BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical implications and prognostic value of EMMPRIN/CD147 and MMP2 expression in pediatric gliomas.

Extracellular matrix metalloproteinase inducer (EMMPRIN), a member of the immunoglobulin superfamily, is present on the surface of tumor cells where it stimulates adjacent fibroblasts to produce matrix metalloproteinases (MMPs).

We have analyzed the clinicopathological characteristics of EMMPRIN and MMP2 expression in normal brain tissue and pediatric gliomas and evaluated their prognostic value in diagnosing the latter.

Immunochemistry analysis revealed EMMPRIN and MMP2 expression in cryo-sections of pediatric gliomas (45 samples) and normal brain tissue (20 samples).

Both EMMPRIN and MMP2 were expressed in normal brain and glioma tissues with different levels of malignancy.

The intensively positive expression rates of EMMPRIN (22/27) and MMP2 (21/27) in anaplastic astrocytoma and glioblastoma tissues were significantly higher than those in normal brain and low-grade astrocytoma tissues (2/28 and (1/2)8, respectively).

The positive expression of EMMPRIN and MMP2 was associated with higher grade gliomas.

Based on these results, we conclude that EMMPRIN and MMP2 are expressed differently in normal brain and pediatric gliomas.

The detection of their co-expression may facilitate the prediction of pediatric gliomas prognosis.

[MeSH-major] Antigens, CD147 / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Matrix Metalloproteinase 2 / metabolism

[MeSH-minor] Child. Child, Preschool. Disease Progression. Female. Humans. Immunohistochemistry. Infant. Male. Prognosis

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Pathol. 2002 Apr;160(4):1215-21 [11943706.001]

[Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]

[Cites] Int J Cancer. 2003 Feb 20;103(5):647-51 [12494473.001]

[Cites] Am J Pathol. 1999 Feb;154(2):417-28 [10027400.001]

[Cites] Cancer Res. 2004 Feb 15;64(4):1229-32 [14983875.001]

[Cites] Am J Pathol. 2001 Jun;158(6):1921-8 [11395366.001]

[Cites] Brain Pathol. 2007 Jul;17(3):276-81 [17465990.001]

[Cites] Cancer Res. 2001 Mar 1;61(5):2276-81 [11280798.001]

[Cites] Pathol Int. 2006 Jul;56(7):359-67 [16792544.001]

[Cites] Rev Recent Clin Trials. 2006 May;1(2):119-31 [18473963.001]

[Cites] Int J Cancer. 2002 May 10;99(2):157-66 [11979428.001]

[Cites] Mol Cancer Res. 2005 Oct;3(10):541-51 [16254188.001]

[Cites] Cancer Gene Ther. 2003 Nov;10(11):823-32 [14605668.001]

[Cites] Cancer. 2004 Nov 1;101(9):1994-2000 [15372476.001]

[Cites] Br J Cancer. 1996 Jun;73(11):1401-8 [8645587.001]

[Cites] Cancer Res. 2005 Apr 15;65(8):3193-9 [15833850.001]

[Cites] Int J Cancer. 2003 Sep 20;106(5):745-51 [12866035.001]

[Cites] Cancer Immunol Immunother. 2008 Sep;57(9):1367-79 [18273614.001]

[Cites] Am J Pathol. 1996 Jul;149(1):273-82 [8686751.001]

[Cites] Cancer Res. 2007 May 1;67(9):4088-97 [17483319.001]

[Cites] Am J Pathol. 2005 Jan;166(1):209-19 [15632013.001]

[Cites] Oncogene. 2007 Aug 9;26(36):5229-37 [17325663.001]

[Cites] Int J Cancer. 2006 Oct 15;119(8):1800-10 [16721788.001]

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

(PMID = 18795327.001).

[ISSN] 1432-1076

[Journal-full-title] European journal of pediatrics

[ISO-abbreviation] Eur. J. Pediatr.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / BSG protein, human; 136894-56-9 / Antigens, CD147; EC 3.4.24.24 / Matrix Metalloproteinase 2

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Neoplasms are a well-established cause of medically intractable or chronic epilepsy.

Certain tumors, including gangliogliomas and dysembryoplastic neuroepithelial tumors, are well known to be associated with cortical dysplasia.

Tumor diagnoses included ganglioglioma (n=29), dysembryoplastic neuroepithelial tumor (n=10), low-grade glial/glioneuronal neoplasm (n=5), low-grade astrocytoma (n=2), angiocentric glioma (n=1), low-grade mixed glioma (n=1), dysembryoplastic neuroepithelial tumor/ganglioglioma mixed tumor (n=1), and meningioangiomatosis (n=1).

Forty-one (82%) tumors represented WHO grade-I neoplasms.

Hamartias were identified in 10 patients (20%), hippocampal sclerosis in four patients (8%), and nodular heterotopia in one patient (2%).

The true incidence of coexistent pathology (17.8% in this study) was likely underrepresented, given the limited extent of adjacent non-tumoral tissue sampling in cases of resected tumor.

Coexistent pathology may account for the incidence of recurrent or residual epilepsy in patients who undergo tumor resection.

[MeSH-major] Brain Neoplasms / pathology. Epilepsy / pathology. Glioma / pathology

[MeSH-minor] Adolescent. Adult. Brain / abnormalities. Child. Child, Preschool. Chronic Disease. Comorbidity. Female. Humans. Infant. Male. Middle Aged. Ohio / epidemiology. Retrospective Studies. Temporal Lobe / pathology. Young Adult

Genetic Alliance. consumer health - Epilepsy.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

MedlinePlus Health Information. consumer health - Epilepsy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20495542.001).

[ISSN] 1530-0285

[Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The infratentorial compartment will be the primary site for 60% to 70% of these tumors, including astrocytomas, medulloblastomas, and ependymomas.

We review current diagnostic and therapeutic approaches and outcome for children harboring the most common pediatric brain tumors: astrocytomas (low-grade and high-grade glioma), ependymoma, medulloblastoma, and craniopharyngioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 1994 Aug;12(8):1607-15 [8040673.001]

[Cites] J Neurooncol. 1994;18(1):69-81 [8057137.001]

[Cites] Cancer. 1994 Oct 15;74(8):2352-60 [7922986.001]

[Cites] N Engl J Med. 1994 Dec 1;331(22):1500-7 [7969301.001]

[Cites] Am J Clin Oncol. 1994 Dec;17(6):475-9 [7977163.001]

[Cites] J Clin Oncol. 1995 Jan;13(1):112-23 [7799011.001]

[Cites] J Neurosurg. 1995 Apr;82(4):536-47 [7897512.001]

[Cites] J Pediatr Oncol Nurs. 1995 Oct;12(4):181-7 [7495523.001]

[Cites] Neurosurgery. 1996 Apr;38(4):696-701; discussion 701-2 [8692387.001]

[Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2734-7 [8675604.001]

[Cites] J Neurosurg. 1996 Oct;85(4):618-24 [8814165.001]

[Cites] J Neurooncol. 1996 Jul;29(1):45-54 [8817415.001]

[Cites] Pediatr Neurosurg. 1996;24(1):9-23 [8817611.001]

[Cites] Pediatr Neurosurg. 1996;24(2):98-102 [8841080.001]

[Cites] Int J Radiat Oncol Biol Phys. 1996 Oct 1;36(3):549-56 [8948338.001]

[Cites] Pediatr Neurosurg. 1996 Jul;25(1):45-53 [9055335.001]

[Cites] Surg Neurol. 1997 Mar;47(3):291-9 [9068702.001]

[Cites] J Neurosurg. 2007 Jul;107(1 Suppl):5-10 [17644914.001]

[Cites] Lancet Neurol. 2007 Dec;6(12):1073-85 [18031705.001]

[Cites] Childs Nerv Syst. 2000 Jan;16(1):15-20 [10672424.001]

[Cites] Int J Radiat Oncol Biol Phys. 1999 May 1;44(2):255-63 [10760417.001]

[Cites] Childs Nerv Syst. 2000 Jun;16(6):341-50 [10933229.001]

[Cites] J Neurosurg. 1997 Aug;87(2):257-61 [9254090.001]

[Cites] J Clin Oncol. 1997 Aug;15(8):2792-9 [9256121.001]

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

[Cites] J Clin Oncol. 1998 Jan;16(1):210-21 [9440745.001]

[Cites] Int J Radiat Oncol Biol Phys. 1998 Mar 1;40(4):845-50 [9531369.001]

[Cites] Pediatr Neurol. 1998 Feb;18(2):103-15 [9535295.001]

[Cites] J Neurosurg. 1998 Jul;89(1):52-9 [9647172.001]

[Cites] Pediatr Neurosurg. 1998 Apr;28(4):215-22 [9732252.001]

[Cites] Pediatr Neurosurg. 1998 May;28(5):273-8 [9732262.001]

[Cites] Clin Neurosurg. 1997;44:559-70 [10080027.001]

[Cites] J Neurooncol. 2004 Aug-Sep;69(1-3):139-50 [15527086.001]

[Cites] Cancer. 2005 Jan 1;103(1):133-9 [15565574.001]

[Cites] Neurosurg Focus. 2003 Feb 15;14(2):e1 [15727422.001]

[Cites] Neurosurg Focus. 2002 Sep 15;13(3):e4 [15844876.001]

[Cites] J Neurosurg. 2005 Apr;102(4):629-36 [15871504.001]

[Cites] Neurosurg Focus. 2005 Jun 15;18(6A):E10 [16048286.001]

[Cites] Lancet Oncol. 2005 Aug;6(8):573-80 [16054568.001]

[Cites] Childs Nerv Syst. 2005 Aug;21(8-9):660-8 [15959733.001]

[Cites] Childs Nerv Syst. 2005 Aug;21(8-9):604-5 [16012874.001]

[Cites] Childs Nerv Syst. 2005 Aug;21(8-9):729-46 [16044343.001]

[Cites] Childs Nerv Syst. 2005 Aug;21(8-9):808-16 [16075214.001]

[Cites] Neurosurg Focus. 2006;20(1):E8 [16459998.001]

[Cites] Cancer. 2004 Aug 15;101(4):817-24 [15305415.001]

[Cites] J Pediatr. 1975 Feb;86(2):254-8 [1111694.001]

[Cites] Cancer. 1976 Apr;37(4):1944-52 [1260697.001]

[Cites] J Neurosurg. 1981 Aug;55(2):174-82 [7252539.001]

[Cites] Int J Radiat Oncol Biol Phys. 1983 Aug;9(8):1231-4 [6347998.001]

[Cites] J Neurosurg. 1984 Mar;60(3):495-9 [6699693.001]

[Cites] Neurosurgery. 1986 May;18(5):568-75 [3714005.001]

[Cites] J Neurosurg. 2006 Feb;104(2 Suppl):108-14 [16506498.001]

[Cites] Childs Nerv Syst. 2006 Oct;22(10):1296-300 [16761160.001]

[Cites] J Neurosurg. 2007 Jan;106(1 Suppl):1-2; discussion 2 [17233304.001]

[Cites] Eur J Cancer. 2007 Apr;43(6):1037-44 [17349783.001]

[Cites] Cancer. 2007 Jul 15;110(2):432-41 [17559078.001]

[Cites] J Neurosurg. 2000 Oct;93(4):605-13 [11014538.001]

[Cites] Am J Pathol. 2001 Apr;158(4):1525-32 [11290570.001]

[Cites] Neuro Oncol. 1999 Jul;1(3):232-50 [11550316.001]

[Cites] Childs Nerv Syst. 2001 Sep;17(9):538-42; discussion 543 [11585328.001]

[Cites] N Engl J Med. 2002 Feb 7;346(6):420-7 [11832530.001]

[Cites] Eur Radiol. 2002 Jun;12(6):1342-8 [12042937.001]

[Cites] J Clin Oncol. 2003 Apr 15;21(8):1581-91 [12697884.001]

[Cites] Med Pediatr Oncol. 2003 Aug;41(2):123-7 [12825216.001]

[Cites] J Clin Oncol. 2003 Aug 1;21(15):2968-73 [12885817.001]

[Cites] Mod Pathol. 2003 Oct;16(10):980-91 [14559980.001]

[Cites] Childs Nerv Syst. 2004 Mar;20(3):143-53 [14669023.001]

[Cites] Pediatr Blood Cancer. 2004 May;42(5):461-4 [15049021.001]

[Cites] J Neurosurg. 1986 Dec;65(6):751-5 [3772472.001]

[Cites] J Neurooncol. 1988 Dec;6(4):309-17 [3221258.001]

[Cites] J Neurooncol. 1989 Jul;7(2):165-77 [2550594.001]

[Cites] Neurosurgery. 1989 Dec;25(6):959-64 [2513523.001]

[Cites] J Neurosurg. 1990 Mar;72(3):408-17 [2303876.001]

[Cites] Neuropediatrics. 1991 Feb;22(1):36-42 [2038426.001]

[Cites] Neurosurgery. 1991 May;28(5):659-64; discussion 664-5 [1876243.001]

[Cites] Neurosurgery. 1991 May;28(5):666-71; discussion 671-2 [1876244.001]

[Cites] J Neurosurg. 1991 Oct;75(4):575-82 [1885975.001]

[Cites] J Neuroradiol. 1991;18(2):201-9 [1919685.001]

[Cites] Pediatr Neurosurg. 1990-1991;16(2):57-65 [2132926.001]

[Cites] J Neurooncol. 1992 Jul;13(3):283-90 [1517804.001]

[Cites] J Neurosurg. 1992 Oct;77(4):545-50 [1527612.001]

[Cites] Radiother Oncol. 1993 Jan;26(1):1-10 [8438080.001]

[Cites] Childs Nerv Syst. 1993 Feb;9(1):7-9 [8481945.001]

[Cites] J Neurooncol. 1993 Feb;15(2):125-31 [8509817.001]

[Cites] Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30 [8133987.001]

[Cites] Neurosurgery. 1994 Feb;34(2):350-2; discussion 352-3 [8177398.001]

(PMID = 18952580.001).

