genes, p53. Glioblastoma / genetics. Mutation. Telomere / genetics

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  • (PMID = 16818615.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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49. Larysz D, Blamek S, Larysz P, Pietras K, Mandera M: Posterior fossa brain tissue injury: developmental, neuropsychological, and neurological consequences of brain tumors in children. Acta Neurochir Suppl; 2010;106:271-4
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  • The aim of the study was the functional neurodevelopmental assessment of children with posterior fossa tumors, specifically examining whether tumor location in particular cerebellar structures determines particular neuropsychological deficits.
  • There were 21 total and 8 subtotal resections of tumor, and marsupialization was performed in cases of arachnoid cysts.
  • Histopathological diagnoses of tumors were as follows: 4 medulloblastomas, 8 pilocytic astrocytomas, 6 fibrillary astrocytomas, 1 anaplastic astrocytoma, 2 oligodendrogliomas, 4 anaplastic ependymomas, 1 choroid plexus papilloma, and 5 arachnoid cysts.

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  • (PMID = 19812963.001).
  • [ISSN] 0065-1419
  • [Journal-full-title] Acta neurochirurgica. Supplement
  • [ISO-abbreviation] Acta Neurochir. Suppl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
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50. Ahmed N, Bhurgri Y, Sadiq S, Shakoor KA: Pediatric brain tumours at a tertiary care hospital in Karachi. Asian Pac J Cancer Prev; 2007 Jul-Sep;8(3):399-404
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  • The morphological distribution of cases was astrocytoma (28 cases, 34.6%), primitive neuroectodermal tumor or PNET (40 cases; 49.4%), ependymoma (8 cases, 10%), mixed glioma (4 cases; 5%) and a case of oligodendroglioma.
  • The morphological categorization of supratentorial tumors was astrocytoma (17 cases; 63%), ependymoma (5 cases; 18.5%), mixed glioma (2 cases; 7.4%).
  • The 17 supratentorial astrocytoma were sub-categorized as follows - pilocytic astrocytoma (5 cases; 29.4%), grade II astrocytoma (6 cases; 35.3%); grade III astrocytoma (2 cases; 11.8%), anaplastic astrocytoma (1 case; 5.9%) and glioblastoma multiforme (3 cases; 17.7%).
  • The morphological categorization of infratentorial tumors was astrocytoma (11 cases; 20.4%), medulloblastoma (38 cases; 70.4%), ependymoma (3 cases; 5.6%) and mixed glioma - astroependymoma (2 cases, 3.7%).
  • The morphological sub-categorization of infratentorial astrocytoma was pilocytic astrocytoma (7 cases, 63.6%), with gemistocytic astrocytoma, grade II, grade III and anaplastic astrocytoma comprising 1 (9.1%) case each.
  • The morphological categorization of medulloblastoma was classical medulloblastoma (15 cases; 39.5%), desmoplastic medulloblastoma (8 cases; 21.1%), medulloblastoma with astrocytic differentiation (12 cases; 31.5%), medulloblastoma with neural differentiation (2 cases; 5.3%), and neuroblastic medulloblastoma (1 case; 2.6%).
  • There is a predominance of medulloblastoma and a paucity of astrocytomas.

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  • (PMID = 18159977.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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51. Arjona D, Rey JA, Taylor SM: Early genetic changes involved in low-grade astrocytic tumor development. Curr Mol Med; 2006 Sep;6(6):645-50
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  • [Title] Early genetic changes involved in low-grade astrocytic tumor development.
  • Astrocytomas represent the most common form of glial tumors.
  • The most malignant grade of these tumors, glioblastoma multiforme, may arise as a malignant progression from low-grade astrocytoma through anaplastic astrocytoma to secondary GBM, or else it may arise "de novo" as primary GBM.
  • Since malignant transformation is a multistep process, we summarize in this review the earliest genetic changes that seem to be involved in the appearance and development of low-grade astrocytic tumors, where early detection and treatment could be possible.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. Models, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 17022734.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins
  • [Number-of-references] 80
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52. Jang FF, Wei W, De WM: Vascular endothelial growth factor and basic fibroblast growth factor expression positively correlates with angiogenesis and peritumoural brain oedema in astrocytoma. J Ayub Med Coll Abbottabad; 2008 Apr-Jun;20(2):105-9
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  • [Title] Vascular endothelial growth factor and basic fibroblast growth factor expression positively correlates with angiogenesis and peritumoural brain oedema in astrocytoma.
  • BACKGROUND: Astrocytoma is the most malignant intracranial neoplasm and is characterized by high neovascularization and peritumoural brain oedema.
  • METHODS: The expression of two angiogenic growth factors, vascular endothelial growth factor and basic fibroblast growth factor were investigated using immunohistochemistry for astrocytoma from 82 patients and 11 normal human tissues.
  • RESULTS: The expression of vascular endothelial growth factor and basic fibroblast growth factor positively correlate with the pathological grade of astrocytoma, microvessel density numbers and brain oedema, which may be responsible for the increased tumour neovascularization and peritumoural brain oedema.
  • CONCLUSION: The results support the idea that inhibiting vascular endothelial growth factor and basic fibroblast growth factor are useful for the treatment of human astrocytoma and to improve patient's clinical outcomes and prognosis.
  • [MeSH-major] Astrocytoma / blood supply. Brain Edema / etiology. Brain Neoplasms / blood supply. Fibroblast Growth Factor 2 / biosynthesis. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 19385471.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
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53. Ohgaki H, Kleihues P: Genetic alterations and signaling pathways in the evolution of gliomas. Cancer Sci; 2009 Dec;100(12):2235-41
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  • Most frequent and malignant are glioblastomas.
  • The vast majority (>90%) develops rapidly after a short clinical history and without evidence of a less malignant precursor lesion (primary or de novo glioblastoma).
  • Secondary glioblastomas develop more slowly through progression from low-grade or anaplastic astrocytoma.
  • Recently, isocitrate dehydrogenase 1 (IDH1) mutations have been identified as a very early and frequent genetic alteration in the pathway to secondary glioblastomas as well as that in oligodendroglial tumors, providing the first evidence that low-grade astrocytomas and oligodendrogliomas may share common cells of origin.
  • In this review, we summarize the current status of genetic alterations and signaling pathways operative in the evolution of astrocytic and oligodendroglial tumors.
  • [MeSH-minor] Animals. Cyclin-Dependent Kinase Inhibitor p16 / physiology. Gene Expression Profiling. Humans. Isocitrate Dehydrogenase / physiology. Loss of Heterozygosity. PTEN Phosphohydrolase / physiology. Phosphatidylinositol 3-Kinases / physiology. Tumor Suppressor Protein p14ARF / physiology. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19737147.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 92
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54. Dall'oglio S, D'Amico A, Pioli F, Gabbani M, Pasini F, Passarin MG, Talacchi A, Turazzi S, Maluta S: Dose-intensity temozolomide after concurrent chemoradiotherapy in operated high-grade gliomas. J Neurooncol; 2008 Dec;90(3):315-9
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  • [Title] Dose-intensity temozolomide after concurrent chemoradiotherapy in operated high-grade gliomas.
  • PURPOSE: We performed a new phase II trial enrolling patients with newly diagnosed high-grade glioma (HGG) to test the efficacy of a weekly alternating temozolomide (TMZ) schedule after surgery and concomitant chemoradiotherapy.
  • There were 32 glioblastoma multiforme and two anaplastic astrocytoma.
  • Hematological toxicity was seen in six patients (18%): grade 1 neutropenia in four, grade 2 thrombocytopenia in one, and grade 4 thrombocytopenia plus grade 1 neutropenia in one.

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  • (PMID = 18688571.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
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55. Greco Crasto S, Soffietti R, Rudà R, Cassoni P, Ducati A, Davini O, De Lucchi R, Rizzo L: Diffusion-Weighted Magnetic Resonance Imaging and ADC Maps in the Diagnosis of Intracranial Cystic or Necrotic Lesions. A Retrospective Study on 49 Patients. Neuroradiol J; 2007 Dec 31;20(6):666-75
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  • Eleven tumours (11/44) appeared hyperintense on DWI: eight metastases from lung cancer (mean ADC value 0.86 mm(2)/s, range 0.75-1.2 mm(2)/s), two GBMs (mean 0.7 mm(2)/s, range 0.67-0.76 mm(2)/s) and one anaplastic astrocytoma (ADC value 1.24 mm(2)/s).

