[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 119
1. Okada H, Low KL, Kohanbash G, McDonald HA, Hamilton RL, Pollack IF: Expression of glioma-associated antigens in pediatric brain stem and non-brain stem gliomas. J Neurooncol; 2008 Jul;88(3):245-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of glioma-associated antigens in pediatric brain stem and non-brain stem gliomas.
  • We investigated the protein expression of three glioma-associated antigens (GAAs) in pediatric brain stem glioma (BSG) and non-brain stem glioma (NBSG) cases with a view to their possible use in immunotherapy.
  • Thirteen of 15 BSGs and all 12 NBSGs expressed at least one of GAAs; and 7 BSGs and 9 NBSGs expressed at least two of these GAAs at higher levels than non-neoplastic brain.
  • There was no association between the tumor grade and levels of GAA expression.
  • These results suggest that EphA2, IL-13Ralpha2 and Survivin are suitable targets for developing vaccine strategies for pediatric glioma.

  • 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.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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] Nat Med. 2002 Sep;8(9):987-94 [12172543.001]
  • [Cites] Clin Cancer Res. 2002 Sep;8(9):2851-5 [12231526.001]
  • [Cites] Oncogene. 2002 Oct 10;21(46):7011-26 [12370823.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):613-8 [12576426.001]
  • [Cites] Blood. 2003 Jul 15;102(2):571-6 [12576330.001]
  • [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] Cancer. 2004 Sep 1;101(5):1036-42 [15329913.001]
  • [Cites] Cancer. 1982 Mar 15;49(6):1294-6 [6277461.001]
  • [Cites] Neurosurgery. 1983 Mar;12(3):298-302 [6302553.001]
  • [Cites] J Neurooncol. 1988 Dec;6(4):309-17 [3221258.001]
  • [Cites] Cancer. 1993 Aug 15;72(4):1414-21 [8339232.001]
  • [Cites] Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30 [8133987.001]
  • [Cites] N Engl J Med. 1994 Dec 1;331(22):1500-7 [7969301.001]
  • [Cites] Int J Cancer. 1996 May 16;66(4):470-6 [8635862.001]
  • [Cites] J Neurooncol. 1996 May-Jun;28(2-3):207-22 [8832463.001]
  • [Cites] Int J Cancer. 1998 Oct 5;78(2):196-201 [9754652.001]
  • [Cites] Childs Nerv Syst. 1999 May;15(5):235-7; discussion 238 [10392494.001]
  • [Cites] Gene Ther. 1999 Feb;6(2):219-26 [10435106.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9160-6 [15604287.001]
  • [Cites] Vaccine. 2005 Jan 4;23(7):884-9 [15603888.001]
  • [Cites] J Neurooncol. 2005 May;72(3):231-8 [15937645.001]
  • [Cites] Clin Cancer Res. 2005 Aug 1;11(15):5515-25 [16061868.001]
  • [Cites] Neoplasia. 2005 Aug;7(8):717-22 [16207473.001]
  • [Cites] Mol Cancer Res. 2005 Oct;3(10):541-51 [16254188.001]
  • [Cites] Nat Med. 2006 Jan;12(1):99-106 [16327802.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5883-91 [16740728.001]
  • [Cites] Cancer Immunol Immunother. 2006 Oct;55(10):1294-8 [16315030.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10815-23 [17090523.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):62-9 [10655584.001]
  • [Cites] Cancer Res. 2000 May 1;60(9):2449-57 [10811123.001]
  • [Cites] Mol Med. 2000 May;6(5):440-9 [10952023.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5614-9 [11114742.001]
  • [Cites] Cancer Lett. 2001 Mar 10;164(1):97-104 [11166921.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):869-72 [11221872.001]
  • [Cites] Hum Gene Ther. 2001 Mar 20;12(5):575-95 [11268289.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2625-31 [11289140.001]
  • [Cites] Nat Cell Biol. 2001 May;3(5):527-30 [11331884.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):5964-8 [11507035.001]
  • [Cites] Gene Ther. 2001 Aug;8(15):1157-66 [11509946.001]
  • (PMID = 18324354.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P01 NS 40923; United States / NINDS NIH HHS / NS / NS040923-06A15462; United States / NINDS NIH HHS / NS / P01 NS040923; United States / NCI NIH HHS / CA / P01 CA 100327; United States / NCI NIH HHS / CA / P01 CA100327; United States / NINDS NIH HHS / NS / P01 NS040923-06A15462
  • [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 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; EC 2.7.10.1 / Receptor, EphA2
  • [Other-IDs] NLM/ NIHMS70086; NLM/ PMC2561297
  •  go-up   go-down


2. Evers P, Lee PP, DeMarco J, Agazaryan N, Sayre JW, Selch M, Pajonk F: Irradiation of the potential cancer stem cell niches in the adult brain improves progression-free survival of patients with malignant glioma. BMC Cancer; 2010 Jul 21;10:384
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Irradiation of the potential cancer stem cell niches in the adult brain improves progression-free survival of patients with malignant glioma.
  • BACKGROUND: Glioblastoma is the most common brain tumor in adults.
  • The mechanisms leading to glioblastoma are not well understood but animal studies support that inactivation of tumor suppressor genes in neural stem cells (NSC) is required and sufficient to induce glial cancers.
  • This suggests that the NSC niches in the brain may harbor cancer stem cells (CSCs), Thus providing novel therapy targets.
  • METHODS: 55 adult patients with Grade 3 or Grade 4 glial cancer treated with radiotherapy at UCLA between February of 2003 and May of 2009 were included in this retrospective study.
  • CONCLUSIONS: Our study leads us to hypothesize that in glioma targeted radiotherapy of the stem cell niches in the adult brain could yield significant benefits over radiotherapy of the primary tumor mass alone and that damage caused by smaller fractions of radiation maybe less efficiently detected by the DNA repair mechanisms in CSCs.

  • Genetic Alliance. consumer health - Glioma.
  • Genetic Alliance. consumer health - Brain Stem Cancer.
  • Genetic Alliance. consumer health - Brain Cancer.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Radiat Biol. 1999 Nov;75(11):1341-8 [10597908.001]
  • [Cites] J Cancer Res Clin Oncol. 2009 Sep;135(9):1239-44 [19277712.001]
  • [Cites] Radiother Oncol. 2002 Sep;64(3):259-73 [12242114.001]
  • [Cites] J Comp Neurol. 2003 Apr 14;458(4):381-8 [12619072.001]
  • [Cites] Int J Cancer. 2003 May 20;105(1):33-40 [12672027.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Brain Res. 2004 Jan 23;996(2):213-26 [14697499.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(1):103-8 [1309203.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] J Neurosci. 1992 Nov;12(11):4565-74 [1432110.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11879-83 [8524867.001]
  • [Cites] Neurosurgery. 1998 Apr;42(4):709-20; discussion 720-3 [9574634.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Novartis Found Symp. 2005;265:66-80; discussion 82-97 [16050251.001]
  • [Cites] Cell Death Differ. 2006 Jul;13(7):1238-41 [16456578.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 20;98(24):1777-85 [17179479.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jul 15;68(4):978-85 [17467925.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):45-56 [19111880.001]
  • [Cites] EMBO J. 2009 Jan 7;28(1):8-20 [19037256.001]
  • [Cites] Nature. 2009 Jan 29;457(7229):608-11 [19092804.001]
  • [Cites] Nature. 2009 Jan 29;457(7229):603-7 [19092805.001]
  • [Cites] Am J Clin Oncol. 2009 Feb;32(1):20-2 [19194118.001]
  • [Cites] J Clin Oncol. 2009 Mar 10;27(8):1275-9 [19188675.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):459-66 [19269895.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2008;73:421-6 [19022744.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • (PMID = 20663133.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA137110; United States / NCI NIH HHS / CA / R01CA137110-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2918578
  •  go-up   go-down


3. Rhee W, Ray S, Yokoo H, Hoane ME, Lee CC, Mikheev AM, Horner PJ, Rostomily RC: Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology. Glia; 2009 Apr 1;57(5):510-23
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of mitotic Olig2 cells in adult human brain and gliomas: implications for glioma histogenesis and biology.
  • The capacity of adult human glial progenitor cells (AGPs), to proliferate and undergo multipotent differentiation, positions them as ideal candidate cells of origin for human gliomas.
  • To investigate this potential role we identified AGPs as mitotically active Olig2 cells in nonneoplastic adult human brain and gliomas.
  • Extrapolating from a mean Olig2/Mib-1 labeling index (LI) of 52% and total cell number of 100 billion, we estimated the overall prevalence of mitotic Olig2 AGPs in nonneoplastic human brain parenchyma at 10 million.
  • In the most malignant Grade IV glioma, or glioblastoma multiforme (GBM), the prevalence of Olig2/Mib-1 cells was significantly decreased (24.5%).
  • The novel framework provided by this quantitative and comparative analysis supports future studies to examine the histogenetic role of Olig2 AGPs in adult gliomas, their potential contribution to the tumor stroma and the molecular role of Olig2 in glioma pathogenesis.

  • Genetic Alliance. consumer health - Glioma.
  • 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] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18837053.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / T32 NS007144; United States / NINDS NIH HHS / NS / T32 NS007144-25; United States / NINDS NIH HHS / NS / T32 NS007144-28; United States / NINDS NIH HHS / NS / T32 NS 0007144
  • [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 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / MIB-1 antibody; 0 / Nerve Growth Factors; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human
  • [Other-IDs] NLM/ NIHMS77469; NLM/ PMC4415884
  •  go-up   go-down


Advertisement
4. Liu Q, Liu R, Kashyap MV, Agarwal R, Shi X, Wang CC, Yang SH: Brainstem glioma progression in juvenile and adult rats. J Neurosurg; 2008 Nov;109(5):849-55

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brainstem glioma progression in juvenile and adult rats.
  • OBJECT: Brainstem gliomas are common in children and have the worst prognosis of any brain tumor in this age group.
  • On the other hand, brainstem gliomas are rare in adults, and the authors of some clinical studies have suggested that this lesion behaves differently in adults than in children.
  • In the present study, the authors test an orthotopic C6 brainstem glioma model in juvenile and adult rats, and investigate the biological behavior of this lesion in the 2 age groups.
  • METHODS: The C6 glioma cells were stereotactically implanted into the pons of juvenile or adult male rats.
  • Tumor proliferation and the number of apoptotic cells in brainstem gliomas of young and adult rats were determined by immunohistochemical staining with Ki 67 and terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate-mediated nick-end labeling assay.
  • RESULTS: Striking differences in the onset of neurological signs, duration of symptoms, survival time, tumor growth pattern, tumor proliferation, and number of apoptotic cells were found between the gliomas in the 2 groups of rats.
  • The lesions were relatively focal in adult rats but more diffuse in young rats.
  • Furthermore, brainstem gliomas in adult rats were less proliferative and had more apoptotic cells than those in young rats.
  • CONCLUSIONS: The authors found that the C6 brainstem glioma model in young and adult rats closely imitates the course of brainstem glioma in humans both in neurological findings and histopathological characteristics.
  • Their findings also suggest that the different growth pattern and invasiveness of these lesions in children compared with that in adults could be due to different cellular environments in the 2 age groups, and warrants further investigation into the difference in the host response to brainstem gliomas in children and adults.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Age Factors. Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Disease Progression. Kaplan-Meier Estimate. Male. Neoplasm Transplantation / pathology. Rats. Rats, Sprague-Dawley

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Acta Neurochir (Wien). 1985;76(1-2):12-7 [4003123.001]
  • [Cites] Oncologist. 2004;9(2):197-206 [15047924.001]
  • [Cites] J Neurosurg. 1987 Oct;67(4):483-7 [3309202.001]
  • [Cites] J Neurooncol. 1988 Dec;6(4):309-17 [3221258.001]
  • [Cites] Neurosurg Clin N Am. 1990 Jan;1(1):111-21 [2135963.001]
  • [Cites] J Neurotrauma. 1994 Apr;11(2):187-96 [7932797.001]
  • [Cites] J Neurooncol. 1998 Jan;36(1):91-102 [9525831.001]
  • [Cites] Hum Gene Ther. 1999 Jan 1;10(1):95-101 [10022534.001]
  • [Cites] Arch Dis Child. 1999 Jun;80(6):558-64 [10332008.001]
  • [Cites] Cancer. 1999 Sep 15;86(6):1064-9 [10491535.001]
  • [Cites] Cancer. 2005 Jan 1;103(1):133-9 [15565574.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):217-28 [15674479.001]
  • [Cites] Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2005 Feb;27(1):7-12 [15782484.001]
  • [Cites] Childs Nerv Syst. 2005 May;21(5):399-403 [15702357.001]
  • [Cites] Neurosurg Focus. 2005 Jun 15;18(6A):E11 [16048287.001]
  • [Cites] J Neurosci Res. 2005 Aug 1;81(3):447-55 [15959903.001]
  • [Cites] Br J Neurosurg. 2005 Apr;19(2):128-36 [16120515.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):253-66 [16195805.001]
  • [Cites] Lancet Oncol. 2006 Mar;7(3):241-8 [16510333.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1364-71 [16463390.001]
  • [Cites] J Clin Neurosci. 2006 May;13(4):431-7 [16678721.001]
  • [Cites] Cancer Sci. 2006 Jun;97(6):546-53 [16734735.001]
  • [Cites] Childs Nerv Syst. 2006 Sep;22(9):1127-35 [16568342.001]
  • [Cites] J Neurooncol. 2006 Sep;79(3):281-7 [16598416.001]
  • [Cites] Childs Nerv Syst. 2006 Dec;22(12):1519-25 [17021732.001]
  • [Cites] Pediatr Neurosurg. 2007;43(3):192-201 [17409788.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Jun;36(6):1046-69 [15094120.001]
  • [Cites] J Cell Physiol. 2000 Mar;182(3):311-22 [10653597.001]
  • [Cites] J Neurooncol. 2000;46(3):193-203 [10902851.001]
  • [Cites] Neurosurgery. 2000 Oct;47(4):993-9; discussion 999-1000 [11014444.001]
  • [Cites] Cancer. 2000 Oct 1;89(7):1569-76 [11013373.001]
  • [Cites] Neurosurgery. 2001 Mar;48(3):616-24; discussion 624-5 [11270553.001]
  • [Cites] Pediatr Neurosurg. 2001 Apr;34(4):206-14 [11359114.001]
  • [Cites] Brain. 2001 Dec;124(Pt 12):2528-39 [11701605.001]
  • [Cites] J Neurooncol. 2001 Jul;53(3):275-87 [11718260.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):711-5 [11723378.001]
  • [Cites] Vet Pathol. 2002 May;39(3):293-9 [12014493.001]
  • [Cites] Cell Tissue Res. 2002 Dec;310(3):257-70 [12457224.001]
  • [Cites] Childs Nerv Syst. 2004 Mar;20(3):143-53 [14669023.001]
  • [Cites] J Neurosurg. 1986 Jan;64(1):11-5 [3941334.001]
  • (PMID = 18976074.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS054651; United States / NINDS NIH HHS / NS / R01 NS054651-01A2; United States / NINDS NIH HHS / NS / R01 NS054687; United States / NINDS NIH HHS / NS / R01 NS054687-01A2
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS75237; NLM/ PMC2693119
  •  go-up   go-down


5. Varghese M, Olstorn H, Sandberg C, Vik-Mo EO, Noordhuis P, Nistér M, Berg-Johnsen J, Moe MC, Langmoen IA: A comparison between stem cells from the adult human brain and from brain tumors. Neurosurgery; 2008 Dec;63(6):1022-33; discussion 1033-4
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparison between stem cells from the adult human brain and from brain tumors.
  • OBJECTIVE: To directly compare stem cells from the normal adult human brain (adult human neural stem cells [AHNSC]), Grade II astrocytomas (AC II), and glioblastoma multiforme (GBM), with respect to proliferative and tumor-forming capacity and differentiation potential.
  • METHODS: Cells were isolated from tissue obtained during epilepsy surgery (AHNSCs) or tumor surgery (glioma stem cells [GSC]).
  • 1) GBM stem cells formed tumors after orthotopic transplantation; AHNSCs showed no sign of tumor formation;.
  • 5) both AHNSCs and stem cells from AC II and GBM responded to differentiation cues with a dramatic decrease in the proliferation index (Ki-67);.
  • CONCLUSION: AHNSCs and stem cells from AC II and GBM differ with respect to proliferation, tumor-forming capacity, and rate and pattern of differentiation.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / physiopathology. Neurons / pathology. Neurons / physiology. Stem Cells / pathology. Stem Cells / physiology
  • [MeSH-minor] Adult. Cell Differentiation. Cell Proliferation. Cells, Cultured. Female. Humans. Male

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 = 19057315.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


6. Panagiotakos G, Tabar V: Brain tumor stem cells. Curr Neurol Neurosci Rep; 2007 May;7(3):215-20
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain tumor stem cells.
  • The concept of brain tumor stem cells is gaining increased recognition in neuro-oncology.
  • Until recently, the paradigm of a tumor-initiating stem cell was confined to hematopoietic malignancies where the hierarchical lineages of stem progenitor cells are well established.
  • The demonstration of persistent stem cells and cycling progenitors in the adult brain, coupled with the expansion of the cancer stem cell concept to solid tumors, has led to the exploration of "stemness" within gliomas.
  • Emerging data are highly suggestive of the subsistence of transformed multipotential cells within a glioma, with a subfraction of cells exhibiting increased efficiency at tumor initiation.
  • However, data in support of true glioma stem cells are inconclusive to date, particularly with respect to functional characterization of these cells.
  • Ongoing work aims at the identification of unique pathways governing self-renewal of these putative stem cells and at their validation as ultimate therapeutic targets.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplastic Stem Cells / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2006 Jun 21;26(25):6781-90 [16793885.001]
  • [Cites] Exp Neurol. 1992 Jan;115(1):110-4 [1728556.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Cancer Res. 1969 Nov;29(11):1927-31 [4311561.001]
  • [Cites] Neuron Glia Biol. 2004 May;1(2):157-63 [17047730.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):114-23 [11150363.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] Acta Neuropathol. 1977 Apr 29;38(1):1-6 [193346.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):895-902 [14737120.001]
  • [Cites] Neuron. 1993 Feb;10(2):201-12 [8439409.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):425-36 [16723989.001]
  • [Cites] J Comp Neurol. 2006 Jan 20;494(3):415-34 [16320258.001]
  • [Cites] Immunity. 1994 Nov;1(8):661-73 [7541305.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Annu Rev Cell Dev Biol. 2001;17:387-403 [11687494.001]
  • [Cites] J Neurosci. 2002 Feb 1;22(3):612-3 [11826087.001]
  • [Cites] Acta Neuropathol. 1977 Sep 26;40(1):63-71 [199034.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] Cell. 2000 Jan 7;100(1):157-68 [10647940.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):823-6 [16799564.001]
  • [Cites] J Neurosci. 1997 Jul 1;17(13):5046-61 [9185542.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] Annu Rev Neurosci. 2001;24:385-428 [11283316.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7445-52 [16885340.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2804-8 [1372992.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):2074-7 [8446631.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):964-8 [15959516.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):323-35 [16226707.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7843-8 [16912155.001]
  • [Cites] Mol Cancer. 2006 Dec 02;5:67 [17140455.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Exp Neurol. 2001 Nov;172(1):1-16 [11681836.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Nat Med. 2000 Apr;6(4):447-50 [10742153.001]
  • [Cites] J Neurosci. 2002 Feb 1;22(3):629-34 [11826091.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14895-900 [8962152.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] J Neurobiol. 1998 Aug;36(2):221-33 [9712306.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Nature. 2004 Feb 19;427(6976):740-4 [14973487.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11619-24 [10500226.001]
  • [Cites] Curr Biol. 2007 Jan 23;17 (2):165-72 [17196391.001]
  • [Cites] Nat Med. 1998 Nov;4(11):1313-7 [9809557.001]
  • [Cites] Nat Med. 2003 Apr;9(4):439-47 [12627226.001]
  • (PMID = 17488587.001).
  • [ISSN] 1528-4042
  • [Journal-full-title] Current neurology and neuroscience reports
  • [ISO-abbreviation] Curr Neurol Neurosci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
  •  go-up   go-down