[ISSN] 1708-8283

[Journal-full-title] Journal of child neurology

[ISO-abbreviation] J. Child Neurol.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R13 NS040925; United States / NINDS NIH HHS / NS / 5R13NS040925-09

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

[Publication-country] United States

[Number-of-references] 92

[Other-IDs] NLM/ NIHMS487102; NLM/ PMC3714852

   

Advertisement

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Quantitative PCR analysis of the expression profile of genes related to multiple drug resistance in tumors of the central nervous system.

METHODS: Eighty microdissected brain tumor samples from 79 patients were analyzed by RQ-PCR for the genes MDR1, MRP1, MRP3, LRP and BCRP.

Histological diagnoses: 21 astrocytomas I and II, 28 astrocytomas III and glioblastomas, 17 medulloblastomas, 8 ependymomas, and 6 oligodendrogliomas.

Low-grade astrocytomas expressed high MDR1 (P = 0.001), MRP3 (P = 0.01) and LRP (P = 0.02) levels.

The profile of gene expression of primary pilocytic astrocytomas of the hypothalamus and of the other locations was similar.

Increased expression of resistance genes, separately or jointly, was not correlated with shorter overall survival in patients with medulloblastomas/PNET and malignant gliomas.

CONCLUSIONS: Drug resistance genes do not explain the higher sensitivity of gliomas of the hypothalamus/pituitary/optic pathways to chemotherapy.

The increased expression of resistance genes had no impact on the overall survival of patients with medulloblastomas/PNET and high grade gliomas.

High MDR1, MRP3 and LRP levels may be implicated in the primary resistance of pilocytic astrocytomas to chemotherapy.

[MeSH-major] Central Nervous System Neoplasms / genetics. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / physiology. Reverse Transcriptase Polymerase Chain Reaction / methods

[MeSH-minor] Adolescent. Adult. Aged. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Brain Neoplasms / mortality. Calibration. Child. Child, Preschool. DNA Primers. Female. Gene Expression Profiling. Glioma / drug therapy. Glioma / genetics. Glioma / mortality. Humans. Immunohistochemistry. Infant. Male. Medulloblastoma / drug therapy. Medulloblastoma / genetics. Medulloblastoma / mortality. Middle Aged. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Survival Analysis

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375.001]

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

[Cites] Clin Neuropathol. 2004 Jan-Feb;23(1):21-7 [14986930.001]

[Cites] Clin Chem. 2002 Jun;48(6 Pt 1):811-7 [12028995.001]

[Cites] Pediatr Neurosurg. 1995;23(6):283-91; discussion 291-2 [8743996.001]

[Cites] Blood. 1999 Aug 1;94(3):1086-99 [10419902.001]

[Cites] Blood. 1998 Mar 15;91(6):2092-8 [9490695.001]

[Cites] Int J Cancer. 2001 Nov 1;94(3):377-82 [11745417.001]

[Cites] Nat Struct Mol Biol. 2004 Oct;11(10):918-26 [15452563.001]

[Cites] Epilepsia. 2005 Jun;46(6):849-57 [15946326.001]

[Cites] Annu Rev Biochem. 1993;62:385-427 [8102521.001]

[Cites] Anticancer Drugs. 1999 Nov;10(10):861-72 [10630353.001]

[Cites] Br J Cancer. 1996 Oct;74(8):1263-8 [8883415.001]

[Cites] Acta Neuropathol. 1997 Dec;94(6):605-11 [9444363.001]

[Cites] Int J Cancer. 2001 Jul 1;93(1):62-6 [11391622.001]

[Cites] Br J Neurosurg. 1994;8(5):585-91 [7857540.001]

[Cites] Virchows Arch. 1994;425(2):133-8 [7952498.001]

[Cites] J Neurooncol. 2005 Sep;74(2):113-21 [16193381.001]

[Cites] J Neurosurg. 1990 Jan;72(1):96-101 [2294193.001]

[Cites] Biol Pharm Bull. 2002 Nov;25(11):1391-400 [12419946.001]

[Cites] An Acad Bras Cienc. 2001 Mar;73(1):57-69 [11246270.001]

[Cites] J Neurosurg. 1994 Nov;81(5):690-8 [7931615.001]

[Cites] J Neurooncol. 1998 Oct;40(1):11-8 [9874181.001]

[Cites] J Cell Sci. 1993 Sep;106 ( Pt 1):23-9 [8270627.001]

[Cites] Pediatr Pathol Lab Med. 1996 Jul-Aug;16(4):551-61 [9025853.001]

[Cites] Brain Tumor Pathol. 1999;16(1):23-7 [10532420.001]

[Cites] Int J Cancer. 2002 Mar 10;98 (2):173-80 [11857404.001]

[Cites] Cancer Res. 2005 Dec 15;65(24):11419-28 [16357150.001]

[Cites] Curr Drug Deliv. 2004 Jan;1(1):27-42 [16305368.001]

(PMID = 17429576.001).

[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 / DNA Primers; 0 / RNA, Neoplasm

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cdk9 regulates neural differentiation and its expression correlates with the differentiation grade of neuroblastoma and PNET tumors.

Cdk9 and Cyclin T1 expression levels were monitored during the differentiation program of neuroblastoma and astrocytoma cell lines.

Our results suggest that Cdk9/Cyclin T1 complex may be required for neuron differentiation induced by retinoic acid, because the expression level of the complex varies during differentiation, but no significant changes were observed in its expression in the astrocytoma cell line.

In addition, the expression of Cdk9 and Cyclin T1 was evaluated by immunohistochemistry in samples of neuroblastoma, PNET (Primary Neuroectodermal Tumor) and astrocytoma tumors of different grades, in order to assess whether there was a correlation between Cdk9 expression and tumor grading.

Our results show that in neuroblastoma and PNET tumor samples Cdk9 is more expressed the more differentiated the tumor is.

Conversely, no significant alteration of Cdk9 expression was observed in astrocytoma tumor samples of different grades, thus confirming the results obtained for the cell lines.

[MeSH-minor] Astrocytes / cytology. Astrocytes / drug effects. Astrocytes / pathology. Cell Differentiation. Cell Line, Tumor. Cyclin T. Cyclins / analysis. Cyclins / genetics. Cyclins / metabolism. Humans. Immunohistochemistry. RNA, Messenger / analysis. RNA, Messenger / metabolism. Tretinoin / pharmacology

Genetic Alliance. consumer health - Neuroblastoma.

MedlinePlus Health Information. consumer health - Neuroblastoma.

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15753651.001).

[ISSN] 1538-4047

[Journal-full-title] Cancer biology & therapy

[ISO-abbreviation] Cancer Biol. Ther.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / CCNT1 protein, human; 0 / Cyclin T; 0 / Cyclins; 0 / RNA, Messenger; 5688UTC01R / Tretinoin; EC 2.7.11.22 / Cyclin-Dependent Kinase 9

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Altered expression of immune defense genes in pilocytic astrocytomas.

Pilocytic astrocytoma (WHO grade I) is a circumscribed, slowly growing, benign astrocytoma that most frequently develops in the cerebellar hemispheres and in midline structures and occurs predominantly in childhood and adolescence.

In contrast to diffusely infiltrating gliomas in adults (e.g. grade II astrocytomas, oligodendrogliomas), survival of patients with pilocytic astrocytoma is excellent after surgical intervention.

To search for potential molecular mechanisms underlying its benign biologic behavior, we compared gene expression profiles of pilocytic astrocytomas (8 cases) with those of normal cerebellum (4 cases), low-grade astrocytomas (WHO grade II; 15 cases), and oligodendrogliomas (WHO grade II; 17 cases) by cDNA array analysis.

A number of immune system-related genes such as HLA-DRalpha, HLA-DPB1, HLA-DQB1, IgG3, IgGK, FCER1G, A2M, FCRN, IFI-56K, and DAP12 were upregulated in pilocytic astrocytomas relative to normal cerebellum, grade II astrocytomas, and oligodendrogliomas.

Genes expressed at higher levels in pilocytic astrocytomas than in grade II astrocytomas and oligodendrogliomas include HLA-DRalpha, HLA-DPA1, HLA-DPB1, HLA-DQB1, A2M, TIMP1, TIMP2, CDKN1A, and SOCS3 and those expressed at lower levels include EGFR and PDGFRA.

Hierarchical clustering analysis using the entire set of 1176 genes distinguished pilocytic astrocytomas from grade II astrocytomas and oligodendrogliomas.

Clustering analysis using selected subgroups of genes based on their molecular functions revealed that immune system-related genes (75 genes) or cell adhesion, migration, and angiogenesis-related genes (69 genes) showed similar power to the entire gene set for separation of pilocytic astrocytomas from diffusely infiltrating low-grade gliomas.

Immunohistochemistry revealed that HLA-DRalpha is expressed diffusely in neoplastic cells in pilocytic astrocytomas, whereas in oligodendrogliomas, expression was limited to scattered reactive astrocytes.

These results suggest that gene expression profiles of pilocytic astrocytomas differ significantly from those of diffusely infiltrating low-grade gliomas and that their benign biologic behavior may be related to upregulation of immune defense-associated genes.

[MeSH-major] Astrocytoma / genetics. Astrocytoma / immunology. Brain Neoplasms / genetics. Brain Neoplasms / immunology. Gene Expression. Immunity / genetics

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16215461.001).

[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 / HLA-DR Antigens; 0 / RNA, Messenger

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade.

In this study, we investigated the expression of Kir 4.1 mRNA and protein in 80 cases of human astrocytic tumors by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry, respectively.

The correlation between Kir 4.1 expression and pathologic grade of astrocytic tumors was further analyzed.

The results showed that the expression of Kir 4.1 mRNA and protein, as well as the Kir 4.1 immunoreactivity score (IRS), increased markedly with increasing pathologic grade.

Therefore, Kir 4.1 may be a new biomarker for astrocytic tumors.

It may also be an attractive therapy target for human astrocytic tumors.

[MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism. Potassium Channels, Inwardly Rectifying / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Statistics as Topic. Tumor Cells, Cultured

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18191638.001).

[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 / Kcnj10 (channel); 0 / Neoplasm Proteins; 0 / Potassium Channels, Inwardly Rectifying

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Brain tumors, especially high-grade gliomas, can present with focal or generalized signs due to mass effect, parenchymal infiltration and destruction.

Microscopic total tumor excision was done and histopathological analysis revealed that these tumors were glioblastoma multiforme.

CONCLUSIONS: Physicians should keep brain tumors in mind in the case of patients who present with atypical symptoms such as those reported here.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Arch Neurol. 2003 Mar;60(3):437-40 [12633158.001]

[Cites] Expert Rev Neurother. 2007 Apr;7(4):343-9 [17425489.001]

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

[Cites] Neurology. 2010 Feb 16;74(7):610-2 [20157165.001]

[Cites] Neurology. 1984 Jun;34(6):837-9 [6539452.001]

[Cites] J Neurosurg. 1960 Jul;17:736-50 [14439403.001]

[Cites] J Formos Med Assoc. 2003 Oct;102(10):737-40 [14691602.001]

[Cites] JAMA. 2005 Feb 2;293(5):557-64 [15687310.001]

[Cites] Mayo Clin Proc. 2007 Oct;82(10):1271-86 [17908533.001]

[Cites] West J Med. 1995 Jul;163(1):19-25 [7667978.001]

[Cites] Acta Neurol Scand. 1994 Sep;90(3):218-21 [7847064.001]

[Cites] Neurology. 1993 Sep;43(9):1678-83 [8414011.001]

[Cites] Am Fam Physician. 2008 May 15;77(10):1423-30 [18533376.001]

[Cites] Neurosurgery. 1996 Aug;39(2):253-8; discussion 258-9 [8832661.001]

[Cites] J Neurosurg. 1958 Sep;15(5):489-503 [13576192.001]

(PMID = 21206896.001).

[ISSN] 2152-7806

[Journal-full-title] Surgical neurology international

[ISO-abbreviation] Surg Neurol Int

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Other-IDs] NLM/ PMC3011111

[Keywords] NOTNLM ; Astrocytoma / brain tumor / glioblastoma multiforme / presentation / symptom

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Inhibition of all-trans retinoic acid on MDM2 gene expression in astrocytoma cell line SHG-44.

OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in astrocytoma cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human astrocytoma.