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  • (PMID = 24300002.001).
  • [ISSN] 1971-4009
  • [Journal-full-title] The neuroradiology journal
  • [ISO-abbreviation] Neuroradiol J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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56. Serrano J, Rayo JI, Infante JR, Domínguez L, García-Bernardo L, Durán C, Fernández Portales I, Cabezudo JM: Radioguided surgery in brain tumors with thallium-201. Clin Nucl Med; 2008 Dec;33(12):838-40
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  • RATIONALE: Malignant astrocytomas show thallium uptake with a high target-to-background ratio, allowing the use of radioguided surgery.
  • METHOD: We report on 6 patients (3 men) diagnosed with malignant astrocytoma.
  • With the gamma probe we confirmed the tumor uptake, and a biopsy sample was taken.
  • After conventional tumor resection, we scanned the surgical bed with the gamma probe.
  • RESULTS: In all patients the biopsy confirmed a high-grade astrocytoma.
  • In all cases we found residual uptake in the surgical bed that was confirmed as residual tumor by pathologic examination.

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  • (PMID = 19033782.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Thallium Radioisotopes
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57. Xiang C, Sarid R, Cazacu S, Finniss S, Lee HK, Ziv-Av A, Mikkelsen T, Brodie C: Cloning and characterization of human RTVP-1b, a novel splice variant of RTVP-1 in glioma cells. Biochem Biophys Res Commun; 2007 Oct 26;362(3):612-8
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  • In contrast, RTVP-1 and RTVP-1b showed similar patterns of expression in astrocytic tumors; highly expressed in glioblastomas as compared to normal brains, low-grade astrocytomas and anaplastic oligodendrogliomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Nerve Tissue Proteins / biosynthesis. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Alternative Splicing. Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Cell Movement. Cell Proliferation. Cloning, Molecular. Humans. Molecular Sequence Data. Protein Isoforms. Tissue Distribution

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  • (PMID = 17825796.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-R21-96965; United States / NCI NIH HHS / CA / R24 CA095809
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLIPR1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms
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58. Argyriou AA, Giannopoulou E, Kalofonos HP: Angiogenesis and anti-angiogenic molecularly targeted therapies in malignant gliomas. Oncology; 2009;77(1):1-11
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  • [Title] Angiogenesis and anti-angiogenic molecularly targeted therapies in malignant gliomas.
  • Angiogenesis is considered to be a regulating factor of vascular development and growth for malignant gliomas, including glioblastoma multiforme (GBM) and anaplastic astrocytomas.
  • The VEGF/VEGFR-2 is the predominant angiogenic signalling pathway in malignant gliomas.
  • Our aim is to review current knowledge on angiogenesis as a molecular pathogenetic mechanism of malignant gliomas and to critically look at and discuss antiangiogenic molecularly targeted therapies for these brain malignancies.

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19439998.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 98
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59. Arakawa Y, Tachibana O, Hasegawa M, Miyamori T, Yamashita J, Hayashi Y: Frequent gene amplification and overexpression of decoy receptor 3 in glioblastoma. Acta Neuropathol; 2005 Mar;109(3):294-8
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  • DcR3 has been demonstrated to produce a secreted member of the tumor necrosis factor receptor superfamily that negatively regulates Fas-mediated apoptosis.
  • In this study we examined DcR3 gene amplification, DcR3 mRNA expression, and DcR3 protein expression in 46 human astrocytic brain tumors by quantitative genomic PCR, quantitative reverse transcription-PCR, and immunohistochemistry, respectively.
  • The DcR3 gene amplification was detected in none of 6 (0%) low-grade astrocytomas, 1 of 16 (6%) anaplastic astrocytomas, and 6 of 24 ( 25%) glioblastomas.
  • We thus concluded that high DcR3 mRNA expression and protein expression may be positively related to the gene amplification in astrocytic brain tumors, especially glioblastomas.
  • Further, we speculated that the DcR3 gene amplification with overexpression may be responsible for malignant features in glioblastomas.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. RNA, Messenger / biosynthesis. Receptors, Tumor Necrosis Factor. Receptors, Tumor Necrosis Factor, Member 6b. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 15627206.001).
  • [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 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human
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60. Chamberlain MC, Johnston S: Salvage chemotherapy with bevacizumab for recurrent alkylator-refractory anaplastic astrocytoma. J Neurooncol; 2009 Feb;91(3):359-67
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  • [Title] Salvage chemotherapy with bevacizumab for recurrent alkylator-refractory anaplastic astrocytoma.
  • A retrospective study of bevacizumab only in adults with recurrent temozolomide (TMZ)-refractory anaplastic astrocytoma (AA) with a primary objective of determining progression free survival (PFS).
  • Bevacizumab-related toxicity included fatigue (14 patients; 2 grade 3), leukopenia (7; 1 grade 3), deep vein thrombosis (5; 2 grade 3), hypertension (5; 1 grade 3), anemia (4; 0 grade 3) and wound dehiscence (1; 1 grade 3).
  • Time to tumor progression ranged from 1 to 20 months (median: 7).
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Neoplasm Recurrence, Local

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  • (PMID = 18953491.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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61. Bozinov O, Kalk JM, Krayenbühl N, Woernle CM, Sure U, Bertalanffy H: Decreasing expression of the interleukin-13 receptor IL-13Ralpha2 in treated recurrent malignant gliomas. Neurol Med Chir (Tokyo); 2010;50(8):617-21
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  • [Title] Decreasing expression of the interleukin-13 receptor IL-13Ralpha2 in treated recurrent malignant gliomas.
  • This gene is highly expressed in various types of human tumors including malignant gliomas.
  • The expression level of IL-13Ralpha2 was examined in a total of 45 tissue samples of anaplastic astrocytomas (AAs) World Health Organization (WHO) grade III, glioblastomas (GBMs) WHO grade IV, and first-recurrent glioblastomas (frGBMs) after treatment with radiation and chemotherapy.
  • The expression level of IL-13Ralpha2 (15 fold) was significantly reduced in frGBMs compared to the primary GBMs (p = 0.014), and significantly reduced by more than 15 fold (p = 0.003) in all untreated malignant astrocytomas (AAs and GBMs) compared with treated frGBMs.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Interleukin-13 Receptor alpha2 Subunit / metabolism. Neoplasm Recurrence, Local / metabolism

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  • (PMID = 20805641.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Actins; 0 / Exotoxins; 0 / IL13-PE38QQR; 0 / Immunotoxins; 0 / Interleukin-13; 0 / Interleukin-13 Receptor alpha2 Subunit; 0S726V972K / Nimustine; 63231-63-0 / RNA; 957E6438QA / Teniposide
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62. Khalatbari M, Borghei-Razavi H, Shayanfar N, Behzadi AH, Sepehrnia A: Collision tumor of meningioma and malignant astrocytoma. Pediatr Neurosurg; 2010;46(5):357-61
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  • [Title] Collision tumor of meningioma and malignant astrocytoma.
  • The pathology of tumors reported collision tumors composed of meningioma and malignant astrocytoma.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Meningeal Neoplasms / surgery. Meningioma / surgery

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  • [Copyright] Copyright © 2011 S. Karger AG, Basel.
  • (PMID = 21389747.001).
  • [ISSN] 1423-0305
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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63. Pavon LF, Marti LC, Sibov TT, Malheiros SM, Oliveira DM, Guilhen DD, Camargo-Mathias MI, Amaro Junior E, Gamarra LF: The ultrastructural study of tumorigenic cells using nanobiomarkers. Cancer Biother Radiopharm; 2010 Jun;25(3):289-98
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  • Despite recent advances, patients with malignant brain tumors still have a poor prognosis.
  • Glioblastoma (WHO grade 4 astrocytoma), the most malignant brain tumor, represents 50% of all astrocytomas, with a median survival rate of <1 year.
  • The process of tumor cell labeling using nanoparticles can successfully contribute to the identification of tumorigenic cells and consequently for better understanding of glioblastoma genesis and recurrence.
  • In addition, this method may help further studies in tumor imaging, diagnosis, and prognostic markers detection.
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / metabolism. Antigens, CD / immunology. Antigens, CD / metabolism. Antigens, CD29 / immunology. Antigens, CD29 / metabolism. Antigens, CD44 / immunology. Antigens, CD44 / metabolism. Biomarkers / analysis. Biomarkers / chemistry. Cell Line, Tumor. Cell Membrane / metabolism. Cell Nucleus / metabolism. Cytoplasm / metabolism. Cytoplasmic Vesicles / metabolism. Endocytosis / immunology. Flow Cytometry. Forkhead Transcription Factors / chemistry. Forkhead Transcription Factors / metabolism. Glycoproteins / immunology. Glycoproteins / metabolism. Humans. Immunophenotyping. Magnetite Nanoparticles / chemistry. Microscopy, Electron, Transmission. Nanomedicine / methods. Peptides / immunology. Peptides / metabolism. Quantum Dots. Receptors, Cell Surface / immunology. Receptors, Cell Surface / metabolism. Tumor Cells, Cultured

