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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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[Title] Temozolomide: The evidence for its therapeutic efficacy in malignant astrocytomas.

INTRODUCTION: Malignant gliomas are a heterogeneous group of primary central nervous system neoplasms that represent less than 2% of all cancers yet carry a significant burden to society.

Temozolomide (TMZ) is a new second generation DNA alkylating agent that has become part of malignant astrocytoma management paradigms because of its proven efficacy, ease of administration, and favorable toxicity profile.

AIMS: To review the role of TMZ in the management of malignant astrocytomas (World Health Organization grades III and IV) including newly diagnosed (n) and recurrent (r) anaplastic astrocytomas (AA) and glioblastomas.

EVIDENCE REVIEW: A series of pivotal clinical trials have established a role for TMZ in the treatment of malignant astrocytomas.

A recent large prospective randomized phase III trial showed that the addition of TMZ during and after radiation therapy (RT) in newly diagnosed (nGBM) patients prolonged median overall survival by 2.5 months; perhaps more importantly, the 2-year survival rate for patients receiving TMZ and RT was 26% compared with 10% for those receiving RT alone.

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[Cites] Ann Intern Med. 2000 May 16;132(10):769-79 [10819699.001]

[Cites] Cancer. 2004 Nov 1;101(9):2098-105 [15389472.001]

[Cites] Oncol Rep. 2000 Jul-Aug;7(4):899-904 [10854567.001]

[Cites] Cancer. 2003 May 1;97(9):2262-6 [12712481.001]

[Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]

[Cites] J Clin Oncol. 2004 May 1;22(9):1598-604 [15117981.001]

[Cites] J Clin Oncol. 2005 Apr 1;23(10):2372-7 [15800329.001]

[Cites] Br J Cancer. 2003 Apr 7;88(7):1004-11 [12671695.001]

[Cites] J Clin Oncol. 2004 May 1;22(9):1583-8 [15051755.001]

[Cites] J Oncol Pharm Pract. 2006 Jun;12(2):105-11 [16984749.001]

[Cites] N Engl J Med. 1980 Dec 4;303(23):1323-9 [7001230.001]

[Cites] Neurosurgery. 1998 Aug;43(2):398-9 [9696102.001]

[Cites] Neuro Oncol. 2002 Jan;4(1):39-43 [11772431.001]

[Cites] Cancer. 2004 May 15;100(10):2208-14 [15139066.001]

[Cites] Qual Life Res. 1996 Feb;5(1):139-50 [8901377.001]

[Cites] J Natl Cancer Inst. 1993 May 5;85(9):704-10 [8478956.001]

[Cites] J Clin Oncol. 2001 Jan 15;19(2):509-18 [11208845.001]

[Cites] J Neurosurg. 1993 May;78(5):767-75 [8468607.001]

[Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):191-200 [15072467.001]

[Cites] Ann Oncol. 2001 Feb;12(2):259-66 [11300335.001]

[Cites] Trends Biochem Sci. 1995 Oct;20(10):421-6 [8533156.001]

[Cites] Health Technol Assess. 2001;5(13):1-73 [11359682.001]

[Cites] Cancer. 1993 Oct 1;72(7):2227-33 [8374881.001]

[Cites] Mayo Clin Proc. 2007 Jun;82(6):771-3 [17550757.001]

[Cites] Int J Cancer. 1999 Mar 1;80(5):764-72 [10048980.001]

[Cites] Anticancer Drugs. 2004 Jun;15(5):499-502 [15166625.001]

[Cites] Brain Pathol. 1995 Apr;5(2):145-51 [7670655.001]

[Cites] Radiother Oncol. 2001 May;59(2):127-37 [11325440.001]

[Cites] Eur J Cancer. 1996 Dec;32A(13):2236-41 [9038604.001]

[Cites] Crit Rev Oncol Hematol. 2007 Jul;63(1):72-80 [17478095.001]

[Cites] Nat Clin Pract Oncol. 2006 Jun;3(6):339-43; quiz following 343 [16757971.001]

[Cites] Cancer Treat Rev. 2006 Oct;32(6):483-6 [16730911.001]

[Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]

[Cites] Neuro Oncol. 2005 Apr;7(2):189-95 [15831237.001]

[Cites] Neuro Oncol. 1999 Apr;1(2):124-37 [11550308.001]

[Cites] J Clin Oncol. 2006 Jun 1;24(16):2563-9 [16735709.001]

[Cites] Semin Radiat Oncol. 2001 Apr;11(2):163-9 [11285554.001]

[Cites] Expert Rev Anticancer Ther. 2006 Nov;6(11):1593-607 [17134364.001]

[Cites] Br J Cancer. 1992 Feb;65(2):287-91 [1739631.001]

[Cites] N Engl J Med. 2007 Apr 12;356(15):1527-35 [17429084.001]

[Cites] J Clin Oncol. 2006 Jan 1;24(1):4-5 [16314613.001]

[Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]

[Cites] J Natl Cancer Inst. 1993 Mar 3;85(5):365-76 [8433390.001]

[Cites] Oncology (Williston Park). 1998 Apr;12(4):537-43, 547; discussion 547-8, 553 [9575527.001]

[Cites] Mol Cancer Ther. 2002 Nov;1(13):1229-36 [12479704.001]

[Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]

[Cites] Oncology. 2002;63(1):38-41 [12187069.001]

[Cites] J Natl Cancer Inst. 2006 Nov 1;98(21):1528-37 [17077355.001]

[Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]

[Cites] Int J Radiat Oncol Biol Phys. 2005 Feb 1;61(2):380-6 [15667956.001]

[Cites] No Shinkei Geka. 1992 Apr;20(4):493-7 [1570077.001]

[Cites] Eur J Cancer. 1993;29A(7):940-2 [8499146.001]

[Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]

[Cites] Neuro Oncol. 1999 Jul;1(3):169-76 [11550311.001]

[Cites] Acta Oncol. 2004;43(6):579-84 [15370616.001]

[Cites] Ann Oncol. 1998 Jun;9(6):589-600 [9681071.001]

[Cites] J BUON. 2002 Jan-Mar;7(1):35-41 [17577258.001]

[Cites] Oncologist. 2006 Feb;11(2):165-80 [16476837.001]

[Cites] Cancer. 1983 Sep 15;52(6):997-1007 [6349785.001]

[Cites] Br J Neurosurg. 2002 Aug;16(4):335-42 [12389885.001]

[Cites] J Clin Oncol. 2005 Oct 1;23(28):7178-87 [16192602.001]

[Cites] Ann Oncol. 2005 Jun;16(6):942-9 [15870090.001]

[Cites] J Pharmacol Exp Ther. 2000 Aug;294(2):664-71 [10900246.001]

[Cites] Cancer. 2006 Jan 1;106(1):172-9 [16323194.001]

[Cites] J Clin Oncol. 2007 Jun 20;25(18):2601-6 [17577040.001]

[Cites] Anticancer Res. 2006 Nov-Dec;26(6C):4675-86 [17214326.001]

[Cites] J Clin Oncol. 1998 Jan;16(1):139-44 [9440735.001]

[Cites] J Neurosurg. 1989 Jul;71(1):1-9 [2661738.001]

[Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]

[Cites] Acta Neurochir (Wien). 2003 Jan;145(1):5-10 [12545256.001]