7. Ehtesham M, Stevenson CB, Thompson RC: Stem cell therapies for malignant glioma. Neurosurg Focus; 2005 Sep 15;19(3):E5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell therapies for malignant glioma.
  • The prognosis for patients with malignant glioma, which is the most common primary intracranial neoplasm, remains dismal despite significant progress in neurooncological therapies and technology.
  • Malignant glial cells often disseminate throughout the brain, making it exceedingly difficult to target and treat all intracranial neoplastic foci, with the result that tumor recurrence is inevitable despite aggressive surgery and adjuvant radiotherapy and/or chemotherapy.
  • The use of neural stem cells (NSCs) as delivery vehicles for tumor-toxic molecules represents the first experimental strategy aimed specifically at targeting disseminated tumor pockets.
  • Investigators have demonstrated that NSCs possess robust tropism for infiltrating tumor cells, and that they can be used to deliver therapeutic agents directly to tumor satellites, with significant therapeutic benefit.
  • With the aim of developing these findings into a clinically viable technology that would not be hindered by ethical and tissue rejection-related concerns, the use of adult tissue-derived stem cells has recently been explored.
  • These technologies represent important progress in the development of a treatment strategy that can specifically target disseminated neoplastic pockets within the brain.
  • Key among these are an inadequate understanding of the specific tropic mechanisms that govern NSC migration toward invasive tumor, and the need to refine the processes used to generate tumor-tropic stem cells from adult tissues so that this can be accomplished in a clinically practicable fashion.
  • Despite these limitations, the use of stem cell therapies for brain tumors holds significant promise and may emerge as an important therapeutic modality for patients with malignant glioma.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy. Stem Cell Transplantation / methods. Stem Cells / physiology

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16190604.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
  •  go-up   go-down


8. Park HJ, Kim JK, Jeon HM, Oh SY, Kim SH, Nam DH, Kim H: The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells. Mol Cells; 2010 Nov;30(5):403-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The neural stem cell fate determinant TLX promotes tumorigenesis and genesis of cells resembling glioma stem cells.
  • A growing body of evidence indicates that deregulation of stem cell fate determinants is a hallmark of many types of malignancies.
  • The neural stem cell fate determinant TLX plays a pivotal role in neurogenesis in the adult brain by maintaining neural stem cells.
  • Here, we report a tumorigenic role of TLX in brain tumor initiation and progression.
  • Increased TLX expression was observed in a number of glioma cells and glioma stem cells, and correlated with poor survival of patients with gliomas.
  • Ectopic expression of TLX in the U87MG glioma cell line and Ink4a/Arf-deficient mouse astrocytes (Ink4a/Arf(-/-) astrocytes) induced cell proliferation with a concomitant increase in cyclin D expression, and accelerated foci formation in soft agar and tumor formation in in vivo transplantation assays.
  • Furthermore, overexpression of TLX in Ink4a/Arf(-/-) astrocytes inhibited cell migration and invasion and promoted neurosphere formation and Nestin expression, which are hallmark characteristics of glioma stem cells, under stem cell culture conditions.
  • Our results indicate that TLX is involved in glioma stem cell genesis and represents a potential therapeutic target for this type of malignancy.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Glioma / pathology. Neoplastic Stem Cells / pathology. Neural Stem Cells / pathology. Receptors, Cytoplasmic and Nuclear / physiology
  • [MeSH-minor] Adult. Animals. Astrocytes / metabolism. Astrocytes / pathology. Astrocytoma / genetics. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Movement / physiology. Central Nervous System Neoplasms. Cyclin D / genetics. Humans. Intermediate Filament Proteins / genetics. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis. Nerve Tissue Proteins / genetics. Nestin. Neurogenesis. Prognosis. Up-Regulation

  • Genetic Alliance. consumer health - Glioma.
  • 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
  • [ErratumIn] Mol Cells. 2011 Feb ;31(2):199. Park, Myung-Jin [removed]; Soeda, Akio [removed]
  • (PMID = 20814749.001).
  • [ISSN] 0219-1032
  • [Journal-full-title] Molecules and cells
  • [ISO-abbreviation] Mol. Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin D; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / NR2E1 protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Cytoplasmic and Nuclear
  •  go-up   go-down


9. Kang SK, Park JB, Cha SH: Multipotent, dedifferentiated cancer stem-like cells from brain gliomas. Stem Cells Dev; 2006 Jun;15(3):423-35
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multipotent, dedifferentiated cancer stem-like cells from brain gliomas.
  • In modern cancer biology, external factors and niches can act on differentiated tissue cells to cause cancer by inducing dedifferentiation of mature adult cells.
  • Recently, we discovered that dedifferentiation of glioma cancer cells alters the expression of mature and neural stem cell (NSC)-related genes, in that cancer cells adjust to the serum-deprived environment and cell-to-cell interaction by down-regulating genes associated with neural mature markers and up-regulating genes that are primitive NSC markers.
  • Neurogenesis of dedifferentiated glioma cancer cells also showed a highly increased neuronal marker associated with highly decreased glial and oligodendrocyte cell markers.
  • After grafting to severe combined immunodeficient (SCID) mouse brains, dedifferentiated cancer stem cells migrated and continued active proliferation for more than 4 weeks.
  • We also performed microarray analysis and characterized the gene expression patterns in control cancer cells with dedifferentiated cancer stem-like cells.
  • In this report, we propose that the dedifferentiation process of brain tumor and normal tissue may contribute to the malignancy and aggressiveness of the brain cancer.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Cell Differentiation. Glioma / pathology. Multipotent Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Movement. Cell Proliferation. DNA, Complementary / genetics. Drug Resistance. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes / genetics. Humans. Mice. Mice, SCID. Neoplasm Metastasis. Neurons / cytology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Brain Stem Cancer.
  • Genetic Alliance. consumer health - Brain Cancer.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Stem Cells Dev. 2006 Oct;15(5):749
  • (PMID = 16846378.001).
  • [ISSN] 1547-3287
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Messenger
  •  go-up   go-down


10. Suzuki T, Izumoto S, Wada K, Fujimoto Y, Maruno M, Yamasaki M, Kanemura Y, Shimazaki T, Okano H, Yoshimine T: Inhibition of glioma cell proliferation by neural stem cell factor. J Neurooncol; 2005 Sep;74(3):233-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of glioma cell proliferation by neural stem cell factor.
  • Neural stem cells (NSC) have unique differentiation-, proliferation-, and motility properties.
  • To investigate whether they secrete factors that interfere with the proliferation of glioma cells, we grew glioma cells in conditioned medium (CM) obtained from cultures of neurospheres including neural stem / progenitor cells (NSPC) isolated from embryonic (E14)- or adult mouse brain or fetal human brain.
  • 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and BrdU-labeling assays showed that CM from NSPC (NSPC/CM) contained factor(s) that inhibited the proliferation of glioma cells by 28-87%.
  • On the basis of these observations we transplanted 203G glioma cells and/or NSPC into the intrathecal space of the cisterna magna of mice to investigate whether NSPC interfere with the proliferation of glioma cells in vivo.
  • We concluded that NSPC secrete factor(s) that may control glioma cell proliferation.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Proliferation / drug effects. Culture Media, Conditioned / pharmacology. Glioma / pathology. Stem Cells / secretion
  • [MeSH-minor] Animals. Cell Line, Tumor. Corpus Striatum / cytology. Embryo, Mammalian. Humans. Immunohistochemistry. Mice. Neurons / cytology. Rats. Stem Cell Transplantation

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • [Cites] Dev Biol. 1996 Aug 25;178(1):77-89 [8812110.001]
  • [Cites] Acta Pathol Microbiol Scand. 1968;74(4):465-86 [4313504.001]
  • [Cites] Science. 1968 Jul 26;161(3839):370-1 [4873531.001]
  • [Cites] Development. 1990 Dec;110(4):1001-20 [2100251.001]
  • [Cites] Dev Biol. 1999 Nov 1;215(1):118-29 [10525354.001]
  • [Cites] Adv Pharmacol. 1997;37:35-67 [8891099.001]
  • [Cites] Acta Neuropathol. 1999 Apr;97(4):393-8 [10208279.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Matrix Biol. 2000 Sep;19(5):377-87 [10980414.001]
  • [Cites] J Neurosci. 1998 Oct 1;18(19):7869-80 [9742155.001]
  • [Cites] J Neurosci Res. 1993 Aug 1;35(5):567-76 [8377226.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5657-63 [12384520.001]
  • [Cites] Acta Neuropathol. 1980;51(1):23-31 [7435138.001]
  • [Cites] J Natl Cancer Inst. 1973 Nov;51(5):1417-23 [4357758.001]
  • [Cites] Cancer Res. 1973 May;33(5):976-86 [4703128.001]
  • [Cites] J Cell Physiol. 1979 Apr;99(1):43-54 [222778.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1440-4 [8640837.001]
  • [Cites] Eur J Neurosci. 1999 Feb;11(2):503-16 [10051751.001]
  • [Cites] J Neurosci. 1995 Aug;15(8):5765-78 [7643217.001]
  • [Cites] Development. 2000 Nov;127(22):4993-5005 [11044412.001]
  • [Cites] Nat Med. 2000 Apr;6(4):447-50 [10742153.001]
  • [Cites] J Neurosci. 1999 Oct 15;19(20):8954-65 [10516314.001]
  • [Cites] Can J Neurol Sci. 1983 May;10(2):105-9 [6861007.001]
  • [Cites] Acta Neuropathol. 1992;84(2):190-7 [1523973.001]
  • [Cites] Differentiation. 2001 Sep;68(2-3):141-52 [11686236.001]
  • (PMID = 16187020.001).
  • [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 / Culture Media, Conditioned
  •  go-up   go-down


11. Tanaka S, Kobayashi I, Utsuki S, Iwamoto K, Takanashi J: Biopsy of brain stem glioma using motor-evoked potential mapping by direct peduncular stimulation and individual adjuvant therapy. Case report. Neurol Med Chir (Tokyo); 2005 Jan;45(1):49-55
Genetic Alliance. consumer health - Glioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biopsy of brain stem glioma using motor-evoked potential mapping by direct peduncular stimulation and individual adjuvant therapy. Case report.
  • A 23-year-old man presented with a brain stem glioma manifesting as a 6-month history of right hemiparesis and diplopia.
  • Serial magnetic resonance imaging showed an intrinsic diffuse brain stem glioma that gradually localized to the left cerebral peduncle after initial adjuvant therapy.
  • Partial resection of the tumor was safely performed, with slight temporary neurological worsening.
  • Individual adjuvant therapy based on the results of real-time reverse transcription-polymerase chain reaction of O6-methylguanine-deoxyribonucleic acid methyltransferase achieved an almost complete tumor response.
  • Surgery under pyramidal tract mapping and intensive postoperative adjuvant therapy resulted in a good outcome despite the presence of a generally intractable intrinsic brain stem glioma.
  • [MeSH-major] Astrocytoma / surgery. Brain Mapping. Brain Stem Neoplasms / surgery. Evoked Potentials, Motor. Mesencephalon / physiopathology. Neurosurgical Procedures / methods
  • [MeSH-minor] Adult. Biopsy / methods. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15699622.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


12. Liu HK, Wang Y, Belz T, Bock D, Takacs A, Radlwimmer B, Barbus S, Reifenberger G, Lichter P, Schütz G: The nuclear receptor tailless induces long-term neural stem cell expansion and brain tumor initiation. Genes Dev; 2010 Apr 1;24(7):683-95
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The nuclear receptor tailless induces long-term neural stem cell expansion and brain tumor initiation.
  • Malignant gliomas are the most common primary brain tumors, and are associated with frequent resistance to therapy as well as poor prognosis.
  • Here we demonstrate that the nuclear receptor tailless (Tlx), which in the adult is expressed exclusively in astrocyte-like B cells of the subventricular zone, acts as a key regulator of neural stem cell (NSC) expansion and brain tumor initiation from NSCs.
  • Overexpression of Tlx antagonizes age-dependent exhaustion of NSCs in mice and leads to migration of stem/progenitor cells from their natural niche.
  • The increase of NSCs persists with age, and leads to efficient production of newborn neurons in aged brain tissues.
  • These cells initiate the development of glioma-like lesions and gliomas.
  • Glioma development is accelerated upon loss of the tumor suppressor p53.
  • Tlx-induced NSC expansion and gliomagenesis are associated with increased angiogenesis, which allows for the migration and maintenance of brain tumor stem cells in the perivascular niche.
  • We also demonstrate that Tlx transcripts are overexpressed in human primary glioblastomas in which Tlx expression is restricted to a subpopulation of nestin-positive perivascular tumor cells.
  • Our study clearly demonstrates how NSCs contribute to brain tumorgenesis driven by a stem cell-specific transcription factor, thus providing novel insights into the histogenesis and molecular pathogenesis of primary brain tumors.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Neurons / cytology. Receptors, Cytoplasmic and Nuclear / metabolism. Stem Cells / cytology
  • [MeSH-minor] Aging. Animals. Brain / cytology. Brain / growth & development. Brain / pathology. Cell Proliferation. Gene Expression. Genes, p53 / genetics. Humans. Mice. Mice, Inbred C57BL. Mutation / genetics. Neovascularization, Pathologic / physiopathology. Neurogenesis


13. Germano I, Swiss V, Casaccia P: Primary brain tumors, neural stem cell, and brain tumor cancer cells: where is the link? Neuropharmacology; 2010 May;58(6):903-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary brain tumors, neural stem cell, and brain tumor cancer cells: where is the link?
  • The discovery of brain tumor-derived cells (BTSC) with the properties of stem cells has led to the formulation of the hypothesis that neural stem cells could be the cell of origin of primary brain tumors (PBT).
  • In this review we present the most common molecular changes in PBT, define the criteria of identification of BTSC and discuss the similarities between the characteristics of these cells and those of the endogenous population of neural stem cells (NPCs) residing in germinal areas of the adult brain.
  • Finally, we propose possible mechanisms of cancer initiation and progression and suggest a model of tumor initiation that includes intrinsic changes of resident NSC and potential changes in the microenvironment defining the niche where the NSC reside.

  • Genetic Alliance. consumer health - Brain Stem Cancer.
  • Genetic Alliance. consumer health - Brain Cancer.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • [Cites] Lab Invest. 2002 Nov;82(11):1481-92 [12429808.001]
  • [Cites] J Cell Biochem. 2003 Jan 1;88(1):11-9 [12461769.001]
  • [Cites] Cancer. 2003 Feb 1;97(3):644-8 [12548606.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Neuro Oncol. 2003 Apr;5(2):79-88 [12672279.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7331-6 [12777630.001]
  • [Cites] J Neurosurg. 2003 Aug;99(2):344-50 [12924709.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):145-57 [15013214.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):488-98 [15183728.001]
  • [Cites] Histopathology. 2004 Jun;44(6):555-60 [15186270.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4783-9 [15256447.001]
  • [Cites] Cell. 2004 Aug 20;118(4):409-18 [15315754.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Acta Neuropathol. 1979 Mar 15;45(3):167-75 [442982.001]
  • [Cites] Neurosurgery. 1980 Nov;7(5):435-9 [6255368.001]
  • [Cites] Lancet. 1982 Apr 17;1(8277):885-7 [6122104.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2390-4 [6572982.001]
  • [Cites] Tumori. 1986 Apr 30;72(2):163-70 [3705189.001]
  • [Cites] Cancer Res. 1991 Apr 15;51(8):2164-72 [2009534.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5334-41 [1382841.001]
  • [Cites] J Neurosci. 1992 Nov;12(11):4565-74 [1432110.001]
  • [Cites] Cancer Res. 1997 Sep 15;57(18):4130-40 [9307304.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):193-209 [9440020.001]
  • [Cites] Cell. 1999 Jan 8;96(1):25-34 [9989494.001]
  • [Cites] Cell Death Differ. 2006 Jul;13(7):1238-41 [16456578.001]
  • [Cites] J Neurosci. 2006 Jun 21;26(25):6781-90 [16793885.001]
  • [Cites] Cell. 2006 Aug 25;126(4):663-76 [16904174.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8655-61 [16951180.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):973-8 [17210912.001]
  • [Cites] Curr Biol. 2007 Jan 23;17(2):165-72 [17196391.001]
  • [Cites] J Neurosurg. 2007 Mar;106(3):417-27 [17367064.001]
  • [Cites] Br J Cancer. 2007 Apr 23;96(8):1293-301 [17375044.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4010-5 [17483311.001]
  • [Cites] Tissue Antigens. 2007 Jun;69(6):602-6 [17498271.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Surg Neurol. 2007 Aug;68(2):133-43; discussion 143-4 [17537489.001]
  • [Cites] Oncogene. 2007 Aug 23;26(39):5752-61 [17353902.001]
  • [Cites] Mol Cancer Res. 2007 Sep;5(9):891-7 [17855658.001]
  • [Cites] J Mol Neurosci. 2007;32(1):53-63 [17873288.001]
  • [Cites] Stem Cells. 2007 Oct;25(10):2524-33 [17628016.001]
  • [Cites] Stem Cells Dev. 2007 Oct;16(5):837-47 [17999604.001]
  • [Cites] Int J Cancer. 2008 Feb 15;122(4):761-8 [17955491.001]
  • [Cites] Cell. 2009 May 15;137(4):606-8 [19450510.001]
  • [Cites] Stem Cells. 2009 Jan;27(1):40-8 [18948646.001]
  • [Cites] J Neurosci. 2009 Jul 15;29(28):8884-96 [19605626.001]
  • [Cites] Cancer Res. 1997 Feb 15;57(4):646-50 [9044841.001]
  • [Cites] Cell. 1997 Feb 7;88(3):287-98 [9039255.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):123-9 [18172261.001]
  • [Cites] Oncol Rep. 2008 Mar;19(3):639-43 [18288395.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2241-9 [18381430.001]
  • [Cites] Neurosurgery. 2008 Feb;62(2):505-14; discussion 514-5 [18382330.001]
  • [Cites] PLoS One. 2008;3(4):e1936 [18398462.001]
  • [Cites] J Biol Chem. 2008 Apr 18;283(16):10958-66 [18292095.001]
  • [Cites] Stem Cells. 2008 Jun;26(6):1506-16 [18403753.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3015-24 [18565887.001]
  • [Cites] Lab Invest. 2008 Aug;88(8):808-15 [18560366.001]
  • [Cites] Stem Cells. 2008 Aug;26(8):1931-8 [18388306.001]
  • [Cites] Cell Stem Cell. 2008 Sep 11;3(3):265-78 [18786414.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6426-38 [18710938.001]
  • [Cites] PLoS One. 2008;3(11):e3769 [19020659.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8205-12 [19088037.001]
  • [Cites] Stem Cells. 2008 Dec;26(12):3018-26 [18787206.001]
  • [Cites] Nat Med. 2009 Jan;15(1):110-6 [19122659.001]
  • [Cites] Neuro Oncol. 2009 Feb;11(1):9-21 [18812521.001]
  • [Cites] Anticancer Res. 2009 Feb;29(2):597-603 [19331209.001]
  • [Cites] Glia. 2009 May;57(7):724-33 [18985733.001]
  • [Cites] J Neurooncol. 2009 May;93(1):49-60 [19430882.001]
  • [Cites] Neurosurgery. 2009 Aug;65(2):237-49; discussion 249-50; quiz N6 [19625901.001]
  • [Cites] Cancer Treat Rev. 2009 Aug;35(5):403-8 [19369008.001]
  • [Cites] Dev Cell. 2009 Aug;17(2):210-21 [19686682.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10361-6 [10468613.001]
  • [Cites] Nature. 1964 Dec 19;204:1161-3 [14264369.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Neurobiol Dis. 2005 Feb;18(1):218-25 [15649712.001]
  • [Cites] Dev Neurosci. 2004 Mar-Aug;26(2-4):148-65 [15711057.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Eur J Pharmacol. 2005 May 2;514(1):1-15 [15878319.001]
  • [Cites] Genes Dev. 2005 May 15;19(10):1129-55 [15905405.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1438-43 [15964995.001]
  • [Cites] J Neurobiol. 2005 Sep 15;64(4):476-90 [16041742.001]
  • [Cites] Nature. 2005 Oct 6;437(7060):894-7 [16208373.001]
  • [Cites] J Natl Cancer Inst. 2005 Nov 2;97(21):1589-600 [16264179.001]
  • [Cites] J Neurosci. 2006 Jan 25;26(4):1107-16 [16436596.001]
  • [Cites] Int J Cancer. 2006 Aug 1;119(3):527-38 [16496386.001]
  • [Cites] J Neurooncol. 2006 May;77(3):273-7 [16614947.001]
  • [Cites] Stem Cells. 2009 Aug;27(8):1722-33 [19544433.001]
  • [Cites] Br J Cancer. 2009 Sep 15;101(6):973-82 [19707201.001]
  • [Cites] Nat Neurosci. 2009 Oct;12(10):1248-56 [19734891.001]
  • [Cites] Mol Cell Neurosci. 2010 Jan;43(1):51-9 [18761091.001]
  • [Cites] Cancer Lett. 2010 Mar 1;289(1):1-10 [19643532.001]
  • [Cites] Int J Biochem Cell Biol. 2010 Mar;42(3):421-4 [19733254.001]
  • [Cites] Toxicol Pathol. 2000 Jan-Feb;28(1):193-201 [10669007.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):109-13 [10973261.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14720-5 [11121071.001]
  • [Cites] Glia. 2001 Apr 1;34(1):1-7 [11284014.001]
  • [Cites] Ann Oncol. 2001 Feb;12(2):259-66 [11300335.001]
  • [Cites] Acta Neuropathol. 2001 Apr;101(4):334-40 [11355304.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8281-6 [11781843.001]
  • [Cites] Am J Surg Pathol. 2002 Apr;26(4):472-8 [11914625.001]
  • [Cites] Lancet. 2002 Mar 23;359(9311):1011-8 [11937180.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] J Neurosci Res. 2002 Sep 15;69(6):976-86 [12205691.001]
  • (PMID = 20045420.001).
  • [ISSN] 1873-7064
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS052738-04; United States / NINDS NIH HHS / NS / R01 NS052738; United States / NINDS NIH HHS / NS / NS042925-07; United States / NINDS NIH HHS / NS / R01 NS042925-07; United States / NINDS NIH HHS / NS / R01 NS042925; United States / NINDS NIH HHS / NS / NS052738-04; United States / NINDS NIH HHS / NS / R01NS42925-07; United States / NCI NIH HHS / CA / 1R01 CA129489-01; United States / NCI NIH HHS / CA / R01 CA129489; United States / NINDS NIH HHS / NS / R01NS052738-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Number-of-references] 118
  • [Other-IDs] NLM/ NIHMS168590; NLM/ PMC2839061
  •  go-up   go-down