The expressions of MDM2 protein in WHO grade II and grade IV astrocytomas were determined by immunohistochemical streptavidin-peroxidase method.

Moreover, the percentages of MDM2-positive protein were 24.00% (6/25) and 56.52% (13/23) (chi(2) = 5.298, P = 0.021) in WHO grade II and grade IV astrocytomas, respectively, suggesting that the expression of MDM2 protein may increase along with the elevation of astrocytoma malignancy.

CONCLUSION: ATRA can inhibit MDM2 gene expression in SHG-44 cells, and MDM2 is related to astrocytoma progression.

[MeSH-minor] Astrocytoma / metabolism. Astrocytoma / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Size / drug effects. Humans. Oligonucleotide Array Sequence Analysis / methods. Time Factors

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

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

[Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):731-6 [15644444.001]

[Cites] Ai Zheng. 2006 Dec;25(12):1470-6 [17166369.001]

[Cites] Gene. 2000 Jan 25;242(1-2):15-29 [10721693.001]

[Cites] Mol Cancer Ther. 2006 Sep;5(9):2358-65 [16985070.001]

[Cites] Neurosurgery. 2000 Feb;46(2):419-30 [10690732.001]

[Cites] Cancer Res. 2005 Jul 1;65(13):5481-4 [15994915.001]

[Cites] Cancer Res. 2005 Sep 15;65(18):8200-8 [16166295.001]

[Cites] FEBS Lett. 2005 Jul 18;579(18):3965-9 [15996664.001]

[Cites] Mol Cell Biol. 2006 Jan;26(1):192-8 [16354690.001]

[Cites] Zhonghua Zhong Liu Za Zhi. 1984 Jul;6(4):241-3 [6525937.001]

[Cites] Brain Res Mol Brain Res. 2001 Feb 19;87(1):100-8 [11223164.001]

[Cites] Mol Cancer Res. 2003 Dec;1(14 ):993-1000 [14707282.001]

(PMID = 18839023.001).

[ISSN] 1673-7067

[Journal-full-title] Neuroscience bulletin

[ISO-abbreviation] Neurosci Bull

[Language] eng

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

[Publication-country] Singapore

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

An increasing body of evidence suggests that astrocytic gliomas of the central nervous system may be derived from gliotypic neural stem cells.

However, when induced to differentiate, neural stem cells give rise to intermediate progenitors that transiently exhibit multiple glioma characteristics, including aneuploidy, loss of growth-contact inhibition, alterations in cell cycle, and growth factor insensitivity.

Further examination of progenitor populations revealed a subset of cells defined by the aberrant expression of (the pathological glioma marker) class III beta-tubulin that exhibit intrinsic parental properties of gliomas, including multilineage differentiation and continued proliferation in the absence of a complex cellular regulatory environment.

MedlinePlus Health Information. consumer health - Stem Cells.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18988710.001).

[ISSN] 1549-4918

[Journal-full-title] Stem cells (Dayton, Ohio)

[ISO-abbreviation] Stem Cells

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01 HL070143; United States / NICHD NIH HHS / HD / T32 HD043730; United States / NINDS NIH HHS / NS / NS055165; United States / NINDS NIH HHS / NS / NS37556; United States / NICHD NIH HHS / HD / T32HD043730; United States / NHLBI NIH HHS / HL / HL70143; United States / NINDS NIH HHS / NS / NS46384; United States / NINDS NIH HHS / NS / R01 NS037556; United States / NINDS NIH HHS / NS / R01 NS055165; United States / NINDS NIH HHS / NS / R21 NS046384

[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 / Biomarkers, Tumor; 0 / Tubulin

[Other-IDs] NLM/ NIHMS686089; NLM/ PMC4425277

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Magnetic resonance imaging is a routine diagnostic measure for a suspected intracerebral mass.

Further diagnostic procedures as well as the interpretation of the findings vary depending on the tumor location.

Supratentorial tumors include astrocytoma, differentiated by their circumscribed and diffuse growth, ganglioglioma, ependyoma, neurocytoma, primitive neuroectodermal tumors (PNET), oligodendroglioma, dysem-bryoplastic neuroepithelial tumors (DNET), meningoangiomatosis, pineal tumors, hamatoma, lymphoma, craniopharyngeoma and metastases.

The most common sub-forms, especially of astrocytoma, will also be presented.

MedlinePlus Health Information. consumer health - CT Scans.

MedlinePlus Health Information. consumer health - MRI Scans.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Childs Nerv Syst. 2006 Jun;22(6):577-85 [16555075.001]

[Cites] Cancer. 2004 Jul 1;101(1):146-55 [15222000.001]

[Cites] Pediatr Dev Pathol. 1999 Nov-Dec;2(6):582-7 [10508884.001]

[Cites] J Neurosurg Sci. 2005 Sep;49(3):73-6 [16288189.001]

[Cites] Childs Nerv Syst. 2003 Jun;19(5-6):292-7 [12750935.001]

[Cites] Neurology. 1996 Jun;46(6):1669-73 [8649567.001]

[Cites] Childs Nerv Syst. 1998 Aug;14(8):357-61 [9753400.001]

[Cites] Nat Clin Pract Neurol. 2007 Jan;3(1):24-35 [17205072.001]

[Cites] Endocr Rev. 2006 Jun;27(4):371-97 [16543382.001]

[Cites] J Neurooncol. 2001 Sep;54(3):251-61 [11767291.001]

[Cites] AJNR Am J Neuroradiol. 1999 Nov-Dec;20(10):1839-41 [10588106.001]

[Cites] AJNR Am J Neuroradiol. 2006 Jan;27(1):85-93 [16418363.001]

[Cites] J Neurooncol. 1997 Aug;34(1):61-78 [9210053.001]

[Cites] AJNR Am J Neuroradiol. 2001 Sep;22(8):1632 [11559521.001]

[Cites] J Neurooncol. 1997 Aug;34(1):37-59 [9210052.001]

[Cites] Childs Nerv Syst. 2005 Aug;21(8-9):635-9 [16078078.001]

[Cites] J Neurooncol. 2004 Nov;70(2):161-81 [15674476.001]

[Cites] Australas Radiol. 2005 Oct;49(5):433-7 [16174188.001]

[Cites] Acta Neurochir (Wien). 2000;142(7):829-31 [10955682.001]

[Cites] Mo Med. 1990 Dec;87(12):889-91 [2270072.001]

[Cites] Neurocirugia (Astur). 2005 Dec;16(6):518-22 [16378134.001]

[Cites] Childs Nerv Syst. 2003 Sep;19(9):650-4 [12720031.001]

[Cites] J Neurol Neurosurg Psychiatry. 1994 Dec;57(12):1497-502 [7798980.001]

[Cites] J Comput Assist Tomogr. 2004 May-Jun;28(3):407-13 [15100549.001]

[Cites] Arq Neuropsiquiatr. 2006 Sep;64(3A):613-8 [17119805.001]

[Cites] J Neuroimaging. 2006 Jan;16(1):52-8 [16483277.001]

[Cites] Childs Nerv Syst. 2006 May;22(5):514-6 [16369853.001]

[Cites] Cell Tissue Res. 2002 Dec;310(3):257-70 [12457224.001]

[Cites] J Neurooncol. 1999;44(3):275-81 [10720207.001]

[Cites] Neurology. 1998 Oct;51(4):1046-50 [9781527.001]

[Cites] J Nippon Med Sch. 2000 Oct;67(5):388-91 [11031374.001]

[Cites] Neurology. 2002 Sep 24;59(6):947-9 [12297589.001]

[Cites] Neuroradiology. 1992;34(3):173-8 [1630604.001]

[Cites] Semin Oncol. 2004 Oct;31(5):595-604 [15497113.001]

[Cites] Radiology. 2003 Jul;228(1):193-9 [12832582.001]

[Cites] Neuroradiology. 2006 Jan;48(1):1-7 [16237548.001]

[Cites] AJR Am J Roentgenol. 1998 Mar;170(3):804-5 [9490984.001]

[Cites] Cancer Imaging. 2006 Oct 31;6:S178-84 [17114073.001]

[Cites] Radiographics. 2002 Sep-Oct;22(5):1177-89 [12235346.001]

[Cites] Curr Neurol Neurosci Rep. 2003 May;3(3):193-9 [12691623.001]

[Cites] Curr Opin Neurol. 1993 Dec;6(6):882-7 [8293162.001]

[Cites] Semin Oncol. 2000 Jun;27(3 Suppl 6):1-10 [10866344.001]

[Cites] Lancet. 2004 May 8;363(9420):1535-43 [15135603.001]

[Cites] Arch Iran Med. 2007 Apr;10 (2):194-8 [17367223.001]

[Cites] J Neurooncol. 2004 Nov;70(2):183-202 [15674477.001]

[Cites] Am J Dis Child. 1988 May;142(5):486 [3358385.001]

[Cites] Neurosurgery. 2005 Nov;57(5 Suppl):S10-23; discusssion S1-4 [16237282.001]

[Cites] Eur Radiol. 2002 Jul;12 (7):1829-36 [12111075.001]

[Cites] Expert Rev Neurother. 2006 Apr;6(4):519-32 [16623651.001]

[Cites] Clin Radiol. 2006 Apr;61(4):348-57 [16546465.001]

[Cites] Australas Radiol. 2000 Nov;44(4):460-3 [11103549.001]

[Cites] Surg Neurol. 1998 Feb;49(2):197-204 [9457271.001]

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

[Cites] Curr Opin Investig Drugs. 2005 Dec;6(12 ):1200-14 [16370386.001]

[Cites] AJNR Am J Neuroradiol. 2000 Sep;21(8):1470-7 [11003281.001]

[Cites] J Neurooncol. 1996 Jul;29(1):1-7 [8817411.001]

[Cites] Cancer J. 2006 Jan-Feb;12(1):1-13 [16613654.001]

[Cites] Neurosurg Focus. 2005 Jun 15;18(6A):E7 [16048293.001]

[Cites] Clin Neurol Neurosurg. 2006 Jun;108(4):363-8 [15893874.001]

[Cites] J Belge Radiol. 1994 Oct;77(5):221 [7961378.001]

(PMID = 17541538.001).

[ISSN] 0033-832X

[Journal-full-title] Der Radiologe

[ISO-abbreviation] Radiologe

[Language] ger

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

[Publication-country] Germany

[Number-of-references] 30

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Neuropathologic diagnoses were cavernoma in three cases, astrocytoma (grade 2) in two cases, arteriovenous malformation in two cases, gliosis in two cases and ganglioglioma in one case.

Patients who had post-operative seizures may also achieve long-term seizure decrease or freedom in three cases: case 5 (E4-E2), case 6 (E4-E2) and case 7 (E3-E1).

Genetic Alliance. consumer health - Epilepsy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17535567.001).

[ISSN] 0161-6412

[Journal-full-title] Neurological research

[ISO-abbreviation] Neurol. Res.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] England

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Application of (1)H MR spectroscopic imaging in radiation oncology: choline as a marker for determining the relative probability of tumor progression after radiation of glial brain tumors].

PURPOSE: To determine the relative signal intensity ratios of choline (Cho), phosphocreatine (CR) and N-acetyl-aspartate (NAA) in MR spectroscopic imaging (proton-MRSI) for differentiating progressive tumors (PT) from non-progressive tumors (nPT) in follow-up and treatment planning of gliomas.

Threshold values to indicate the probability of a progressive tumor were also calculated.

MATERIAL AND METHODS: Thirty-four patients with histologically proven gliomas showing a suspicious brain lesion in MRI after stereotactic radiotherapy were evaluated on a 1.5 Tesla unit (Magnetom Vision, Siemens, Erlangen, Germany) using 2D proton MRSI (repetition time/echo time = 1500/135 msec, PRESS; voxel size 9 x 9 x 15 mm (3)).

PT and nPT were differentiated between on the basis of clinical course and follow-up by MRI, CT and positron emission tomography.

RESULTS: The Cho parameter and the relative signal intensity ratios of Cr and NAA were most effective in differentiating between PT and nPT.

CONCLUSION: (1)H-MRSI has a high sensitivity and specificity for differentiating between therapy-related effects and the relapse of irradiated gliomas.

[MeSH-major] Aspartic Acid / analogs & derivatives. Astrocytoma / diagnosis. Astrocytoma / radiotherapy. Brain / radiation effects. Brain Neoplasms / diagnosis. Brain Neoplasms / radiotherapy. Choline / metabolism. Cranial Irradiation. Glioblastoma / diagnosis. Glioblastoma / radiotherapy. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy. Neoplasm Recurrence, Local / diagnosis. Oligodendroglioma / diagnosis. Oligodendroglioma / radiotherapy. Phosphocreatine / metabolism. Stereotaxic Techniques

[MeSH-minor] Adult. Chemotherapy, Adjuvant. Combined Modality Therapy. Contrast Media. Diagnosis, Differential. Disease Progression. Female. Follow-Up Studies. Gadolinium DTPA. Humans. Male. Middle Aged. Neoadjuvant Therapy. Predictive Value of Tests. Radiotherapy Planning, Computer-Assisted. Radiotherapy, Adjuvant. Reference Values

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - MRI Scans.