[Cites] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324.001]

[Cites] Qual Life Res. 1996 Dec;5(6):555-67 [8993101.001]

[Cites] J Neurooncol. 2007 Feb;81(3):295-303 [17001519.001]

[Cites] J Clin Oncol. 2002 Mar 1;20(5):1375-82 [11870182.001]

[Cites] J Clin Oncol. 1999 Sep;17(9):2762-71 [10561351.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4412-7 [16983109.001]

[Cites] Nat Rev Cancer. 2004 Apr;4(4):296-307 [15057289.001]

[Cites] Biochemistry. 1994 Aug 9;33(31):9045-51 [8049205.001]

[Cites] Cancer. 2004 Apr 15;100(8):1712-6 [15073861.001]

[Cites] Am J Clin Oncol. 2002 Dec;25(6):606-11 [12478010.001]

[Cites] N Engl J Med. 1977 Mar 31;296(13):716-21 [402576.001]

[Cites] Int J Radiat Oncol Biol Phys. 2000 Jun 1;47(3):779-84 [10837964.001]

[Cites] J Clin Oncol. 2000 Apr;18(7):1481-91 [10735896.001]

[Cites] Lancet. 2002 Mar 23;359(9311):1011-8 [11937180.001]

[Cites] Anticancer Drugs. 1997 Jan;8(1):92-7 [9147618.001]

[Cites] Br J Cancer. 2004 Sep 13;91(6):1038-44 [15305187.001]

[Cites] J Neurooncol. 2007 Feb;81(3):271-7 [17031561.001]

[Cites] Br J Cancer. 2000 Sep;83(5):588-93 [10944597.001]

[Cites] Int J Radiat Oncol Biol Phys. 1996 Sep 1;36(2):433-41 [8892469.001]

[Cites] Neuro Oncol. 2004 Jan;6(1):38-43 [14769139.001]

[Cites] Neuroepidemiology. 2006;27(1):55-6 [16825795.001]

[Cites] Br J Cancer. 2003 Jul 21;89(2):248-51 [12865911.001]

[Cites] Curr Mol Med. 2003 Feb;3(1):73-84 [12558076.001]

[Cites] J Neurooncol. 1994;21(2):135-40 [7861189.001]

[Cites] J Clin Oncol. 2002 Mar 1;20(5):1383-8 [11870183.001]

[Cites] Eur J Cancer. 2000 Sep;36(14):1788-95 [10974627.001]

[Cites] J Neurooncol. 2004 Jan;66(1-2):203-8 [15015788.001]

[Cites] J Neurosurg. 2003 Sep;99(3):467-73 [12959431.001]

[Cites] Pharmacoeconomics. 2005;23(8):803-15 [16097842.001]

[Cites] J Neurooncol. 2007 Mar;82(1):85-9 [17031555.001]

[Cites] J Health Econ. 1988 Sep;7(3):289-90 [10291478.001]

[Cites] Clin Cancer Res. 2004 Jun 1;10(11):3728-36 [15173079.001]

[Cites] J Neurosurg. 2001 Aug;95(2):190-8 [11780887.001]

[Cites] Int J Radiat Biol. 2002 Oct;78(10):931-6 [12465658.001]

(PMID = 20694068.001).

[ISSN] 1555-175X

[Journal-full-title] Core evidence

[ISO-abbreviation] Core Evid

[Language] eng

[Publication-type] Journal Article

[Publication-country] New Zealand

[Other-IDs] NLM/ PMC2899776

[Keywords] NOTNLM ; anaplastic astrocytoma / evidence / glioblastoma / glioma / malignant astrocytoma / temozolomide

   

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[Title] [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors].

Cyclooxygenase (COX)-2 of astrocytic tumors was studied by immunohistochemistry.

COX-2 was expressed in 8 of 12 (75%) glioblastoma multiforme, 1 of 7 (14%) anaplastic astrocytoma, but none in astrocytoma.

The result showed that COX-2 expression may be related with histological grades and COX-2 inhibitors will be one of promising therapeutic tools in human astrocytic tumors.

[MeSH-major] Astrocytoma / enzymology. Cyclooxygenase 2 / analysis. Cyclooxygenase 2 Inhibitors / therapeutic use

[MeSH-minor] Adult. Aged. Etodolac / pharmacology. Female. Glioblastoma / drug therapy. Glioblastoma / enzymology. Humans. Immunoblotting. Immunohistochemistry. Male. Middle Aged. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured

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(PMID = 16482921.001).

[ISSN] 0006-8969

[Journal-full-title] Nō to shinkei = Brain and nerve

[ISO-abbreviation] No To Shinkei

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2

   

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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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[Title] PBEF1/NAmPRTase/Visfatin: a potential malignant astrocytoma/glioblastoma serum marker with prognostic value.

Malignant astrocytomas comprise anaplastic astrocytoma (AA; grade III) and Glioblastoma (GBM; grade IV).

GBM is the most malignant with a median survival of 10-12 months in patients.

Using cDNA microarray based expression profiling of different grades of astrocytomas, we identified several fold increased levels of PBEF1 transcripts in GBM samples.

Further validation using real time RT-qPCR on an independent set of tumor samples (n=91) and normal brain samples (n=9), GBM specific higher expression of PBEF1 was confirmed.

We carried out ELISA analysis on serum samples of astrocytoma patients to determine whether this protein levels would correlate with the presence of tumor and tumor grade.

Statistical analysis of these data indicates that in patients with astrocytoma, serum PBEF1 levels correlate with tumor grade and is highest in GBM.

Immunohistochemical analysis of an independent set of 51 retrospective GBM cases with known survival data revealed that PBEF1 expression in the tumor tissue along with its co-expression with p53 was associated with poor survival.

Thus, we have identified PBEF1 as a potential malignant astrocytoma serum marker and prognostic indicator among GBMs.

[MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor. Brain / metabolism. Brain Neoplasms / metabolism. Cytokines / physiology. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. Nicotinamide Phosphoribosyltransferase / metabolism

[MeSH-minor] Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry / methods. Oligonucleotide Array Sequence Analysis. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / metabolism

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(PMID = 18728403.001).

[ISSN] 1555-8576

[Journal-full-title] Cancer biology & therapy

[ISO-abbreviation] Cancer Biol. Ther.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / Tumor Suppressor Protein p53; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human

   

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[Title] Neuropeptide Y receptors in primary human brain tumors: overexpression in high-grade tumors.

World Health Organization Grade IV glioblastomas showed a remarkably high expression of the NPY receptor subtype Y2 with respect to both incidence (83%) and density (mean, 4,886 dpm/mg tissue); astrocytomas World Health Organization Grades I to III and oligodendrogliomas also exhibited high Y2 incidences but low Y2 densities.

In conclusion, Y2 receptors in glioblastomas that are activated by NPY originating from intratumoral nerve fibers might mediate functional effects on the tumor cells.

Moreover, identification of the high expression of NPY receptors in high-grade gliomas and embryonal brain tumors provides the basis for in vivo targeting.

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(PMID = 18648328.001).