14. Xu Q, Yuan X, Xu M, McLafferty F, Hu J, Lee BS, Liu G, Zeng Z, Black KL, Yu JS: Chemokine CXC receptor 4--mediated glioma tumor tracking by bone marrow--derived neural progenitor/stem cells. Mol Cancer Ther; 2009 Sep;8(9):2746-53
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemokine CXC receptor 4--mediated glioma tumor tracking by bone marrow--derived neural progenitor/stem cells.
  • Malignant gliomas manifest frequent tumor recurrence after surgical resection and/or other treatment because of their nature of invasiveness and dissemination.
  • The recognized brain tumor-tracking property of neural progenitor/stem cells opened the possibility of targeting malignant brain tumors using neural progenitor/stem cells.
  • We and others have previously shown that fetal neural progenitor/stem cells can be used to deliver therapeutic molecules to brain tumors.
  • Our recent work has further shown that gene delivery by bone marrow-derived neural progenitor/stem cells achieves therapeutic effects in a glioma model.
  • In this study, we isolate and characterize bone marrow-derived neural progenitor/stem cells, which also express the chemokine receptor chemokine CXC receptor 4 (CXCR4).
  • We show that CXCR4 is required for their chemotaxis and extracellular matrix invasion against a gradient of glioma soluble factors.
  • Furthermore, beta-galactosidase-labeled bone marrow-derived neural progenitor/stem cells implanted in the contralateral side of the brain were shown to track gliomas as early as day 1 and increased through days 3 and 7.
  • Intracranial glioma tracking by bone marrow-derived neural progenitor/stem cells is significantly inhibited by preincubation of bone marrow-derived neural progenitor/stem cells with a blocking anti-CXCR4 antibody, suggesting a CXCR4-dependent tracking mechanism.
  • Glioma tracking bone marrow-derived neural progenitor/stem cells were found to express progenitor/stem cell markers, as well as CXCR4.
  • Although bromodeoxyuridine incorporation assays and proliferating antigen staining indicated that tumor tracking bone marrow-derived neural progenitor/stem cells were mostly nonproliferating, these cells survive in the local tumor environment with little apoptosis.
  • Elucidating the molecular mechanism of brain tumor tracking by adult source stem cells may provide basis for the development of future targeted therapy for malignant brain tumors.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci Res. 2007 Feb 1;85(2):310-20 [17131390.001]
  • [Cites] Immunity. 2006 Dec;25(6):977-88 [17174120.001]
  • [Cites] Ann N Y Acad Sci. 2007 Jun;1106:1-19 [17360804.001]
  • [Cites] Neuroreport. 2007 Oct 29;18(16):1713-7 [17921874.001]
  • [Cites] Stem Cells. 2008 Jan;26(1):223-34 [17932420.001]
  • [Cites] Stem Cells. 2008 Dec;26(12):3018-26 [18787206.001]
  • [Cites] Nat Med. 2000 Apr;6(4):447-50 [10742153.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Nat Immunol. 2002 Jul;3(7):687-94 [12068293.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5657-63 [12384520.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7170-4 [12499252.001]
  • [Cites] Hum Gene Ther. 2003 Sep 1;14(13):1247-54 [12952596.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8877-89 [14695205.001]
  • [Cites] Neoplasia. 2004 May-Jun;6(3):287-93 [15153341.001]
  • [Cites] Lancet Oncol. 2004 Aug;5(8):511-4 [15288241.001]
  • [Cites] Neuroimage. 2004 Sep;23(1):281-7 [15325375.001]
  • [Cites] Ann Neurol. 2005 Jan;57(1):34-41 [15622535.001]
  • [Cites] J Neurooncol. 2005 Feb;71(3):245-55 [15735912.001]
  • [Cites] Neuroscience. 2005;133(1):85-95 [15893633.001]
  • [Cites] Neurosci Lett. 2005 Aug 26;384(3):282-7 [15941621.001]
  • [Cites] Stem Cells. 2005 Aug;23(7):879-94 [15888687.001]
  • [Cites] Brain. 2005 Sep;128(Pt 9):2200-11 [15947066.001]
  • [Cites] J Neurooncol. 2005 Sep;74(3):233-9 [16187020.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2630-8 [16510582.001]
  • [Cites] Exp Cell Res. 2006 May 1;312(8):1265-76 [16434036.001]
  • [Cites] Stem Cells. 2006 May;24(5):1254-64 [16410389.001]
  • [Cites] Exp Neurol. 2006 Jun;199(2):301-10 [16574102.001]
  • [Cites] Blood. 2006 Aug 1;108(3):812-20 [16537807.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8887-96 [16951206.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3928-37 [16912231.001]
  • [Cites] Brain Res. 2006 Dec 6;1123(1):27-33 [17064670.001]
  • [Cites] Exp Cell Res. 2007 Mar 10;313(5):1008-23 [17289022.001]
  • (PMID = 19723878.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS048959; United States / NINDS NIH HHS / NS / NS048959-01; United States / NINDS NIH HHS / NS / R21 NS048879-02; United States / NINDS NIH HHS / NS / NS048879-02; United States / NINDS NIH HHS / NS / R21 NS048879; United States / NINDS NIH HHS / NS / NS048879; United States / NINDS NIH HHS / NS / R01 NS048959-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cxcr4 protein, rat; 0 / Receptors, CXCR4
  • [Other-IDs] NLM/ NIHMS140357; NLM/ PMC2760002
  •  go-up   go-down


15. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells in pediatric brain tumors.
  • Central nervous system (CNS) tumors remain the leading cause of death among pediatric neoplasms.
  • Although standard therapies cure many pediatric CNS tumors, the long-term cognitive and physical consequences of these therapies are devastating.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


16. Das S, Srikanth M, Kessler JA: Cancer stem cells and glioma. Nat Clin Pract Neurol; 2008 Aug;4(8):427-35
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer stem cells and glioma.
  • Recent data suggest that progression of these brain tumors is driven by a small subpopulation of tumor cells, which are termed cancer stem cells (CSCs) because of their capability to self-renew, proliferate and give rise to progeny of multiple neuroepithelial lineages.
  • According to the CSC hypothesis, current therapies that are extremely cytotoxic to the bulk of highly proliferative tumor cells fail to obliterate the relatively quiescent and resistant CSC compartment, thereby allowing these cells to survive and drive tumor recurrence.
  • This Review summarizes current knowledge regarding neural stem cells in the normal adult brain and CSCs in glial tumors and discusses the implications of the CSC hypothesis for the development of future therapies for brain tumors.
  • [MeSH-major] Glioma / pathology. Neoplastic Stem Cells / pathology

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18628751.001).
  • [ISSN] 1745-8358
  • [Journal-full-title] Nature clinical practice. Neurology
  • [ISO-abbreviation] Nat Clin Pract Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 91
  •  go-up   go-down


17. Tabatabai G, Bähr O, Möhle R, Eyüpoglu IY, Boehmler AM, Wischhusen J, Rieger J, Blümcke I, Weller M, Wick W: Lessons from the bone marrow: how malignant glioma cells attract adult haematopoietic progenitor cells. Brain; 2005 Sep;128(Pt 9):2200-11
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lessons from the bone marrow: how malignant glioma cells attract adult haematopoietic progenitor cells.
  • Stem and progenitor cells (PCs) of various lineages have become attractive vehicles to improve therapeutic gene delivery to cancers, notably glioblastoma.
  • Here we report that adult human and murine haematopoietic PCs display a tropism for intracerebral gliomas but not for normal brain tissue in mice.
  • Organotypic hippocampal slice culture and spheroid confrontation assays confirm a directed PC migration towards glioma cells ex vivo and in vitro.
  • RNA interference-mediated disruption of transforming growth factor beta (TGF-beta) synthesis by the glioma cells strongly inhibits PC migration.
  • We delineate a CXC chemokine ligand (CXCL) 12-dependent pathway of TGF-beta-induced PC migration that is facilitated by MMP-9-mediated stem cell factor cleavage in vitro.
  • Thus, we define here the molecular mechanism underlying the glioma tropism of the probably most easily accessible PC population suitable for cancer therapy, that is, adult haematopoietic PC.
  • [MeSH-major] Brain Neoplasms / pathology. Chemotaxis. Glioma / pathology. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / cytology
  • [MeSH-minor] Adult. Animals. Chemokine CXCL12. Chemokines, CXC / physiology. Humans. Matrix Metalloproteinase 9 / physiology. Mice. Mice, Nude. Neoplasm Transplantation. Stem Cell Factor / physiology. Transforming Growth Factor beta / physiology. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15947066.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Stem Cell Factor; 0 / Transforming Growth Factor beta; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


18. Giussani C, Poliakov A, Ferri RT, Plawner LL, Browd SR, Shaw DW, Filardi TZ, Hoeppner C, Geyer JR, Olson JM, Douglas JG, Villavicencio EH, Ellenbogen RG, Ojemann JG: DTI fiber tracking to differentiate demyelinating diseases from diffuse brain stem glioma. Neuroimage; 2010 Aug 1;52(1):217-23
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DTI fiber tracking to differentiate demyelinating diseases from diffuse brain stem glioma.
  • OBJECT: Intrinsic diffuse brainstem tumors and demyelinating diseases primarily affecting the brainstem can share common clinical and radiological features, sometimes making the diagnosis difficult especially at the time of first clinical presentation.
  • To explore the potential usefulness of new MRI sequences in particular diffusion tensor imaging fiber tracking in differentiating these two pathological entities, we review a series of brainstem tumors and demyelinating diseases treated at our institution.
  • MATERIAL AND METHODS: The clinical history including signs and symptoms and MRI findings of three consecutive demyelinating diseases involving the brainstem that presented with diagnostic uncertainty and three diffuse intrinsic brainstem tumors were reviewed, along with a child with a supratentorial tumor for comparison.
  • RESULTS: Routine MR imaging was unhelpful in differentiating between intrinsic tumor and demyelination.
  • In contrast, retrospective DTI fiber tracking clearly differentiated the pathology showing deflection of the pyramidal tracts posteriorly and laterally in the case of intrinsic brainstem tumors and, in the case of demyelinating disease, poorly represented and truncated fibers.
  • CONCLUSION: DTI fiber tracking of the pyramid tracts in patients with suspected intrinsic brainstem tumor or demyelinating disease presents two clearly different patterns that may help in differentiating between these two pathologies when conventional MRI and clinical data are inconclusive.
  • [MeSH-major] Brain Diseases / pathology. Brain Stem Neoplasms / pathology. Demyelinating Diseases / pathology. Diagnosis, Computer-Assisted / methods. Diffusion Tensor Imaging / methods. Glioma / pathology
  • [MeSH-minor] Adolescent. Brain Stem / pathology. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging / methods. Male. Pyramidal Tracts / pathology. Retrospective Studies. Supratentorial Neoplasms / diagnosis. Supratentorial Neoplasms / pathology. Young Adult

  • Genetic Alliance. consumer health - Demyelinating Diseases.
  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20363335.001).
  • [ISSN] 1095-9572
  • [Journal-full-title] NeuroImage
  • [ISO-abbreviation] Neuroimage
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Pisati F, Belicchi M, Acerbi F, Marchesi C, Giussani C, Gavina M, Javerzat S, Hagedorn M, Carrabba G, Lucini V, Gaini SM, Bresolin N, Bello L, Bikfalvi A, Torrente Y: Effect of human skin-derived stem cells on vessel architecture, tumor growth, and tumor invasion in brain tumor animal models. Cancer Res; 2007 Apr 1;67(7):3054-63
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of human skin-derived stem cells on vessel architecture, tumor growth, and tumor invasion in brain tumor animal models.
  • New experimental approaches have shown tumor regression after the grafting of neural stem cells and human mesenchymal stem cells into experimental intracranial gliomas of adult rodents.
  • In the present study, we evaluated the tumor targeting and antitumor activity of human skin-derived stem cells (hSDSCs) in human brain tumor models.
  • The hSDSCs exhibit tumor targeting characteristics in vivo when injected into the controlateral hemisphere or into the tail vein of mice.
  • When implanted directly into glioblastomas, hSDSCs distributed themselves extensively throughout the tumor mass, reduced tumor vessel density, and decreased angiogenic sprouts.
  • In addition, transplanted hSDSCs differentiate into pericyte cell and release high amounts of human transforming growth factor-beta1 with low expression of vascular endothelial growth factor, which may contribute to the decreased tumor cell invasion and number of tumor vessels.
  • In long-term experiments, the hSDSCs were also able to significantly inhibit tumor growth and to prolong animal survival.
  • Similar behavior was seen when hSDSCs were implanted into two different tumor models, the chicken embryo experimental glioma model and the transgenic Tyrp1-Tag mice.
  • Taken together, these data validate the use of hSDSCs for targeting human brain tumors.
  • [MeSH-major] Brain Neoplasms / blood supply. Brain Neoplasms / therapy. Glioblastoma / blood supply. Glioblastoma / therapy. Skin / cytology. Stem Cell Transplantation. Stem Cells / physiology
  • [MeSH-minor] Animals. Cell Growth Processes / physiology. Cell Line, Tumor. Chick Embryo. Chorioallantoic Membrane / blood supply. Humans. Mice. Mice, Nude. Mice, Transgenic. Neoplasm Invasiveness. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Neovascularization, Pathologic / therapy. Transforming Growth Factor beta1 / biosynthesis. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17409412.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1
  •  go-up   go-down


20. Mori K, Iwata J, Miyazaki M, Osada H, Tange Y, Yamamoto T, Aiko Y, Tamura M, Shiroishi T: Bystander killing effect of tymidine kinase gene-transduced adult bone marrow stromal cells with ganciclovir on malignant glioma cells. Neurol Med Chir (Tokyo); 2010;50(7):545-53
Hazardous Substances Data Bank. GANCICLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bystander killing effect of tymidine kinase gene-transduced adult bone marrow stromal cells with ganciclovir on malignant glioma cells.
  • Transduction of the suicide gene of Herpes simplex virus thymidine kinase (Hsv-tk) into glioma cells or neural stem cells combined with pro-drug ganciclovir (GCV) treatment has been effective to treat experimental glioma in the rat through the bystander effect.
  • Bone marrow stromal cells (MSCs) in the adult bone marrow have tropism for brain tumors and act as tumor stromal cells.
  • Whether adult MSCs expressing Hsv-tk can also act as effector cells of the bystander killing effect on murine glioma cells was investigated.
  • In vitro study of co-culture between 9L/LacZ (9L) glioma cells and Hsv-tk-transduced MSCs (MSCs/tk(+)) followed by GCV administration in the culture medium resulted in apparent nuclear morphological changes in the 9L glioma cells surrounding the MSCs/tk(+).
  • 9L glioma cell survival in the presence of MSCs/tk(+) and GCV treatment was quantitatively measured and showed significant decrease of 9L glioma cell proliferation with higher MSCs/tk(+) ratio and GCV concentration.
  • Intracerebral co-inoculation experiments in Fisher rats used 9L glioma cells and either MSCs/tk(+) or Hsv-tk-non-transduced MSCs (MSCs/tk(-)) followed by intraperitoneal injection of GCV (100 mg/kg, daily for 7 days).
  • The animals co-inoculated with 9L glioma cells and MSCs/tk(+) showed significant retardation of tumor growth and prolongation of survival time compared with the animals with 9L glioma cells and MSCs/tk(-).
  • Quantitative findings were established of the novel effects of adult MSCs/tk(+) as effector cells of the bystander killing effect on glioma cells.
  • [MeSH-major] Antiviral Agents / pharmacology. Bone Marrow Cells. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Bystander Effect / genetics. Cell Survival / genetics. Ganciclovir / pharmacology. Genes, Transgenic, Suicide / genetics. Genetic Therapy / methods. Glioma / genetics. Glioma / pathology. Simplexvirus / enzymology. Simplexvirus / genetics. Stromal Cells. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / genetics. Cell Line, Tumor. Humans. In Vitro Techniques. Lac Operon / genetics. Male. Mice. Neoplasm Transplantation. Rats. Rats, Inbred F344

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20671379.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
  •  go-up   go-down


21. Zhang M, Song T, Yang L, Chen R, Wu L, Yang Z, Fang J: Nestin and CD133: valuable stem cell-specific markers for determining clinical outcome of glioma patients. J Exp Clin Cancer Res; 2008;27:85
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nestin and CD133: valuable stem cell-specific markers for determining clinical outcome of glioma patients.
  • AIM: Gliomas represent the most frequent neoplasm of the central nervous system.
  • Unfortunately, surgical cure of it is practically impossible and their clinical course is primarily determined by the biological behaviors of the tumor cells.
  • The aim of this study was to investigate the correlation of the stem cell markers Nestin and CD133 expression with the grading of gliomas, and to evaluate their prognostic value.
  • METHODS: The tissue samples consisted of 56 low- (WHO grade II), 69 high- (WHO grade III, IV) grade gliomas, and 10 normal brain tissues.
  • RESULTS: Immunohistochemical analysis with anti-Nestin and anti-CD133 antibodies revealed dense and spotty staining in the tumor cells and their expression levels became significantly higher as the glioma grade advanced (p < 0.05).
  • The low expression of the two markers significantly correlated with long survival of the glioma patients (p < 0.05).
  • A combined detection of Nestin/CD133 co-expression may benefit us in the prediction of aggressive nature of this tumor.
  • [MeSH-major] Antigens, CD / biosynthesis. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Glioma / metabolism. Glycoproteins / biosynthesis. Intermediate Filament Proteins / biosynthesis. Neoplastic Stem Cells / metabolism. Nerve Tissue Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. Nestin. Peptides. Prognosis. Young Adult