Hazardous Substances Data Bank. (L)-ASPARTIC ACID .

Hazardous Substances Data Bank. CHOLINE CHLORIDE .

Hazardous Substances Data Bank. GADOPENTETATE DIMEGLUMINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16703499.001).

[ISSN] 1438-9029

[Journal-full-title] RöFo : Fortschritte auf dem Gebiete der Röntgenstrahlen und der Nuklearmedizin

[ISO-abbreviation] Rofo

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Contrast Media; 020IUV4N33 / Phosphocreatine; 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; K2I13DR72L / Gadolinium DTPA; N91BDP6H0X / Choline

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We analyzed the genomic region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7 pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83 oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23 pituitary adenomas.

A total of 221 somatic IDH1 mutations were detected and the highest frequencies occurred in diffuse astrocytomas (68%), oligodendrogliomas (69%), oligoastrocytomas (78%) and secondary glioblastomas (88%).

The very high frequency of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas suggests a role in early tumor development.

[MeSH-minor] Astrocytoma / genetics. Astrocytoma / pathology. Base Sequence. DNA Mutational Analysis. Disease Progression. Gene Frequency. Glioblastoma / genetics. Glioblastoma / pathology. Glioma / etiology. Glioma / pathology. Humans. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Polymerase Chain Reaction

MedlinePlus Health Information. consumer health - Brain Tumors.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18985363.001).

[ISSN] 1432-0533

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

To further address the role of NDRG2 as a candidate tumor suppressor in human gliomas, we analyzed 67 astrocytic tumors (10 diffuse astrocytomas, 11 anaplastic astrocytomas, 34 primary glioblastomas and 12 secondary glioblastomas) for NDRG2 gene mutation, promoter methylation and expression at the mRNA and protein levels.

Using real-time reverse transcription PCR analysis, we found decreased NDRG2 mRNA levels in primary glioblastomas as compared to diffuse and anaplastic astrocytomas.

Mutational analysis of the entire NDRG2 coding sequence did not reveal any tumor-associated DNA sequence alterations.

In contrast to primary glioblastomas, NDRG2 promoter hypermethylation was detected in only 1 of 11 anaplastic astrocytomas (9%) and was absent in 10 diffuse astrocytomas and 12 secondary glioblastomas.

Taken together, our data support NDRG2 as a candidate tumor suppressor gene that is epigenetically silenced in the majority of primary glioblastomas, but not in lower grade astrocytomas and secondary glioblastomas.

[MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 14. DNA Methylation. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics

[MeSH-minor] Down-Regulation. Gene Silencing. Genes, Tumor Suppressor. Humans. Immunohistochemistry. RNA, Messenger / analysis

Genetic Alliance. consumer health - Glioblastoma.

MedlinePlus Health Information. consumer health - Brain Tumors.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2008 Wiley-Liss, Inc.

(PMID = 18709645.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / NDRG2 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Whole-genome profiling of pediatric diffuse intrinsic pontine gliomas highlights platelet-derived growth factor receptor alpha and poly (ADP-ribose) polymerase as potential therapeutic targets.

PURPOSE: Diffuse intrinsic pontine glioma (DIPG) is one of the most devastating of pediatric malignancies and one for which no effective therapy exists.

A major contributor to the failure of therapeutic trials is the assumption that biologic properties of brainstem tumors in children are identical to cerebral high-grade gliomas of adults.

A better understanding of the biology of DIPG itself is needed in order to develop agents targeted more specifically to these children's disease.

Herein, we address this lack of knowledge by performing the first high-resolution single nucleotide polymorphism (SNP) -based DNA microarray analysis of a series of DIPGs.

RESULTS: Analysis of DIPG copy number alterations showed recurrent changes distinct from those of pediatric supratentorial high-grade astrocytomas.

Our findings of recurrent involvement of the PDGFR pathway as well as defects in DNA repair pathways coupled with gain of PARP-1 highlight two potential, biologically based, therapeutic targets directed specifically at this devastating disease.

[MeSH-major] Brain Stem Neoplasms / genetics. Glioma / genetics. Poly(ADP-ribose) Polymerases / genetics. Polymorphism, Single Nucleotide. Receptor, Platelet-Derived Growth Factor alpha / genetics

[MeSH-minor] Autopsy. Case-Control Studies. Child. Child, Preschool. DNA Repair / genetics. DNA, Neoplasm / analysis. Female. Gene Dosage. Humans. Infant. Infant, Newborn. Loss of Heterozygosity. Male. Oligonucleotide Array Sequence Analysis

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20142589.001).

[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] Canada / Canadian Institutes of Health Research / / MOP 82727

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

High-resolution magic angle spinning (HRMAS) (1)H NMR of biopsy tissue provides a biochemical profile that has potential diagnostic and prognostic value, and can aid interpretation of the lower-resolution (1)H-NMR spectra obtained in vivo.

In addition, we have compared biochemical changes that occur in normal rat brain during HRMAS (spun continuously at 5 kHz for 4 h at 4 degrees C as could be required for a two-dimensional acquisition) with those that occur in biopsy samples from low-grade and high-grade adult human astrocytomas, during the same HRMAS procedure.

In particular, the 18% total creatine increase observed is unlikely to be de novo synthesis of creatine.

[MeSH-major] Biomarkers, Tumor / analysis. Brain Ischemia / metabolism. Brain Ischemia / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Magnetic Resonance Spectroscopy / methods. Specimen Handling / methods

[MeSH-minor] Animals. Biopsy / methods. Cell Line, Tumor. Female. Glioma / metabolism. Glioma / pathology. Humans. Protons. Rats. Rats, Wistar. Reproducibility of Results. Sensitivity and Specificity. Spin Labels

MedlinePlus Health Information. consumer health - Brain Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.

(PMID = 18666093.001).

[ISSN] 0952-3480

[Journal-full-title] NMR in biomedicine

[ISO-abbreviation] NMR Biomed

[Language] eng

[Grant] United Kingdom / Cancer Research UK / / C1459/A2592

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

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protons; 0 / Spin Labels

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cerebrospinal fluid cytologic findings of a pleomorphic xanthoastrocytoma: a case report.

BACKGROUND: Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic neoplasm with a relatively favorable prognosis.

Characteristic histologic features include pleomorphic tumor cells and lipidized cells expressing glial fibrillary acidic protein (GFAP), corresponding to a World Health Organization grade 2 tumor.

Computed tomography of the central nervous system revealed a supracallous periventricular tumor mass suggestive of either a lymphoma or a metastatic carcinoma.

CSF revealed 18 cells/mm3 and contained numerous tumor cells highly pleomorphic in size and shape.

Some atypical cells of moderate size were closely packed with well-defined cytoplasmic limits and a vacuolated appearance, suggesting an epithelial proliferation.

A primitive glial proliferation was found, and paraffin-embedded tumor tissue obtained by biopsy confirmed the diagnosis of anaplastic PXA.

[MeSH-major] Astrocytoma / cerebrospinal fluid. Astrocytoma / pathology. Brain Neoplasms / cerebrospinal fluid. Brain Neoplasms / pathology

Genetic Alliance. consumer health - Pleomorphic xanthoastrocytoma.

MedlinePlus Health Information. consumer health - Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21053559.001).

[ISSN] 0001-5547

[Journal-full-title] Acta cytologica

[ISO-abbreviation] Acta Cytol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Operative case of isomorphic astrocytoma].

Diffuse astrocytomas are classified as WHO Grade II tumors.

Recently, a subtype presenting with better prognosis has been proposed, and it is known as "isomorphic astrocytoma."

A clinical case that we encountered was believed to be categorized as this subtype; it has been presented in this report.

The tumor was resected under awake surgery.

The pathological diagnosis was diffuse astrocytoma, but this tumor was considered to be the isomorphic subtype.

Some parts of the tumor showed a relatively high MIB-1 labeling index (LI) of 9.2%, and additional 50-Gy radiotherapy was performed.

Isomorphic astrocytoma is characterized by prolonged epileptic seizures, a low MIB-1 LI, and better prognosis.

In our case, since the MIB-1 LI was higher in some parts of the tumor, the appropriate therapy for WHO Grade II tumors was performed.

However, this case was considered representative of isomorphic astrocytoma.

No reports of this tumor subtype have been previously described in Japan.

Therefore, this report is the first case of isomorphic astrocytoma reported to Japanese literature.

[MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

MedlinePlus Health Information. consumer health - Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17713125.001).

[ISSN] 1881-6096

[Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo

[ISO-abbreviation] Brain Nerve

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Aberrant hypermethylation of p14ARF and O6-methylguanine-DNA methyltransferase genes in astrocytoma progression.

The aim of the present study was to elucidate genetic alterations that are critically involved in astrocytoma progression.

We characterized 27 World Health Organization grade II fibrillary astrocytomas which later underwent recurrence or progression, paying specific attention to the CpG island methylation status of critical growth regulatory genes. p14(ARF) and O(6)-methylguanine-DNA methyltransferase (MGMT) hypermethylation represented frequent events (26% and 63%, respectively), which were mutually exclusive except in one case, with alternate or simultaneous methylation of these two genes occurring in 85% of our tumor series.

Methylation of the p21(Waf1/Cip1), p27(Kip1) and p73 genes and homozygous deletion of the p16(INK4a), p15(INK4b) and p14(ARF) genes were not detected in any of the primary low-grade tumors.

On analysis of their respective recurrent tumors, five of six patients whose primary low-grade tumors carried p14(ARF) methylation exhibited homozygous co-deletions of the p14(ARF), p15(INK4b) and p16(INK4a) genes, which were restricted to glioblastoma as the most malignant end point.

Our findings suggest that p14(ARF) hypermethylation and MGMT hypermethylation constitute distinct molecular pathways of astrocytoma progression, which could differ in biological behavior and clinical outcome.

[MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. CpG Islands / physiology. Neoplasm Recurrence, Local / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Tumor Suppressor Protein p14ARF / metabolism

[MeSH-minor] Adult. Aged. Female. Humans. Male. Methylation. Middle Aged. Mutation / genetics. Promoter Regions, Genetic / physiology. Survival Analysis. Tumor Suppressor Protein p53 / genetics

MedlinePlus Health Information. consumer health - Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17493032.001).

[ISSN] 1015-6305

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

[ISO-abbreviation] Brain Pathol.

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Alpha-actinin 1 and alpha-actinin 4: contrasting roles in the survival, motility, and RhoA signaling of astrocytoma cells.

Here, we have examined whether the two highly homologous non-muscle alpha-actinin isoforms 1 and 4 exhibit functional differences in astrocytoma cells.

The protein levels of these isoforms were differentially regulated during the development and progression of astrocytomas, as alpha-actinin 1 was higher in astrocytomas compared to normal brains whereas alpha-actinin 4 was elevated in high-grade astrocytomas compared to normal brains and low grade astrocytomas.

RNAi demonstrated contrasted contributions of alpha-actinin 1 and 4 to the malignant behavior of U-373, U-87 and A172 astrocytoma cells.

While alpha-actinin 1 appeared to favor the expansion of U-373, U-87 and A172 astrocytoma cell populations, alpha-actinin 4 played this role only for U-373 cells.

Finally, in the three astrocytoma cell lines examined, alpha-actinin 1 and 4 had contrasted biochemical properties as alpha-actinin 4 was significantly more abundant in the actin cytoskeleton than alpha-actinin 1.

Collectively, these findings suggest that alpha-actinin 1 and 4 are differentially regulated during the development and progression of astrocytomas because each of these isoforms uniquely contributes to distinct malignant properties of astrocytoma cells.

[MeSH-major] Actinin / physiology. Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Movement / genetics. rhoA GTP-Binding Protein / physiology

[MeSH-minor] Brain / metabolism. Cell Proliferation. Cell Survival / genetics. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Signal Transduction / genetics. Signal Transduction / physiology. Time Factors. Tumor Cells, Cultured

MedlinePlus Health Information. consumer health - Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Published by Elsevier Inc.

(PMID = 20156433.001).

[ISSN] 1090-2422

[Journal-full-title] Experimental cell research

[ISO-abbreviation] Exp. Cell Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / ACTN1 protein, human; 0 / ACTN4 protein, human; 11003-00-2 / Actinin; EC 3.6.5.2 / rhoA GTP-Binding Protein

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] B7-H4 is preferentially expressed in non-dividing brain tumor cells and in a subset of brain tumor stem-like cells.

B7-H4, a newly discovered member of B7 family that negatively regulates T cell-mediated immunity, may facilitate tumor progression by undermining host immunity.

Recent studies show that brain tumor stem-like cells (TSCs) contribute to tumorigenesis.

In this study, we found that B7-H4 was expressed in cultured tumor cells from human gliomas (n = 5) and medulloblastomas (n = 3).

Double immunostaining indicated that B7-H4 was primarily restricted to non-dividing (Ki67(-)) cultured tumor cells.

Tumor cells cultured under medium conditions favoring the growth of neural stem cells were able to form primary and secondary spheres, along with expression of neural stem/progenitor cell markers.

These cells differentiated into different neural lineages when cultured in differentiation medium, indicating that these cells have TSCs characteristics.