[ISSN] 0022-3069

[Journal-full-title] Journal of neuropathology and experimental neurology

[ISO-abbreviation] J. Neuropathol. Exp. Neurol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / BIIE 0246; 0 / Benzazepines; 0 / Iodine Radioisotopes; 0 / Peptides; 0 / Receptors, Neuropeptide Y; 37589-80-3 / Guanosine 5'-O-(3-Thiotriphosphate); 94ZLA3W45F / Arginine

   

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[Title] [Anaplastic glioma. Neuropathology, molecular diagnostics and current study concepts].

According to the current WHO classification anaplastic gliomas comprise pure astrocytomas and oligodendrogliomas and mixed tumors.

This review summarizes findings, discusses problems and defines new questions from the phase III trials on anaplastic gliomas.

Therefore, marker profiles should be included into the next WHO brain tumor classification.

The current standard of care for first-line treatment in anaplastic gliomas is radiotherapy or chemotherapy.

Inclusion in this trial is already based on the WHO grade and the 1p/19q status and not on the histopathological subtype.

Furthermore, anaplastic gliomas are an important group of brain tumors for developing future molecular targeted therapies and should therefore be in the main focus of academic and industrial drug development, which aims at improved efficacy and avoiding long-term side-effects.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Oligodendroglioma / pathology

[MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Brain / pathology. Chromosome Deletion. Clinical Trials as Topic. Clinical Trials, Phase III as Topic. Combined Modality Therapy. Cranial Irradiation. DNA Modification Methylases / genetics. DNA Mutational Analysis. DNA Repair Enzymes / genetics. Disease-Free Survival. Humans. Isocitrate Dehydrogenase / genetics. Promoter Regions, Genetic / genetics. Survival Rate. Tumor Suppressor Proteins / genetics

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[Cites] Lancet Oncol. 2009 May;10 (5):459-66 [19269895.001]

[Cites] J Neurol. 2009 May;256(5):734-41 [19240962.001]

[Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]

[Cites] Cancer Res. 2009 May 15;69(10 ):4502-9 [19366800.001]

[Cites] Eur J Cancer. 2008 Jun;44(9):1210-6 [18248979.001]

[Cites] J Neurooncol. 2009 May;92(3):401-15 [19357966.001]

[Cites] J Clin Oncol. 2010 Apr 20;28(12 ):2051-7 [20308655.001]

[Cites] Nat Rev Neurol. 2010 Jan;6(1):39-51 [19997073.001]

[Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]

[Cites] N Engl J Med. 2000 Nov 9;343(19):1350-4 [11070098.001]

[Cites] Lancet Oncol. 2006 May;7(5):392-401 [16648043.001]

[Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]

[Cites] J Clin Oncol. 2003 Sep 1;21(17):3276-84 [12947063.001]

[Cites] Neuro Oncol. 2008 Dec;10 (6):1019-24 [18676355.001]

[Cites] J Clin Oncol. 2009 Dec 10;27(35):5881-6 [19901104.001]

[Cites] J Clin Oncol. 2010 Apr 10;28(11):1963-72 [20231676.001]

[Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]

[Cites] J Neuropathol Exp Neurol. 2006 Oct;65(10):988-94 [17021403.001]

[Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]

[Cites] Neuro Oncol. 2009 Dec;11(6):737-46 [19224764.001]

[Cites] Cancer Res. 2006 Oct 15;66(20):9852-61 [17047046.001]

[Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]

[Cites] Cancer Cell. 2010 May 18;17(5):510-22 [20399149.001]

[Cites] Clin Cancer Res. 2008 Nov 1;14 (21):7068-73 [18981004.001]

[Cites] J Clin Oncol. 2007 Aug 1;25(22):3357-61 [17664483.001]

[Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]

[Cites] Brain Pathol. 2002 Apr;12(2):257-9 [11958379.001]

[Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]

[Cites] J Clin Oncol. 2009 Dec 10;27(35):5874-80 [19901110.001]

[Cites] Acta Neuropathol. 2009 Oct;118(4):469-74 [19554337.001]

[Cites] J Clin Oncol. 2006 Mar 10;24(8):1281-8 [16525183.001]

[Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]

[Cites] J Neurosurg. 2008 Feb;108(2):330-5 [18240930.001]

[Cites] N Engl J Med. 2005 Mar 10;352(10 ):997-1003 [15758010.001]

[Cites] Clin Cancer Res. 2007 Dec 1;13(23):6933-7 [18056167.001]

[Cites] N Engl J Med. 2005 Mar 10;352(10 ):987-96 [15758009.001]

[Cites] Neurology. 2006 Jan 24;66(2):239-42 [16434662.001]

(PMID = 20635074.001).

[ISSN] 1433-0407

[Journal-full-title] Der Nervenarzt

[ISO-abbreviation] Nervenarzt

[Language] ger

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes

   

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[Transliterated title] Guide de prescription et de bon usage du témozolomide dans les tumeurs cérébrales.

Malignant gliomas are the most frequent primary brain tumors in adults.

Temozolomide is an oral alkylating cytotoxic agent of second generation, used in the treatment of high-grade gliomas.

It is indicated in newly diagnosed glioblastoma multiform as well as in recurrent or progressive malignant gliomas, such as glioblastoma multiform or anaplastic astrocytoma.

The literature review was analysed by experts who determined the evidence level (A to E) according to the scale of recommendations adopted by the "Haute Autorité de santé--HAS--(French National Authority for Health)".

For high-grade and low-grade gliomas, based on the level of evidence from the literature, the use of temozolomide can be justified, with a B2 score attributed to these indications.

[MeSH-minor] Age Factors. Astrocytoma / drug therapy. Drug Administration Schedule. Drug Labeling. Glioblastoma / drug therapy. Humans

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(PMID = 19467988.001).

[ISSN] 1769-6917

[Journal-full-title] Bulletin du cancer

[ISO-abbreviation] Bull Cancer

[Language] fre

[Publication-type] English Abstract; Journal Article; Practice Guideline; Review

[Publication-country] France

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide

[Number-of-references] 55

   

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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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[Title] Clinicopathologic features of recurrent dysembryoplastic neuroepithelial tumor and rare malignant transformation: a report of 5 cases and review of the literature.

More recently, case reports have described malignant gliomas arising after irradiation and recurrences following subtotal or even gross total resection.

Nonetheless, a probably radiation induced anaplastic astrocytoma was encountered in one case 7 years after therapy.

These findings suggest that these patients may need closer follow-up than initially suggested, lending further support to the notion that this tumor behaves more like a benign neoplasm, rather than a dysplastic or hamartomatous lesion.