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1383-7 [10728703.001]
  • [Cites] Exp Neurol. 2000 Feb;161(2):585-96 [10686078.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14720-5 [11121071.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2387-95 [11489817.001]
  • [Cites] J Physiol Paris. 2002 Jan-Mar;96(1-2):81-90 [11755786.001]
  • [Cites] Exp Neurol. 2002 Mar;174(1):89-95 [11869037.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2055-61 [14630820.001]
  • [Cites] Curr Neurol Neurosci Rep. 2004 May;4(3):228-33 [15102349.001]
  • [Cites] J Neurooncol. 2004 Jun;68(2):113-21 [15218947.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Cell. 1990 Feb 23;60(4):585-95 [1689217.001]
  • [Cites] Radiother Oncol. 1991 Feb;20(2):99-110 [1851573.001]
  • [Cites] Lab Invest. 1992 Mar;66(3):303-13 [1538585.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12425-30 [9356465.001]
  • [Cites] J Mol Med (Berl). 2004 Oct;82(10):656-70 [15316624.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] J Clin Pathol. 2005 Feb;58(2):222-3 [15677549.001]
  • [Cites] Stem Cells. 2005 Jun-Jul;23(6):791-804 [15917475.001]
  • [Cites] BMC Cancer. 2006;6:32 [16457706.001]
  • [Cites] Virchows Arch. 2006 Apr;448(4):485-92 [16418842.001]
  • [Cites] Acta Neuropathol. 2006 Mar;111(3):272-7 [16538520.001]
  • [Cites] Neurosci Lett. 2006 May 29;400(1-2):80-5 [16529857.001]
  • [Cites] J Neurooncol. 2006 Dec;80(3):227-33 [16826367.001]
  • [Cites] Surg Neurol. 2007 Aug;68(2):133-43; discussion 143-4 [17537489.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6970-7 [18056172.001]
  • [Cites] J Neurooncol. 2008 Jan;86(1):31-45 [17611714.001]
  • [Cites] J Clin Pathol. 2008 Apr;61(4):467-73 [17873113.001]
  • [Cites] Brain Pathol. 2008 Jul;18(3):370-7 [18371181.001]
  • (PMID = 19108713.001).
  • [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
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Peptides
  • [Other-IDs] NLM/ PMC2633002
  •  go-up   go-down


22. Okamoto K, Furusawa T, Ishikawa K, Sasai K, Tokiguchi S: Focal T2 hyperintensity in the dorsal brain stem in patients with vestibular schwannoma. AJNR Am J Neuroradiol; 2006 Jun-Jul;27(6):1307-11
MedlinePlus Health Information. consumer health - MRI Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Focal T2 hyperintensity in the dorsal brain stem in patients with vestibular schwannoma.
  • BACKGROUND AND PURPOSE: The vestibular nucleus cannot be visualized on MR imaging, but some patients with vestibular schwannoma show a tiny area of hyperintensity in the dorsal brain stem on T2-weighted images.
  • METHODS: We retrospectively reviewed the postoperative MR images of 53 patients with cerebellopontine angle tumor.
  • Surgical and histopathologic diagnosis was vestibular schwannoma (41/53 = 77%), meningioma (7/53 = 13%), epidermoid cyst (3/53 = 6%), glioma with exophytic growth (1/53 = 2%), and chordoma (1/53 = 2%).
  • If such hyperintensity is seen in a patient with a large cerebellopontine angle tumor, a diagnosis of vestibular schwannoma is suggested.
  • [MeSH-major] Brain Stem / pathology. Magnetic Resonance Imaging. Neuroma, Acoustic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Cerebellar Neoplasms / diagnosis. Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / surgery. Cerebellopontine Angle. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Schwannoma.
  • MedlinePlus Health Information. consumer health - Acoustic Neuroma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16775286.001).
  • [ISSN] 0195-6108
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


23. Chu L, Huang Q, Zhai DZ, Zhu Q, Huo HM, Dong J, Qian ZY, Wang AD, Lan Q, Gao YL: [Expression and significance of ABCG2 in human malignant glioma]. Ai Zheng; 2007 Oct;26(10):1090-4
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression and significance of ABCG2 in human malignant glioma].
  • BACKGROUND & OBJECTIVE: ATP-binding cassette transporter protein ABCG2 is a marker derived from hematopoietic stem cells.
  • However, its role in tumorigenesis and malignant progression of glioma is unclear.
  • METHODS: A microarray chip containing glioma tissues of different malignant grades, implanted glioma xenografts in nude mice, spheroids of glioma cell lines and glioma stem cells was prepared and examined for the expression of ABCG2 with immunohistochemical staining.
  • RESULTS: The positive rate of ABCG2 was 26.8% in the 71 specimens of human glioma tissues, with 11.1% in grade I gliomas, 8% in grade II gliomas, 43.5% in grade III gliomas, and 42.9% in grade IV gliomas; it was significantly higher in grade III-IV gliomas than in grade I-II gliomas (chi2=10.710, P=0.001).
  • The positive rate of ABCG2 was 100% in implanted glioma xenografts in nude mice, gliomas stem cells, and neural stem cells.
  • The positive cells surrounded and invaded into vessels in glioma tissues.
  • CONCLUSIONS: ABCG2 is overexpressed in glioma stem cells, glioma tissues of higher grades, and implanted glioma xenografts.
  • The positive cells distribute around vessels in glioma tissues.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Neoplasm Proteins / metabolism. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Bone Marrow Cells / metabolism. Brain / metabolism. Brain / pathology. Cell Line, Tumor. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Middle Aged. Neoplasm Transplantation. Stem Cells / metabolism. Tissue Array Analysis. Young Adult

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17927879.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Neoplasm Proteins
  •  go-up   go-down


24. Amano S, Li S, Gu C, Gao Y, Koizumi S, Yamamoto S, Terakawa S, Namba H: Use of genetically engineered bone marrow-derived mesenchymal stem cells for glioma gene therapy. Int J Oncol; 2009 Dec;35(6):1265-70
Hazardous Substances Data Bank. GANCICLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of genetically engineered bone marrow-derived mesenchymal stem cells for glioma gene therapy.
  • In our previous study, we successfully treated an established C6 brain tumor using neural stem cells transduced with the herpes simplex virus-thymidine kinase gene (HSVtk) and ganciclovir in the rat.
  • In the present study, we investigated the use of mesenchymal stem cells (MSCs), obtained from adult rats and transduced with HSVtk (MSCtk cells), instead of neural stem cells because MSCs are much easier to obtain from the adult subjects.
  • Those cells were used for in vitro co-culture study and in vivo co-implantation study with C6 rat glioma cells to examine bystander tumoricidal effect, which revealed a sufficient bystander effect and only 1/32 MSCtk cells were needed for complete tumor eradication.
  • In vitro bystander effect was also observed in a real-time fashion using a culture microscope and it was shown that only tumor cells that had contact with MSCtk cells died.
  • In vivo treatment study of an established C6 brain tumor with an intratumoral injection of MSCtk cells followed by systemic ganciclovir administration demonstrated a significant reduction of the tumor size and a significant survival prolongation.
  • The treatment strategy using MSCtk and ganciclovir (MSCtk therapy) is more feasible and practical for clinical application than the method using neural stem cells.
  • [MeSH-major] Antiviral Agents / therapeutic use. Brain Neoplasms / therapy. Ganciclovir / therapeutic use. Genetic Therapy / methods. Glioma / therapy. Mesenchymal Stem Cell Transplantation

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19885548.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
  •  go-up   go-down


25. Strojnik T, Røsland GV, Sakariassen PO, Kavalar R, Lah T: Neural stem cell markers, nestin and musashi proteins, in the progression of human glioma: correlation of nestin with prognosis of patient survival. Surg Neurol; 2007 Aug;68(2):133-43; discussion 143-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neural stem cell markers, nestin and musashi proteins, in the progression of human glioma: correlation of nestin with prognosis of patient survival.
  • BACKGROUND: The IF protein nestin and the RNA-binding protein musashi are expressed by neural progenitor cells during CNS development.
  • METHODS: The levels of nestin, musashi, and cathepsins B and L were assessed by immunohistochemical analysis of biopsies from 87 patients with primary CNS tumors.
  • To confirm the immunohistochemical data, nestin expression was analyzed by real-time PCR in 12 brain tumor biopsies.
  • The exact location of nestin-positive cells was determined by mapping the distribution of nestin in a highly invasive human glioma xenograft model.
  • IHC staining of nestin in a xenograft model showed that its expression is localized mainly in the invasive tumor cells at the tumor periphery.
  • CONCLUSIONS: Nestin is shown to be a strong prognostic marker for glioma malignancy.
  • The presented data links the invasive glioma cells to CNS precursor cells, indicating that the most malignant cells in the gliomas may well be closely related to the glioma stem cells.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioma / metabolism. Glioma / pathology. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Cathepsin B / metabolism. Cathepsin L. Cathepsins / metabolism. Child. Child, Preschool. Cysteine Endopeptidases / metabolism. Female. Humans. Male. Middle Aged. Nestin. RNA, Messenger / metabolism. RNA-Binding Proteins / metabolism. Rats. Survival Rate

  • 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 = 17537489.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / MSI1 protein, human; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L; EC 3.4.22.15 / Ctsl protein, rat
  •  go-up   go-down


26. Fomchenko EI, Holland EC: Platelet-derived growth factor-mediated gliomagenesis and brain tumor recruitment. Neurosurg Clin N Am; 2007 Jan;18(1):39-58, viii
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet-derived growth factor-mediated gliomagenesis and brain tumor recruitment.
  • Platelet-derived growth factor (PDGF) is a growth factor family of ligands and receptors known to activate phosphatidylinositol 3-kinase, mitogen-activated protein kinase, Jak family kinase, Src family kinase, and phospholipase Cgamma signal transduction pathways, some of which have been causally linked to glioma formation.
  • Many researchers view brain tumors as clonal entities derived from the cancer stem cell; however, recent documentation of the importance of the tumor microenvironment for glioma initiation and progression as well as the ability of neural stem or progenitor cells to migrate toward the sites of injury or tumor formation reveals additional complexities in brain tumorigenesis.
  • Paracrine effects of PDGF in animal models of gliomagenesis, continued adult neurogenesis capable of increasing in response to brain injury, and the growth factor-rich environment of brain tumors suggest that recruitment may play a role in gliomagenesis.
  • In this view, glioma formation involves recruitment of cells from the adjacent brain and possibly other sites.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / physiopathology. Glioma / pathology. Glioma / physiopathology. Platelet-Derived Growth Factor / metabolism. Stem Cells / pathology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 = 17244553.001).
  • [ISSN] 1042-3680
  • [Journal-full-title] Neurosurgery clinics of North America
  • [ISO-abbreviation] Neurosurg. Clin. N. Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099489; United States / NCI NIH HHS / CA / R01 CA100688; United States / NCI NIH HHS / CA / U01 CA894314-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor
  • [Number-of-references] 179
  •  go-up   go-down


27. Gururangan S, Chi SN, Young Poussaint T, Onar-Thomas A, Gilbertson RJ, Vajapeyam S, Friedman HS, Packer RJ, Rood BN, Boyett JM, Kun LE: Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study. J Clin Oncol; 2010 Jun 20;28(18):3069-75
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study.
  • PURPOSE: A phase II study of bevacizumab (BVZ) plus irinotecan (CPT-11) was conducted in children with recurrent malignant glioma (MG) and intrinsic brainstem glioma (BSG).
  • Toxicities related to BVZ included grade 1 to 3 fatigue in seven patients, grade 1 to 2 hypertension in seven patients, grade 1 CNS hemorrhage in four patients, and grade 4 CNS ischemia in two patients.
  • CONCLUSION: BVZ plus CPT-11 was well-tolerated but had minimal efficacy in children with recurrent malignant glioma and brainstem glioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Child. Diffusion Magnetic Resonance Imaging. Humans. Phosphorylation. Survival Rate. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Young Adult

  • 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.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Nat Rev Cancer. 2008 Apr;8(4):309-16 [18337733.001]
  • [Cites] Neuro Oncol. 2008 Aug;10(4):624-30 [18539884.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Oct 1;72(2):383-9 [18793954.001]
  • [Cites] Pediatr Blood Cancer. 2008 Dec;51(6):806-11 [18802947.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6371-5 [18927275.001]
  • [Cites] J Neurooncol. 2009 Feb;91(3):329-36 [18953493.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1878-86 [10766175.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5598-605 [11114740.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):2064-72 [11597385.001]
  • [Cites] NMR Biomed. 2002 Feb;15(1):6-17 [11840548.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):237-53 [12187958.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3542; author reply 3543 [12972536.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 [1688381.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):271-5 [8508417.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1516-25 [10334539.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] Am J Health Syst Pharm. 2004 Nov 1;61(21 Suppl 5):S21-6 [15552623.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):172-87 [15687360.001]
  • [Cites] Neurol Res. 2005 Jun;27(4):371-7 [15949234.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2347-55 [15985545.001]
  • [Cites] Oncology. 2005;69 Suppl 3:25-33 [16301833.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1364-71 [16463390.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • (PMID = 20479404.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01 CA081457; United States / NCRR NIH HHS / RR / M01RR00188; United States / NCI NIH HHS / CA / U01CA81457
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2903337
  •  go-up   go-down


28. Demeter K, Zádori A, Agoston VA, Madarász E: Studies on the use of NE-4C embryonic neuroectodermal stem cells for targeting brain tumour. Neurosci Res; 2005 Nov;53(3):331-42
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Studies on the use of NE-4C embryonic neuroectodermal stem cells for targeting brain tumour.
  • Neural stem cells were suggested to migrate to and invade intracranial gliomas.
  • In the presented studies, interactions of NE-4C embryonic neural stem cells were investigated with C6 and Gl261, LL and U87, glioblastoma cells or with primary astrocytes.
  • Glioma-derived humoral factors did not influence the proliferation of stem cells.
  • In chimera-aggregates, all types of glioma cells co-aggregated with astrocytes, but most of them segregated from stem cells.
  • Complete intercalation of stem and tumour cells was detected only in chimera-aggregates of Gl261 glioma and NE-4C cells.
  • If mixed suspensions of NE-4C and Gl261 cells were injected into the brain, stem cells survived and grew inside the tumour mass.
  • NE-4C stem cells, however, did not migrate towards the tumour, if implanted near to Gl261 tumours established in the adult mouse forebrain.
  • The observations indicate that not all types of stem cells could be used for targeting all sorts of brain tumours.
  • [MeSH-major] Brain Neoplasms / therapy. Brain Tissue Transplantation / methods. Ectoderm / transplantation. Stem Cell Transplantation / methods. Stem Cells / physiology
  • [MeSH-minor] Animals. Astrocytes / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation / drug effects. Coculture Techniques. Glioblastoma / physiopathology. Glioblastoma / therapy. Graft Survival / physiology. Growth Substances / metabolism. Growth Substances / pharmacology. Humans. Mice. Neoplasm Invasiveness / physiopathology. Rats

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16183159.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Growth Substances
  •  go-up   go-down


29. Jacques TS, Swales A, Brzozowski MJ, Henriquez NV, Linehan JM, Mirzadeh Z, O' Malley C, Naumann H, Alvarez-Buylla A, Brandner S: Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes. EMBO J; 2010 Jan 6;29(1):222-35
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes.
  • It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor cell population in the subventricular zone of the post-natal brain.
  • However, the influence of the initial genetic mutation on the phenotype as well as the contribution of mature astrocytes to the formation of brain tumours is still not understood.
  • We deleted Rb/p53, Rb/p53/PTEN or PTEN/p53 in adult subventricular stem cells; in ectopically neurografted stem cells; in mature parenchymal astrocytes and in transplanted astrocytes.
  • We found that only stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.
  • This suggests a cell autonomous mechanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form brain tumours in adults.
  • Our study underlines an important role of stem cells and the relevance of initial genetic mutations in the pathogenesis and phenotype of brain tumours.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 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] Nature. 2008 Oct 23;455(7216):1129-33 [18948956.001]
  • [Cites] Cancer Cell. 2008 Aug 12;14(2):135-45 [18691548.001]
  • [Cites] Nat Med. 2009 Jan;15(1):110-6 [19122659.001]
  • [Cites] Genes Dev. 2009 Jan 15;23(2):157-70 [19171780.001]
  • [Cites] Cancer Cell. 2009 Jun 2;15(6):514-26 [19477430.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2008;73:357-65 [19022766.001]
  • [Cites] Neurosci Lett. 1999 Dec 10;276(3):197-200 [10612639.001]
  • [Cites] Curr Opin Genet Dev. 2000 Feb;10(1):94-9 [10679383.001]
  • [Cites] Genes Dev. 2000 Apr 15;14(8):994-1004 [10783170.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Nat Neurosci. 2000 Nov;3(11):1091-7 [11036265.001]
  • [Cites] Nat Rev Genet. 2001 Feb;2(2):120-9 [11253051.001]
  • [Cites] EMBO Rep. 2001 Apr;2(4):292-7 [11306549.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3826-36 [11325859.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9209-14 [11481484.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6674-8 [11559533.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):157-68 [12086874.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Development. 2002 Jul;129(14):3513-22 [12091320.001]
  • [Cites] Cancer Lett. 2002 Dec 15;188(1-2):1-7 [12406541.001]
  • [Cites] Neuron. 2002 Dec 19;36(6):1021-34 [12495619.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):453-8 [12778135.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):133-46 [12957288.001]
  • [Cites] Neuron. 2004 Jun 24;42(6):885-8 [15207233.001]
  • [Cites] Nucleic Acids Res. 1997 May 1;25(9):1766-73 [9108159.001]
  • [Cites] Oncogene. 1998 Jul 9;17(1):1-12 [9671308.001]
  • [Cites] Development. 1998 Aug;125(16):3167-77 [9671589.001]
  • [Cites] J Neurobiol. 1998 Aug;36(2):105-10 [9712298.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3644-9 [9851971.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6937-41 [10359817.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2065-9 [15781613.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5172-80 [15958561.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Development. 2005 Dec;132(24):5577-88 [16314489.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] J Neurosci. 2006 Sep 13;26(37):9593-602 [16971543.001]
  • [Cites] Methods Enzymol. 2006;419:3-23 [17141049.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Science. 2007 Jul 20;317(5836):381-4 [17615304.001]
  • [Cites] Cancer Cell. 2007 Oct;12(4):328-41 [17936558.001]
  • [Cites] Genesis. 2007 Dec;45(12):768-75 [18064676.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3286-94 [18451155.001]
  • [Cites] Neuron. 2008 Jun 26;58(6):832-46 [18579075.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):45-56 [19111880.001]
  • (PMID = 19927122.001).
  • [ISSN] 1460-2075
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD032116; United States / NICHD NIH HHS / HD / R37 HD032116; United States / NICHD NIH HHS / HD / HD-32116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / glial fibrillary astrocytic protein, mouse; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2808375
  •  go-up   go-down


30. Christensen K, Aaberg-Jessen C, Andersen C, Goplen D, Bjerkvig R, Kristensen BW: Immunohistochemical expression of stem cell, endothelial cell, and chemosensitivity markers in primary glioma spheroids cultured in serum-containing and serum-free medium. Neurosurgery; 2010 May;66(5):933-47
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of stem cell, endothelial cell, and chemosensitivity markers in primary glioma spheroids cultured in serum-containing and serum-free medium.
  • METHODS: Paraffin sections of the original surgical specimens, primary glioma spheroids, and U87 derived spheroids were stained immunohistochemically with the stem cell markers CD133, podoplanin, Sox2, Bmi-1, and nestin; the endothelial cell markers CD31, CD34, and Von Willebrand Factor (VWF); the chemosensitivity markers P-glycoprotein and tissue inhibitor of metalloproteinases-1 (TIMP-1); and glial fibrillary acidic protein, neural cell adhesion molecule CD56, and the proliferation marker Ki67.
  • CONCLUSION: In this first study of the influence of SFM on primary glioma spheroids, the conditions favored an in vivo-like phenotype with increased expression of CD133.
  • More vascular structures were found in SFM, suggesting that the close relationship between blood vessels and tumor stem-like cells was better preserved in this medium.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cell Culture Techniques / methods. Culture Media, Serum-Free / pharmacology. Glioma / metabolism. Spheroids, Cellular / cytology
  • [MeSH-minor] Adult. Aged. Culture Media. Endothelial Cells / cytology. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Epidermal Growth Factor / pharmacology. Female. Fibroblast Growth Factor 2 / pharmacology. Humans. Immunohistochemistry. Male. Middle Aged. Phenotype. Stem Cells / cytology. Stem Cells / drug effects. Stem Cells / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • 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
  • (PMID = 20404698.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Culture Media; 0 / Culture Media, Serum-Free; 103107-01-3 / Fibroblast Growth Factor 2; 62229-50-9 / Epidermal Growth Factor
  •  go-up   go-down