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  • (PMID = 20578834.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD29; 0 / Antigens, CD44; 0 / Biomarkers; 0 / CD44 protein, human; 0 / ENG protein, human; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Glycoproteins; 0 / Magnetite Nanoparticles; 0 / Peptides; 0 / Receptors, Cell Surface
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64. Arjona D, Bello MJ, Alonso ME, Aminoso C, Isla A, De Campos JM, Sarasa JL, Gutierrez M, Villalobo A, Rey JA: Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations. Neuropathol Appl Neurobiol; 2005 Aug;31(4):384-94
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  • [Title] Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations.
  • This report investigates the presence of mutations, amplification and/or over-expression of the EGFR gene in 86 glial tumours including 44 glioblastomas, 21 anaplastic astrocytomas, and 21 WHO grade II astrocytomas, using polymerase chain reaction/single-strand conformation polymorphism, semiquantitative reverse-transcription-polymerase chain reaction (RT-PCR) and Southern Blot techniques.
  • These findings corroborate that EGFR is non-randomly involved in malignant glioma development and that different mutant forms participate in aberrant activation of tyrosine kinase pathways.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Epidermal Growth Factor / genetics. Gene Amplification


65. Krzyszkowski T, Dziedzic T, Czepko R, Szczudlik A: Decreased levels of interleukin-10 and transforming growth factor-beta 2 in cerebrospinal fluid of patients with high grade astrocytoma. Neurol Res; 2008 Apr;30(3):294-6
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  • [Title] Decreased levels of interleukin-10 and transforming growth factor-beta 2 in cerebrospinal fluid of patients with high grade astrocytoma.
  • It is unknown if production of these cytokines is limited to the site of tumor or these molecules are also released to cerebrospinal fluid and blood.
  • The goal of our study was to determine if patients with astrocytoma have increased levels of IL-10 and TGF-beta 2 in cerebrospinal fluid (CSF) and serum.
  • METHODS: CSF and serum samples were taken from 16 patients with astrocytoma of grade III or grade IV according to the WHO classification and from 28 age- and gender-matched controls (patients with normal pressure hydrocephalus or with lumbar disk herniation).
  • Patients with astrocytoma had decreased levels of IL-10 (0.9 +/- 1.2 versus 3.5 +/- 9.2 pg/ml, p=0.01) and TGF-beta 2 (0.0 +/- 0.0 versus 5.4 +/- 9.4 pg/ml, p=0.05) in CSF compared to controls.
  • Because serum IL-10 and TGF-beta 2 levels are similar in patients with astrocytoma and in controls, these cytokines are probably not directly involved in peripheral monocyte and T cell deactivation.
  • [MeSH-major] Astrocytoma / blood. Astrocytoma / cerebrospinal fluid. Interleukin-10 / blood. Interleukin-10 / cerebrospinal fluid. Transforming Growth Factor beta2 / blood. Transforming Growth Factor beta2 / cerebrospinal fluid

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  • (PMID = 17848206.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta2; 130068-27-8 / Interleukin-10
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66. Swinnen LJ, Rankin C, Carraway H, Albain KS, Townsend JJ, Budd GT, Kish JA, Rivkin SE, Blumenthal DT: A phase II study of cisplatin preceded by a 12-h continuous infusion of concurrent hydroxyurea and cytosine arabinoside (Ara-C) for adult patients with malignant gliomas (Southwest Oncology Group S9149). J Neurooncol; 2008 Feb;86(3):353-8
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  • [Title] A phase II study of cisplatin preceded by a 12-h continuous infusion of concurrent hydroxyurea and cytosine arabinoside (Ara-C) for adult patients with malignant gliomas (Southwest Oncology Group S9149).
  • A Phase II study in patients with relapsed or progressive anaplastic astrocytoma (AA) or glioblastoma multiforme (GBM) was performed in the Southwest Oncology Group.
  • Twenty-three patients (33%) experienced Grade 4 toxicities, primarily hematological.
  • Although benefit might be possible in a more platinum-sensitive tumor type, further clinical trials with this regimen for patients with glioblastoma multiforme or anaplastic astrocytoma are not justified.

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  • (PMID = 18175205.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01 CA004919; United States / NCI NIH HHS / CA / CA37981; United States / NCI NIH HHS / CA / CA58416; United States / NCI NIH HHS / CA / U10 CA027057; United States / NCI NIH HHS / CA / CA45560; United States / NCI NIH HHS / CA / CA28862; United States / NCI NIH HHS / CA / CA04920; United States / NCI NIH HHS / CA / CA46136; United States / NCI NIH HHS / CA / CA45807; United States / NCI NIH HHS / CA / CA35261; United States / NCI NIH HHS / CA / U10 CA004919; United States / NCI NIH HHS / CA / CA22433; United States / NCI NIH HHS / CA / U10 CA045560; United States / NCI NIH HHS / CA / CA12644; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / U10 CA063845; United States / NCI NIH HHS / CA / U10 CA063850; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / P01 CA053996; United States / NCI NIH HHS / CA / CA58658; United States / NCI NIH HHS / CA / N01 CA045807; United States / NCI NIH HHS / CA / CA63845; United States / NCI NIH HHS / CA / N01 CA046441; United States / NCI NIH HHS / CA / CA58882; United States / NCI NIH HHS / CA / U10 CA074647; United States / NCI NIH HHS / CA / CA63850; United States / NCI NIH HHS / CA / CA58861; United States / NCI NIH HHS / CA / CA52772; United States / NCI NIH HHS / CA / N01 CA063844; United States / NCI NIH HHS / CA / CA46282; United States / NCI NIH HHS / CA / U10 CA035261; United States / NCI NIH HHS / CA / CA16385; United States / NCI NIH HHS / CA / CA46441; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / U10 CA046282; United States / NCI NIH HHS / CA / CA46368; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / N01 CA038926; United States / NCI NIH HHS / CA / U10 CA067575; United States / NCI NIH HHS / CA / N01 CA027057; United States / NCI NIH HHS / CA / U10 CA046441; United States / NCI NIH HHS / CA / U10 CA058882; United States / NCI NIH HHS / CA / CA74647; United States / NCI NIH HHS / CA / U10 CA020319; United States / NCI NIH HHS / CA / CA46113; United States / NCI NIH HHS / CA / U10 CA038926; United States / NCI NIH HHS / CA / CA58686; United States / NCI NIH HHS / CA / CA63844; United States / NCI NIH HHS / CA / U10 CA042777; United States / NCI NIH HHS / CA / CA27057; United States / NCI NIH HHS / CA / CA42777; United States / NCI NIH HHS / CA / CA52654; United States / NCI NIH HHS / CA / U10 CA046368; United States / NCI NIH HHS / CA / N01 CA067575; United States / NCI NIH HHS / CA / U10 CA052654; United States / NCI NIH HHS / CA / CA76429; United States / NCI NIH HHS / CA / CA04919; United States / NCI NIH HHS / CA / CA67575; United States / NCI NIH HHS / CA / U10 CA063844; United States / NCI NIH HHS / CA / U10 CA045807; United States / NCI NIH HHS / CA / N01 CA045560
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS591247; NLM/ PMC4051205
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67. Hayatsu N, Kaneko MK, Mishima K, Nishikawa R, Matsutani M, Price JE, Kato Y: Podocalyxin expression in malignant astrocytic tumors. Biochem Biophys Res Commun; 2008 Sep 19;374(2):394-8
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  • [Title] Podocalyxin expression in malignant astrocytic tumors.
  • Recently, we revealed that highly sulfated KS or another mucin-like transmembrane sialoglycoprotein podoplanin/aggrus is upregulated in malignant astrocytic tumors.
  • The aim of this study is to examine the relationship between podocalyxin expression and malignant progression of astrocytic tumors.
  • In this study, 51 astrocytic tumors were investigated for podocalyxin expression using immunohistochemistry, Western blot analysis, and quantitative real-time PCR.
  • Immunohistochemistry detected podocalyxin on the surface of tumor cells in six of 14 anaplastic astrocytomas (42.9%) and in 17 of 31 glioblastomas (54.8%), especially around proliferating endothelial cells.
  • In diffuse astrocytoma, podocalyxin expression was observed only in vascular endothelial cells.
  • Podocalyxin might be associated with the malignant progression of astrocytic tumors, and be a useful prognostic marker for astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Central Nervous System Neoplasms / pathology. Sialoglycoproteins / analysis
  • [MeSH-minor] Blotting, Western. Humans. Immunohistochemistry. Polymerase Chain Reaction. Prognosis. RNA, Messenger / analysis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 18639524.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Sialoglycoproteins; 0 / podocalyxin
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68. Shen CF, Yuan XR, Qin ZQ: [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2007 Oct;32(5):836-9
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  • [Title] [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors].
  • OBJECTIVE: To determine the mRNA and protein expressions of RCAS1 in human astrocytic tumors, and to explore the relation between their expression and the genesis and development of tumor.
  • METHODS: The RCAS1 mRNA expression in human astrocytic tumors was evaluated by RT-PCR, and the RCAS1 protein expression was studied by immunohistochemical staining.
  • RESULTS: The quantities of RCAS1 mRNA expression between diffusive astrocytoma(Grade II) and anaplastic astrocytoma(Grade III), anaplastic astrocytoma and glioblastoma(Grade IV) were significantly different(P<0.05), while the expression scores of RCAS1 protein were different only between the anaplastic astrocytoma and glioblastoma(P<0.01).
  • RCAS1 protein expression was positively correlated with the tumor grade (r=0.573,P<0.001).
  • CONCLUSION: The RCAS1 expression is related to the histological grade of astrocytic tumor.
  • In astrocytic tumors, the RCAS1 expression is regulated transcriptionally and posttranscriptionally.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism

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  • (PMID = 18007080.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / EBAG9 protein, human; 0 / RNA, Messenger
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69. Ehling R, Sterlacci W, Maier H, Berger T: A 45-year old male with left-sided hemihypesthesia. Brain Pathol; 2010 Mar;20(2):515-8
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  • Extensive immunological and radiological investigations were not able to differentiate between an intrinsic brain tumor and a demyelinating disease.
  • Stereotactic biopsies of the brainstem were performed; the findings of abundant Rosenthal fibers, interjacent spindle-shaped and gemistocytic cells partially with dark and irregularly formed nuclei favored primarily the diagnosis of a malignant astrocytoma, although a demyelinating disease could not be definitely excluded.

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  • (PMID = 20438473.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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70. Comincini S, Ferrara V, Arias A, Malovini A, Azzalin A, Ferretti L, Benericetti E, Cardarelli M, Gerosa M, Passarin MG, Turazzi S, Bellazzi R: Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy. Oncol Rep; 2007 May;17(5):989-96
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  • [Title] Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy.
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • In order to address clinical important issues, PRND mRNA expression was investigated in a panel of 111 astrocytoma tissue samples, histologically classified according to the World Health Organization (WHO) criteria (6 grade I pilocytic astrocytomas, 15 grade II low-grade astrocytomas, 26 grade III anaplastic astrocytomas and 64 grade IV glioblastoma multiforme).
  • Real-time PRND gene expression profiling, after normalisation with GAPDH, revealed large differences between low (WHO I and II) and high grade (III and IV) of malignancy (P<0.001).
  • Extensive differences in PRND gene expression were also found within each grade of malignancy, suggesting that PRND mRNA quantitation might be useful to distinguish astrocytoma subtypes, and important in disease stratification and in the assessment of specific treatment strategies.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Prions / biosynthesis

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  • (PMID = 17390034.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions
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71. Anselmo NP, Rey JA, Almeida LO, Custódio AC, Almeida JR, Clara CA, Santos MJ, Casartelli C: Concurrent sequence variation of TP53 and TP73 genes in anaplastic astrocytoma. Genet Mol Res; 2009;8(4):1257-63
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  • [Title] Concurrent sequence variation of TP53 and TP73 genes in anaplastic astrocytoma.
  • Disruption or loss of tumor suppressor gene TP53 is implicated in the development or progression of almost all different types of human malignancies.
  • Using PCR-SSCP and gene sequencing, we analyzed the TP53 and TP73 genes in a case of a grade III anaplastic astrocytoma that progressed to glioblastoma.
  • The mutation found at exon 6 of the gene TP53 could be associated with the rapid tumoral progression found in this case, since the mutated p53 may inactivate the wild-type p53 and the p73alpha protein, which was conserved here, leading to an increase in cellular instability.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. DNA-Binding Proteins / genetics. Nuclear Proteins / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 19876867.001).
  • [ISSN] 1676-5680
  • [Journal-full-title] Genetics and molecular research : GMR
  • [ISO-abbreviation] Genet. Mol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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72. Chamberlain MC, Chowdhary SA, Glantz MJ: Anaplastic astrocytomas: biology and treatment. Expert Rev Neurother; 2008 Apr;8(4):575-86
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  • [Title] Anaplastic astrocytomas: biology and treatment.
  • Anaplastic astrocytomas (AA), WHO grade III gliomas, comprise 10-15% of all glial neoplasms.
  • The most important predictor of response to therapy and survival in AA tumors is the presence or absence of the 1p19q co-deletion, a translocation that defines a subset of oligodendroglial tumors, and anaplastic oligodendrogliomas in particular.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Clinical Trials as Topic

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  • (PMID = 18416660.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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73. Reardon DA, Akabani G, Coleman RE, Friedman AH, Friedman HS, Herndon JE 2nd, McLendon RE, Pegram CN, Provenzale JM, Quinn JA, Rich JN, Vredenburgh JJ, Desjardins A, Gururangan S, Badruddoja M, Dowell JM, Wong TZ, Zhao XG, Zalutsky MR, Bigner DD: Salvage radioimmunotherapy with murine iodine-131-labeled antitenascin monoclonal antibody 81C6 for patients with recurrent primary and metastatic malignant brain tumors: phase II study results. J Clin Oncol; 2006 Jan 1;24(1):115-22
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  • [Title] Salvage radioimmunotherapy with murine iodine-131-labeled antitenascin monoclonal antibody 81C6 for patients with recurrent primary and metastatic malignant brain tumors: phase II study results.
  • PURPOSE: To assess the efficacy and toxicity of intraresection cavity iodine-131-labeled murine antitenascin monoclonal antibody 81C6 (131I-m81C6) among recurrent malignant brain tumor patients.
  • PATIENTS AND METHODS: In this phase II trial, 100 mCi of 131I-m81C6 was injected directly into the surgically created resection cavity (SCRC) of 43 patients with recurrent malignant glioma (glioblastoma multiforme [GBM], n = 33; anaplastic astrocytoma [AA], n = 6; anaplastic oligodendroglioma [AO], n = 2; gliosarcoma [GS], n = 1; and metastatic adenocarcinoma, n = 1) followed by chemotherapy.
  • CONCLUSION: In this single-institution phase II study, administration of 100 mCi of 131I-m81C6 to recurrent malignant glioma patients followed by chemotherapy is associated with a median survival that is greater than that of historical controls treated with surgery plus iodine-125 brachytherapy.
  • A phase III multicenter trial with patient-specific dosing is planned.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / radiotherapy. Iodine Radioisotopes / therapeutic use. Neoplasm Recurrence, Local / radiotherapy. Radioimmunotherapy. Tenascin / immunology
  • [MeSH-minor] Adult. Aged. Biopsy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Salvage Therapy