[MeSH-major] Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Neoplasm Recurrence, Local / diagnosis. Neoplasms, Neuroepithelial / pathology

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[Cites] Clin Radiol. 1993 Apr;47(4):255-8 [8495572.001]

[Cites] Clin Neuropathol. 2004 Sep-Oct;23(5):223-31 [15581025.001]

[Cites] Brain. 1994 Jun;117 ( Pt 3):461-75 [8032857.001]

[Cites] J Neurooncol. 1999 Feb;41(3):267-80 [10359147.001]

[Cites] Neurosurgery. 1988 Nov;23(5):545-56 [3143922.001]

[Cites] Cancer. 1990 Jan 15;65(2):333-6 [2403835.001]

[Cites] Pediatr Radiol. 2003 Mar;33(3):207-10 [12612823.001]

[Cites] J Neuropathol Exp Neurol. 2003 May;62(5):530-7 [12769192.001]

[Cites] Pediatr Neurosurg. 2008;44(2):153-8 [18230932.001]

[Cites] Brain Tumor Pathol. 1999;16(2):81-5 [10746965.001]

[Cites] Brain Pathol. 2009 Jan;19(1):81-90 [18452568.001]

[Cites] Ann Diagn Pathol. 2003 Aug;7(4):240-4 [12913847.001]

[Cites] Neurology. 2004 Jun 22;62(12):2270-6 [15210893.001]

[Cites] Cancer. 2007 Dec 15;110(12 ):2799-808 [17973253.001]

[Cites] Pediatr Neurosurg. 1997 Jul;27(1):1-11 [9486830.001]

[Cites] AJNR Am J Neuroradiol. 2003 May;24(5):829-34 [12748079.001]

[Cites] J Neurol Neurosurg Psychiatry. 2001 Apr;70(4):450-8 [11254766.001]

[Cites] Front Biosci. 2003 Jan 01;8:a1-9 [12456321.001]

[Cites] J Neurosurg. 2007 Jun;106(6 Suppl):509-12 [17566412.001]

[Cites] Acta Neuropathol. 1993;86(5):466-72 [8310797.001]

[Cites] Pediatr Neurosurg. 2008;44(4):333-6 [18552517.001]

[Cites] J Neurosurg. 2000 Apr;92(4):722-5 [10761668.001]

[Cites] Am J Clin Pathol. 1992 Mar;97(3):398-401 [1543164.001]

[Cites] J Neurooncol. 2006 May;78(1):59-62 [16314940.001]

(PMID = 19267228.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 25

   

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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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[Title] Induction of gliosarcoma and atypical meningioma 13 years after radiotherapy of residual pilocytic astrocytoma in childhood.

BACKGROUND: Malignant transformation of pilocytic astrocytomas in children is rare and often linked to previous radiotherapy.

METHODS AND RESULTS: We report a patient who underwent subtotal resection of a right temporal and insular pilocytic astrocytoma at age 8 in 1988 followed by high-dose radiation therapy.

A local recurrence, grade WHO III, with signs of focal sarcomatous transformation, was subtotally resected 13 years later in 2001.

A new and fast growing right frontal meningioma, grade WHO II, was removed in 2003.

Another tumor mass reduction in 2005 was followed by stereotactic radiotherapy.

CONCLUSION: Most of the reported cases of malignant transformation of pilocytic astrocytomas received radiation therapy beforehand.

Irradiation-induced meningiomas in children are known to occur, however not following radiotherapy of low-grade hemispheric gliomas.

The presented case illustrates why adjuvant radiotherapy of residual pilocytic astrocytoma in children is not recommended anymore.

[MeSH-major] Astrocytoma / radiotherapy. Gliosarcoma / etiology. Meningeal Neoplasms / etiology. Meningioma / etiology. Neoplasms, Radiation-Induced / etiology

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(PMID = 18230932.001).

[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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[Title] Meta-analysis of glioblastoma multiforme versus anaplastic astrocytoma identifies robust gene markers.

BACKGROUND: Anaplastic astrocytoma (AA) and its more aggressive counterpart, glioblastoma multiforme (GBM), are the most common intrinsic brain tumors in adults and are almost universally fatal.

A deeper understanding of the molecular relationship of these tumor types is necessary to derive insights into the diagnosis, prognosis, and treatment of gliomas.

Although genomewide profiling of expression levels with microarrays can be used to identify differentially expressed genes between these tumor types, comparative studies so far have resulted in gene lists that show little overlap.

CONCLUSION: We have performed a meta-analysis of genome-scale mRNA expression data for 289 human malignant gliomas and have identified a list of >900 probe sets and >20 pathways that are significantly different between GBM and AA.

These feature lists could be utilized to aid in diagnosis, prognosis, and grade reduction of high-grade gliomas and to identify genes that were not previously suspected of playing an important role in glioma biology.

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[Cites] Br J Cancer. 1999 Dec;81(8):1371-7 [10604735.001]

[Cites] Mol Endocrinol. 2000 Jun;14(6):848-62 [10847587.001]

[Cites] J Biol Chem. 2000 Jul 7;275(27):20315-23 [10783396.001]

[Cites] BMC Bioinformatics. 2008;9:63 [18226260.001]

[Cites] Genomics. 2008 May;91(5):395-406 [18343632.001]

[Cites] Mol Cancer Ther. 2008 May;7(5):1013-24 [18445660.001]

[Cites] Biochem Biophys Res Commun. 2008 Sep 5;373(4):539-44 [18590702.001]

[Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]

[Cites] BMC Bioinformatics. 2009;10:1 [19118496.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]

[Cites] FASEB J. 2001 Feb;15(2):458-66 [11156961.001]

[Cites] Am J Pathol. 2002 Apr;160(4):1279-92 [11943713.001]

[Cites] Cancer Res. 2002 Aug 1;62(15):4427-33 [12154050.001]

[Cites] Am J Pathol. 2002 Nov;161(5):1695-700 [12414516.001]

[Cites] Cancer Res. 2002 Nov 1;62(21):6205-10 [12414648.001]

[Cites] Acta Neuropathol. 2003 Jan;105(1):49-57 [12471461.001]

[Cites] Pancreas. 2003 Jan;26(1):56-64 [12499918.001]

[Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e15 [12582260.001]

[Cites] Cancer Res. 2003 Mar 1;63(5):1138-43 [12615733.001]

[Cites] Cancer Res. 2003 Apr 1;63(7):1602-7 [12670911.001]

[Cites] Oncogene. 2003 Apr 17;22(15):2361-73 [12700671.001]

[Cites] Genome Biol. 2003;4(4):210 [12702200.001]

[Cites] Nat Genet. 2003 Jul;34(3):267-73 [12808457.001]

[Cites] Bioinformatics. 2003;19 Suppl 1:i84-90 [12855442.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]

[Cites] Surg Neurol. 2003 Nov;60(5):402-6; discussion 406 [14572960.001]

[Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):212-21 [14734472.001]

[Cites] Bioinformatics. 2004 Feb 12;20(3):307-15 [14960456.001]

[Cites] Nat Biotechnol. 2004 May;22(5):615-21 [15122300.001]

[Cites] FEBS Lett. 2004 Aug 27;573(1-3):83-92 [15327980.001]

[Cites] Cancer Res. 2004 Sep 15;64(18):6503-10 [15374961.001]

[Cites] Genome Biol. 2004;5(10):R80 [15461798.001]

[Cites] Mol Cell Biol. 1996 Sep;16(9):4604-13 [8756616.001]

[Cites] J Biol Chem. 1996 Dec 20;271(51):32529-37 [8955077.001]

[Cites] Cancer Res. 1999 Feb 15;59(4):895-900 [10029081.001]

[Cites] Cancer Res. 1999 Aug 15;59(16):3915-8 [10463582.001]

[Cites] BMC Bioinformatics. 2004 Oct 25;5:159 [15504239.001]

[Cites] Bioinformatics. 2004 Nov 22;20(17):3166-78 [15231529.001]

[Cites] Genome Biol. 2005;6(2):R16 [15693945.001]

[Cites] Cancer Res. 2005 Mar 1;65(5):1678-86 [15753362.001]

[Cites] Clin Cancer Res. 2005 May 1;11(9):3326-34 [15867231.001]