31. Yuan X, Hu J, Belladonna ML, Black KL, Yu JS: Interleukin-23-expressing bone marrow-derived neural stem-like cells exhibit antitumor activity against intracranial glioma. Cancer Res; 2006 Mar 1;66(5):2630-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-23-expressing bone marrow-derived neural stem-like cells exhibit antitumor activity against intracranial glioma.
  • Neural progenitor-like cells have been isolated from bone marrow and the cells have the ability of tracking intracranial tumor.
  • However, the capacity of the cells to deliver molecules for activating immune response against intracranial tumor and the identity of cellular and molecular factors that are involved in such immune responses have yet to be elucidated.
  • Here, we isolated neural stem-like cells from the bone marrow of adult mice.
  • The isolated cells were capable of producing progenies of three lineages, neurons, astrocytes, and oligodendrocytes, in vitro and tracking glioma in vivo.
  • By genetically manipulating bone marrow-derived neural stem-like cells (BM-NSC) to express a recently discovered cytokine, interleukin (IL)-23, the cells showed protective effects in intracranial tumor-bearing C57BL/6 mice.
  • Furthermore, the IL-23-expressing BM-NSC-treated survivors were resistant to the same tumor rechallenge associated with enhanced IFN-gamma, but not IL-17, expression in the brain tissue.
  • [MeSH-major] Bone Marrow Cells / immunology. Brain Neoplasms / therapy. Glioma / therapy. Immunotherapy, Adoptive / methods. Interleukins / biosynthesis. Neurons / immunology. Stem Cells / immunology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16510582.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1K23 NS02232; United States / NINDS NIH HHS / NS / 1R01 NS048959; United States / NINDS NIH HHS / NS / 1R21 NS048879
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Il23a protein, mouse; 0 / Interleukin-23; 0 / Interleukin-23 Subunit p19; 0 / Interleukins
  •  go-up   go-down


32. Ligon KL, Huillard E, Mehta S, Kesari S, Liu H, Alberta JA, Bachoo RM, Kane M, Louis DN, Depinho RA, Anderson DJ, Stiles CD, Rowitch DH: Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma. Neuron; 2007 Feb 15;53(4):503-17
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Olig2-regulated lineage-restricted pathway controls replication competence in neural stem cells and malignant glioma.
  • Recent studies have identified stem cells in brain cancer.
  • However, their relationship to normal CNS progenitors, including dependence on common lineage-restricted pathways, is unclear.
  • We observe expression of the CNS-restricted transcription factor, OLIG2, in human glioma stem and progenitor cells reminiscent of type C transit-amplifying cells in germinal zones of the adult brain.
  • Olig2 function is required for proliferation of neural progenitors and for glioma formation in a genetically relevant murine model.
  • Moreover, we show p21(WAF1/CIP1), a tumor suppressor and inhibitor of stem cell proliferation, is directly repressed by OLIG2 in neural progenitors and gliomas.
  • Our findings identify an Olig2-regulated lineage-restricted pathway critical for proliferation of normal and tumorigenic CNS stem cells.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BROMODEOXYURIDINE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2006 Jul 26;26(30):7907-18 [16870736.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Nature. 2006 Sep 28;443(7110):448-52 [16957738.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Genes Dev. 2004 Mar 15;18(6):629-40 [15075291.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Oct;62(10):1052-9 [14575240.001]
  • [Cites] Neuron. 2003 Oct 30;40(3):485-99 [14642274.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 3;101(5):1374-9 [14734810.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Feb;63(2):170-9 [14989603.001]
  • [Cites] Development. 2004 Mar;131(6):1289-98 [14960493.001]
  • [Cites] Science. 2004 Apr 23;304(5670):554 [15016963.001]
  • [Cites] Nat Rev Drug Discov. 2004 May;3(5):430-46 [15136790.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 May;63(5):499-509 [15198128.001]
  • [Cites] Science. 2004 Sep 3;305(5689):1466-70 [15353804.001]
  • [Cites] J Cell Biol. 2004 Sep 27;166(7):963-8 [15452140.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Brain Res. 1972 Aug 25;43(2):429-35 [4559710.001]
  • [Cites] Cancer Res. 1988 Oct 1;48(19):5433-9 [3416300.001]
  • [Cites] Cell. 2002 Apr 5;109(1):61-73 [11955447.001]
  • [Cites] Cell. 2002 Apr 5;109(1):75-86 [11955448.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):125-8 [12086870.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Curr Biol. 2002 Jul 9;12(13):1157-63 [12121626.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):237-53 [12187958.001]
  • [Cites] J Neurooncol. 2002 Sep;59(2):143-9 [12241107.001]
  • [Cites] Science. 2002 Oct 18;298(5593):597-600 [12228720.001]
  • [Cites] Science. 2002 Oct 18;298(5593):601-4 [12228721.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] J Neurosurg. 2003 Aug;99(2):344-50 [12924709.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] J Neurosci. 2003 Oct 22;23(29):9547-56 [14573534.001]
  • [Cites] Neuron. 1997 Apr;18(4):553-62 [9136765.001]
  • [Cites] Cancer Res. 1997 Oct 1;57(19):4187-90 [9331072.001]
  • [Cites] Oncogene. 1998 Apr 30;16(17):2259-64 [9619835.001]
  • [Cites] Curr Opin Cell Biol. 1998 Dec;10(6):791-7 [9914179.001]
  • [Cites] Curr Opin Oncol. 1999 May;11(3):162-7 [10328589.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23):2963-72 [15574597.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9392-400 [15558011.001]
  • [Cites] Science. 2004 Dec 17;306(5704):2111-5 [15604411.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):565-76 [15607961.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D91-7 [15608292.001]
  • [Cites] N Engl J Med. 2004 Dec 30;351(27):2883 [15625347.001]
  • [Cites] Genes Dev. 2005 Jan 15;19(2):282-94 [15655114.001]
  • [Cites] J Neurosci. 2005 Feb 9;25(6):1354-65 [15703389.001]
  • [Cites] Genes Dev. 2005 Mar 15;19(6):756-67 [15769947.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 19;102(16):5814-9 [15827123.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):3980-5 [15899785.001]
  • [Cites] BMC Bioinformatics. 2005;6:79 [15799782.001]
  • [Cites] Exp Neurol. 2005 Aug;194(2):320-32 [15992799.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Nat Neurosci. 2005 Jul;8(7):865-72 [15951811.001]
  • [Cites] Development. 2006 Jan;133(2):363-9 [16368933.001]
  • [Cites] J Cell Sci. 2006 Apr 1;119(Pt 7):1433-41 [16554441.001]
  • [Cites] Dev Biol. 2006 May 15;293(2):348-57 [16537079.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 16;103(20):7853-8 [16682644.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):425-36 [16723989.001]
  • [Cites] Nucleic Acids Res. 1990 Jun 25;18(12):3587-96 [2194165.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] Science. 1995 Aug 4;269(5224):682-5 [7624798.001]
  • [Cites] Science. 1996 Mar 29;271(5257):1861-4 [8596954.001]
  • [Cites] Mol Cell Biol. 1996 Aug;16(8):4327-36 [8754833.001]
  • [Cites] J Neurooncol. 1997 Jan;31(1-2):17-23 [9049826.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3497-502 [10737801.001]
  • [Cites] Neuron. 2001 Apr;30(1):19-35 [11343642.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] J Neurooncol. 2001 Feb;51(3):245-64 [11407596.001]
  • [Cites] Lancet. 2001 Jul 28;358(9278):298-300 [11498220.001]
  • [Cites] J Neurooncol. 2001 May;52(3):263-72 [11519857.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10851-6 [11526205.001]
  • [Cites] Neuron. 2001 Sep 13;31(5):757-71 [11567615.001]
  • [Cites] Neuron. 2001 Sep 13;31(5):773-89 [11567616.001]
  • [Cites] Nat Neurosci. 2001 Oct;4(10):973-4 [11574831.001]
  • [Cites] Clin Immunol. 2002 Jan;102(1):84-95 [11781071.001]
  • [Cites] J Neurooncol. 2001 Oct;55(1):29-37 [11804280.001]
  • [Cites] Mol Cell. 2002 Mar;9(3):601-10 [11931767.001]
  • [Cites] Methods Mol Biol. 2002;198:15-27 [11951618.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):151-3 [16846849.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] Nat Rev Cancer. 2006 Aug;6(8):593-602 [16862190.001]
  • (PMID = 17296553.001).
  • [ISSN] 1097-4199
  • [Journal-full-title] Neuron
  • [ISO-abbreviation] Neuron
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS040511; United States / NINDS NIH HHS / NS / K08NS047213; United States / NINDS NIH HHS / NS / NS05563; United States / NCI NIH HHS / CA / P01 CA095616; United States / NINDS NIH HHS / NS / F32 NS055631; United States / NCI NIH HHS / CA / P01 CA95616; United States / NINDS NIH HHS / NS / P01 NS047572; United States / Howard Hughes Medical Institute / / ; United States / NINDS NIH HHS / NS / P01NS047572; United States / NINDS NIH HHS / NS / R01NS40511; United States / NINDS NIH HHS / NS / K08 NS047213
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Nerve Tissue Proteins; 0 / Olig2 protein, mouse; 147336-22-9 / Green Fluorescent Proteins; EC 1.13.12.- / Luciferases; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ NIHMS18231; NLM/ PMC1810344
  •  go-up   go-down


33. Tabatabai G, Herrmann C, von Kürthy G, Mittelbronn M, Grau S, Frank B, Möhle R, Weller M, Wick W: VEGF-dependent induction of CD62E on endothelial cells mediates glioma tropism of adult haematopoietic progenitor cells. Brain; 2008 Oct;131(Pt 10):2579-95
Zurich Open Access Repository and Archive. Full text from .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF-dependent induction of CD62E on endothelial cells mediates glioma tropism of adult haematopoietic progenitor cells.
  • This attraction is further enhanced by irradiation or hypoxic preconditioning of the glioma cells.
  • Adhesive interactions might be critical to the preferential accumulation of HPC within the glioma tissue.
  • Exposure of human cerebral endothelial cells (SV-HCEC), human microvascular endothelial cells (HMEC) and brain tumour endothelial cells derived from human glioblastomas (BTEC) to supernatants of glioma cells and primary glioma cells (SN-G) induced the expression of E-selectin (CD62E).
  • CD62E expression was further enhanced when the glioma cells had been exposed to irradiation or hypoxia prior to the collection of supernatants, as well as by irradiation or exposure to hypoxia of the endothelial cells.
  • Tissue microarray sampling normal brain tissue and astrocytomas of WHO grades II-IV revealed a selective expression of CD62E on endothelial cells of tumour vessels.
  • SN-G-induced CD62E expression on endothelial cells in vitro required transforming growth factor (TGF)-beta signalling in glioma cells and vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGF-R2) signalling in endothelial cells.
  • Further, we observed a nuclear factor kappa B-dependent activation of the CD62E promoter peaking at 12 h after VEGF-R2 activation by glioma-derived VEGF.
  • Taken together, we identify glioma cell-induced CD62E expression on endothelial cells as one mediator of the glioma tropism of HPC.
  • [MeSH-major] Adult Stem Cells / metabolism. E-Selectin / metabolism. Endothelial Cells / metabolism. Glioma / metabolism. Hematopoietic Stem Cells / metabolism. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Animals. Autoantibodies / pharmacology. Cell Hypoxia. Cell Line, Tumor. Cell Migration Inhibition. Cell Movement. Coculture Techniques. Gene Expression. Humans. Mice. Mice, Mutant Strains. NF-kappa B / metabolism. Neoplasm Transplantation. Signal Transduction / physiology. Transforming Growth Factor beta / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • 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 = 18689869.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / E-Selectin; 0 / NF-kappa B; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


34. Chen H, Huang Q, Zhai DZ, Dong J, Wang AD, Lan Q: [CDK1 expression and effects of CDK1 silencing on the malignant phenotype of glioma cells]. Zhonghua Zhong Liu Za Zhi; 2007 Jul;29(7):484-8
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [CDK1 expression and effects of CDK1 silencing on the malignant phenotype of glioma cells].
  • OBJECTIVE: Our previous cDNA array data have shown that expression level of CDK1 increased along with the malignant progression of ganglioglioma, and decreased with the differentiation process of neural stem cells.
  • The purpose of this study was to investigate the CDK1 expression levels in gliomas and the effects of CDK1 knockdown on phenotype of glioma cells.
  • METHODS: Glioma tissue array was constructed, which was composed of surgical specimens of gliomas with different malignancy grades, glioma xenografts in nude mice, cellular spheroids of brain tumor stem cells, normal neural stem cells and glioma cell line.
  • CDK1 expression was detected in glioma tissue array with immunohistochemical techniques.
  • CDK1 expression in human brain glioma cell line and relevant xenogeneic graft tumor was inhibited by retroviral vectors expressing short hairpin RNAs (shRNAs).
  • RESULTS: The expression level of CDK1 increased along with the malignancy progression of glioma in clinical specimens.
  • The positive expression rates of CDK1 in human brain glioma tissues were 22.2% (grade I), 40.0% (grade II), 69.6% (grade III) and 78.6% (grade IV), P = 0.01, respectively.
  • The positive expression rate of CDK1 in glioma cell line and implanted xenografts was similar as the clinical tumors with high malignancy, and higher than those in neural stem cells and brain tumor stem cells (P = 0.0014).
  • Expression of CDK1 was high in human fetal brain tissues and bone marrows of nude mice, but low in normal adult human brain tissues.
  • Downregulation of CDK1 inhibited the proliferation activities notably both in SHG-44 cells in vitro and relevant xenogeneic graft tumors, and induced apoptosis of tumor cells prominantly as well.
  • [MeSH-major] Brain Neoplasms / metabolism. CDC2 Protein Kinase / metabolism. Cell Differentiation / drug effects. Gene Silencing. Glioma / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / pathology. Brain Stem Neoplasms / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Ganglioglioma / genetics. Ganglioglioma / metabolism. Ganglioglioma / pathology. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Nude. Neoplasm Staging. Neoplasm Transplantation. RNA, Messenger / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18069625.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.11.22 / CDC2 Protein Kinase
  •  go-up   go-down


35. Malakootian M, Mowla SJ, Saberi H, Asadi MH, Atlasi Y, Shafaroudi AM: Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors. Mol Carcinog; 2010 Sep;49(9):818-25
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors.
  • Nucleostemin (NS) is implicated in the control of stem and cancer cell proliferation.
  • In the present study, we have examined the expression of NS and its spliced variants in various brain tumors.
  • Total RNA was extracted from 59 brain tumor samples, and the expression of different NS spliced variants was measured by semi-quantitative RT-PCR.
  • The subcellular distribution of NS protein in brain tumors was further examined by immunohistochemistry.
  • Furthermore, to decipher the potential involvement of NS in brain tumorogenesis, its expression was knocked-down by means of RNA interference (RNAi) in two malignant glioma (U-87MG and A172), one astrocytoma (1321N1) and one medulloblastoma (DAOY) cell lines.
  • Our data revealed that NS and its variants are widely expressed in different types of brain tumors.
  • Among the NS spliced variants, variant "1" and variant "3" were detected in the majority of tumor samples, whereas variant "2" was only detectable in few samples.
  • As expected, a nucleolar/nucleoplasmic localization of NS protein was observed in the examined tumor samples.
  • All in all, our data suggest a potential role for NS in tumorogenesis of brain cancers.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Glioma / metabolism
  • [MeSH-minor] Adult. Brain / metabolism. Cell Cycle / genetics. Cell Line. Cell Proliferation. Female. Humans. Immunohistochemistry. Male. Medulloblastoma / genetics. Medulloblastoma / metabolism. Medulloblastoma / pathology. Middle Aged. Proteins / genetics. Proteins / metabolism. RNA Interference. RNA Splicing. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / metabolism. Stem Cells / pathology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20572164.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / RNA, Small Interfering
  •  go-up   go-down


36. Duntsch C, Zhou Q, Weimar JD, Frankel B, Robertson JH, Pourmotabbed T: Up-regulation of neuropoiesis generating glial progenitors that infiltrate rat intracranial glioma. J Neurooncol; 2005 Feb;71(3):245-55
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Up-regulation of neuropoiesis generating glial progenitors that infiltrate rat intracranial glioma.
  • To investigate adult neural stem cell (NSC) biology in relation to glioma, the C6 glioma cell line was tagged with green fluorescent protein (GFP) and inoculated into the brain of adult rats.
  • The in vivo biological response of the brain to glioma was studied using immunohistochemical analysis of the subventricular zone (SVZ), peritumoral areas, and glioma.
  • Nestin immunoreactive cells were found infiltrating glioma, but the distribution of abnormal immunoreactivity was restricted to the dorsal and medial border of the tumor relative to the ipsilateral ventricle.
  • Furthermore, a dense contiguous population of nestin immunoreactive cells could be found streaming from ipsilateral dorsal tip of the SVZ, tracking along the ventral margin of the corpus callosum, and fanning out to encompass and infiltrate the proximal tumor border.
  • Although most cells were either nestin or glial fibrillary acidic protein (GFAP) immunoreactive in the SVZ and along the ventral margin of the corpus callosum, the number of cells co-expressing both markers increased proportionally as the tumor was approached so that the predominant cell population along the proximal tumor border was GFAP immunoreactive.
  • In summary, there is an induction of neuropoietic activity in a rat intracranial glioma model that results in an infiltration and accumulation of abnormal nestin and GFAP expressing cells with proliferative potential along the dorsal and medial border of intracranial C6 glioma.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioma / metabolism. Glioma / pathology. Neuroglia / metabolism. Neuroglia / pathology. Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Lineage. Cell Movement. Cerebral Ventricles / pathology. Disease Models, Animal. Fluorescent Antibody Technique. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Intermediate Filament Proteins / metabolism. Neoplasm Transplantation. Nerve Tissue Proteins / metabolism. Nestin. Rats. Rats, Inbred WF. Rats, Sprague-Dawley. Up-Regulation