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  • [ErratumIn] J Clin Oncol. 2006 Mar 20;24(9):1484. Guruangan, Sri [corrected to Gururangan, Sridharan]
  • (PMID = 16382120.001).
  • [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 / 1-P50-CA108786-01; United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / NS20023
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Iodine Radioisotopes; 0 / Tenascin
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74. Heimberger AB, McGary EC, Suki D, Ruiz M, Wang H, Fuller GN, Bar-Eli M: Loss of the AP-2alpha transcription factor is associated with the grade of human gliomas. Clin Cancer Res; 2005 Jan 1;11(1):267-72
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  • [Title] Loss of the AP-2alpha transcription factor is associated with the grade of human gliomas.
  • PURPOSE: The activator protein (AP)-2alpha transcription factor plays a crucial role in the progression of several human tumors, including malignant melanoma, prostate, and breast cancer.
  • Anderson Cancer Center since 1986 to include 72 glioblastomas, 49 anaplastic astrocytomas, 9 low-grade astrocytoma, 37 oligodendrogliomas, 37 anaplastic oligodendrogliomas, 15 mixed oligoastrocytomas, 20 anaplastic mixed oligoastrocytomas, and 7 gliosarcomas.
  • RESULTS: AP-2alpha expression was lost on 99% (P < 0.001) and 98% (P < 0.001) of glioblastomas and anaplastic astrocytomas, respectively, compared with grade 2 astrocytomas and normal brain, all of which (100%) maintained expression of AP-2alpha.
  • However, there was no significant effect of loss of AP-2alpha expression on survival observed after adjustment for patient age, Karnofsky Performance Scale score, tumor grade, and extent of resection (rate ratio, 1.2; 95% confidence interval, 0.6-2.2; P = 0.6).
  • CONCLUSIONS: AP-2alpha expression correlates inversely with glioma grade, suggesting a direct role in glioma tumorigenicity, possibly through subsequent deregulation of target genes.
  • Of all the previously characterized markers of progression, the loss of AP-2alpha would be the most common (96.2%) molecular marker as an astrocytic tumor evolves from grade 2 to 3.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Motifs. Antigens, CD / biosynthesis. Antigens, CD146. Astrocytoma / metabolism. Brain / metabolism. Cell Cycle Proteins / biosynthesis. Cell Line, Tumor. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p21. Disease Progression. Humans. Immunohistochemistry. Matrix Metalloproteinase 2 / biosynthesis. Middle Aged. Neural Cell Adhesion Molecules / biosynthesis. Oligodendroglioma / metabolism. Oligonucleotide Array Sequence Analysis. Prognosis. Proportional Hazards Models. Proto-Oncogene Proteins c-kit / biosynthesis. Time Factors. Transcription Factor AP-2. Treatment Outcome. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 15671555.001).
  • [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 States / PHS HHS / / T-32-09666
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD146; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / MCAM protein, human; 0 / Neural Cell Adhesion Molecules; 0 / TFAP2A protein, human; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.24.24 / Matrix Metalloproteinase 2
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75. Seifert G, Reindl T, Lobitz S, Seeger K, Henze G: Fatal course after administration of rituximab in a boy with relapsed all: a case report and review of literature. Haematologica; 2006 Jun;91(6 Suppl):ECR23
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  • We are reporting on a 14-year-old boy with a very early relapse of pre-B acute lymphoblastic leukemia (ALL) and anaplastic astrocytoma WHO degrees III; the astrocytoma was subtotally resected and subsequently treated with irradiation and chemotherapy.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Burkitt Lymphoma / drug therapy

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  • (PMID = 16785126.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 27
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76. Limentani SA, Asher A, Heafner M, Kim JW, Fraser R: A phase I trial of surgery, Gliadel wafer implantation, and immediate postoperative carboplatin in combination with radiation therapy for primary anaplastic astrocytoma or glioblastoma multiforme. J Neurooncol; 2005 May;72(3):241-4
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  • [Title] A phase I trial of surgery, Gliadel wafer implantation, and immediate postoperative carboplatin in combination with radiation therapy for primary anaplastic astrocytoma or glioblastoma multiforme.
  • Two types of chemotherapy used in the treatment of patients with malignant glioma are carboplatin and Gliadel wafer [(3.85% 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU)].
  • The purpose of this study was to evaluate combination chemotherapy with Gliadel wafer and carboplatin in patients with high-grade, malignant glioma.
  • Fourteen (88%) patients had glioblastoma multiforme and 2 (12%) had anaplastic astrocytoma.
  • No grade 3 or 4 toxicities were noted in this study.
  • We conclude that administering systemic carboplatin is safe and well tolerated in the postoperative period immediately following resection and implantation of Gliadel wafer for the treatment of malignant glioma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Carboplatin / therapeutic use. Decanoic Acids / therapeutic use. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Polyesters / therapeutic use
  • [MeSH-minor] Adult. Aged. Carmustine. Combined Modality Therapy. Disease Progression. Drug Implants. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Neoplasm Staging. Neurosurgical Procedures. Survival Analysis

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  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Decanoic Acids; 0 / Drug Implants; 0 / Polyesters; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; BG3F62OND5 / Carboplatin; U68WG3173Y / Carmustine
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77. Dunlap SM, Celestino J, Wang H, Jiang R, Holland EC, Fuller GN, Zhang W: Insulin-like growth factor binding protein 2 promotes glioma development and progression. Proc Natl Acad Sci U S A; 2007 Jul 10;104(28):11736-41
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  • Our studies show that IGFBP2 coexpression results in progression to a higher-grade glioma in platelet-derived growth factor beta (PDGFB)-driven tumors.
  • These anaplastic oligodendrogliomas are characterized by increased cellularity, vascular proliferation, small regions of necrosis, increased mitotic activity, and increased activation of the Akt pathway.
  • Combined expression of IGFBP2 or Akt with K-Ras was required to form astrocytomas, indicating that activation of two separate pathways is necessary for gliomagenesis.

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  • (PMID = 17606927.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098503; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA- 16672; United States / NCI NIH HHS / CA / R01 CA98503; United States / NIDDK NIH HHS / DK / 5 T90 DK070109-02; United States / NIDDK NIH HHS / DK / T90 DK070109
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin-Like Growth Factor Binding Protein 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC1913900
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78. Ghosh S, Duigou GJ: Decreased replication ability of E1-deleted adenoviruses correlates with increased brain tumor malignancy. Cancer Res; 2005 Oct 1;65(19):8936-43
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  • [Title] Decreased replication ability of E1-deleted adenoviruses correlates with increased brain tumor malignancy.
  • To address this, freshly cultured cells from normal human brain and common brain tumors (astrocytomas and meningiomas) were infected using wild-type species C adenoviruses and adenoviruses missing E1A (H5dl312) or E1A plus E1B (H5dl434).
  • Wild-type adenoviruses grew efficiently in normal brain and brain tumor cells.
  • In comparison, E1-deleted adenovirus DNA replication was delayed and lower in cells derived from normal brain tissues, meningiomas, and low-grade astrocytomas.
  • However, in contrast, E1-deleted adenovirus DNA replication did not occur or was extremely low in cells derived from malignancy grade III and IV astrocytic tumors.
  • Because wild-type adenoviruses infected and replicated in all cells, the malignancy grade-based differential E1-deleted adenovirus DNA replication was not explained by differential virus uptake.
  • Compared with a 5-day average for wild-type infections, advanced cytopathology was noted approximately 4 weeks after H5dl312 or H5dl434 infection of meningioma, astrocytoma, and normal brain cells.
  • Cytopathology was not observed after H5dl312 or H5dl434 infection of glioblastoma, anaplastic astrocytoma, and gliosarcoma cells.
  • Because of this tumor grade-based differential growth, the E1-deleted adenoviruses may represent novel tools for studies of brain tumor malignancy.
  • [MeSH-minor] Astrocytoma / pathology. Astrocytoma / virology. Cell Line, Tumor. Cytopathogenic Effect, Viral. Disease Progression. Glioblastoma / pathology. Glioblastoma / virology. Gliosarcoma / pathology. Gliosarcoma / virology. Humans. Meningioma / pathology. Meningioma / virology

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  • (PMID = 16204066.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1 Proteins
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79. Roselli F, Pisciotta NM, Aniello MS, Niccoli-Asabella A, Defazio G, Livrea P, Rubini G: Brain F-18 Fluorocholine PET/CT for the assessment of optic pathway glioma in neurofibromatosis-1. Clin Nucl Med; 2010 Oct;35(10):838-9
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  • Magnetic resonance imaging, magnetic resonance spectroscopy (MRS), and F-18 fluorocholine revealed a splenial mass with imaging features compatible with malignant astrocytoma.