Secondary glioma cells derived from CD133(+) or CD133(-) cell xenografts expressed B7-H4 as well.

Our data suggest B7-H4 is preferentially expressed in non-dividing brain tumor cells and in a subpopulation of brain TSCs, and CD133(-) tumor cells also have the capacity to initiate brain formation in vivo.

[MeSH-major] Antigens, CD80 / metabolism. Astrocytoma / pathology. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Medulloblastoma / pathology. Neoplastic Stem Cells / metabolism

[MeSH-minor] Adolescent. Aged. Animals. Antigens, CD / metabolism. Child. Female. Flow Cytometry. Humans. Ki-67 Antigen / metabolism. Male. Mice. Mice, SCID. Middle Aged. Neoplasm Metastasis. Nerve Tissue Proteins / metabolism. Tumor Cells, Cultured. V-Set Domain-Containing T-Cell Activation Inhibitor 1

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Physiol Cell Physiol. 2005 Apr;288(4):C805-12 [15601754.001]

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

[Cites] Brain Res Brain Res Rev. 2003 May;42(2):97-122 [12738053.001]

[Cites] Exp Cell Res. 2005 May 15;306(1):128-41 [15878339.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10388-92 [12920180.001]

[Cites] Clin Neuropathol. 2002 Nov-Dec;21(6):252-7 [12489673.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]

[Cites] Eur J Cancer. 2007 Jul;43(10 ):1502-7 [17524637.001]

[Cites] Lung Cancer. 2006 Aug;53(2):143-51 [16782226.001]

[Cites] Front Biosci. 2007 Jan 01;12:2252-9 [17127461.001]

[Cites] J Immunol. 2003 Nov 1;171(9):4650-4 [14568939.001]

[Cites] J Immunother. 2007 Apr;30(3):251-60 [17414316.001]

[Cites] J Exp Med. 2006 Apr 17;203(4):871-81 [16606666.001]

[Cites] J Immunol. 1984 Oct;133(4):1710-5 [6206131.001]

[Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]

[Cites] Immunity. 2003 Jun;18(6):849-61 [12818165.001]

[Cites] Leukemia. 2003 Oct;17 (10 ):2049-51 [14513057.001]

[Cites] Mol Cancer. 2006 Dec 02;5:67 [17140455.001]

[Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]

[Cites] Immunity. 2003 Jun;18(6):863-73 [12818166.001]

[Cites] Cancer Res. 2007 May 1;67(9):4010-5 [17483311.001]

[Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]

[Cites] Neurosurgery. 2002 Jun;50(6):1238-44; discussion 1244-5 [12015841.001]

[Cites] Cancer. 1996 Jan 15;77(2):373-80 [8625247.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10391-6 [16798883.001]

(PMID = 18478183.001).

[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 / Antigens, CD; 0 / Antigens, CD80; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / VTCN1 protein, human

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Reappraisal of the Sainte-Anne Hospital classification of oligodendrogliomas in view of retrospective studies].

[Transliterated title] Classification des oligodendrogliomes de l'hôpital Sainte-Anne. Mise au point à l'usage des études rétrospectives.

PURPOSE: Definition of homogeneous tumor groups of oligodendrogliomas or oligo-astrocytomas is a basic condition for an adequate evaluation and comparison of the results of treatments in patients from various institutions.

The main goal of this study is to assess whether, for retrospective studies, MRI data may serve as a common basis for encompassing asymmetry in diagnosis established according to the WHO or Ste-Anne (SA) classification.

PATIENTS AND METHODS: This study included 251 adult patients in whom a SA grade A or B oligodendroglioma or oligo-astrocytoma was newly diagnosed at our institution from 1984 to 2003.

Routine histological preparations and post-contrast preoperative MRI/CT-scan were simultaneously reviewed in order to assess the impact on survival of the following features: presence or absence of a polymorphous or gemistocytic astrocytic component, of necrosis and of contrast enhancement (CH); endothelial hyperplasia (EH) assessed as absent, present minor (HE+) or (HE++) when conform to the threshold of HE defined in the SA grading system of oligodendrogliomas.

RESULTS: 70.1% of the tumors were classified as "pure" oligodendroglioma, 19.5% as "polymorphous oligo-astroastrocytoma" and 10.3% as "gemistocytic oligo-astrocytoma".

In grade A, or B tumors, the presence of a polymorphous or a gemistocytic component had no significant influence on survival; however respectively 53% and 65% of these tumours versus 32% of "pure" oligodendrogliomas were grade B at the time of diagnosis.

After regrouping of the histological subtypes and of the tumors with HE+ or absent, the series included 153 oligodendrogliomas grade A and 98 grade B.

Survival in patients with grade A versus grade B tumors was respectively 142 versus 52 months (p<0.0001).

In grade B tumors, necrosis had no significant influence on survival.

On post contrast MRI done in 235 patients, only 7 tumors (3%) were grade A/B (EH++ but no CH).

CONCLUSIONS: From these results and our previous observation that, according to the SA classification of gliomas, only oligodendrogliomas or oligo-astrocytomas may not show CE, we propose that for retrospective studies:.

1) tumors diagnosed according to the Ste-Anne classification as oligodendroglioma or oligo-astrocytoma be regrouped in a unique category, 2) independent of their histological type and grade according to the WHO, gliomas that do not show CE be regrouped with SA oligodendrogliomas grade A, 3) concerning gliomas that show CE on MRI: oligodendrogliomas or oligo-astrocytomas WHO grade II or III, as well as WHO secondary glioblastomas or glioblastomas with an oligodendroglial component, be regrouped with SA oligodendrogliomas grade B; however tumors that show ring-like CE surrounding large foci of necrosis and finger-like "peritumoral" edema should be excluded or analysed separately.

[MeSH-major] Brain / pathology. Brain / radiography. Brain Neoplasms / classification. Glioma / classification. Oligodendroglioma / classification

[MeSH-minor] Adult. France. Hospitals. Humans. Magnetic Resonance Imaging. Neoplasm Staging. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed

MedlinePlus Health Information. consumer health - Brain Tumors.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16292168.001).

[ISSN] 0028-3770

[Journal-full-title] Neuro-Chirurgie

[ISO-abbreviation] Neurochirurgie

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Temozolomide in children with progressive low-grade glioma.

We conducted a phase II study to assess the efficacy of oral temozolomide (TMZ) in children with progressive low-grade glioma.

Best responses in the 26 patients (86%) with optic pathway glioma (OPG)/pilocytic astrocytoma (PA) included partial response in 3 patients (11%), minor response in 1 (4%), stable disease in 10 (38%), and progressive disease in 12 (46%).

Only one of four patients with fibrillary astrocytoma had stable disease for 29 months after TMZ.

The overall disease stabilization rate in patients with OPG/PA was 54%, and disease control was maintained for a median interval of 34 months.

Seventeen of 26 patients had progressive disease either on or off therapy, and three have died of disease.

Worst toxicity related to TMZ in all 30 patients included grade 2-4 thrombocytopenia in seven patients, grade 2-4 neutropenia in seven, grade 2 skin rash in one, and intratumor hemorrhage in one.

TMZ given in this schedule was successful in stabilizing disease in a significant proportion of the patients with OPG/PA, with manageable toxicity.

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

Genetic Alliance. consumer health - Glioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. DACARBAZINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Cancer. 1999 Nov;81(6):1022-30 [10576660.001]

[Cites] Neuro Oncol. 2006 Jan;8(1):79-82 [16443951.001]

[Cites] Semin Radiat Oncol. 2001 Apr;11(2):152-62 [11285553.001]

[Cites] J Clin Oncol. 2002 May 1;20(9):2388-99 [11981013.001]

[Cites] J Clin Oncol. 2002 Jul 1;20(13):2951-8 [12089224.001]

[Cites] Mol Cancer Ther. 2002 Sep;1(11):943-8 [12481416.001]

[Cites] J Clin Oncol. 2003 Feb 15;21(4):646-51 [12586801.001]

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

[Cites] J Pediatr Hematol Oncol. 2003 May;25(5):372-8 [12759623.001]

[Cites] Ann Oncol. 2003 Dec;14(12):1715-21 [14630674.001]

[Cites] Ann Oncol. 2003 Dec;14(12):1722-6 [14630675.001]

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

[Cites] J Clin Oncol. 2004 Aug 1;22(15):3133-8 [15284265.001]

[Cites] Neurol Clin. 1991 May;9(2):479-95 [1944111.001]

[Cites] J Neurooncol. 1997 May;32(3):235-41 [9049885.001]

[Cites] J Neurosurg. 1997 May;86(5):747-54 [9126887.001]

[Cites] J Clin Oncol. 1998 Sep;16(9):3037-43 [9738573.001]

[Cites] Ann Neurol. 1999 Mar;45(3):393-6 [10072056.001]

[Cites] Clin Cancer Res. 2005 Apr 1;11(7):2747-55 [15814657.001]

[Cites] Ann Hematol. 2005 Oct;84(11):760-2 [16044311.001]

[Cites] J Clin Oncol. 2005 Oct 20;23(30):7646-53 [16234526.001]

[Cites] J Neurooncol. 2005 Dec;75(3):301-7 [16195800.001]

[Cites] Clin Cancer Res. 2000 Jul;6(7):2585-97 [10914698.001]

(PMID = 17347491.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study

[Publication-country] United States

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

[Other-IDs] NLM/ PMC1871667

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Malignant astrocytoma is the most common primary brain tumor in adults.

The median survival time of patients with high-grade malignant astrocytoma is about 1 year, despite aggressive treatment with surgical resection, radiotherapy, and cytotoxic chemotherapy.

Immunotherapy is one such novel approach that has been investigated for application with different types of tumors, including brain tumors.

The author reviews immunotherapeutic approaches for malignant gliomas and the relevance of recent clinical trials and their outcomes.

A number of potentially targetable antigens have been identified in gliomas.

DCs have been investigated in several clinical trials in patients with malignant tumors including malignant gliomas.

So far, seven papers concerning immunotherapy with DCs against malignant gliomas have been published.

These reports demonstrate that immunotherapy with DCs induces immune responses and clinically antitumor effects in some patients with malignant glioma.

[MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Glioma / therapy. Immunotherapy

MedlinePlus Health Information. consumer health - Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15853209.001).

[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 / Immunotoxins; 0 / Interleukin-13; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

[Number-of-references] 23

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Anaplastic astrocytoma presenting as reversible posterior leukoencephalopathy syndrome.

We report a 60-year-old man with grade III astrocytoma, who presented with status epilepticus.

The initial MRI did not demonstrate typical findings of an astrocytoma but rather showed reversible posterior leukoencephalopathy syndrome (RPLS).

A brain tumor should be considered and the patient carefully followed by MRI, even if the MRI white matter lesion pattern suggests RPLS.

[MeSH-major] Astrocytoma / diagnosis. Brain Diseases / diagnosis. Occipital Lobe / pathology

Genetic Alliance. consumer health - Anaplastic Astrocytoma.

MedlinePlus Health Information. consumer health - Brain Diseases.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17122727.001).

[ISSN] 1074-7931

[Journal-full-title] The neurologist

[ISO-abbreviation] Neurologist

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pathological and molecular progression of astrocytomas in a GFAP:12 V-Ha-Ras mouse astrocytoma model.

We previously characterized a genetically engineered mouse astrocytoma model with embryonic astrocyte-specific, activated (12)V-Ha-RAS (GFAP-RAS) transgenesis.

The GFAP-RAS line Ras-B8 appears normal at birth, but 50% of mice die by 4 months from low- and high-grade astrocytomas.

We examined the development and progression of astrocytomas in the Ras-B8 genetically engineered mouse.

From 3 to 8 weeks the incidence of low-grade astrocytomas progressively increased with 85% of 12-week-old mice harboring low- or high-grade astrocytomas, the latter characterized by increased proliferation, nuclear atypia, and angiogenesis.

Tp 53 mutations were detected in both astrocytoma grades, with high-grade astrocytomas expressing elevated levels of epidermal growth factor receptor and vascular endothelial growth factor, plus decreased levels of PTEN and p16, similar to human astrocytomas.

Of interest, many of these acquired alterations occur in human astrocytomas, further validating GFAP-RAS as a useful model for studying astrocytoma development and progression.