[Cites] Nat Methods. 2005 May;2(5):345-50 [15846361.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13544-9 [16174746.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]

[Cites] J Bioinform Comput Biol. 2005 Oct;3(5):1171-89 [16278953.001]

[Cites] Nat Rev Genet. 2006 Jan;7(1):55-65 [16369572.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):159-67 [16397228.001]

[Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]

[Cites] Cancer Cell. 2006 Apr;9(4):287-300 [16616334.001]

[Cites] J Neurooncol. 2006 Jul;78(3):233-47 [16612574.001]

[Cites] Biom J. 2006 Jun;48(3):435-50 [16845907.001]

[Cites] BMC Bioinformatics. 2006;7:359 [16872483.001]

[Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D760-5 [17099226.001]

[Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]

[Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Jul 10;104(28):11736-41 [17606927.001]

[Cites] Cancer Res. 2007 Nov 1;67(21):10296-303 [17974971.001]

[Cites] Neurosurg Rev. 2008 Jan;31(1):83-9; discussion 89-90 [17917751.001]

[Cites] Comput Biol Chem. 2008 Feb;32(1):38-46 [17988949.001]

[Cites] Bioinformatics. 2008 Feb 1;24(3):374-82 [18204063.001]

[Cites] Ann Vasc Surg. 2008 Mar;22(2):273-84 [18346582.001]

(PMID = 19732454.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] ENG

[Grant] United States / NIGMS NIH HHS / GM / R01 GM082798; United States / NIH HHS / OD / DP2 OD002319; United States / NIH HHS / OD / DP2OD002319; United States / NLM NIH HHS / LM / U54 LM008748; United States / NLM NIH HHS / LM / U54LM008748

[Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A

[Other-IDs] NLM/ PMC2743637

   

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[Title] Evaluation of invasiveness of astrocytoma using 1H-magnetic resonance spectroscopy: correlation with expression of matrix metalloproteinase-2.

INTRODUCTION: Even low-grade astrocytomas infiltrate the entire brain, a feature that precludes their successful therapy.

So to assess the invasive potential of astrocytoma is very important.

The aim of this study was determine whether there is a significant correlation between the results of (1)H-magnetic resonance spectroscopy ((1)H-MRS) and tumor invasive potential of astrocytoma, which is reflected by expression of matrix metalloproteinase-2 (MMP-2).

METHODS: The (1)H-MRS spectra of 41 histologically verified astrocytomas were obtained on a 3-T MR scanner.

According to the World Health Organization classification criteria for central nervous system tumors, there were 16 low-grade astrocytomas (2 pilocytic astrocytomas, 14 grade II astrocytomas) and 25 high-grade astrocytomas (5 anaplastic astrocytomas, 20 glioblastomas).The choline/N-acetylaspartate (Cho/NAA) and choline/creatine (Cho/Cr) ratios were calculated.

Of the 41 astrocytomas, 19 (8 low-grade and 11 high-grade) were analyzed immunohistochemically.

The correlations between metabolite ratios and the quantitative data from the immunohistochemical tests in the 19 astrocytomas were determined.

RESULTS: The Cho/NAA and Cho/Cr ratios of high-grade astrocytoma were both significantly greater than those of low-grade astrocytoma (t = -6.222, P = 0.000; t = -6.533, P = 0.000, respectively).

MMP-2 COD values of high-grade astrocytomas were also significantly greater than those of low-grade astrocytomas (t = -5.892, P = 0.000).

CONCLUSION: (1)H-MRS is helpful in evaluating the invasiveness of astrocytomas and predicting prognosis preoperatively by determining the Cho/NAA and Cho/Cr ratios.

[MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Magnetic Resonance Spectroscopy. Matrix Metalloproteinase 2 / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Aspartic Acid / analogs & derivatives. Aspartic Acid / metabolism. Choline / metabolism. Creatine / metabolism. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Predictive Value of Tests. Treatment Outcome

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[Cites] Nat Rev Mol Cell Biol. 2002 Mar;3(3):207-14 [11994741.001]

[Cites] Int J Dev Neurosci. 1999 Aug-Oct;17(5-6):495-502 [10571411.001]

[Cites] Neuroradiology. 2006 May;48(5):312-8 [16552583.001]

[Cites] Radiology. 2006 Mar;238(3):958-69 [16424238.001]

[Cites] Pharmacol Res. 2002 Aug;46(2):155-63 [12220955.001]

[Cites] J Neurooncol. 2000 Dec;50(3):215-26 [11263501.001]

[Cites] NMR Biomed. 2004 Feb;17(1):10-20 [15011246.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8904-9 [12861074.001]

[Cites] AJNR Am J Neuroradiol. 1999 Jan;20(1):117-23 [9974066.001]

[Cites] Br J Cancer. 2000 Jan;82(1):52-5 [10638966.001]

[Cites] J Neurooncol. 2003 Jul;63(3):233-45 [12892229.001]

[Cites] Stereotact Funct Neurosurg. 2004;82(2-3):90-7 [15305081.001]

[Cites] Am J Pathol. 1998 Aug;153(2):429-37 [9708803.001]

[Cites] Neuroradiology. 2002 May;44(5):371-81 [12012120.001]

[Cites] AJNR Am J Neuroradiol. 2001 Apr;22(4):604-12 [11290466.001]

[Cites] Nat Rev Neurosci. 2001 Jul;2(7):502-11 [11433375.001]

[Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):659-65 [10782774.001]

[Cites] AJNR Am J Neuroradiol. 2002 Nov-Dec;23 (10 ):1775-8 [12427638.001]

(PMID = 17763847.001).

[ISSN] 0028-3940

[Journal-full-title] Neuroradiology

[ISO-abbreviation] Neuroradiology

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; EC 3.4.24.24 / Matrix Metalloproteinase 2; MU72812GK0 / Creatine; N91BDP6H0X / Choline

   

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Ependymoma was the most common tumor (83%), and 55% were located in the thoracic spine.

There were two deaths due tumor progression (both malignant tumors) and one recurrence (anaplastic astrocytoma).

All three patients in whom malignant astrocytomas were diagnosed underwent postoperative radiation therapy.

The authors recommend motor evoked potential-guided aggressive microsurgical resection, because the long-term outcome of benign lesions is excellent (good functional recovery and no tumor recurrence).

[MeSH-minor] Aged. Astrocytoma / surgery. Chi-Square Distribution. Female. Humans. Male. Middle Aged. Quality of Life. Retrospective Studies. Survival Rate. Treatment Outcome

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(PMID = 15796348.001).

[ISSN] 1547-5654

[Journal-full-title] Journal of neurosurgery. Spine

[ISO-abbreviation] J Neurosurg Spine

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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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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[Title] Regulation of progesterone receptor isoforms content in human astrocytoma cell lines.

Both PR isoforms have been detected in human astrocytomas, the most common and aggressive primary brain tumours, but their regulation and function are unknown.

We studied the effects of estradiol, progesterone and their receptor antagonists (ICI 182,780 and RU 486) on PR isoforms content in U373 and D54 human astrocytoma cell lines, respectively derived from grades III and IV astrocytomas, by Western blot analysis.

Our results suggest a differential PR isoforms regulation depending on the evolution grade of human astrocytoma cells, and an inhibitory role of PR-A on progesterone effects on astrocytomas cell growth.