80. Nakagawa Y, Kageji T, Mizobuchi Y, Kumada H, Nakagawa Y: Clinical results of BNCT for malignant brain tumors in children. Appl Radiat Isot; 2009 Jul;67(7-8 Suppl):S27-30
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  • [Title] Clinical results of BNCT for malignant brain tumors in children.
  • It is very difficult to treat the patients with malignant brain tumor in children, especially under 3 years, because the conventional irradiation cannot be applied due to the damage of normal brain tissue.
  • However, boron neutron capture therapy (BNCT) has tumor selectivity such that it can make damage only in tumor cells.
  • We evaluated the clinical results and courses in patients with malignant glioma under 15 years.
  • There were 3 glioblastomas (GBM), 6 anaplastic astrocytomas(AAS), 7 primitive neuroectodermal tumors (PNET), 6 pontine gliomas and 1 anaplastic ependymoma.
  • All GBM and PNET patients died due to CSF and/or CNS dissemination without local tumor regrowth.
  • All pontine glioma patients died due to regrowth of the tumor.
  • Four of 6 anaplastic astrocytoma and 1 anaplastic ependymoma patients alive without tumor recurrence.
  • BNCT can be applied to malignant brain tumors in children, especially under 3 years instead of conventional radiation.
  • [MeSH-minor] Adolescent. Astrocytoma / pathology. Astrocytoma / radiotherapy. Child. Child, Preschool. Ependymoma / pathology. Ependymoma / radiotherapy. Fatal Outcome. Female. Glioblastoma / pathology. Glioblastoma / radiotherapy. Humans. Infant. Magnetic Resonance Angiography. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Neuroectodermal Tumors, Primitive / pathology. Neuroectodermal Tumors, Primitive / radiotherapy

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  • (PMID = 19406652.001).
  • [ISSN] 1872-9800
  • [Journal-full-title] Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine
  • [ISO-abbreviation] Appl Radiat Isot
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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81. Panigrahy A, Nelson MD Jr, Finlay JL, Sposto R, Krieger MD, Gilles FH, Blüml S: Metabolism of diffuse intrinsic brainstem gliomas in children. Neuro Oncol; 2008 Feb;10(1):32-44
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  • The purpose of this study was to compare the metabolic profile of DIBSGs with that of astrocytomas elsewhere in the CNS and to determine whether the measurement of metabolic features can improve the assessment of disease status.
  • Control data for baseline studies of DIBSGs were obtained from 14 untreated regular and anaplastic astrocytomas.
  • At baseline, creatine and total choline (tCho) were significantly lower in DIBSGs than in astrocytomas elsewhere in the CNS (4.3 +/- 1.1 vs. 7.5 +/- 1.9 mmol/kg, p < 0.001; 1.9 +/- 0.7 vs. 4.2 +/- 2.6, p < 0.001).
  • Subsequent metabolic changes that have been associated with malignant degeneration preceded clinical deterioration.

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  • (PMID = 18003889.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA097452; United States / NCI NIH HHS / CA / U01 CA97452-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2600836
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82. Shirahata M, Oba S, Iwao-Koizumi K, Saito S, Ueno N, Oda M, Hashimoto N, Ishii S, Takahashi JA, Kato K: Using gene expression profiling to identify a prognostic molecular spectrum in gliomas. Cancer Sci; 2009 Jan;100(1):165-72
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  • The expression levels of these genes in 152 gliomas (100 glioblastomas, 21 anaplastic astrocytomas, 19 diffuse astrocytomas, and 12 anaplastic oligodendrogliomas) were measured using adapter-tagged competitive polymerase chain reaction, a high-throughput reverse transcription-polymerase chain reaction technique.
  • The gene expression profiling identified clinically informative prognostic molecular features in astrocytic and oligodendroglial tumors that were more reliable than the traditional histological classification scheme.

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  • (PMID = 19038000.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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83. Gil-Benso R, Lopez-Gines C, Benito R, López-Guerrero JA, Callaghan RC, Pellín A, Roldán P, Cerdá-Nicolas M: Concurrent EGFR amplification and TP-53 mutation in glioblastomas. Clin Neuropathol; 2007 Sep-Oct;26(5):224-31
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  • A genetic alteration that is significantly more frequent in primary than in secondary glioblastomas, the latter arising from preceding low-grade gliomas, is epidermal growth factor receptor gene (EGFR) amplification, whereas TP-53 mutations are significantly more frequent in low-grade gliomas and secondary glioblastomas derived there- from.
  • We report the histological and genetic study of two glioblastomas, one case arising de novo and the other case arising 3 years after a previously diagnosed anaplastic astrocytoma, with concurrent EGFR amplification and TP-53 mutation.
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / pathology. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation


84. Kawarabuki K, Ohta T, Hashimoto N, Wada K, Maruno M, Yamaki T, Ueda S: Cerebellar glioblastoma genetically defined as a secondary one. Clin Neuropathol; 2005 Mar-Apr;24(2):64-8
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  • In the present case, tumor lesions were observed in each cerebellar hemisphere.
  • The left-side lesion was diagnosed as glioblastoma, and the right-side lesion as malignant astrocytoma by histopathology.
  • Immunohistochemistry revealed that the tumor cells of the left-side lesion was positive for p53, whereas epidermal growth factor receptors (EGFR) were negative in tumor cells from both sides.
  • Genetic alterations were investigated using a genome DNA microarray (GenoSensor Array 300), which has led us to define this tumor as a secondary glioblastoma.


85. Choi K, Ryu SW, Song S, Choi H, Kang SW, Choi C: Caspase-dependent generation of reactive oxygen species in human astrocytoma cells contributes to resistance to TRAIL-mediated apoptosis. Cell Death Differ; 2010 May;17(5):833-45
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  • [Title] Caspase-dependent generation of reactive oxygen species in human astrocytoma cells contributes to resistance to TRAIL-mediated apoptosis.
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF family of cytokines, causes apoptosis by caspase activation in various cell types, particularly in transformed cells.
  • We report here a new signal transduction pathway involving protein kinase Cdelta (PKCdelta), NADPH oxidase 4 (NOX4) and reactive oxygen species (ROS), that inhibits caspase-dependent cell death induced by TRAIL ligation in human malignant astrocytoma cells.
  • [MeSH-major] Apoptosis / physiology. Astrocytoma / metabolism. Caspase 3 / metabolism. Reactive Oxygen Species / metabolism. TNF-Related Apoptosis-Inducing Ligand / metabolism
  • [MeSH-minor] Cell Line, Tumor. Electrophoresis, Gel, Two-Dimensional. Humans. Immunoblotting. NADPH Oxidase / metabolism

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  • (PMID = 19876066.001).
  • [ISSN] 1476-5403
  • [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
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 1.6.3.- / NOX4 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 3.4.22.- / Caspase 3
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86. Opstad KS, Ladroue C, Bell BA, Griffiths JR, Howe FA: Linear discriminant analysis of brain tumour (1)H MR spectra: a comparison of classification using whole spectra versus metabolite quantification. NMR Biomed; 2007 Dec;20(8):763-70
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  • A total of 145 histologically diagnosed brain tumour spectra were acquired [14 astrocytoma grade II (AS2), 15 astrocytoma grade III (AS3), 42 glioblastoma (GBM), 41 metastases (MET) and 33 meningioma (MNG)], and linear discriminant analyses (LDA) were performed on the LCModel analysis of the spectra and the original spectra.
  • LDA of AS2, MNG and high-grade tumours (HG, comprising GBM and MET) correctly classified 94% using the LCModel dataset compared with 93% using the spectral dataset.

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  • (PMID = 17326043.001).
  • [ISSN] 0952-3480
  • [Journal-full-title] NMR in biomedicine
  • [ISO-abbreviation] NMR Biomed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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87. Hiremath GK, Bingaman WE, Prayson RA, Nair D: Oligoastrocytoma presenting with intractable epilepsy. Epileptic Disord; 2007 Sep;9(3):315-22
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  • OBJECTIVE: Oligoastrocytomas (OA) are mixed gliomas with distinct oligodendroglial and astrocytic neoplastic components.
  • Surgical pathology revealed low-grade OA (WHO II) in five patients, and anaplastic OA in one.
  • There were no surgical complications, clinical or radiographic tumor recurrence at a mean follow up period of 3.2 years (range 2-8).
  • CONCLUSION: As a result of our small sample size, general conclusions may be imprecise, but this review suggests that OA behave similar to other tumors related to intractable epilepsy: they usually have a preoperative seizure course of many years, an excellent rate of seizure-freedom following surgery, and are in general, low-grade tumors with an indolent course for which serial imaging is sufficient follow-up.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Epilepsy / drug therapy. Epilepsy / etiology
  • [MeSH-minor] Adolescent. Adult. Anticonvulsants / therapeutic use. Craniotomy. Drug Resistance. Epilepsy, Complex Partial / etiology. Epilepsy, Complex Partial / surgery. Female. Humans. Magnetic Resonance Imaging. Male. Memory / physiology. Neoplasm Recurrence, Local. Neurosurgical Procedures. Temporal Lobe / pathology. Temporal Lobe / surgery