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Res. 2001 May 1;61(9):3826-36 [11325859.001]

[Cites] Exp Neurol. 1999 Jun;157(2):327-37 [10364444.001]

[Cites] J Neurooncol. 2001 Jul;53(3):289-96 [11718261.001]

[Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]

[Cites] Oncogene. 2002 Oct 24;21(49):7453-63 [12386807.001]

[Cites] Carcinogenesis. 2003 Feb;24(2):335-42 [12584185.001]

[Cites] Cancer Res. 2003 Mar 1;63(5):1106-13 [12615729.001]

[Cites] Acta Neuropathol. 1978 Jan 19;41(1):27-31 [636834.001]

[Cites] Acta Neuropathol. 1979 Mar 15;45(3):167-75 [442982.001]

[Cites] Oncogene. 1999 Dec 9;18(52):7514-26 [10602510.001]

[Cites] Oncogene. 2000 Aug 10;19(34):3948-54 [10951588.001]

[Cites] Brain Res. 2000 Nov 10;883(1):87-97 [11063991.001]

[Cites] Neuro Oncol. 2001 Jan;3(1):1-10 [11305411.001]

[Cites] J Cell Biol. 1980 Jun;85(3):890-902 [6248568.001]

[Cites] Cancer Res. 1986 Nov;46(11):5836-41 [3756925.001]

[Cites] Cancer Res. 1991 Nov 15;51(22):6202-5 [1933879.001]

[Cites] Cancer Res. 1992 Apr 1;52(7):1974-80 [1551126.001]

[Cites] Cancer Res. 1992 Oct 1;52(19):5334-41 [1382841.001]

[Cites] Cancer Res. 1993 Jun 1;53(11):2614-7 [8495424.001]

[Cites] J Clin Endocrinol Metab. 1993 Oct;77(4):1054-8 [8408453.001]

[Cites] Proc Natl Acad Sci U S A. 1994 May 24;91(11):5124-8 [8197195.001]

[Cites] Gynecol Oncol. 1995 Dec;59(3):423-6 [8522268.001]

[Cites] Br J Cancer. 1996 Jul;74(2):165-71 [8688317.001]

[Cites] Cancer Res. 1996 Nov 15;56(22):5141-5 [8912848.001]

[Cites] Neurosurgery. 1997 May;40(5):1016-26 [9149260.001]

[Cites] Oncogene. 1997 Dec 4;15(23):2755-65 [9419966.001]

[Cites] Int J Cancer. 1999 Mar 31;81(1):118-24 [10077162.001]

[Cites] Cancer Res. 2001 Jun 1;61(11):4425-31 [11389071.001]

(PMID = 16127163.001).

[ISSN] 0002-9440

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS041097; United States / NINDS NIH HHS / NS / NS41097

[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 / Glial Fibrillary Acidic Protein; 0 / Growth Substances; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53

[Other-IDs] NLM/ PMC1698742

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We aimed to prospectively analyze correlations between clinical features and histological classification of multi-segment intramedullary spinal cord tumors (MSICTs), and the extent of microsurgical resection and functional outcomes.

Fifty-six patients with MSICTs underwent microsurgery for tumor removal using a posterior approach.

The tumor was exposed through a dorsal myelotomy.

Pre-operative and post-operative nervous function was scored using the Improved Japanese Orthopaedic Association (IJOA) grading system.

Correlation analyses were performed between functional outcome (IJOA score) and histological features, age, tumor location, and the longitudinal extent of spinal cord involvement.

Ependymoma was the most frequent MSICT type, seen in 22 of 56 patients (39%), followed by low grade astrocytoma (17 patients, 30%) and glioblastoma multiforme (3 patients, 5%).

Gross total tumor removal was achieved in 33 cases (58%), subtotal resection in 4 (7%), and partial resection in 16 (28%).

The histological classification of the tumor was the most important factor influencing the extent of surgical removal (chi2=22.17, p=0.00).

Thus, MSICTs were most commonly seen in the medullo cervical and cervicothoracic regions, with ependymoma and low grade astrocytoma the most common tumour types.

[MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neurologic Examination / methods. Outcome Assessment (Health Care). Prospective Studies. Spinal Cord / pathology. Spinal Cord / surgery. Young Adult

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19303302.001).

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

[Publication-country] Scotland

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Overexpression of Aurora B kinase, which regulates cell progression through mitosis and cytokinesis, has been shown to be associated with higher-grade tumors and shortened survival in astrocytomas.

The association between Aurora B expression and World Health Organization grade II/III tumors was statistically significant (P<0.0001).

Aurora B expression was not associated with patient age, sex, tumor location, tumor recurrence, or death from tumor.

In contrast to astrocytomas, elevated Aurora B expression in higher-grade ependymomas does not seem to correlate with clinical course, although it may be a potential target of Aurora kinase inhibitors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18301241.001).

[ISSN] 1533-4058

[Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM

[ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] J1-31 protein expression in astrocytes and astrocytomas.

J1-31 is one of the astrocytic proteins, the expression of which has not been evaluated in astrocytomas.

In the present study, we studied the expression of J1-31 protein in astrocytes and astrocytomas in comparison with GFAP, p53 and Ki-67.

Materials consisted of formalin-fixed paraffin-embedded tissue specimens that included five cases of normal brain, 17 of gliosis, 15 of pilocytic astrocytoma (WHO grade I), 26 of low-grade diffuse astrocytoma (WHO grade II), four of anaplastic astrocytoma (WHO grade III), and eight of glioblastoma (WHO grade IV).

The antibody showed reactivity with tumor cells in 12/15 (80%) cases of pilocytic astrocytoma, although intensity of staining was generally weaker and more focal than observed in reactive gliosis.

J1-31-positive tumor cells were detected in only 9/26 (35%) cases of the low-grade diffuse astrocytoma and none of the cases of anaplastic astrocytoma and glioblastoma.

Increasing Ki-67 indices paralleled advancing tumor grades. p53 protein was expressed more commonly in infiltrating astrocytomas compared to pilocytic astrocytoma.

In conclusion, down-regulation of J1-31 expression correlates with advancing grade of astrocytomas.

The anti-J1-31 antibody may help further our understanding of astrocytes in disease and may be useful as an aid in the pathologic diagnosis of astrocytic lesions.

[MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Nerve Tissue Proteins / metabolism

[MeSH-minor] Cytoplasm / metabolism. Down-Regulation. Glial Fibrillary Acidic Protein / metabolism. Glioblastoma / metabolism. Gliosis / metabolism. Humans. Ki-67 Antigen / metabolism. Neoplasm Staging. Tumor Suppressor Protein p53 / metabolism

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19019178.001).

[ISSN] 1440-1789

[Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology

[ISO-abbreviation] Neuropathology

[Language] eng

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

[Publication-country] Australia

[Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / J1-31 protein, human; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial using proteasome inhibitor bortezomib and concurrent temozolomide and radiotherapy for central nervous system malignancies.

PURPOSE: To evaluate the toxicity and response rate of bortezomib with concurrent radiotherapy and temozolomide in the treatment of patients with central nervous system malignancies.

PATIENTS AND METHODS: This open-label, dose-escalation, Phase I clinical study evaluated the safety of three dose levels of intravenously administered bortezomib (0.7, 1.0, and 1.3 mg/m(2)/dose) on Days 1, 4, 8, and 11 of a 21-day cycle, in addition to concurrent radiotherapy and temozolomide at a daily dose of 75 mg/m(2) starting on Day 1.

The primary endpoint was dose-limiting toxicity, defined as any Grade 4-5 toxicity or Grade 3 toxicity directly attributable to protocol treatment, requiring hospitalization and/or radiotherapy interruption.

RESULTS: A total of 27 patients were enrolled, 23 of whom had high-grade glioma (10 recurrent and 13 newly diagnosed).

The most frequent toxicities were Grade 1 and 2 stomatitis, erythema, and alopecia.

At a median follow-up of 15.0 months, 9 patients were still alive, with a median survival of 17.4 months for all patients and 15.0 months for patients with high-grade glioma.

CONCLUSION: Bortezomib administered at its typical "systemic" dose (1.3 mg/m(2)) is well tolerated and safe combined with temozolomide and radiotherapy when used in the treatment of central nervous system malignancies.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. BORTEZOMIB .

Hazardous Substances Data Bank. DACARBAZINE .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 2006 Nov 1;24(31):5025-33 [17075122.001]

[Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]

[Cites] Anticancer Res. 2006 Nov-Dec;26(6B):4499-503 [17201170.001]

[Cites] Clin Cancer Res. 2007 Feb 15;13(4):1208-15 [17317831.001]

[Cites] J Thorac Oncol. 2006 Feb;1(2):126-34 [17409841.001]

[Cites] J Thorac Oncol. 2006 Nov;1(9):996-1001 [17409985.001]

[Cites] Clin Cancer Res. 2007 Jun 1;13(11):3403-12 [17545549.001]

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

[Cites] N Engl J Med. 2001 Jan 11;344(2):114-23 [11150363.001]

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

[Cites] Cancer Res. 2004 Jul 15;64(14):4912-8 [15256463.001]

[Cites] Lab Invest. 2004 Aug;84(8):941-51 [15184909.001]

[Cites] Clin Cancer Res. 2004 Aug 15;10(16):5595-603 [15328202.001]

[Cites] J Neurosurg. 1978 Sep;49(3):333-43 [355604.001]

[Cites] Cancer Treat Rep. 1983 Feb;67(2):121-32 [6337710.001]

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

[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] N Engl J Med. 2005 Jun 16;352(24):2487-98 [15958804.001]

[Cites] Ann Oncol. 2006 May;17(5):813-7 [16403809.001]

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

[Cites] Ann Oncol. 2006 Jun;17 Suppl 7:vii115-23 [16760273.001]

[Cites] Cancer. 2006 Dec 1;107(11):2688-97 [17075878.001]

(PMID = 19084346.001).

[ISSN] 1879-355X

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA056036-08; United States / NCI NIH HHS / CA / P30 CA056036-08

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

[Publication-country] United States

[Chemical-registry-number] 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide

[Other-IDs] NLM/ NIHMS117014; NLM/ PMC2697394

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Forniceal glioma in children. Clinical article.

The aim of this study was to review the clinical, radiological, and histopathological features as well as the feasibility of surgical excision and the outcomes in these patients.

METHODS: From a retrospective analysis of 250 cases of supratentorial pediatric glioma, the records of 8 children presenting with forniceal lesions were selected and reviewed.

On histological review, the tumors were confirmed as pilocytic astrocytoma (4 lesions), WHO Grade II astrocytoma (3), and ganglioglioma (1).

Additional treatment was required for 5 patients for tumor progression, with a median interval of 19 months from surgery.

At a median follow-up duration of 4.9 years, all patients had stable disease.

CONCLUSIONS: In this series, forniceal gliomas were found to be low-grade gliomas.

Due to the high rate of progression of residual disease, adjuvant therapy is recommended for infiltrative tumors, and it yielded excellent results.

[MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Fornix, Brain. Glioma / diagnosis. Glioma / surgery

Genetic Alliance. consumer health - Glioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19772409.001).

[ISSN] 1933-0707

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

[ISO-abbreviation] J Neurosurg Pediatr

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Incidence and prognostic impact of FoxP3+ regulatory T cells in human gliomas.

PURPOSE: The incidence of regulatory T cells (Treg) in intrinsic central nervous system malignancies is unknown.

Immunotherapeutic approaches that inhibit the Treg population may be limited to a subset of patients with gliomas.

Our hypothesis is that only the most malignant gliomas have a prominent glioma-infiltrating Treg population that contributes to the immunosuppressive biology and that the presence of Tregs is a negative prognostic variable.

EXPERIMENTAL DESIGN: We measured the incidence of Tregs in 135 glial tumors (including all pathologic types) in a glioma microarray using immunohistochemical analysis.

RESULTS: Tregs were not present in normal brain tissue and were very rarely found in low-grade gliomas and oligodendrogliomas.

We observed significant differences in the prevalence of Tregs between astrocytic and oligodendroglial tumors, between tumors of different grades, and between different pathologic types of tumors.

We identified Tregs most frequently in glioblastoma multiforme (GBM) but very rarely in low-grade astrocytomas.

CONCLUSIONS: Treg infiltration differed significantly in the tumors according to lineage, pathology, and grade.

Tregs seemed to have the highest predilection for tumors of the astrocytic lineage and specifically in the high-grade gliomas, such as GBM.

[MeSH-major] Biomarkers, Tumor / immunology. Brain Neoplasms / immunology. Forkhead Transcription Factors / metabolism. Glioma / immunology. Lymphocytes, Tumor-Infiltrating / immunology. T-Lymphocytes, Regulatory / immunology

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18698034.001).

[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 / NCI NIH HHS / CA / R01 CA120813-01A1

[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 / Biomarkers, Tumor; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Glioblastoma multiforme (GBM) is the most aggressive form of primary brain tumours known collectively as gliomas.

Gliomas are graded by their microscopic appearance.

As a rule, their behaviour can be predicted from histology: Grade I (pilocytic astrocytomas) and Grade II (benign astrocytomas) tumours are of low grade and grow slowly over many years.

Grade IV tumours (GBM) are the most aggressive and, unfortunately, also the most common in humans, growing rapidly, invading and altering brain function.

Most patients with GBM die of their disease in less than a year and none have long term survival.Extracranial metastases from GBM are extremely rare, with a reported frequency of only 0.44% because of the absence of lymphatics in the brain and the difficulty of tumours to penetrate blood vessels.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Res. 1995 Nov 1;55(21):4833-6 [7585516.001]

[Cites] Cancer. 1980 Jan 1;45(1):112-25 [6985826.001]

[Cites] J Neurosurg. 1970 Jul;33(1):88-94 [4316740.001]

[Cites] Cancer. 1992 Apr 15;69(8):2149-53 [1311985.001]

[Cites] J Neurosurg. 2000 Nov;93(5):887-90 [11059674.001]

[Cites] Clin Imaging. 1994 Oct-Dec;18(4):386-9 [8000959.001]

(PMID = 21614314.001).