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Brain Res. 1999 Sep 4;840(1-2):153-7 [10517963.001]
  • [Cites] J Neurooncol. 1999 Mar;42(1):59-67 [10360479.001]
  • [Cites] J Neurosci. 1988 Apr;8(4):1144-51 [3357014.001]
  • [Cites] Trends Neurosci. 1997 Dec;20(12):570-7 [9416670.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Neuron. 1993 Jul;11(1):173-89 [8338665.001]
  • [Cites] Exp Neurol. 2002 Mar;174(1):89-95 [11869037.001]
  • [Cites] Science. 1968 Jul 26;161(3839):370-1 [4873531.001]
  • [Cites] Brain Res. 1999 Aug 14;838(1-2):1-10 [10446310.001]
  • [Cites] CA Cancer J Clin. 2002 Jan-Feb;52(1):23-47 [11814064.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Virchows Arch B Cell Pathol. 1978 Jul 14;28(1):77-85 [97859.001]
  • [Cites] Neuroreport. 1994 Oct 3;5(15):1885-8 [7841369.001]
  • [Cites] J Neurosci. 1996 Dec 1;16(23):7599-609 [8922416.001]
  • [Cites] Neurosurgery. 1990 Apr;26(4):622-8 [2330084.001]
  • [Cites] J Neurosurg. 1981 Apr;54(4):461-7 [7205347.001]
  • [Cites] Neurosurgery. 2001 Jul;49(1):168-75; discussion 175-6 [11440439.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] J Neurooncol. 2003 Aug-Sep;64(1-2):31-44 [12952284.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5334-41 [1382841.001]
  • [Cites] Neuroreport. 1999 Apr 6;10(5):1007-11 [10321476.001]
  • [Cites] Brain Res. 1997 Sep 12;768(1-2):1-9 [9369294.001]
  • [Cites] J Neurosci. 1997 Jul 1;17(13):5046-61 [9185542.001]
  • [Cites] Pediatr Neurosurg. 1992;18(5-6):310-4 [1476942.001]
  • [Cites] J Cell Biol. 1995 Oct;131(2):453-64 [7593171.001]
  • [Cites] J Neurosci. 1996 Apr 15;16(8):2649-58 [8786441.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):683-8 [11723374.001]
  • [Cites] Trends Neurosci. 1994 Apr;17(4):138-42 [7517589.001]
  • [Cites] Mol Cell Neurosci. 1995 Oct;6(5):474-86 [8581317.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):151-60 [9892097.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):779-86 [11549567.001]
  • [Cites] J Neurosurg. 2001 Sep;95(3):459-65 [11565868.001]
  • [Cites] J Neurosci Res. 2000 Aug 15;61(4):421-9 [10931528.001]
  • [Cites] Neuron. 1994 Nov;13(5):1071-82 [7946346.001]
  • [Cites] Cell. 1990 Feb 23;60(4):585-95 [1689217.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):565-71 [9250169.001]
  • [Cites] Carcinogenesis. 1998 Sep;19(9):1529-37 [9771921.001]
  • [Cites] J Neurosurg. 1980 Dec;53(6):808-15 [7003068.001]
  • (PMID = 15735912.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin
  •  go-up   go-down


37. Santra M, Liu XS, Santra S, Zhang J, Zhang RL, Zhang ZG, Chopp M: Ectopic expression of doublecortin protects adult rat progenitor cells and human glioma cells from severe oxygen and glucose deprivation. Neuroscience; 2006 Oct 27;142(3):739-52
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ectopic expression of doublecortin protects adult rat progenitor cells and human glioma cells from severe oxygen and glucose deprivation.
  • DCX expression is increased in subventricular zone (SVZ) cells migrating to the boundary of an ischemic lesion after induction of middle cerebral artery occlusion (MCAO) in adult rats and mice.
  • Using gene transfer technology, we overexpressed DCX in rat SVZ and U-87 human glioma cells.
  • In NIH3T3 cells, DCX overexpression had no effect on cell survival against OGD, and indicating that the protective effects of DCX was restricted to brain cells e.g.
  • Our data suggest a novel and an important role for DCX as a protective agent for migrating neuroblasts and tumor cells.
  • [MeSH-major] Anoxia / metabolism. Gene Expression Regulation / physiology. Glioma / metabolism. Glucose / deficiency. Microtubule-Associated Proteins / physiology. Neuropeptides / physiology. Stem Cells / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Apoptosis / drug effects. Apoptosis / physiology. Brain / cytology. Cadherins / classification. Cadherins / metabolism. Cell Movement / drug effects. Cell Movement / physiology. Cells, Cultured. Humans. In Situ Nick-End Labeling / methods. Intermediate Filament Proteins / metabolism. Male. Mice. Nerve Tissue Proteins / metabolism. Nestin. RNA, Small Interfering / pharmacology. Rats. Rats, Wistar. Time Factors. Transfection / methods. beta-Galactosidase / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLUCOSE .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16962712.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS23393
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Intermediate Filament Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nes protein, rat; 0 / Nestin; 0 / Neuropeptides; 0 / RNA, Small Interfering; 0 / doublecortin protein; EC 3.2.1.23 / beta-Galactosidase; IY9XDZ35W2 / Glucose
  •  go-up   go-down


38. Miletic H, Fischer Y, Litwak S, Giroglou T, Waerzeggers Y, Winkeler A, Li H, Himmelreich U, Lange C, Stenzel W, Deckert M, Neumann H, Jacobs AH, von Laer D: Bystander killing of malignant glioma by bone marrow-derived tumor-infiltrating progenitor cells expressing a suicide gene. Mol Ther; 2007 Jul;15(7):1373-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bystander killing of malignant glioma by bone marrow-derived tumor-infiltrating progenitor cells expressing a suicide gene.
  • Adult stem cells are promising cellular vehicles for therapy of malignant gliomas as they have the ability to migrate into these tumors and even track infiltrating tumor cells.
  • In the present study, a bone marrow-derived, highly proliferative subpopulation of mesenchymal stem cells (MSCs)-here termed bone marrow-derived tumor-infiltrating cells (BM-TICs)-was genetically modified for the treatment of malignant glioma.
  • Upon injection into the tumor or the vicinity of the tumor, BM-TICs infiltrated solid parts as well as the border of rat 9L glioma.
  • A therapeutic effect was demonstrated in vitro and in vivo by BM-TICs expressing HSV-tk through bystander-mediated glioma cell killing.
  • In conclusion, BM-TICs expressing a suicide gene were highly effective in the treatment of malignant glioma in a rat model and therefore hold great potential for the therapy of malignant brain tumors in humans.
  • [MeSH-major] Bone Marrow Cells / cytology. Bystander Effect / genetics. Cell Movement. Genes, Transgenic, Suicide / genetics. Glioma / pathology. Mesenchymal Stromal Cells / cytology. Mesenchymal Stromal Cells / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17457322.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.21 / Thymidine Kinase
  •  go-up   go-down


39. Jackson EL, Garcia-Verdugo JM, Gil-Perotin S, Roy M, Quinones-Hinojosa A, VandenBerg S, Alvarez-Buylla A: PDGFR alpha-positive B cells are neural stem cells in the adult SVZ that form glioma-like growths in response to increased PDGF signaling. Neuron; 2006 Jul 20;51(2):187-99
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PDGFR alpha-positive B cells are neural stem cells in the adult SVZ that form glioma-like growths in response to increased PDGF signaling.
  • Neurons and oligodendrocytes are produced in the adult brain subventricular zone (SVZ) from neural stem cells (B cells), which express GFAP and have morphological properties of astrocytes.
  • We report here on the identification B cells expressing the PDGFRalpha in the adult SVZ.
  • Conditional ablation of PDGFRalpha in a subpopulation of postnatal stem cells showed that this receptor is required for oligodendrogenesis, but not neurogenesis.
  • The work demonstrates that PDGFRalpha signaling occurs early in the adult stem cell lineage and may help regulate the balance between oligodendrocyte and neuron production.
  • Excessive PDGF activation in the SVZ in stem cells is sufficient to induce hallmarks associated with early stages of tumor formation.
  • [MeSH-major] Cell Proliferation. Glioma / metabolism. Lateral Ventricles / metabolism. Neurons / metabolism. Platelet-Derived Growth Factor / physiology. Receptor, Platelet-Derived Growth Factor alpha / biosynthesis. Signal Transduction / physiology. Stem Cells / metabolism


40. Zeppernick F, Ahmadi R, Campos B, Dictus C, Helmke BM, Becker N, Lichter P, Unterberg A, Radlwimmer B, Herold-Mende CC: Stem cell marker CD133 affects clinical outcome in glioma patients. Clin Cancer Res; 2008 Jan 1;14(1):123-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell marker CD133 affects clinical outcome in glioma patients.
  • PURPOSE: The CD133 antigen has been identified as a putative stem cell marker in normal and malignant brain tissues.
  • According to the cancer stem cell hypothesis, CD133-positive cells determine long-term tumor growth and, therefore, are suspected to influence clinical outcome.
  • To date, a correlation between CD133 expression in primary tumor tissues and patients' prognosis has not been reported.
  • EXPERIMENTAL DESIGN: To address this question, we analyzed the expression of the CD133 stem cell antigen in a series of 95 gliomas of various grade and histology by immunohistochemistry on cryostat sections.
  • RESULTS: By multivariate survival analysis, we found that both the proportion of CD133-positive cells and their topological organization in clusters were significant (P < 0.001) prognostic factors for adverse progression-free survival and overall survival independent of tumor grade, extent of resection, or patient age.
  • Furthermore, proportion of CD133-positive cells was an independent risk factor for tumor regrowth and time to malignant progression in WHO grade 2 and 3 tumors.
  • CONCLUSIONS: These findings constitute the first conclusive evidence that CD133 stem cell antigen expression correlates with patient survival in gliomas, lending support to the current cancer stem cell hypothesis.
  • [MeSH-major] Antigens, CD / biosynthesis. Brain Neoplasms / pathology. Glioma / pathology. Glycoproteins / biosynthesis. Stem Cells / metabolism
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Peptides. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18172261.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
  •  go-up   go-down


41. Maderna E, Salmaggi A, Calatozzolo C, Limido L, Pollo B: Nestin, PDGFRbeta, CXCL12 and VEGF in glioma patients: different profiles of (pro-angiogenic) molecule expression are related with tumor grade and may provide prognostic information. Cancer Biol Ther; 2007 Jul;6(7):1018-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nestin, PDGFRbeta, CXCL12 and VEGF in glioma patients: different profiles of (pro-angiogenic) molecule expression are related with tumor grade and may provide prognostic information.
  • Nestin, a marker for multipotential neuroepithelial stem cells, is detected in neuroepithelial tumors and in proliferating endothelial cells (ECs) and is involved in the early stages of lineage commitment, proliferation and differentiation.
  • We performed a retrospective study on the presence and role of nestin-expressing cells in 102 patients with glioma, relating the findings to VEGF, CXCL12, PDGFRbeta expression and to clinical outcome (time to tumor progression-TTP and survival time-ST).
  • [MeSH-major] Brain Neoplasms / chemistry. Chemokine CXCL12 / analysis. Glioma / blood supply. Intermediate Filament Proteins / analysis. Nerve Tissue Proteins / analysis. Receptor, Platelet-Derived Growth Factor beta / analysis. Vascular Endothelial Growth Factor A / analysis
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Nestin. Prognosis

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17611402.001).
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  •  go-up   go-down


42. Wang Y, Yang J, Zheng H, Tomasek GJ, Zhang P, McKeever PE, Lee EY, Zhu Y: Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model. Cancer Cell; 2009 Jun 2;15(6):514-26
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.
  • However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood.
  • By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis.
  • Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]
  • [Cites] Science. 1994 Jul 15;265(5170):346-55 [8023157.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1019-29 [7926784.001]
  • [Cites] Oncogene. 1996 May 16;12(10):2121-7 [8668337.001]
  • [Cites] J Neurosci. 1997 Jul 1;17(13):5046-61 [9185542.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Nat Neurosci. 2005 Jul;8(7):865-72 [15951811.001]
  • [Cites] Development. 2005 Dec;132(24):5577-88 [16314489.001]
  • [Cites] Development. 2006 Jan;133(2):363-9 [16368933.001]
  • [Cites] J Neurosci. 2006 Jan 25;26(4):1107-16 [16436596.001]
  • [Cites] Mol Cell. 2006 Jun 23;22(6):741-53 [16793544.001]
  • [Cites] J Neurosci. 2006 Jul 26;26(30):7907-18 [16870736.001]
  • [Cites] Curr Opin Cell Biol. 2006 Dec;18(6):704-9 [17046226.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Neuro Oncol. 2007 Oct;9(4):424-9 [17622647.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2683-710 [17974913.001]
  • [Cites] Neuron. 2008 Jun 26;58(6):832-46 [18579075.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1129-33 [18948956.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):45-56 [19111880.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):109-13 [10973261.001]
  • [Cites] Genesis. 2001 Oct;31(2):85-94 [11668683.001]
  • [Cites] Neuron. 2003 Mar 6;37(5):751-64 [12628166.001]
  • [Cites] Int J Oncol. 2003 Sep;23(3):641-8 [12888899.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3525-32 [15150107.001]
  • [Cites] Lab Invest. 2004 Aug;84(8):941-51 [15184909.001]
  • [Cites] Nature. 1992 Mar 19;356(6366):215-21 [1552940.001]
  • (PMID = 19477430.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS053900-03; United States / NINDS NIH HHS / NS / R01 NS053900; United States / NINDS NIH HHS / NS / 1R01 NS053900; United States / NINDS NIH HHS / NS / R01 NS053900-01; United States / NINDS NIH HHS / NS / NS053900-01; United States / NINDS NIH HHS / NS / R01 NS053900-02; United States / NINDS NIH HHS / NS / NS053900-02; United States / NINDS NIH HHS / NS / R01 NS073762; United States / NINDS NIH HHS / NS / NS053900-03
  • [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 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS112275; NLM/ PMC2721466
  •  go-up   go-down


43. Ree A, Jain R, Rock J, Rosenblum M, Patel SC: Direct infiltration of brainstem glioma along the cranial nerves. J Neuroimaging; 2005 Apr;15(2):197-9
Genetic Alliance. consumer health - Glioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Direct infiltration of brainstem glioma along the cranial nerves.
  • The authors describe a case of a low-grade brainstem glioma extending along the cranial nerves without any evidence of leptomeningeal spread.
  • The tumor extended directly along the VII-VIIIth cranial nerve complex and also along the trigeminal nerve, which is quite an unusual characteristic of the glial tumors.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Cranial Nerve Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Adult. Facial Nerve Diseases / pathology. Female. Humans. Magnetic Resonance Imaging. Neoplasm Invasiveness. Trigeminal Nerve Diseases / pathology. Vestibulocochlear Nerve Diseases / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15746234.001).
  • [ISSN] 1051-2284
  • [Journal-full-title] Journal of neuroimaging : official journal of the American Society of Neuroimaging
  • [ISO-abbreviation] J Neuroimaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


44. Abel TW, Clark C, Bierie B, Chytil A, Aakre M, Gorska A, Moses HL: GFAP-Cre-mediated activation of oncogenic K-ras results in expansion of the subventricular zone and infiltrating glioma. Mol Cancer Res; 2009 May;7(5):645-53
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GFAP-Cre-mediated activation of oncogenic K-ras results in expansion of the subventricular zone and infiltrating glioma.
  • A subset of neoplastic cells within human high-grade gliomas has features associated with stem cells.
  • These cells may sustain glioma growth, and their stem-like properties may confer resistance to standard glioma treatments.
  • Whether glioma stem cells derive from indigenous neural stem cells (NSC), or from tumor cells that have reacquired stem cell-like properties, is unknown.
  • However, signaling pathways that are tightly regulated and central to NSC biology, including the Ras/Raf/Erk pathway, are hyperactive and pathogenic in gliomagenesis.
  • Furthermore, data in animal models suggests that, in some cases, tumors are initiated in the subventricular zone (SVZ), a stem/progenitor cell niche in the mature brain.
  • We activated oncogenic K-ras in mouse glioneuronal precursor cells and adult SVZ cells using GFAP-Cre.
  • In addition, mice developed intermediate grade, infiltrating glioma with 100% penetrance.
  • Tumor cells expressed markers associated with neural progenitor cells, including Olig2, Bmi-1, and PDGFR-alpha.
  • These data suggest that infiltrating tumor cells may arise from NSC transformed by activation of oncogenic K-ras in vivo.

  • 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 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] Science. 2000 Feb 25;287(5457):1433-8 [10688783.001]
  • [Cites] Neuron. 2008 Jun 26;58(6):832-46 [18579075.001]
  • [Cites] Genesis. 2001 Oct;31(2):85-94 [11668683.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Genesis. 2002 Feb;32(2):73-5 [11857781.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):616-26 [12154354.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5551-8 [12359767.001]
  • [Cites] Neuron. 2002 Dec 19;36(6):1021-34 [12495619.001]
  • [Cites] Neuron. 2003 Mar 6;37(5):751-64 [12628166.001]
  • [Cites] J Neurosci. 2003 Apr 1;23(7):2824-32 [12684469.001]
  • [Cites] Cereb Cortex. 2003 Jun;13(6):580-7 [12764031.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Nature. 2004 Mar 18;428(6980):337-41 [15029199.001]
  • [Cites] Cell. 2004 Aug 20;118(4):409-18 [15315754.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Int J Cancer. 1995 Jan 17;60(2):168-73 [7829210.001]
  • [Cites] Dev Biol. 1996 Apr 10;175(1):1-13 [8608856.001]
  • [Cites] J Neurosci. 1997 Jul 1;17(13):5046-61 [9185542.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 14;101(50):17528-32 [15574494.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9392-400 [15558011.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):236-45 [15665300.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1432-7 [15964994.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Am J Pathol. 2005 Sep;167(3):859-67 [16127163.001]
  • [Cites] J Comp Neurol. 2006 Jan 20;494(3):415-34 [16320258.001]
  • [Cites] J Neurosci. 2006 Jan 25;26(4):1107-16 [16436596.001]
  • [Cites] Semin Pediatr Neurol. 2006 Mar;13(1):21-6 [16818172.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Neuron. 2007 Feb 15;53(4):503-17 [17296553.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):121-33 [17588166.001]
  • [Cites] Prog Neurobiol. 2007 Sep;83(1):24-36 [17196731.001]
  • [Cites] Neuro Oncol. 2007 Oct;9(4):424-9 [17622647.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):733-6 [17882276.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):8980-4 [17908997.001]
  • [Cites] Cancer Cell. 2007 Oct;12(4):328-41 [17936558.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3286-94 [18451155.001]
  • [Cites] Neoplasia. 2008 May;10(5):501-10 [18472967.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3826-36 [11325859.001]
  • (PMID = 19435821.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS062107; United States / NINDS NIH HHS / NS / NS062107-01A1; United States / NCI NIH HHS / CA / P30 CA068485; United States / NINDS NIH HHS / NS / K08 NS062107-01A1
  • [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 / Glial Fibrillary Acidic Protein; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS126139; NLM/ PMC3406747
  •  go-up   go-down


45. Ehtesham M, Sarangi A, Valadez JG, Chanthaphaychith S, Becher MW, Abel TW, Thompson RC, Cooper MK: Ligand-dependent activation of the hedgehog pathway in glioma progenitor cells. Oncogene; 2007 Aug 23;26(39):5752-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-dependent activation of the hedgehog pathway in glioma progenitor cells.
  • We have investigated the activity of this pathway in adult gliomas, and demonstrate that the Hh pathway is operational and activated within grade II and III gliomas, but not grade IV de novo glioblastoma multiforme.
  • Additionally, we demonstrate that Hh signaling in glioma progenitor cells is ligand-dependent and provide evidence documenting the in vivo source of Sonic hedgehog protein.
  • These findings suggest a regulatory role for the Hh pathway in progenitor cells within grade II and III gliomas, and the potential clinical utility of monitoring and targeting this pathway in these primary brain tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Glioma / genetics. Hedgehog Proteins / genetics. Neoplastic Stem Cells / physiology. Signal Transduction
  • [MeSH-minor] Animals. Blotting, Western. Humans. Ligands. Mice. Neoplasm Staging. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, Cell Surface / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / physiology. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • 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
  • (PMID = 17353902.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS02133; United States / NINDS NIH HHS / NS / R01 NS051557
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / Ligands; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Cell Surface; 0 / SHH protein, human; 0 / Transcription Factors; 0 / patched receptors
  •  go-up   go-down


46. An JH, Lee SY, Jeon JY, Cho KG, Kim SU, Lee MA: Identification of gliotropic factors that induce human stem cell migration to malignant tumor. J Proteome Res; 2009 Jun;8(6):2873-81
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of gliotropic factors that induce human stem cell migration to malignant tumor.
  • Neural stem cells are mobile, are attracted to regions of brain damage, and can migrate a considerable distance to reach a glioma site.
  • With the use of clinically and histologically assessed glioma cells, we have assessed their protein and gene profiles via proteomics and microarray approaches, and have identified candidate genes from human glioma tissues.
  • This research is expected to provide clues to the molecular mechanisms underlying the migration of neural stem cells (F3 cell) to glioma sites.
  • The expression of 16 proteins was shown to have increased commonly in human glioma tissues.
  • Among them, the expression of annexin A2, TIMP-1, COL11A1, bax, CD74, TNFSF8, and SPTLC2 were all increased in human glioma cells, as confirmed by Western blotting and immunohistochemical staining.
  • These results demonstrated that 7 candidate proteins may harbor a potential glioma tropism factor relevant to the pathology of malignant glioma.
  • These results reveal that this novel molecular approach to the monitoring of glioma may provide clinically relevant information regarding tumor malignancy, and should also prove appropriate for high-throughput clinical screening applications.
  • [MeSH-major] Cell Movement. Glioma / genetics. Glioma / metabolism. Neurons / cytology. Stem Cells / physiology
  • [MeSH-minor] Adult. Aged. Annexin A2 / genetics. Annexin A2 / metabolism. Blotting, Western. Cell Line. Electrophoresis, Gel, Two-Dimensional. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Oligonucleotide Array Sequence Analysis. Proteomics / methods. Reproducibility of Results. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19351187.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins
  •  go-up   go-down


47. Laks DR, Masterman-Smith M, Visnyei K, Angenieux B, Orozco NM, Foran I, Yong WH, Vinters HV, Liau LM, Lazareff JA, Mischel PS, Cloughesy TF, Horvath S, Kornblum HI: Neurosphere formation is an independent predictor of clinical outcome in malignant glioma. Stem Cells; 2009 Apr;27(4):980-7
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurosphere formation is an independent predictor of clinical outcome in malignant glioma.
  • Renewable neurosphere formation in culture is a defining characteristic of certain brain tumor initiating cells.
  • This retrospective study was designed to assess the relationship among neurosphere formation in cultured human glioma, tumorigenic capacity, and patient clinical outcome.
  • Tumor samples were cultured in neurosphere conditions from 32 patients with glioma, including a subpopulation of 15 patients with primary glioblastoma.
  • A subsample of renewable neurosphere cultures was xenografted into mouse brain to determine if they were tumorigenic.
  • Renewable neurosphere formation in cultured human glioma significantly predicted an increased hazard of patient death and more rapid tumor progression.
  • These results pertained to both the full population of glioma and the subpopulation of primary glioblastoma.
  • Similarly, there was a significant hazard of progression for patients whose glioma had tumorigenic capacity.
  • In addition, multivariate analysis of neurosphere formation, tumor grade and patient age, demonstrated that neurosphere formation was a robust, independent predictor of glioma tumor progression.
  • Although the lengthy duration of this assay may preclude direct clinical application, these results exemplify how neurosphere culture serves as a clinically relevant model for the study of malignant glioma.
  • Furthermore, this study suggests that the ability to propagate brain tumor stem cells in vitro is associated with clinical outcome.