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  • (PMID = 17884756.001).
  • [ISSN] 1294-9361
  • [Journal-full-title] Epileptic disorders : international epilepsy journal with videotape
  • [ISO-abbreviation] Epileptic Disord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anticonvulsants
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88. McCarthy BJ, Propp JM, Davis FG, Burger PC: Time trends in oligodendroglial and astrocytic tumor incidence. Neuroepidemiology; 2008;30(1):34-44
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  • [Title] Time trends in oligodendroglial and astrocytic tumor incidence.
  • BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.
  • METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.
  • RESULTS: Using CBTRUS data, the incidences (per 100,000 person-years) of oligodendrogliomas (APC = 4.7), mixed gliomas (APC = 3.9) and anaplastic oligodendrogliomas (APC = 12.5) have all increased over time, while the incidences of astrocytoma not otherwise specified (APC = -8.1) and fibrillary astrocytoma (APC = -2.1) have decreased.
  • CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18259099.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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89. Liau CT, Wei KC, Tseng CK, Jung SM: Combination chemotherapy with carmustine and cisplatin followed by procarbazine, lomustine, and vincristine for adult high-grade astrocytoma. Chang Gung Med J; 2005 Jan;28(1):16-23
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  • [Title] Combination chemotherapy with carmustine and cisplatin followed by procarbazine, lomustine, and vincristine for adult high-grade astrocytoma.
  • BACKGROUND: We have reported that carmustine (BCNU) and cisplatin administered before, during, and after radiotherapy did not improve the survival of patients with high-grade astrocytomas and were associated with more serious toxicities than radiotherapy plus BCNU.
  • Of these, 20 had glioblastoma multiforme and 22 had anaplastic astrocytoma.
  • The median time to tumor progression was 7.2 months (range, 0-88.7 months) and median survival time was 13.3 months (range, 1.7-88.7 months).
  • This combined modality treatment program was associated with reversible grade 3 to 4 hematological toxicity in 10 patients, with grade 3 ototoxicity in one patient and grade 2 neurotoxicity in one patient.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy

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  • (PMID = 15804144.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
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90. Koul D: PTEN signaling pathways in glioblastoma. Cancer Biol Ther; 2008 Sep;7(9):1321-5
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  • 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.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. PTEN Phosphohydrolase / genetics. Signal Transduction / physiology. Tumor Suppressor Proteins / physiology


91. Narayana A, Yamada J, Berry S, Shah P, Hunt M, Gutin PH, Leibel SA: Intensity-modulated radiotherapy in high-grade gliomas: clinical and dosimetric results. Int J Radiat Oncol Biol Phys; 2006 Mar 1;64(3):892-7
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  • [Title] Intensity-modulated radiotherapy in high-grade gliomas: clinical and dosimetric results.
  • PURPOSE: To report preliminary clinical and dosimetric data from intensity-modulated radiotherapy (IMRT) for malignant gliomas.
  • METHODS AND MATERIALS: Fifty-eight consecutive high-grade gliomas were treated between January 2001 and December 2003 with dynamic multileaf collimator IMRT, planned with the inverse approach.
  • Glioblastoma accounted for 70% of the cases, and anaplastic oligodendroglioma histology (pure or mixed) was seen in 15% of the cases.
  • The median progression-free survival time for anaplastic astrocytoma and glioblastoma histology was 5.6 and 2.5 months, respectively.
  • The overall survival time for anaplastic glioma and glioblastoma was 36 and 9 months, respectively.
  • No Grade IV/V late neurologic toxicities were noted.
  • A comparative dosimetric analysis revealed that regardless of tumor location, IMRT did not significantly improve target coverage compared with three-dimensional planning.
  • CONCLUSIONS: It is unlikely that IMRT will improve local control in high-grade gliomas without further dose escalation compared with conventional radiotherapy.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Brain / radiation effects. Disease Progression. Female. Glioblastoma / radiotherapy. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Oligodendroglioma / radiotherapy. Radiotherapy Dosage. Retrospective Studies

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  • (PMID = 16458777.001).
  • [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
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92. Henriksson R, Malmström A, Bergström P, Bergh G, Trojanowski T, Andreasson L, Blomquist E, Jonsborg S, Edekling T, Salander P, Brännström T, Bergenheim AT: High-grade astrocytoma treated concomitantly with estramustine and radiotherapy. J Neurooncol; 2006 Jul;78(3):321-6
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  • [Title] High-grade astrocytoma treated concomitantly with estramustine and radiotherapy.
  • Experimental and early clinical investigations have demonstrated encouraging results for estramustine in the treatment of malignant glioma.
  • The present study is an open randomized clinical trial comparing estramustine phosphate (Estracyt) in addition to radiotherapy with radiotherapy alone as first line treatment of astrocytoma grade III and IV.
  • For astrocytoma grade III the median survival time was 10.6 (1.3-92.7) months for the radiotherapy only group and 17.3 (0.4-96.9+) months for the estramustine + radiotherapy group.
  • In grade IV the corresponding median survival time was 12.3 (2.1-89.2) and 10.3 (0.3-91.7+) months, respectively.
  • Median time to progress for radiotherapy only and radiotherapy and estramustin group in grade III tumours was 6.5 and 10.1 months, respectively.
  • In grade IV tumours the corresponding figures were 5.1 and 3.3 months, respectively.
  • Although there was a tendency for improved survival in grade III, no statistical significant differences were found between the treatment groups.
  • In conclusion, this first randomized study did not demonstrate any significant improvement of using estramustine in addition to conventional radiotherapy, however, a trend for a positive response for the estramustine group was found in patients with grade III glioma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Estramustine / administration & dosage

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  • (PMID = 16598426.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 35LT29625A / Estramustine
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93. Hatano M, Eguchi J, Tatsumi T, Kuwashima N, Dusak JE, Kinch MS, Pollack IF, Hamilton RL, Storkus WJ, Okada H: EphA2 as a glioma-associated antigen: a novel target for glioma vaccines. Neoplasia; 2005 Aug;7(8):717-22
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  • We demonstrate in the current study that the EphA2 protein is restrictedly expressed in primary glioblastoma multiforme and anaplastic astrocytoma tissues in comparison to normal brain tissues.

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  • (PMID = 16207473.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P01 NS040923; United States / NINDS NIH HHS / NS / P01 NS40923
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / HLA-A2 Antigen; EC 2.7.10.1 / Receptor, EphA2
  • [Other-IDs] NLM/ PMC1501889
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94. Nishikawa R, Shibui S, Maruno M, Sugiyama K, Sato S, Fujimaki T, Takahashi H, Wakabayashi T, Takahashi J, Kochi M, Nakamura H, Sawamura Y, Ikeda J, Hori T, Aoki T, Matsutani M: [Efficacy and safety of monotherapy with temozolomide in patients with anaplastic astrocytoma at first relapse--a phase II clinical study]. Gan To Kagaku Ryoho; 2006 Sep;33(9):1279-85
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  • [Title] [Efficacy and safety of monotherapy with temozolomide in patients with anaplastic astrocytoma at first relapse--a phase II clinical study].
  • The efficacy and safety of temozolomide were evaluated in 32 patients with anaplastic astrocytoma at first relapse.
  • The main laboratory test abnormalities (total incidence and incidence of grade 3/4 change) were lymphocytopenia (50%, 25%), neutropenia (47%, 6%), leukopenia (38%, 3%), thrombocytopenia (31%, 9%), and increased GPT (25%, 3%).
  • Temozolomide was shown to have good efficacy and tolerability in patients with anaplastic astrocytoma at first relapse.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives

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  • (PMID = 16969025.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Clinical Trial, Phase II; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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95. Quant EC, Drappatz J, Wen PY, Norden AD: Recurrent high-grade glioma. Curr Treat Options Neurol; 2010 Jul;12(4):321-33
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  • [Title] Recurrent high-grade glioma.
  • OPINION STATEMENT: Opinions vary on the best treatment options for recurrent high-grade glioma.
  • Age, performance status, histology, tumor size and location, O6-methylguanine-DNA methyltransferase (MGMT) methylation status for glioblastoma, 1p/19q status for oligodendroglial tumors, and the number and types of prior therapies are important considerations.
  • Enrollment in a clinical trial is the optimal choice for most patients with recurrent high-grade glioma after failure of radiation therapy and temozolomide.
  • Involved-field external beam radiation should be considered for patients with anaplastic gliomas who have not received radiation.
  • For patients with anaplastic astrocytoma who progress after radiotherapy, temozolomide may be used.
  • For patients with anaplastic oligodendroglioma who progress after radiotherapy, PCV chemotherapy and temozolomide are options.
  • In the past, carmustine was commonly used to treat recurrent high-grade glioma, but the utility of carmustine in the modern era is unknown because most studies were performed prior to the widespread use of temozolomide.
  • High-precision re-irradiation such as stereotactic radiosurgery is another option in high-grade glioma, especially for patients with poor bone marrow reserve or inability to tolerate chemotherapy, but there is a paucity of studies with adequate controls.