[ISSN] 1823-5530

[Journal-full-title] Biomedical imaging and intervention journal

[ISO-abbreviation] Biomed Imaging Interv J

[Language] eng

[Publication-type] Journal Article

[Publication-country] Malaysia

[Other-IDs] NLM/ PMC3097703

[Keywords] NOTNLM ; GBM / Glioblastoma multiforme / extracranial metastases / glioma

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Knockdown of GluR1 expression by RNA interference inhibits glioma proliferation.

High-grade gliomas release excitotoxic concentrations of glutamate which contributes to their malignant phenotype.

To improve our understanding of the mechanisms by which glutamate enhances tumor growth and invasion, we examined alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-mediated signaling in glioma cell lines. shRNA was used to stably knockdown GluR1, the most abundant AMPA receptor subunit in glioma, to evaluate its role in tumor signaling, proliferation and tumorigenicity.

In a tissue array, there was a statistically significant increase in GluR1 expression in glioblastoma samples compared to anaplastic astrocytoma and low-grade tumors.

Retroviral delivery of GluR1 shRNA in U251 and U87 glioma cells reduced GluR1 protein expression, inhibited AMPA-mediated increases in MAPK phosphorylation, and decreased glioma proliferation in vitro.

These results suggest that AMPA receptors are abundantly expressed in high-grade gliomas and gene silencing of the GluR1 AMPA receptor subunit results in abrogation of AMPA-mediated signaling and tumor growth.

[MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation / drug effects. Glioma / prevention & control. RNA Interference / physiology. RNA, Small Interfering / therapeutic use. Receptors, AMPA / metabolism

[MeSH-minor] Animals. Carcinogenicity Tests. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Down-Regulation / drug effects. Down-Regulation / genetics. Humans. Ki-67 Antigen / metabolism. Mice. Mice, Nude. Microarray Analysis / methods. RNA, Double-Stranded / pharmacology. Signal Transduction / drug effects

Genetic Alliance. consumer health - Glioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Neurosci. 1999 Dec 15;19(24):10767-77 [10594060.001]

[Cites] Nucleic Acids Res. 2003 Nov 1;31(21):e127 [14576327.001]

[Cites] Pharmacol Rev. 1999 Mar;51(1):7-61 [10049997.001]

[Cites] Expert Rev Anticancer Ther. 2003 Oct;3(5):595-614 [14599084.001]

[Cites] J Neurosci. 1993 Sep;13(9):3904-15 [8103555.001]

[Cites] Neuron. 2000 Jun;26(3):603-17 [10896157.001]

[Cites] Annu Rev Cell Biol. 1991;7:601-32 [1667084.001]

[Cites] Neuron. 1994 Jun;12 (6):1207-21 [8011335.001]

[Cites] J Biol Chem. 1994 Mar 4;269(9):7030-5 [8120067.001]

[Cites] Cancer Metastasis Rev. 2003 Dec;22(4):395-403 [12884914.001]

[Cites] J Neurosci. 2005 Aug 3;25(31):7101-10 [16079392.001]

[Cites] Mol Cell. 2003 Oct;12(4):889-901 [14580340.001]

[Cites] Nat Med. 2002 Sep;8(9):971-8 [12172541.001]

[Cites] J Neurooncol. 2001 Feb;51(3):245-64 [11407596.001]

[Cites] Brain Pathol. 2002 Jan;12(1):95-107 [11770905.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14687-92 [11717408.001]

[Cites] Trends Neurosci. 2003 Oct;26(10):543-9 [14522147.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7058-61 [11416187.001]

[Cites] J Neurosci. 2007 Jul 25;27(30):7987-8001 [17652589.001]

[Cites] Nat Methods. 2004 Nov;1(2):163-7 [16144086.001]

[Cites] J Neurooncol. 2003 Jan;61(2):151-60 [12622454.001]

[Cites] J Cereb Blood Flow Metab. 2007 Aug;27(8):1431-43 [17245419.001]

[Cites] J Biol Chem. 1993 Feb 15;268(5):3715-9 [8429046.001]

[Cites] Neuron. 1999 Mar;22(3):511-24 [10197531.001]

[Cites] Genes Dev. 1995 Sep 15;9(18):2279-91 [7557381.001]

[Cites] J Med Chem. 1998 Jul 2;41(14):2513-23 [9651156.001]

[Cites] J Neurochem. 2003 Mar;84(6):1288-95 [12614329.001]

[Cites] Nature. 1998 Dec 10;396(6711):584-7 [9859994.001]

[Cites] Nature. 1999 Jan 7;397(6714):72-6 [9892356.001]

[Cites] Biochem Pharmacol. 2002 Oct 15;64(8):1195-200 [12234599.001]

[Cites] J Neurosci Res. 1998 Dec 15;54(6):814-9 [9856865.001]

[Cites] J Neurooncol. 2000 Mar;47(1):11-22 [10930095.001]

[Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6372-7 [11331750.001]

[Cites] Nat Med. 2001 Sep;7(9):1010-5 [11533703.001]

[Cites] J Neurosci. 2005 Feb 16;25(7):1654-63 [15716401.001]

[Cites] Cancer Res. 2005 Mar 1;65(5):1934-40 [15753393.001]

[Cites] Cancer Res. 1999 Sep 1;59(17):4383-91 [10485487.001]

[Cites] J Cereb Blood Flow Metab. 1998 Apr;18(4):396-406 [9538905.001]

[Cites] Cancer Res. 2003 Aug 1;63(15):4315-21 [12907597.001]

[Cites] Nat Rev Neurosci. 2004 Oct;5(10):771-81 [15378037.001]

[Cites] J Biol Chem. 1995 Sep 29;270(39):22783-7 [7559406.001]

[Cites] Cancer. 2004 Mar 15;100(6):1110-22 [15022276.001]

(PMID = 18317690.001).

[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 / Ki-67 Antigen; 0 / RNA, Double-Stranded; 0 / RNA, Small Interfering; 0 / Receptors, AMPA; 0 / glutamate receptor ionotropic, AMPA 1

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Glioblastoma (GBM; grade IV astrocytoma) is a very aggressive form of brain cancer with a poor survival and few qualified predictive markers.

A system level analysis was used to construct GBM-specific network.

Computation of topological parameters of networks showed scale-free pattern and hierarchical organization.

Real-time quantitative reverse transcription-PCR analysis revealed CSK21 to be moderately upregulated and PP1A to be overexpressed by 20-fold in GBM tumor samples.

Genetic Alliance. consumer health - Glioblastoma.

MedlinePlus Health Information. consumer health - Brain Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c)2010 AACR.

(PMID = 20663907.001).

[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 2.7.11.1 / Casein Kinase II; EC 3.1.3.16 / Protein Phosphatase 1

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Biochemical and cytogenetic analysis of brain tissues in different grades of glioma patients.

BACKGROUND: Glioma, a neoplasm of neuroglial cells, is the most common type of brain tumor, constituting more than 50% of all brain tumors.

PURPOSE: This report summarizes the current knowledge regarding the clinical utility of biochemical enzyme markers for both diagnostic and therapeutic purposes in different grades of glioma.

METHODS: Sixty patients with different grades of glioma include glioblastoma multiforme (n=20), Anaplastic astrocytoma (n=10).

Ependymoma (n=10), Pilocytic astrocytoma (n=10) and patients with benign lesions (n=5) served as controls.

CK, Na-K(+) ATPases, 5'-Nucleotidases showed marked increase in grade IV.

Similarly, Mg2-ATPase, Ca2+ATPases showed significant increase in grade III.

CONCLUSION: The clinical importance for classification and treatment of glioma is governed by biochemical enzyme markers.

The study of enzymes supported by related chromosomal changes is anticipated to provide better appreciation of biological properties in different grades of glioma.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 25205887.001).

[ISSN] 0972-7531

[Journal-full-title] Annals of neurosciences

[ISO-abbreviation] Ann Neurosci

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Other-IDs] NLM/ PMC4116979

[Keywords] NOTNLM ; Antioxidants / Biochemical profile in glioma / Chromosomal aberrations / Enzymes / Glioma

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Spinal cord pilocytic astrocytoma with leptomeningeal dissemination to the brain. Case report and review of the literature.

Leptomeningeal dissemination of low-grade spinal cord gliomas is an uncommon event.

The authors report a unique case of leptomeningeal dissemination of a spinal cord pilocytic astrocytoma (PCA) to the intracranial cerebral subarachnoid spaces in a child.

An intradural intramedullary spinal cord tumor was identified, and the lesion was subtotally resected and diagnosed by the pathology department to be a PCA.

Subsequently, the patient had recurrences of the intradural intramedullary tumor at 6 months and 2 years after his original presentation.

He underwent a repeated resection of the recurrent tumor and fenestration of an associated syrinx on both occasions.

The pathological characteristics of the reresected tumor remained consistent with those of a PCA.

Postoperative imaging after his last surgery revealed diffuse intracranial leptomeningeal dissemination into the cisternal space surrounding the midbrain, the suprasellar region, and the internal auditory canal, as well as nodular subarachnoid disease in the upper cervical region.

The patient then underwent chemotherapy, and total spine magnetic resonance (MR) imaging 2 months later demonstrated stability in the size of the spinal cord tumor and a decrease in the associated syrinx.

However, an MR image of the head demonstrated two new areas of supratentorial subarachnoid leptomeningeal spread of the primary spinal cord tumor at the 2-month follow-up examination.

At the 6-month follow-up examination, MR imaging of the head and spine demonstrated stable metastatic disease.

[MeSH-major] Astrocytoma / secondary. Brain Neoplasms / secondary. Meningeal Neoplasms / secondary. Spinal Cord Neoplasms / pathology

[MeSH-minor] Child, Preschool. Humans. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery

Genetic Alliance. consumer health - Pilocytic astrocytoma.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17184088.001).

[ISSN] 0022-3085

[Journal-full-title] Journal of neurosurgery

[ISO-abbreviation] J. Neurosurg.

[Language] eng

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

[Publication-country] United States

[Number-of-references] 45

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.

PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors.

MATERIALS AND METHODS: Forty-one patients with spinal cord glioma received post-operative radiotherapy between 1979 and 2003.

There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors.

Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.

RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009).

Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%.

The actuarial survival rates at 10 years were 67% for those who received hypofractionated radiotherapy boost for dose escalation, and 20% for those who did not (P=0.47).

DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature.

Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.

[MeSH-major] Dose Fractionation. Glioma / radiotherapy. Spinal Cord Neoplasms / radiotherapy

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 1992 Sep;10(9):1379-85 [1325539.001]

[Cites] J Clin Neurosci. 2002 Mar;9(2):211-6 [11922720.001]

[Cites] Int J Radiat Oncol Biol Phys. 1993 Sep 30;27(2):223-9 [8407395.001]

[Cites] Br J Neurosurg. 2000 Aug;14(4):331-6 [11045198.001]

[Cites] Am J Clin Oncol. 1999 Aug;22(4):344-51 [10440187.001]

[Cites] J Neurooncol. 2001 Mar;52(1):85-94 [11451207.001]

[Cites] Radiology. 1980 May;135(2):473-9 [7367644.001]

[Cites] J Neurosurg. 1995 Oct;83(4):590-5 [7674006.001]

[Cites] J Neurooncol. 1997 Jul;33(3):205-11 [9195492.001]

[Cites] Int J Radiat Oncol Biol Phys. 1997 Jul 1;38(4):805-11 [9240650.001]

[Cites] Radiat Oncol Investig. 1998;6(6):276-80 [9885944.001]

[Cites] Int J Radiat Oncol Biol Phys. 1998 Dec 1;42(5):953-8 [9869215.001]

[Cites] Int J Radiat Oncol Biol Phys. 2000 Sep 1;48(2):421-6 [10974456.001]

[Cites] Childs Nerv Syst. 1997 Jul;13(7):375-82 [9298273.001]

[Cites] Neurosurgery. 1999 Feb;44(2):264-9 [9932879.001]

[Cites] Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1397-403 [2542194.001]

[Cites] Int J Radiat Oncol Biol Phys. 2000 Oct 1;48(3):837-42 [11020582.001]

[Cites] J Clin Oncol. 1995 Jul;13(7):1642-8 [7602353.001]

[Cites] Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):323-8 [7673019.001]

[Cites] Oncol Rep. 2003 Nov-Dec;10(6):2079-82 [14534747.001]

[Cites] Int J Radiat Oncol Biol Phys. 2003 Jan 1;55(1):162-7 [12504049.001]

[Cites] J Neurosurg. 1998 Feb;88(2):215-20 [9452226.001]

[Cites] J Neurosurg. 1989 Jan;70(1):50-4 [2909688.001]

(PMID = 16314938.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Most are syndrome associated and include pilocytic astrocytoma in neurofibromatosis type 1 and subependymal giant cell astrocytoma in tuberous sclerosis complex.

Acquired, more conventional, diffuse astrocytomas are less frequent.

The tumor was sporadic in occurrence and unilateral, low grade, and of cellular type.

The literature regarding retinal glial neoplasia including ependymoma as well as the so-called massive retinal gliosis is discussed.

Genetic Alliance. consumer health - Ependymoma.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18835620.001).