[MeSH-major] Astrocytoma / metabolism. Receptors, Progesterone / metabolism

[MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Protein Isoforms / metabolism. Transfection

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(PMID = 19095059.001).

[ISSN] 0960-0760

[Journal-full-title] The Journal of steroid biochemistry and molecular biology

[ISO-abbreviation] J. Steroid Biochem. Mol. Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Progesterone

   

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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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[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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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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[Title] Methylation of the PTEN promoter defines low-grade gliomas and secondary glioblastoma.

Glioblastoma multiforme (GBM) can present as either de novo or secondary tumors arising from previously diagnosed low-grade gliomas.

Although these tumor types are phenotypically indistinguishable, de novo and secondary GBMs are associated with distinct genetic characteristics.

PTEN mutations, which result in activation of the phosphoinositide 3-kinase (PI3K) signal transduction pathway, are frequent in de novo but not in secondary GBMs or their antecedent low-grade tumors.

Results we present here show that grade II astrocytomas, oligodendrogliomas, and oligoastrocytomas commonly display methylation of the PTEN promoter, a finding that is absent in nontumor brain specimens and rare in de novo GBMs.

Our results also demonstrate frequent methylation of the PTEN promoter in grade III astrocytomas and secondary GBMs, consistent with the hypothesis that these tumors arise from lower grade precursors.

PTEN methylation is rare in de novo GBMs and is mutually exclusive with PTEN mutations.

We conclude that methylation of the PTEN promoter may represent an alternate mechanism by which PI3K signaling is increased in grade II and III gliomas as well as secondary GBMs, a finding that offers new therapeutic approaches in these patients.

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[Cites] Cancer Res. 2001 Feb 1;61(3):1122-8 [11221842.001]

[Cites] Cancer Res. 2006 Jul 1;66(13):6546-52 [16818626.001]

[Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]

[Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]

[Cites] Am J Pathol. 2002 Mar;160(3):795-800 [11891178.001]

[Cites] Gynecol Oncol. 2004 Jun;93(3):621-7 [15196854.001]

[Cites] Genes Chromosomes Cancer. 2004 Oct;41(2):117-24 [15287024.001]

[Cites] Int J Cancer. 2004 Nov 10;112(3):407-10 [15382065.001]

[Cites] J Neurosurg. 1998 Jan;88(1):1-10 [9420066.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5246-50 [9560261.001]

[Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]

[Cites] Clin Cancer Res. 1998 Oct;4(10):2447-54 [9796977.001]

[Cites] Clin Cancer Res. 1998 Dec;4(12):3005-10 [9865913.001]

[Cites] Cancer Res. 1999 Apr 15;59(8):1820-4 [10213484.001]

[Cites] Lab Invest. 2002 Mar;82(3):285-91 [11896207.001]

[Cites] Clin Cancer Res. 2002 May;8(5):1100-6 [12006525.001]

[Cites] Clin Cancer Res. 2002 May;8(5):1178-84 [12006535.001]

[Cites] Cancer Cell. 2002 May;1(4):299-305 [12086841.001]

[Cites] Nat Rev Cancer. 2002 Jul;2(7):489-501 [12094235.001]

[Cites] Genes Chromosomes Cancer. 2002 Sep;35(1):74-80 [12203792.001]

[Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]

[Cites] Drugs R D. 2003;4(3):179-84 [12757405.001]

[Cites] Acta Neuropathol. 2003 Nov;106(5):479-85 [12904991.001]

[Cites] J Biol Chem. 2004 Jan 23;279(4):2737-46 [14576155.001]

[Cites] Clin Cancer Res. 2004 Feb 1;10(3):1013-23 [14871980.001]

[Cites] Cancer Res. 2004 Mar 15;64(6):2000-6 [15026336.001]

[Cites] Cancer Lett. 2004 Apr 30;207(2):215-20 [15072831.001]

[Cites] Cancer Res. 2004 May 1;64(9):3014-21 [15126336.001]

[Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]

[Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]

[Cites] J Neuropathol Exp Neurol. 1999 Nov;58(11):1170-83 [10560660.001]

[Cites] Lab Invest. 2000 Jan;80(1):65-72 [10653004.001]

[Cites] Biochem J. 2000 Mar 15;346 Pt 3:561-76 [10698680.001]

[Cites] Front Biosci. 2000 Jan 1;5:D213-31 [10702383.001]

[Cites] Carcinogenesis. 2000 Nov;21(11):2057-64 [11062168.001]

[Cites] J Neurooncol. 2000 Jun;48(2):89-94 [11083071.001]

[Cites] Int J Cancer. 2001 Jan 1;91(1):22-6 [11149415.001]

[Cites] Am J Clin Pathol. 2001 Jan;115(1):32-8 [11190805.001]

[Cites] Int J Oncol. 2001 Mar;18(3):493-7 [11179477.001]

[Cites] Cancer Res. 2001 Feb 1;61(3):900-2 [11221878.001]

[Cites] Curr Opin Oncol. 1999 May;11(3):162-7 [10328589.001]

[Cites] Oncogene. 2004 Nov 11;23(53):8571-80 [15467756.001]

[Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]

[Cites] Hum Pathol. 2005 Apr;36(4):357-63 [15891996.001]

[Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):880-7 [15956649.001]

[Cites] Hum Pathol. 2005 Jul;36(7):768-76 [16084946.001]

[Cites] N Engl J Med. 2005 Nov 10;353(19):2012-24 [16282176.001]

[Cites] Thyroid. 2006 Jan;16(1):17-23 [16487009.001]

[Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]

[Cites] Exp Cell Res. 2001 Mar 10;264(1):29-41 [11237521.001]

(PMID = 17504928.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA97257; United States / NCI NIH HHS / CA / R01 CA52689; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA082783-06; United States / NCI NIH HHS / CA / R01 CA082783; United States / NCI NIH HHS / CA / CA082783-06; United States / NCI NIH HHS / CA / R01 CA052689

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

[Other-IDs] NLM/ PMC1907411

   

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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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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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[Title] First-line nitrosourea-based chemotherapy in symptomatic non-resectable supratentorial pure low-grade astrocytomas.

At the present time, there are no proven beneficial effects of chemotherapy (CT) for the treatment of pure low-grade astrocytomas.

Brain radiotherapy (RT) still remains the standard treatment in order to reduce or delay tumor progression or symptoms, despite possible long-term neurologic complications.

We report 10 patients, with histologically proven pure low-grade fibrillary astrocytomas, to which we administered a first-line nitrosourea-based CT.

CT was well tolerated; all patients developed myelosuppression with 40% of grade III/IV hematotoxicity.

These results demonstrate that some patients with symptomatic non-resectable fibrillary low-grade astrocytomas can be treated with up-front CT to improve their neurologic status.

[MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Drug Therapy / methods. Nitrosourea Compounds / therapeutic use

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(PMID = 16128869.001).

[ISSN] 1351-5101

[Journal-full-title] European journal of neurology

[ISO-abbreviation] Eur. J. Neurol.

[Language] eng

[Publication-type] Clinical Trial; Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Nitrosourea Compounds

   

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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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[Title] Combined treatment of pediatric high-grade glioma with the oncolytic viral strain MTH-68/H and oral valproic acid.