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  • (PMID = 20842591.001).
  • [ISSN] 1534-3138
  • [Journal-full-title] Current treatment options in neurology
  • [ISO-abbreviation] Curr Treat Options Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Cerveny L, Pavek P, Malakova J, Staud F, Fendrich Z: Lack of interactions between breast cancer resistance protein (bcrp/abcg2) and selected antiepileptic agents. Epilepsia; 2006 Mar;47(3):461-8
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  • In epileptogenic brain tumors such as ganglioma, astrocytoma, anaplastic astrocytomas, or glioma multiforme, strong expression of BCRP in the microvasculature of the BBB was observed.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Anticonvulsants / pharmacokinetics. Blood-Brain Barrier / metabolism. Drug Resistance, Multiple / drug effects. Neoplasm Proteins / metabolism

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  • (PMID = 16529607.001).
  • [ISSN] 0013-9580
  • [Journal-full-title] Epilepsia
  • [ISO-abbreviation] Epilepsia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Anticonvulsants; 0 / Neoplasm Proteins
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97. Server A, Josefsen R, Kulle B, Maehlen J, Schellhorn T, Gadmar Ø, Kumar T, Haakonsen M, Langberg CW, Nakstad PH: Proton magnetic resonance spectroscopy in the distinction of high-grade cerebral gliomas from single metastatic brain tumors. Acta Radiol; 2010 Apr;51(3):316-25
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  • [Title] Proton magnetic resonance spectroscopy in the distinction of high-grade cerebral gliomas from single metastatic brain tumors.
  • BACKGROUND: Brain metastases and primary high-grade gliomas, including glioblastomas multiforme (GBM) and anaplastic astrocytomas (AA), may be indistinguishable by conventional magnetic resonance (MR) imaging.
  • PURPOSE: To assess the value of MR spectroscopy (MRS) using short and intermediate echo time (TE) in differentiating solitary brain metastases and high-grade gliomas on the basis of differences in metabolite ratios in the intratumoral and peritumoral region.
  • MATERIAL AND METHODS: We performed MR imaging and MRS in 73 patients with histologically verified intraaxial brain tumors: 53 patients with high-grade gliomas (34 GBM and 19 AA) and 20 patients with metastatic brain tumors.
  • The differences in the metabolite ratios between high-grade gliomas/GBM/AA and metastases were analyzed statistically.
  • Cutoff values of Cho/Cr, Cho/NAA, and NAA/Cr ratios in the peritumoral edema, as well as Cho/Cr and NAA/Cr ratios in the tumoral core for distinguishing high-grade gliomas/GBM/AA from metastases were determined by receiver operating characteristic (ROC) curve analysis.
  • RESULTS: Significant differences were noted in the peritumoral Cho/Cr, Cho/NAA, and NAA/ Cr ratios between high-grade gliomas/GBM/AA and metastases.
  • ROC analysis demonstrated a cutoff value of 1.24 for peritumoral Cho/Cr ratio to provide sensitivity, specificity, positive (PPV), and negative predictive values (NPV) of 100%, 88.9%, 80.0%, and 100%, respectively, for discrimination between high-grade gliomas and metastases.
  • CONCLUSION: The results of this study demonstrate that MRS can differentiate high-grade gliomas from metastases, especially with peritumoral measurements, supporting the hypothesis that MRS can detect infiltration of tumor cells in the peritumoral edema.

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  • [CommentIn] Acta Radiol. 2010 Apr;51(3):326-8 [20192894.001]
  • (PMID = 20092374.001).
  • [ISSN] 1600-0455
  • [Journal-full-title] Acta radiologica (Stockholm, Sweden : 1987)
  • [ISO-abbreviation] Acta Radiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Contrast Media; 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; K2I13DR72L / Gadolinium DTPA; MU72812GK0 / Creatine; N91BDP6H0X / Choline
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98. Iwamoto FM, Nicolardi L, Demopoulos A, Barbashina V, Salazar P, Rosenblum M, Hormigo A: Clinical relevance of 1p and 19q deletion for patients with WHO grade 2 and 3 gliomas. J Neurooncol; 2008 Jul;88(3):293-8
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  • [Title] Clinical relevance of 1p and 19q deletion for patients with WHO grade 2 and 3 gliomas.
  • PURPOSE: To assess the frequency of chromosomes 1p and 19q deletions in gliomas and to correlate 1p deletion with prognosis in patients with grade 2 and grade 3 gliomas independently of histologic subtype.
  • METHODS: We retrospectively evaluated 208 patients with WHO grade 2 and 3 gliomas who had 1p/19q molecular studies performed between 2000 and 2004.
  • DNA was extracted from tumor tissue and germline material and evaluated by PCR using microsatellite markers for each chromosome.
  • Thirty-eight patients had a low-grade astrocytoma (A2), 58 low-grade oligodendroglioma (O2), 31 low-grade oligoastrocytoma (OA2), 21 anaplastic astrocytoma (A3), 37 anaplastic oligodendroglioma (O3), and 23 had an anaplastic oligoastrocytoma (OA3).
  • On multivariate analyses, chromosome 1p was a prognostic factor for prolonged PFS (HR = 1.75, P = 0.03) and OS (HR = 3.59, P = 0.02) in grade 2 gliomas but not for grade 3 (HR = 0.81, P = 0.7 for PFS; HR = 1.31, P = 0.7 for OS).
  • CONCLUSION: Chromosome 1p deletion is a significant positive prognostic marker in diffuse, grade 2 gliomas regardless of histologic subtype.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Glioma / genetics

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  • (PMID = 18345516.001).
  • [ISSN] 0167-594X
  • [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 / Biomarkers, Tumor
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99. El-Bahy K: Telovelar approach to the fourth ventricle: operative findings and results in 16 cases. Acta Neurochir (Wien); 2005 Feb;147(2):137-42; discussion 142
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  • The inferior medullary velum was infiltrated by the tumour and was not detected as a separate layer in 6 cases (3 cases vermian astrocytomas and 3 cases medulloblastomas).
  • Subtotal removal was achieved in the remaining patients (31.25%); three ependymomas, one medulloblastoma, and one anaplastic astrocytoma.
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / pathology. Astrocytoma / surgery. Cerebellar Ataxia / etiology. Cerebellar Ataxia / pathology. Cerebellar Ataxia / physiopathology. Child. Choroid Plexus / pathology. Choroid Plexus / surgery. Cranial Fossa, Posterior / surgery. Dermoid Cyst / pathology. Dermoid Cyst / surgery. Ependymoma / pathology. Ependymoma / surgery. Female. Humans. Magnetic Resonance Imaging. Male. Medulloblastoma / pathology. Medulloblastoma / surgery. Middle Aged. Neoplasm Recurrence, Local / prevention & control. Papilloma, Choroid Plexus / pathology. Papilloma, Choroid Plexus / surgery. Postoperative Complications / etiology. Postoperative Complications / pathology. Postoperative Complications / physiopathology. Retrospective Studies. Treatment Outcome

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  • (PMID = 15605202.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Austria
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100. Saito T, Arifin MT, Hama S, Kajiwara Y, Sugiyama K, Yamasaki F, Hidaka T, Arita K, Kurisu K: Survivin subcellular localization in high-grade astrocytomas: simultaneous expression in both nucleus and cytoplasm is negative prognostic marker. J Neurooncol; 2007 Apr;82(2):193-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin subcellular localization in high-grade astrocytomas: simultaneous expression in both nucleus and cytoplasm is negative prognostic marker.
  • OBJECTIVE: Subcellularly localized (nuclear and/or cytoplasmic) survivin has various functions, and correlates with prognosis of malignant tumors.
  • However, there have been no reports about the significance of subcellularly localized survivin in high-grade astrocytomas.
  • The aim of the present study was to examine the relationship between prognosis and subcellular localization of survivin in high-grade astrocytoma.
  • METHODS: We immunohistochemically examined the pattern of subcellular localization of survivin expression (nuclear, cytoplasmic, or both) in 51 patients with high-grade astrocytoma (19 anaplastic astrocytomas; 32 glioblastomas).
  • We statistically examined the relationship between survivin localization and prognosis, using multivariate analysis including other clinicopathological factors (age, sex, WHO grade, extent of resection, MIB-1 labeling index, and expression of p53 and epidermal growth factor receptor).
  • CONCLUSIONS: We found that simultaneous expression of survivin in both the nucleus and cytoplasm is an important prognostic factor for high-grade astrocytoma.
  • The present findings indicate that subcellular localization of survivin expression is a reliable prognostic factor for patients with this tumor.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Nucleus / metabolism. Cytoplasm / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Prognosis. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism. Retrospective Studies. Subcellular Fractions. Survival Rate. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 17151933.001).
  • [ISSN] 0167-594X
  • [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] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; 0 / epidermal growth factor receptor-neu receptor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
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