[ISSN] 1532-8392

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Third ventricular chordoid glioma: clinicopathological study of two cases with evidence for a poor clinical outcome despite low grade histological features.

Chordoid glioma of the third ventricle is a rare glial tumour whose precise histogenesis remains uncertain.

The neoplasm tends to occur in women and its clinical presentation is variable, resulting from acute hydrocephalus or impingement upon local structures.

The main differentials for histological diagnosis include chordoid meningiomas, pilocytic astrocytomas and ependymomas.

[MeSH-major] Choroid Plexus Neoplasms / pathology. Choroid Plexus Neoplasms / physiopathology. Glioma / pathology. Glioma / physiopathology. Third Ventricle / pathology

Genetic Alliance. consumer health - Glioma.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16008819.001).

[ISSN] 0305-1846

[Journal-full-title] Neuropathology and applied neurobiology

[ISO-abbreviation] Neuropathol. Appl. Neurobiol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Tumor antigen precursor protein profiles of adult and pediatric brain tumors identify potential targets for immunotherapy.

OBJECTIVES: We evaluated and compared tumor antigen precursor protein (TAPP) profiles in adult and pediatric brain tumors of 31 genes related to tumor associated antigens (TAA) for possible use in immunotherapy.

METHODS: Thirty-seven brain tumor specimens from 11 adult and 26 pediatric patients were analyzed by quantitative real-time PCR for the relative expression of 31 TAPP mRNAs.

Histological diagnoses consisted of 16 glioblastomas, 4 low grade astrocytomas, 10 juvenile pilocytic astrocytomas, and 7 ependymomas.

RESULTS: The adult gliomas expressed 94% (29 of 31) of the TAPP mRNAs evaluated compared with pediatric brain tumors that expressed 55-74% of the TAPP mRNAs, dependent on tumor histological subtype.

The pediatric brain tumors lacked expression of some genes associated with engendering tumor survival, such as hTert and Survivin.

Genetic Alliance. consumer health - Brain Tumor, Adult.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Res. 2002 Aug 1;62(15):4364-8 [12154041.001]

[Cites] Cancer Immunol Immunother. 2001 Sep;50(7):337-44 [11676393.001]

[Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]

[Cites] Cancer. 2003 Feb 15;97(4):1077-83 [12569609.001]

[Cites] J Neurooncol. 2003 Aug-Sep;64(1-2):13-20 [12952282.001]

[Cites] Cancer Res. 2004 Jul 15;64(14):4973-9 [15256471.001]

[Cites] Br J Cancer. 2004 Nov 1;91(9):1656-62 [15477864.001]

[Cites] J Cell Biol. 1989 Dec;109(6 Pt 1):2575-87 [2687284.001]

[Cites] Hum Gene Ther. 1995 May;6(5):591-601 [7578396.001]

[Cites] Cancer Immunol Immunother. 1997 Oct;45(2):77-87 [9390198.001]

[Cites] Lancet. 1998 Mar 21;351(9106):882-3 [9525374.001]

[Cites] J Neurosurg. 1998 Jul;89(1):42-51 [9647171.001]

[Cites] J Biol Chem. 1999 Jan 15;274(3):1359-65 [9880507.001]

[Cites] Br J Cancer. 2005 Jan 31;92(2):359-65 [15655550.001]

[Cites] Neuro Oncol. 2005 Jul;7(3):225-35 [16053697.001]

[Cites] Clin Cancer Res. 2005 Aug 1;11(15):5515-25 [16061868.001]

[Cites] Brain Pathol. 2005 Oct;15(4):342-63 [16389946.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):194-202 [16492905.001]

[Cites] Oncogene. 2006 May 4;25(19):2818-26 [16314830.001]

[Cites] Pediatr Blood Cancer. 2006 Jul;47(1):4-13 [16534789.001]

[Cites] Int J Oncol. 2006 Jun;28(6):1555-60 [16685456.001]

[Cites] Neurosurg Focus. 2000;9(6):e9 [16817692.001]

[Cites] J Neuropathol Exp Neurol. 2006 Sep;65(9):905-13 [16957584.001]

[Cites] Cancer Gene Ther. 2006 Dec;13(12):1052-60 [16826191.001]

[Cites] Neurosurgery. 2006 Nov;59(5):988-99; discussioin 999-1000 [17143233.001]

[Cites] J Neurooncol. 2007 Jan;81(2):139-48 [17004103.001]

[Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):566-75 [17255279.001]

[Cites] Clin Cancer Res. 2007 Sep 1;13(17):4960-3 [17785545.001]

[Cites] Immunology. 2007 Dec;122(4):615-22 [17645496.001]

[Cites] Oncogene. 2000 Feb 3;19(5):617-23 [10698506.001]

[Cites] J Neurooncol. 1999;45(2):141-57 [10778730.001]

[Cites] Clin Cancer Res. 2000 Jun;6(6):2209-18 [10873070.001]

[Cites] Semin Radiat Oncol. 2001 Apr;11(2):152-62 [11285553.001]

[Cites] Clin Cancer Res. 2002 Sep;8(9):2851-5 [12231526.001]

(PMID = 18259692.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA121258; United States / NINDS NIH HHS / NS / NS 046463; United States / NCI NIH HHS / CA / CA 121258; United States / NINDS NIH HHS / NS / R21 NS057829; United States / NINDS NIH HHS / NS / NS 054093; United States / NINDS NIH HHS / NS / NS 056300; United States / NINDS NIH HHS / NS / R21 NS056300; United States / NINDS NIH HHS / NS / R21 NS046463; United States / NINDS NIH HHS / NS / NS 057829

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Protein Precursors; 0 / RNA, Messenger

[Other-IDs] NLM/ NIHMS572988; NLM/ PMC4005736

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Management of tectal glioma in childhood.

Tectal glioma is a topographical diagnosis including tumors of different histology, mainly low-grade astrocytomas.

This report discusses the management of this rare tumor in children.

Clinical charts of 12 children with tectal glioma treated in our department between 1976 and 2001 were retrospectively reviewed.

The duration between first symptoms and the diagnosis of tectal glioma was in the range of 2 days to 9 years.

Ten patients presented with symptoms associated with increased intracranial pressure, one patient presented with ataxia, and in one case tectal glioma was an incidental finding.

First-line therapy was endoscopic third ventriculostomy in 5 cases (42%), ventriculoperitoneal shunting in 6 cases (50%), and combined partial tumor resection and shunting in one case.

Histology was obtained in 5 cases (low-grade astrocytoma, n = 4; ependymoma, n = 1).

Tectal glioma represents a distinct subgroup of brainstem tumors associated with a good (or favorable) prognosis.

Effective treatment for hydrocephalus is essential; the tumor should be monitored by regular clinical examination and magnetic resonance imaging.

Biopsy is warranted in cases with tumor progression.

[MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Glioma / pathology. Glioma / therapy. Superior Colliculi / pathology

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Management. Female. Follow-Up Studies. Humans. Infant. Male. Retrospective Studies

Genetic Alliance. consumer health - Glioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15876519.001).

[ISSN] 0887-8994

[Journal-full-title] Pediatric neurology

[ISO-abbreviation] Pediatr. Neurol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I single-dose study of intracavitary-administered iodine-131-TM-601 in adults with recurrent high-grade glioma.

PURPOSE: TM-601 binds to malignant brain tumor cells with high affinity and does not seem to bind to normal brain tissue.

Preclinical studies suggest that iodine-131 (131I) -TM-601 may be an effective targeted therapy for the treatment of glioma.

We evaluated the safety, biodistribution, and dosimetry of intracavitary-administered 131I-TM-601 in patients with recurrent glioma.

PATIENTS AND METHODS: Eighteen adult patients (17 with glioblastoma multiforme and one with anaplastic astrocytoma) with histologically documented recurrent glioma and a Karnofsky performance status of > or = 60% who were eligible for cytoreductive craniotomy were enrolled.

An intracavitary catheter with subcutaneous reservoir was placed in the tumor cavity during surgery.

Two weeks after surgery, patients received a single dose of 131I-TM-601 from one of three dosing panels (0.25, 0.50, or 1.0 mg of TM-601), each labeled with 10 mCi of 131I.

RESULTS: Intracavitary administration was well tolerated, with no dose-limiting toxicities observed.

131I-TM-601 bound to the tumor periphery and demonstrated long-term retention at the tumor with minimal uptake in any other organ system.

At day 180, four patients had radiographic stable disease, and one had a partial response.

Two of these patients further improved and were without evidence of disease for more than 30 months.

CONCLUSION: A single dose of 10 mCi 131I-TM-601 was well tolerated for 0.25 to 1.0 mg TM-601 and may have an antitumoral effect.

[MeSH-major] Brachytherapy. Brain Neoplasms / radiotherapy. Glioma / radiography. Iodine Radioisotopes / administration & dosage. Iodine Radioisotopes / adverse effects. Scorpion Venoms / administration & dosage. Scorpion Venoms / adverse effects

[MeSH-minor] Adult. Aged. Female. Humans. Karnofsky Performance Status. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / radiotherapy. Radiometry. Radiopharmaceuticals / administration & dosage. Radiopharmaceuticals / adverse effects. Radiotherapy Dosage. Survival Analysis. Time Factors. Tomography, Emission-Computed, Single-Photon. Treatment Outcome

Genetic Alliance. consumer health - Glioma.

MedlinePlus Health Information. consumer health - Brain Tumors.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16877732.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Chlorotoxin; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Scorpion Venoms

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression and aberrant promoter methylation of Wnt inhibitory factor-1 in human astrocytomas.

BACKGROUND: Wnt inhibitory factor-1(WIF-1) acts as a Wnt-antagonists and tumor suppressor, but hypermethylation of WIF-1 gene promoter and low expression activate Wnt signaling aberrantly and induce the development of various human tumors.

With this work we intended to investigate the expression and promoter methylation status of WIF-1 gene in human astrocytomas.

METHODS: The tissue samples consisted of 53 astrocytomas and 6 normal brain tissues.

RESULTS: The average expression levels of WIF-1 protein and mRNA in astrocytomas were decreased significantly compared with normal control tissues.

The protein and mRNA expression of WIF-1 gene in astrocytomas was decreased with the increase of pathological grade.

Furthermore, WIF-1 promoter methylation was observed by MS-PCR in astrocytomas which showed significant reduction of WIF-1 expression.

CONCLUSION: Our results demonstrate that the WIF-1 gene is frequently down-regulated or silenced in astrocytomas by aberrant promoter methylation.

This may be an important mechanism in astrocytoma carcinogenesis.

[MeSH-major] Adaptor Proteins, Signal Transducing / biosynthesis. Astrocytoma / metabolism. Brain Neoplasms / metabolism. DNA Methylation. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Clin Cancer Res. 2003 Jun;9(6):2121-32 [12796377.001]

[Cites] J Cell Sci. 2003 Jul 1;116(Pt 13):2627-34 [12775774.001]

[Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]

[Cites] Cancer Res. 2004 Jul 15;64(14):4717-20 [15256437.001]

[Cites] J Neurooncol. 2004 Jul;68(3):275-83 [15332332.001]

[Cites] Biochem Biophys Res Commun. 2004 Oct 8;323(1):229-34 [15351726.001]

[Cites] Br J Cancer. 1997;75(1):2-8 [9000591.001]

[Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]

[Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]

[Cites] Nature. 1999 Apr 1;398(6726):431-6 [10201374.001]

[Cites] Oncogene. 2005 Nov 24;24(53):7946-52 [16007117.001]

[Cites] Clin Cancer Res. 2006 Jan 15;12(2):383-91 [16428476.001]

[Cites] Biochem Biophys Res Commun. 2006 Mar 10;341(2):635-40 [16427602.001]

[Cites] Pathobiology. 2006;73(5):213-23 [17314492.001]

[Cites] Curr Opin Cell Biol. 2007 Apr;19(2):150-8 [17306971.001]

[Cites] Neuro Oncol. 2007 Jul;9(3):271-9 [17504928.001]

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

[Cites] Cancer Lett. 2007 Nov 18;257(2):172-81 [17709179.001]

[Cites] N Engl J Med. 2008 Jul 31;359(5):492-507 [18669428.001]

[Cites] Gene Expr Patterns. 2008 Sep;8(7-8):515-22 [18586116.001]

[Cites] Cancer Gene Ther. 2009 Apr;16(4):351-61 [18949017.001]

[Cites] Int J Oncol. 2009 Jun;34(6):1743-8 [19424593.001]

[Cites] Neurochem Res. 2009 Jul;34(7):1278-88 [19148749.001]

[Cites] World J Gastroenterol. 2009 Jun 7;15(21):2595-601 [19496188.001]

[Cites] Neoplasia. 2009 Jul;11(7):700-11 [19568415.001]

[Cites] Neurochem Int. 2009 Sep;55(5):307-17 [19576519.001]

[Cites] Cancer Res. 2000 Sep 1;60(17):4926-31 [10987308.001]

[Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]

[Cites] J Pathol. 2003 Oct;201(2):204-12 [14517837.001]

(PMID = 20334650.001).

[ISSN] 1756-9966

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Repressor Proteins; 0 / WIF1 protein, human

[Other-IDs] NLM/ PMC2851677