  • 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.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Lab Invest. 2008 Aug;88(8):808-15 [18560366.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7267-73 [15378086.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Cell. 1974 Dec;3(4):355-9 [4442124.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Nov;72(11):4435-9 [172908.001]
  • [Cites] Cancer Res. 1978 Mar;38(3):624-34 [626967.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Feb;77(2):1039-43 [6928659.001]
  • [Cites] Science. 1992 Mar 27;255(5052):1707-10 [1553558.001]
  • [Cites] J Neurosci. 1992 Nov;12(11):4565-74 [1432110.001]
  • [Cites] Neuropathol Appl Neurobiol. 1998 Oct;24(5):381-8 [9821169.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):425-36 [16723989.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):761-5 [17151667.001]
  • [Cites] Mayo Clin Proc. 2007 Oct;82(10):1271-86 [17908533.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6970-7 [18056172.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):123-9 [18172261.001]
  • [Cites] J Neurosci Res. 2008 Jan;86(1):48-60 [17722061.001]
  • [Cites] Brain Pathol. 2008 Jul;18(3):370-7 [18371181.001]
  • [Cites] Stem Cells. 2008 Jun;26(6):1414-24 [18403755.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • (PMID = 19353526.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R56 NS052563; United States / NINDS NIH HHS / NS / R01 NS050151; United States / NINDS NIH HHS / NS / NS050151; United States / NINDS NIH HHS / NS / R01 NS052563; United States / NINDS NIH HHS / NS / R01 NS052563-03; United States / NINDS NIH HHS / NS / NS052563
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS323660; NLM/ PMC3177534
  •  go-up   go-down


48. Niranjan A, Fellows W, Stauffer W, Burton EA, Hong CS, Lunsford LD, Kondziolka D, Glorioso JC, Gobbel GT: Survival of transplanted neural progenitor cells enhanced by brain irradiation. J Neurosurg; 2007 Aug;107(2):383-91
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival of transplanted neural progenitor cells enhanced by brain irradiation.
  • OBJECT: Authors of previous studies have reported that adult transplanted neural progenitor cells (NPCs) are suitable for brain cell replacement or gene delivery.
  • In this study, the authors evaluated survival and integration of adult rat-derived NPCs after transplantation and explored the potential impact on transplant survival of various mechanical and biological factors of clinical importance.
  • METHODS: Adult female Fischer 344 rats were used both as a source and recipient of transplanted NPCs.
  • Both 9L and RG2 rat glioma cells were used to generate in vivo brain tumor models.
  • On the 5th day after tumor implantation, NPCs expressing green fluorescent protein (GFP) were administered either intravenously (3.5 x 10(7) cells) or by stereotactic injection (1 x 10(4)-1 x 10(6) cells) into normal or tumor-bearing brain.
  • The authors evaluated the effect of delivery method (sharp compared with blunt needles, normal compared with zero-volume needles, phosphate-buffered saline compared with medium as vehicle), delivery sites (intravenous compared with intratumoral compared with intraparenchymal), and pretreatment with an immunosuppressive agent (cyclosporin) or brain irradiation (20-40 Gy) on survival and integration of transplanted NPCs.
  • When 10(5) cells or more were transplanted, only previously administered brain irradiation significantly affected survival and integration of NPCs.
  • Although GFP-containing NPCs could be readily detected 1 day after injection, few cells survived 4 days to 1 week unless preceded by whole-brain radiation (20 or 40 Gy in a single fraction), which increased the number of GFP-containing NPCs within the tissue more than fivefold.
  • CONCLUSIONS: The authors' findings indicate that most NPCs, including those from a syngeneic autologous source, do not survive at the site of implantation, but that brain irradiation can facilitate subsequent survival in both normal and tumor-bearing brain.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy. Multipotent Stem Cells / radiation effects. Multipotent Stem Cells / transplantation. Stem Cell Transplantation. Transplantation Immunology / radiation effects

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17695394.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


49. Broniscer A, Laningham FH, Kocak M, Krasin MJ, Fouladi M, Merchant TE, Kun LE, Boyett JM, Gajjar A: Intratumoral hemorrhage among children with newly diagnosed, diffuse brainstem glioma. Cancer; 2006 Mar 15;106(6):1364-71
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intratumoral hemorrhage among children with newly diagnosed, diffuse brainstem glioma.
  • BACKGROUND: Children with diffuse brainstem glioma (BSG) commonly undergo novel therapies because their outcome is poor with radiation therapy (RT).
  • METHODS: All available brain imaging studies and medical records of 48 consecutive patients with newly diagnosed BSG treated at the study institution over a 10-year interval (1992-2002) were reviewed.
  • At the time of last follow-up, all patients had died of tumor progression.
  • The uniform occurrence of IH among patients treated with various chemotherapeutic regimens and its association with necrotic areas suggests that tumor biology plays a significant role in this event.
  • [MeSH-major] Brain Stem Neoplasms / diagnosis. Cerebral Hemorrhage / diagnosis. Glioma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Female. Humans. Magnetic Resonance Imaging. Male. Necrosis. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome

  • Genetic Alliance. consumer health - Glioma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16463390.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 21765
  • [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 / Antineoplastic Agents
  •  go-up   go-down


50. Zhu Y, Harada T, Liu L, Lush ME, Guignard F, Harada C, Burns DK, Bajenaru ML, Gutmann DH, Parada LF: Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation. Development; 2005 Dec;132(24):5577-88
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation.
  • The gene responsible for neurofibromatosis type 1 (NF1) encodes a tumor suppressor that functions as a negative regulator of the Ras proto-oncogene.
  • Individuals with germline mutations in NF1 are predisposed to the development of benign and malignant tumors of the peripheral and central nervous system (CNS).
  • Children with this disease suffer a high incidence of optic gliomas, a benign but potentially debilitating tumor of the optic nerve; and an increased incidence of malignant astrocytoma, reactive astrogliosis and intellectual deficits.
  • In the present study, we have sought insight into the molecular and cellular basis of NF1-associated CNS pathologies.
  • We show that mice genetically engineered to lack NF1 in CNS exhibit a variety of defects in glial cells.
  • Primary among these is a developmental defect resulting in global reactive astrogliosis in the adult brain and increased proliferation of glial progenitor cells leading to enlarged optic nerves.
  • These data point to hyperproliferative glial progenitors as the source of the optic tumors and provide a genetic model for NF1-associated astrogliosis and optic glioma.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neuropathol Appl Neurobiol. 2000 Aug;26(4):361-7 [10931370.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Sep;59(9):759-67 [11005256.001]
  • [Cites] J Neurosci. 2005 Jun 8;25(23):5584-94 [15944386.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7773-9 [15520182.001]
  • [Cites] Am J Med Genet. 1999 Mar 26;89(1):38-44 [10469435.001]
  • [Cites] Oncogene. 1999 Aug 5;18(31):4450-9 [10442636.001]
  • [Cites] Neuron. 2000 May;26(2):533-41 [10839371.001]
  • [Cites] Science. 2000 Feb 25;287(5457):1433-8 [10688783.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] Nat Rev Cancer. 2005 Jul;5(7):557-64 [16069817.001]
  • [Cites] Development. 2000 Dec;127(24):5253-63 [11076748.001]
  • [Cites] Neuron. 2000 Oct;28(1):69-80 [11086984.001]
  • [Cites] Nature. 2001 Feb 8;409(6821):714-20 [11217860.001]
  • [Cites] Nat Rev Genet. 2001 Feb;2(2):120-9 [11253051.001]
  • [Cites] Nat Rev Neurosci. 2001 Apr;2(4):287-93 [11283751.001]
  • [Cites] Neurology. 2001 Apr 10;56(7):885-90 [11294925.001]
  • [Cites] Genes Dev. 2001 Apr 1;15(7):859-76 [11297510.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Sep;60(9):917-20 [11556548.001]
  • [Cites] Genesis. 2001 Oct;31(2):85-94 [11668683.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):112-7 [11689956.001]
  • [Cites] Cancer Res. 2002 Apr 1;62(7):2085-91 [11929829.001]
  • [Cites] Science. 2002 May 3;296(5569):920-2 [11988578.001]
  • [Cites] Mol Cell Biol. 2002 Jul;22(14):5100-13 [12077339.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):616-26 [12154354.001]
  • [Cites] J Neurosci. 2002 Nov 1;22(21):9228-36 [12417648.001]
  • [Cites] Neuron. 2003 Mar 6;37(5):751-64 [12628166.001]
  • [Cites] J Neurosci. 2003 Aug 6;23(18):7207-17 [12904481.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8573-7 [14695164.001]
  • [Cites] Neuron. 2004 Mar 25;41(6):881-90 [15046721.001]
  • [Cites] Cell. 1990 Feb 23;60(4):585-95 [1689217.001]
  • [Cites] Cell. 1990 Nov 16;63(4):835-41 [2121369.001]
  • [Cites] Cell. 1990 Nov 16;63(4):851-9 [2121371.001]
  • [Cites] Neuron. 1992 Mar;8(3):415-28 [1550670.001]
  • [Cites] Dev Dyn. 1992 Nov;195(3):216-26 [1301085.001]
  • [Cites] Dev Biol. 1994 Feb;161(2):538-51 [8314000.001]
  • [Cites] Neuron. 1994 Apr;12(4):895-908 [8161459.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1019-29 [7926784.001]
  • [Cites] Development. 1994 Sep;120(9):2637-49 [7956838.001]
  • [Cites] J Neuropathol Exp Neurol. 1995 Jul;54(4):588-600 [7602332.001]
  • [Cites] J Cell Biol. 1995 Oct;131(2):453-64 [7593171.001]
  • [Cites] Development. 1995 Nov;121(11):3583-92 [8582272.001]
  • [Cites] Mol Cell Biol. 1997 Feb;17(2):862-72 [9001241.001]
  • [Cites] Ann Neurol. 1997 Feb;41(2):143-9 [9029062.001]
  • [Cites] Trends Neurosci. 1997 Dec;20(12):570-7 [9416670.001]
  • [Cites] Cell. 1998 Sep 18;94(6):703-14 [9753318.001]
  • [Cites] Brain Res. 1999 Jan 16;816(1):111-23 [9878702.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] J Neurosci. 1999 Feb 1;19(3):1049-61 [9920668.001]
  • (PMID = 16314489.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS052606-01; United States / NINDS NIH HHS / NS / P50 NS052606; United States / NINDS NIH HHS / NS / P50 NS052606-01
  • [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] England
  • [Chemical-registry-number] 0 / Neurofibromin 1
  • [Other-IDs] NLM/ NIHMS149022; NLM/ PMC2760350
  •  go-up   go-down


51. Torcuator R, Zuniga R, Loutfi R, Mikkelsen T: Bevacizumab and irinotecan treatment for progressive diffuse brainstem glioma: case report. J Neurooncol; 2009 Jul;93(3):409-12
Genetic Alliance. consumer health - Glioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bevacizumab and irinotecan treatment for progressive diffuse brainstem glioma: case report.
  • Diffuse brainstem glioma carries a dismal prognosis.
  • In this paper, we report our experience in an adult patient with progressive diffuse brainstem glioma treated with bevacizumab and irinotecan.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Combined Modality Therapy. Female. Humans. Magnetic Resonance Imaging. Radiotherapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Neurooncol. 2009 Nov;95(2):299-300 [19506812.001]
  • [Cites] J Clin Oncol. 2010 Jun 20;28(18):3069-75 [20479404.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jan 15;40(2):265-71 [9457808.001]
  • [Cites] Brain. 2001 Dec;124(Pt 12):2528-39 [11701605.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):171-7 [9892099.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4722-9 [17947719.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Apr 1;55(5):1182-5 [12654425.001]
  • [Cites] Arch Neurol. 1999 Apr;56(4):421-5 [10199329.001]
  • [Cites] Pediatr Neurosurg. 1996;24(1):24-34 [8817612.001]
  • [Cites] Childs Nerv Syst. 1998 Apr-May;14(4-5):167-73 [9660117.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(7):721-6; discussion 726-7 [10481783.001]
  • [Cites] Childs Nerv Syst. 1998 Oct;14(10):578-81 [9840382.001]
  • [Cites] Oncology (Williston Park). 2005 Apr;19(4 Suppl 3):7-16 [15934498.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):253-66 [16195805.001]
  • [Cites] Nat Rev Neurosci. 2007 Aug;8(8):610-22 [17643088.001]
  • [Cites] Neurology. 1998 Oct;51(4):1136-9 [9781543.001]
  • [Cites] Cancer. 1996 May 15;77(10):2150-6 [8640684.001]
  • [Cites] Oncologist. 2004;9(2):197-206 [15047924.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] Br J Cancer. 2002 Oct 21;87(9):945-9 [12434281.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;39(4):376-9 [9025780.001]
  • [Cites] Pediatr Neurosurg. 1996;24(2):98-102 [8841080.001]
  • [Cites] J Neurooncol. 2008 May;87(3):355-61 [18217208.001]
  • [Cites] Childs Nerv Syst. 1999 Oct;15(10):545-53 [10550585.001]
  • [Cites] Mol Cell Biochem. 2008 May;312(1-2):71-80 [18259841.001]
  • (PMID = 19139822.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


52. Spreafico F, Gandola L, Marchianò A, Simonetti F, Poggi G, Adduci A, Clerici CA, Luksch R, Biassoni V, Meazza C, Catania S, Terenziani M, Musumeci R, Fossati-Bellani F, Massimino M: Brain magnetic resonance imaging after high-dose chemotherapy and radiotherapy for childhood brain tumors. Int J Radiat Oncol Biol Phys; 2008 Mar 15;70(4):1011-9
Hazardous Substances Data Bank. THIO-TEPA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain magnetic resonance imaging after high-dose chemotherapy and radiotherapy for childhood brain tumors.
  • PURPOSE: Brain necrosis or other subacute iatrogenic reactions has been recognized as a potential complication of radiotherapy (RT), although the possible synergistic effects of high-dose chemotherapy and RT might have been underestimated.
  • METHODS AND MATERIALS: We reviewed the clinical and radiologic data of 49 consecutive children with malignant brain tumors treated with high-dose thiotepa and autologous hematopoietic stem cell rescue, preceded or followed by RT.
  • RESULTS: Of the 49 children, 18 (6 of 25 with high-grade gliomas and 12 of 24 with primitive neuroectodermal tumors) had abnormal brain MRI findings occurring a median of 8 months (range, 2-39 months) after RT and beginning to regress a median of 13 months (range, 2-26 months) after onset.
  • Such findings pose a major diagnostic challenge in terms of their differential diagnosis vis-à-vis recurrent tumor.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Brain. Brain Neoplasms. Glioma. Neuroectodermal Tumors, Primitive. Thiotepa / adverse effects
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cognition / drug effects. Cognition / radiation effects. Combined Modality Therapy / adverse effects. Combined Modality Therapy / methods. Disease-Free Survival. Female. Humans. Infant. Intelligence / drug effects. Intelligence / radiation effects. Magnetic Resonance Imaging. Male. Medulloblastoma / drug therapy. Medulloblastoma / radiotherapy

  • 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 = 17904307.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 905Z5W3GKH / Thiotepa
  •  go-up   go-down


53. Fouladi M, Nicholson HS, Zhou T, Laningham F, Helton KJ, Holmes E, Cohen K, Speights RA, Wright J, Pollack IF, Children's Oncology Group: A phase II study of the farnesyl transferase inhibitor, tipifarnib, in children with recurrent or progressive high-grade glioma, medulloblastoma/primitive neuroectodermal tumor, or brainstem glioma: a Children's Oncology Group study. Cancer; 2007 Dec 1;110(11):2535-41
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of the farnesyl transferase inhibitor, tipifarnib, in children with recurrent or progressive high-grade glioma, medulloblastoma/primitive neuroectodermal tumor, or brainstem glioma: a Children's Oncology Group study.
  • BACKGROUND: An open-label Phase II study of tipifarnib was conducted to evaluate its safety and efficacy in children with recurrent or refractory medulloblastoma (MB)/primitive neuroectodermal tumor (PNET), high-grade glioma (HGG), and diffuse intrinsic brainstem glioma (BSG).
  • CONCLUSIONS: Tipifarnib tolerated well but had little activity as a single agent in children with recurrent central nervous system malignancies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Medulloblastoma / drug therapy. Quinolones / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Female. Humans. Male. Neuroectodermal Tumors / drug therapy. Treatment Outcome


54. Joshi BH, Puri RA, Leland P, Varricchio F, Gupta G, Kocak M, Gilbertson RJ, Puri RK, US Pediatric Brain Tumor Consortium: Identification of interleukin-13 receptor alpha2 chain overexpression in situ in high-grade diffusely infiltrative pediatric brainstem glioma. Neuro Oncol; 2008 Jun;10(3):265-74
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of interleukin-13 receptor alpha2 chain overexpression in situ in high-grade diffusely infiltrative pediatric brainstem glioma.
  • Human malignant glioma cell lines and adult brain tumors overexpress high levels of interleukin-13 receptor alpha2 chain (IL-13Ralpha2).
  • Because the IL-13Ralpha2 chain is an important target for cancer therapy and prognosis for patients with brainstem glioma (BSG) remains dismal, we investigated the expression of this receptor in specimens of diffusely infiltrative pediatric BSG relative to normal brain tissue.
  • Twenty-eight BSG specimens and 15 normal brain specimens were investigated for IL-13Ralpha2 protein expression by immunohistochemical analysis (IHC) using two different antibodies in two different laboratories.
  • By Q-dot IHC or a standard IHC assay, 17 of 28 (61%) tumor specimens showed modest to strong staining for IL-13Ralpha2, while 15 normal brain tissue samples showed weak expression for IL-13Ralpha2 protein.
  • High-level IL-13Ralpha2 RNA expression was detected in tumor samples by Q-dot ISH, but only weak RNA expression was observed in normal brain.
  • IL-13Ralpha2 protein and mRNA are expressed to significantly higher levels in BSG than in normal brain tissue.