The case of a 12-year-old boy with anaplastic astrocytoma of the left thalamus is reported.

Postoperative irradiation and chemotherapy could not repress tumor progression; therefore, treatment was undertaken with an oncolytic virus, MTH-68/H, an attenuated strain of Newcastle disease virus (NDV), and valproic acid (VPA), an antiepileptic drug, which also has antineoplastic properties.

This treatment resulted in a far-reaching regression of the thalamic glioma, but 4 months later a new tumor manifestation, an extension of the thalamic tumor, appeared in the wall of the IVth ventricle, which required a second neurosurgical intervention.

Under continuous MTH-68/H - VPA administration the thalamic tumor remained under control, but the rhombencephalic one progressed relentlessly and led to the fatal outcome.

In the final stage, a third tumor manifestation appeared in the left temporal lobe.

The possible reasons for the antagonistic behavior of the three manifestations of the same type of glioma to the initially most successful therapy are discussed.

The comparative histological study of the thalamic and rhombencephalic tumor manifestations revealed that MTH-68/H treatment induces, similar to in vitro observations, a massive apoptotic tumor cell decline.

In the rhombencephalic tumor, in and around the declining tumor cells, NDV antigen could be demonstrated immunohistochemically, and virus particles have been found in the cytoplasm of tumor cells at electron microscopic investigation.

[MeSH-major] Anticonvulsants / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / therapy. Brain Neoplasms / therapy. Valproic Acid / therapeutic use. Viral Vaccines / therapeutic use

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(PMID = 17004977.001).

[ISSN] 0903-4641

[Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica

[ISO-abbreviation] APMIS

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Anticonvulsants; 0 / Antigens, Viral; 0 / Newcastle disease virus vaccine MTH-68-H; 0 / Viral Vaccines; 614OI1Z5WI / Valproic Acid

   

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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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Heterozygous point mutations of isocitrate dehydrogenase (IDH)1 codon 132 are frequent in grade II and III gliomas.

Here we investigate the capability of this antibody to differentiate wild type and mutated IDH1 protein in central nervous system (CNS) tumors by Western blot and immunohistochemistry.

Intriguing is the ability of mIDH1R132H to detect single infiltrating tumor cells.

The very high frequency and the distribution of this mutation among specific brain tumor entities allow the highly sensitive and specific discrimination of various tumors by immunohistochemistry, such as anaplastic astrocytoma from primary glioblastoma or diffuse astrocytoma World Health Organization (WHO) grade II from pilocytic astrocytoma or ependymoma.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Ependymoma / genetics. Glioma / enzymology. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Isocitrate Dehydrogenase / immunology

[MeSH-minor] Adolescent. Adult. Aged. Antigen-Antibody Reactions. Blotting, Western. Child. Child, Preschool. Cloning, Molecular. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Mutation / genetics. Mutation / physiology. Protein Biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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(PMID = 19903171.001).

[ISSN] 1750-3639

[Journal-full-title] Brain pathology (Zurich, Switzerland)

[ISO-abbreviation] Brain Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human

   

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[Title] WT1 expression distinguishes astrocytic tumor cells from normal and reactive astrocytes.

Particularly in small brain biopsies, it might be difficult to distinguish reactive astrogliosis from low-grade or infiltration zones of high-grade astrocytomas.

Recently, the over-expression of Wilms' tumor gene product WT1 was reported in astrocytic tumor cells.

Therefore, we investigated WT1 expression in paraffin-embedded brain sections from 28 controls, 48 cases with astrogliosis of various etiology and 219 astrocytomas [World Health Organization (WHO) grades I-IV] by immunohistochemistry.

In astrocytomas, WT1-positive tumor cells were found in pilocytic astrocytomas (66.7% of cases), diffuse astrocytomas (52.7%) WHO grade II (52.7%), anaplastic astrocytomas (83.4%) and glioblastomas (98.1%).

Overall, the majority of all astrocytic neoplasms (84.5%) expressed WT1.

Establishing a cut-off value of 0% immunoreactive tumor cells served to recognize neoplastic astrocytes with 100% specificity and 68% sensitivity and was associated with positive and negative predictive values of 1 and 0.68, respectively.

[MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gliosis / metabolism. WT1 Proteins / biosynthesis

[MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Endothelial Cells / metabolism. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged

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(PMID = 18371184.001).

[ISSN] 1015-6305

[Journal-full-title] Brain pathology (Zurich, Switzerland)

[ISO-abbreviation] Brain Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / WT1 Proteins

   

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[Title] Malignant transformation of high-grade astrocytoma associated with neurocysticercosis in a patient with Turcot syndrome.

A 45-year-old woman with anaplastic astrocytoma was clinically diagnosed with Turcot syndrome, and subsequently developed simultaneous neurocysticercosis and malignant transformation to glioblastoma.

The clinical course and histological findings suggest that the parasitic infection and/or genetic changes contributed to the malignant transformation of the astrocytic tumour.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Glioblastoma / pathology. Neurocysticercosis / pathology

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(PMID = 17138070.001).

[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] Case Reports; Journal Article

[Publication-country] Scotland

   

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[Title] Perfusion and diffusion MR imaging in enhancing malignant cerebral tumors.

OBJECTIVE: Common contrast-enhancing malignant tumors of the brain are glioblastoma multiforme (GBMs), anaplastic astrocytomas (AAs), metastases, and lymphomas, all of which have sometimes similar conventional MRI findings.

Our aim was to evaluate the role of perfusion MR imaging (PWI) and diffusion-weighted imaging (DWI) in the differentiation of these contrast-enhancing malignant cerebral tumors.

Minimum ADC values (ADC(min)) of each tumor was later calculated from ADC map images.

PWI was applied using dynamic susceptibility contrast technique and maximum relative cerebral blood volume (rCBV(max)) was calculated from each tumor, given in ratio with contralateral normal white matter.

CONCLUSION: Combination of DWI and PWI, with ADC(min) and rCBV(max) calculations, may aid routine MR imaging in the differentiation of common cerebral contrast-enhancing malignant tumors.

[MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / diagnosis. Image Enhancement / methods. Lymphoma / diagnosis. Magnetic Resonance Angiography / methods

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(PMID = 16527438.001).

[ISSN] 0720-048X

[Journal-full-title] European journal of radiology

[ISO-abbreviation] Eur J Radiol

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Ireland

[Chemical-registry-number] 0 / Contrast Media

   

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We report a patient after resection of anaplastic astrocytoma and 5,580 cGy of total external-beam radiation treatments with brain radiation necrosis who underwent HBO2 therapy and developed a partial seizure during treatment.

[MeSH-minor] Astrocytoma / radiotherapy. Astrocytoma / surgery. Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Combined Modality Therapy. Humans. Male. Middle Aged. Necrosis / etiology. Necrosis / pathology. Necrosis / therapy. Radiotherapy, Conformal / adverse effects

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(PMID = 15946345.001).

[ISSN] 0013-9580

[Journal-full-title] Epilepsia

[ISO-abbreviation] Epilepsia

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Anaplastic astrocytoma in adults.

Anaplastic astrocytoma is an uncommon disease in the adult population.

Based on randomized data available, chemotherapy has consistently failed to improve the outcome of patients with anaplastic astrocytoma, while a meta-analysis showed a small, but significant improvement in survival favouring the use of chemotherapy.

In recurrent disease, chemotherapy with temozolomide has been proven to be active and well-tolerated in phase II trials, but no comparative phase III trials of other cytotoxic drugs have been conducted.

[MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives

[MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Female. Humans. Incidence. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Prognosis. Risk Factors. Survival Analysis

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(PMID = 17478095.001).

[ISSN] 1040-8428

[Journal-full-title] Critical reviews in oncology/hematology

[ISO-abbreviation] Crit. Rev. Oncol. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Review

[Publication-country] Ireland

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide

[Number-of-references] 69

   

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[Title] A congenital brain tumor associated with assisted in vitro fertilization. Case report.

In this report the authors describe the clinical features of a rare neonatal anaplastic astrocytoma in the setting of in vitro fertilization (IVF).

Grosstotal resection of an anaplastic astrocytoma was followed by chemotherapy with temozolomide and vincristine.

[MeSH-major] Astrocytoma / congenital. Brain Neoplasms / congenital. Fertilization in Vitro / adverse effects

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[CommentIn] J Neurosurg. 2007 May;106(5 Suppl):418; author reply 418-9 [17566216.001]

(PMID = 16302619.001).

[ISSN] 0022-3085

[Journal-full-title] Journal of neurosurgery

[ISO-abbreviation] J. Neurosurg.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 5J49Q6B70F / Vincristine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide

   

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[Title] Multifocal anaplastic astrocytoma in a patient with hereditary colorectal cancer, transcobalamin II deficiency, agenesis of the corpus callosum, mental retardation, and inherited PMS2 mutation.

We describe the case of a patient with transcobalamin II deficiency, hypogammaglobulinemia, absent corpus callosum, and mental retardation who presented at an early age with colorectal cancer and multifocal anaplastic astrocytoma.

He was found to have a possible germline mutation of the PMS2 gene, as evidenced by absent protein expression in both normal and tumor tissues.

[MeSH-major] Abnormalities, Multiple / genetics. Adenosine Triphosphatases / genetics. Astrocytoma / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Repair Enzymes / genetics. DNA-Binding Proteins / genetics

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[Cites] Vitam Horm. 2000;59:337-66 [10714245.001]

[Cites] Oncogene. 2000 Mar 23;19(13):1719-23 [10763829.001]

[Cites] Am J Pathol. 2002 Jun;160(6):1953-8 [12057899.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):919-32 [12621137.001]

[Cites] Am J Hum Genet. 2004 May;74(5):954-64 [15077197.001]

[Cites] Cancer Res. 2004 Jul 15;64(14):4721-7 [15256438.001]

[Cites] Cancer Res. 2006 Aug 1;66(15):7810-7 [16885385.001]

[Cites] Nature. 1994 Sep 1;371(6492):75-80 [8072530.001]

[Cites] N Engl J Med. 1995 Mar 30;332(13):839-47 [7661930.001]

[Cites] Arch Dis Child. 1995 Mar;72(3):237-8 [7741573.001]

[Cites] Curr Probl Surg. 2005 Apr;42(4):195-256 [15821699.001]

[Cites] Clin Invest Med. 2005 Oct;28(5):267-82 [16265999.001]

[Cites] Hum Mutat. 2006 May;27(5):490-5 [16619239.001]

[Cites] Br J Haematol. 1992 Jan;80(1):117-20 [1536799.001]

(PMID = 17993636.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Transcobalamins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 6.5.1.- / DNA Repair Enzymes

[Other-IDs] NLM/ PMC2600843

   

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[Title] Preoperative grading of presumptive low-grade astrocytomas on MR imaging: diagnostic value of minimum apparent diffusion coefficient.

BACKGROUND AND PURPOSE: Histopathologic grade of glial tumors is inversely correlated with the minimum apparent diffusion coefficient (ADC).

We assessed the diagnostic values of minimum ADC for preoperative grading of supratentorial astrocytomas that were diagnosed as low-grade astrocytomas on conventional MR imaging.

MATERIALS AND METHODS: Among 118 patients with astrocytomas (WHO grades II-IV), 16 who showed typical MR imaging findings of low-grade supratentorial astrocytomas on conventional MR imaging were included.

The minimum ADC value of each tumor was determined from several regions of interest in the tumor on ADC maps.

To assess the relationship between the minimum ADC and tumor grade, we performed the Mann-Whitney U test.

A receiver operating characteristic (ROC) analysis was used to determine the cutoff value of the minimum ADC that had the best combination of sensitivity and specificity for distinguishing low- and high-grade astrocytomas.

RESULTS: Eight of the 16 patients (50%) were confirmed as having high-grade astrocytomas (WHO grades III and IV), and the other 8 patients were confirmed as having low-grade astrocytomas (WHO grade II).

The median minimum ADC of the high-grade astrocytoma (1.035 x 10(-3) mm(2) .

sec(-1)) group was significantly lower than that of the low-grade astrocytoma group (1.19 x 10(-3) mm(2) .

CONCLUSION: Measuring minimum ADC can provide valuable diagnostic information for the preoperative grading of presumptive low-grade supratentorial astrocytomas.

[MeSH-major] Algorithms. Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods

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(PMID = 18719036.001).

[ISSN] 1936-959X

[Journal-full-title] AJNR. American journal of neuroradiology

[ISO-abbreviation] AJNR Am J Neuroradiol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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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.

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(PMID = 20838306.001).

[ISSN] 1536-0229

[Journal-full-title] Clinical nuclear medicine

[ISO-abbreviation] Clin Nucl Med

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / fluorocholine; N91BDP6H0X / Choline

   

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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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[Title] Immunohistochemical appearance of HNE-protein conjugates in human astrocytomas.

Those of astrocytic origin are the most widespread of primary brain tumors and account for more then 60% of all CNS neoplasms.

The current state of knowledge on the associations between tumor etiology and oxidative stress suggests that environmental factors that cause oxidative stress could also induce and promote cancer, especially in case of hereditary predisposition.

The aim of present study was to investigate by immunohistochemistry the presence of HNE-modified proteins in different types of astrocytoma.

Our study comprised 45 astrocytic tumors.

These tumors were graded in accordance with the WHO classification as diffuse astrocytomas (DA), anaplastic astrocytomas (AA) and glioblastomas (GB), while each group comprised 15 tumors.

Slides of paraffin-embedded tumor tissue were stained with hematoxylin-eosin or were prepared for immunohistochemistry with monoclonal antibodies to HNE-histidine conjugate.

HNE positivity was proportional with malignancy of astrocytomas.

Lowest intensity of HNE immunopositivity was present in tumor cells of almost all DA, predominantly around blood vessels.

In malignant variants of astrocytoma, AA and GB, HNE positivity was moderate to strong, and diffusely distributed in all tumors.

[MeSH-major] Aldehydes / analysis. Aldehydes / metabolism. Astrocytoma / chemistry. Immunohistochemistry. Proteins / analysis. Proteins / metabolism

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(PMID = 16403961.001).

[ISSN] 0951-6433

[Journal-full-title] BioFactors (Oxford, England)

[ISO-abbreviation] Biofactors

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Aldehydes; 0 / Antibodies, Monoclonal; 0 / Proteins; 29343-52-0 / 4-hydroxy-2-nonenal

   

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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