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Gene Ther. 2000 Sep 1;11(13):1829-35 [10986556.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3506-13 [10828036.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6194-200 [11507072.001]
  • [Cites] Cancer Gene Ther. 2001 Nov;8(11):861-8 [11773976.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1103-9 [11861389.001]
  • [Cites] Oncol Res. 2001;12(11-12):459-67 [11939409.001]
  • [Cites] Curr Treat Options Oncol. 2001 Dec;2(6):529-36 [12057098.001]
  • [Cites] J Clin Oncol. 2002 Aug 15;20(16):3431-7 [12177103.001]
  • [Cites] J Immunol. 2002 Dec 15;169(12):7119-26 [12471149.001]
  • [Cites] J Exp Med. 2003 Mar 17;197(6):703-9 [12642602.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3620-4 [14506149.001]
  • [Cites] J Neurooncol. 2003 Oct;65(1):37-48 [14649884.001]
  • [Cites] Cancer. 2004 Sep 1;101(5):1036-42 [15329913.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):2200-5 [2005905.001]
  • [Cites] J Neurosurg. 1993 Oct;79(4):569-76 [7692018.001]
  • [Cites] Int J Cancer. 1994 Aug 15;58(4):574-81 [8056454.001]
  • [Cites] J Biol Chem. 1995 Apr 14;270(15):8797-804 [7721786.001]
  • [Cites] J Biol Chem. 1995 Jul 14;270(28):16775-80 [7622490.001]
  • [Cites] J Immunol. 1996 Apr 15;156(8):2972-8 [8609418.001]
  • [Cites] J Biol Chem. 1996 Sep 13;271(37):22428-33 [8798406.001]
  • [Cites] Pediatr Neurosurg. 1996;24(4):185-92 [8873160.001]
  • [Cites] Cancer Res. 1996 Dec 15;56(24):5631-7 [8971168.001]
  • [Cites] J Immunol. 1997 Jan 15;158(2):756-64 [8992992.001]
  • [Cites] Mol Med. 1997 May;3(5):327-38 [9205948.001]
  • [Cites] Cancer Res. 1997 Aug 1;57(15):3272-80 [9242460.001]
  • [Cites] J Biol Chem. 1997 Aug 8;272(32):20251-8 [9242704.001]
  • [Cites] J Urol. 1997 Sep;158(3 Pt 1):948-53 [9258124.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Sep 8;238(1):90-4 [9299458.001]
  • [Cites] Nat Med. 1997 Dec;3(12):1362-8 [9396606.001]
  • [Cites] Int Immunol. 1998 Aug;10(8):1103-10 [9723696.001]
  • [Cites] J Natl Cancer Inst. 1998 Sep 2;90(17):1269-77 [9731733.001]
  • [Cites] Clin Cancer Res. 1995 Nov;1(11):1253-8 [9815919.001]
  • [Cites] Clin Cancer Res. 1997 Feb;3(2):151-6 [9815666.001]
  • [Cites] Int J Mol Med. 1998 Mar;1(3):551-7 [9852261.001]
  • [Cites] Biophys J. 1999 Jul;77(1):154-72 [10388747.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2956-63 [15805299.001]
  • [Cites] Nat Med. 2006 Jan;12(1):99-106 [16327802.001]
  • [Cites] Technol Cancer Res Treat. 2006 Jun;5(3):239-50 [16700620.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3145-51 [16707614.001]
  • [Cites] Vitam Horm. 2006;74:479-504 [17027527.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):837-44 [17327604.001]
  • [Cites] Int J Hematol. 1999 Jan;69(1):13-20 [10641437.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1168-72 [10728667.001]
  • [Cites] Int J Cancer. 2001 Apr 15;92(2):168-75 [11291041.001]
  • (PMID = 18430795.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA081457; United States / NCI NIH HHS / CA / U01 CA81457
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2563049
  •  go-up   go-down


55. Burzynski SR, Janicki TJ, Weaver RA, Burzynski B: Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma. Integr Cancer Ther; 2006 Mar;5(1):40-7
Hazardous Substances Data Bank. Glutamine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma.
  • BACKGROUND: Brainstem glioma carries the worst prognosis of all malignancies of the brain.
  • Most patients with brainstem glioma fail standard radiation therapy and chemotherapy and do not survive longer than 2 years.
  • Treatment is even more challenging when an inoperable tumor is of high-grade pathology (HBSG).
  • CONCLUSION: Antineoplastons contributed to more than a 5-year survival in recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of the brainstem in a small group of patients.
  • [MeSH-major] Benzeneacetamides / administration & dosage. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Glutamine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy. Phenylacetates / administration & dosage. Piperidones / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Combinations. Female. Follow-Up Studies. Humans. Injections, Intravenous. Magnetic Resonance Imaging. Male. Maximum Tolerated Dose. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Glioma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16484713.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzeneacetamides; 0 / Drug Combinations; 0 / Phenylacetates; 0 / Piperidones; 0RH81L854J / Glutamine; 104624-98-8 / antineoplaston AS 2-1; 91531-30-5 / antineoplaston A10
  •  go-up   go-down


56. Shiras A, Chettiar ST, Shepal V, Rajendran G, Prasad GR, Shastry P: Spontaneous transformation of human adult nontumorigenic stem cells to cancer stem cells is driven by genomic instability in a human model of glioblastoma. Stem Cells; 2007 Jun;25(6):1478-89
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous transformation of human adult nontumorigenic stem cells to cancer stem cells is driven by genomic instability in a human model of glioblastoma.
  • The presence of a CD133+/nestin+ population in brain tumors suggests that a normal neural stem cell may be the cell of origin for gliomas.
  • We have identified human CD133-positive NSCs from adult glioma tissue and established them as long-term in vitro cultures human neuroglial culture (HNGC)-1.
  • Replicative senescence in HNGC-1 led to a high level of genomic instability and emergence of a spontaneously immortalized clone that developed into cell line HNGC-2 with features of cancer stem cells (CSCs), which include the ability for self-renewal and the capacity to form CD133-positive neurospheres and develop intracranial tumors.
  • The activated forms of Notch and Hes isoforms were expressed in both non-neoplastic neural stem cells and brain tumor stem cells derived from it.
  • Importantly, a significant overexpression of these molecules was found in the brain tumor stem cells.
  • These findings suggest that this model comprised of HNGC-1 and HNGC-2 cells would be a useful system for studying pathways involved in self-renewal of stem cells and their transformation to cancer stem cells.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / genetics. Genomic Instability / physiology. Glioblastoma / pathology. Models, Biological. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Aging / genetics. Cell Proliferation. Humans. Mice. Mice, Nude. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Telomerase / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17332509.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  •  go-up   go-down


57. Ogden AT, Waziri AE, Lochhead RA, Fusco D, Lopez K, Ellis JA, Kang J, Assanah M, McKhann GM, Sisti MB, McCormick PC, Canoll P, Bruce JN: Identification of A2B5+CD133- tumor-initiating cells in adult human gliomas. Neurosurgery; 2008 Feb;62(2):505-14; discussion 514-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of A2B5+CD133- tumor-initiating cells in adult human gliomas.
  • OBJECTIVE: Several studies have shown that human gliomas contain a small population of cells with stem cell-like features.
  • It has been proposed that these "cancer stem cells" may be uniquely responsible for glioma formation and recurrence.
  • METHODS: To investigate the contributions of stem-like and progenitor-like cells in human gliomas, we used flow cytometry to characterize the expression of a cancer stem cell marker (CD133) and a glial progenitor marker (A2B5) in 25 tumors.
  • RESULTS: We found that the capacity for these different populations to form tumors varied depending on the human tumor specimen from which they were isolated.
  • Of the six human gliomas tested, four contained A2B5+/CD133- cells that formed tumors when transplanted into nude rats, three contained A2B5+/CD133+ cells that formed tumors, and only one glioma contained A2B5-/CD133- cells with the capacity to form tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Gangliosides / metabolism. Glioma / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adult. Animals. Antigens, CD / metabolism. Flow Cytometry. Glycoproteins / metabolism. Humans. Peptides / metabolism. Rats. Rats, Nude


58. De Toni A, Zbinden M, Epstein JA, Ruiz i Altaba A, Prochiantz A, Caillé I: Regulation of survival in adult hippocampal and glioblastoma stem cell lineages by the homeodomain-only protein HOP. Neural Dev; 2008 May 28;3:13
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of survival in adult hippocampal and glioblastoma stem cell lineages by the homeodomain-only protein HOP.
  • BACKGROUND: Homeodomain proteins play critical roles in shaping the development of the embryonic central nervous system in mammals.
  • After birth, neurogenic activities are relegated to stem cell niches, which include the subgranular layer of the dentate gyrus of the hippocampus.
  • Here, we have analyzed the function of HOP (Homeodomain only protein) in this stem cell niche and in human glioblastomas.
  • RESULTS: We find that HOP is strongly expressed by radial astrocytes of the dentate gyrus in mice, which are stem cells that give rise to hippocampal granular neurons throughout adulthood.
  • Deletion or down-regulation of HOP results in a decrease of apoptosis of these stem cells without changes in proliferation, and in an increase in the number of newly formed granule neurons.
  • We also find that human glioblastomas largely lack HOP expression and that reintroduction of HOP function in glioma cells cultured as gliomaspheres leads to enhanced apoptosis in a subset of cases.
  • CONCLUSION: These data suggest that HOP participates in the regulation of the adult mouse hippocampal stem cell niche by negatively affecting cell survival.
  • In addition, HOP may work as a tumor suppressor in a subset of glioblastomas.
  • HOP function thus appears to be critical in the adult brain in a region of continued plasticity, and its deregulation may contribute to disease.

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2001 Oct 1;21(19):7691-704 [11567059.001]
  • [Cites] Neurosci Lett. 2000 Sep 8;291(1):17-20 [10962143.001]
  • [Cites] Prog Neurobiol. 2002 Jan;66(1):1-18 [11897403.001]
  • [Cites] Nat Rev Cancer. 2002 May;2(5):361-72 [12044012.001]
  • [Cites] J Neurosci. 2002 Jul 15;22(14):6106-13 [12122071.001]
  • [Cites] Cell. 2002 Sep 20;110(6):713-23 [12297045.001]
  • [Cites] Cell. 2002 Sep 20;110(6):725-35 [12297046.001]
  • [Cites] Eur J Neurosci. 2002 Nov;16(9):1681-9 [12431220.001]
  • [Cites] Development. 2003 Jan;130(2):391-9 [12466205.001]
  • [Cites] Genomics. 2003 Jan;81(1):15-25 [12573257.001]
  • [Cites] J Comp Neurol. 2003 Jun 9;460(4):563-72 [12717714.001]
  • [Cites] Oncology. 2003;64(4):450-8 [12759545.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] J Neurosci. 2003 Dec 3;23(35):11112-9 [14657169.001]
  • [Cites] Development. 2003 Dec;130(26):6635-42 [14627719.001]
  • [Cites] EMBO J. 2004 Apr 21;23(8):1834-44 [15057274.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(12):5281-9 [15169892.001]
  • [Cites] Br J Cancer. 2004 Jul 19;91(2):258-61 [15213722.001]
  • [Cites] Development. 2004 Aug;131(15):3805-19 [15240551.001]
  • [Cites] Trends Neurosci. 2004 Aug;27(8):447-52 [15271491.001]
  • [Cites] J Comp Neurol. 2004 Oct 25;478(4):359-78 [15384070.001]
  • [Cites] Nat Neurosci. 2004 Nov;7(11):1233-41 [15494728.001]
  • [Cites] Trends Cell Biol. 1998 Feb;8(2):84-7 [9695814.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Neuron. 1999 Jun;23(2):247-56 [10399932.001]
  • [Cites] Neuron. 1999 Jun;23(2):257-71 [10399933.001]
  • [Cites] J Neurosci. 2004 Nov 10;24(45):10040-6 [15537872.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17132-7 [15569937.001]
  • [Cites] Development. 2005 Jan;132(2):335-44 [15604099.001]
  • [Cites] Physiol Rev. 2005 Apr;85(2):523-69 [15788705.001]
  • [Cites] Dev Biol. 2005 Jul 15;283(2):522-34 [15967424.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] EMBO Rep. 2005 Sep;6(9):885-90 [16113652.001]
  • [Cites] J Biol Chem. 2005 Sep 16;280(37):32531-8 [15929941.001]
  • [Cites] Eur J Neurosci. 2005 Oct;22(8):1907-15 [16262630.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):780-5 [16407118.001]
  • [Cites] Nat Rev Neurosci. 2006 Mar;7(3):179-93 [16495940.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):425-36 [16723989.001]
  • [Cites] Curr Biol. 2007 Jan 23;17(2):165-72 [17196391.001]
  • [Cites] J Neurosci. 2001 Sep 15;21(18):7153-60 [11549726.001]
  • [Cites] Trends Neurosci. 2000 Jul;23(7):291-7 [10856938.001]
  • [Cites] J Neurosci. 2002 Mar 15;22(6):2255-64 [11896165.001]
  • (PMID = 18507846.001).
  • [ISSN] 1749-8104
  • [Journal-full-title] Neural development
  • [ISO-abbreviation] Neural Dev
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL071546-05A1; United States / NHLBI NIH HHS / HL / R01 HL071546; United States / NHLBI NIH HHS / HL / R01 HL071546-05A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOP protein, human; 0 / Homeodomain Proteins; 0 / Hop protein, mouse; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2416439
  •  go-up   go-down


59. Barth RF, Kaur B: Rat brain tumor models in experimental neuro-oncology: the C6, 9L, T9, RG2, F98, BT4C, RT-2 and CNS-1 gliomas. J Neurooncol; 2009 Sep;94(3):299-312
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rat brain tumor models in experimental neuro-oncology: the C6, 9L, T9, RG2, F98, BT4C, RT-2 and CNS-1 gliomas.
  • In this review we will describe eight commonly used rat brain tumor models and their application for the development of novel therapeutic and diagnostic modalities.
  • The C6, 9L and T9 gliomas were induced by repeated injections of methylnitrosourea (MNU) to adult rats.
  • The C6 glioma has been used extensively for a variety of studies, but since it arose in an outbred Wistar rat, it is not syngeneic to any inbred strain, and its potential to evoke an alloimmune response is a serious limitation.
  • The 9L gliosarcoma has been used widely and has provided important information relating to brain tumor biology and therapy.
  • The T9 glioma, although not generally recognized, was and probably still is the same as the 9L.
  • The RG2 and F98 gliomas were both chemically induced by administering ethylnitrosourea (ENU) to pregnant rats, the progeny of which developed brain tumors that subsequently were propagated in vitro and cloned.
  • The CNS-1 glioma was induced by administering MNU to a Lewis rat.
  • Finally, the BT4C glioma was induced by administering ENU to a BD IX rat, following which brain cells were propagated in vitro until a tumorigenic clone was isolated.
  • This tumor has been used for a variety of studies to evaluate new therapeutic modalities.
  • The Avian Sarcoma Virus (ASV) induced tumors, and a continuous cell line derived from one of them designated RT-2, have been useful for studies in which de novo tumor induction is an important requirement.
  • [MeSH-major] Brain Neoplasms. Glioma
  • [MeSH-minor] Animals. Cell Line, Tumor / pathology. Disease Models, Animal. Gene Expression Regulation, Neoplastic. Mice. Rats

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cell lines described in this publication .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosurg. 2004 Nov;101(5):826-31 [15540922.001]
  • [Cites] Mol Ther. 2004 Dec;10(6):1071-84 [15564139.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8561-76 [15623640.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):341-50 [15671565.001]
  • [Cites] J Immunol. 2005 Mar 1;174(5):2533-43 [15728459.001]
  • [Cites] Mol Cancer. 2005;4(1):12 [15762988.001]
  • [Cites] Brain Res Mol Brain Res. 2005 Apr 27;135(1-2):93-103 [15857672.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3475-84 [15867250.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3821-7 [15897582.001]
  • [Cites] J Neurooncol. 2005 May;72(3):209-15 [15937642.001]
  • [Cites] Brain Res. 2005 Jun 14;1047(1):56-64 [15893739.001]
  • [Cites] Am J Pathol. 2005 Aug;167(2):565-76 [16049340.001]
  • [Cites] J Neurosurg. 2005 Jan;102(1 Suppl):53-8 [16206734.001]
  • [Cites] Neurosurg Focus. 2005 Oct 15;19(4):E1 [16241103.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Feb 1;64(2):603-11 [16338098.001]
  • [Cites] Mol Cancer Ther. 2006 Jan;5(1):52-9 [16432162.001]
  • [Cites] J Neurosurg. 2006 Jan;104(1):118-28 [16509155.001]
  • [Cites] J Neurooncol. 2007 Nov;85(2):133-48 [17874037.001]
  • [Cites] Neurochem Res. 2007 Dec;32(12):2235-42 [17701349.001]
  • [Cites] Free Radic Biol Med. 2008 Jan 1;44(1):63-72 [18045548.001]
  • [Cites] J Natl Cancer Inst. 2007 Dec 5;99(23):1768-81 [18042934.001]
  • [Cites] J Neurooncol. 2008 Jan;86(1):13-21 [17611717.001]
  • [Cites] Clin Cancer Res. 2008 Feb 1;14(3):883-91 [18245552.001]
  • [Cites] J Neurosurg. 2008 Feb;108(2):320-9 [18240929.001]
  • [Cites] Phys Med Biol. 2008 Feb 21;53(4):861-78 [18263945.001]
  • [Cites] Int J Immunopathol Pharmacol. 2008 Jan-Mar;21(1):227-31 [18336750.001]
  • [Cites] Z Krebsforsch Klin Onkol Cancer Res Clin Oncol. 1977 Aug 15;89(3):273-95 [198983.001]
  • [Cites] J Neurosurg. 1979 Mar;50(3):298-304 [217977.001]
  • [Cites] Acta Neuropathol. 1980;51(1):23-31 [7435138.001]
  • [Cites] J Neurosurg. 1980 Dec;53(6):808-15 [7003068.001]
  • [Cites] Eur J Cancer Clin Oncol. 1982 Sep;18(9):891-5 [6891332.001]
  • [Cites] J Neuropathol Exp Neurol. 1983 Mar;42(2):122-35 [6600780.001]
  • [Cites] J Neuropathol Exp Neurol. 1984 Jul;43(4):426-38 [6610726.001]
  • [Cites] Cancer Res. 1986 Oct;46(10):5276-81 [3019523.001]
  • [Cites] Cancer. 1987 Jan 15;59(2):266-70 [3026604.001]
  • [Cites] Ann Neurol. 1987 Sep;22(3):300-5 [3118762.001]
  • [Cites] Cancer Res. 1991 May 1;51(9):2373-8 [2015600.001]
  • [Cites] Cancer Res. 1991 May 1;51(9):2430-7 [2015604.001]
  • [Cites] J Clin Neurosci. 2008 May;15(5):545-51 [18378459.001]
  • [Cites] J Neurooncol. 2008 May;88(1):1-9 [18228115.001]
  • [Cites] Neuroimage. 2008 Apr 1;40(2):973-83 [18441552.001]
  • [Cites] J Neurosurg. 2008 May;108(5):972-8 [18447715.001]
  • [Cites] J Chemother. 2008 Apr;20(2):253-62 [18467254.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2008 Jun;35(6):1192-203 [18264706.001]
  • [Cites] Toxicol Lett. 2008 Jun 10;179(1):29-33 [18485629.001]
  • [Cites] Cancer Res. 2008 Jul 15;68(14):5508-11 [18632599.001]
  • [Cites] Neuro Oncol. 2008 Jun;10(3):292-9 [18430796.001]
  • [Cites] J Cereb Blood Flow Metab. 2008 Aug;28(8):1431-9 [18414496.001]
  • [Cites] Brain Res. 2008 Aug 28;1227:198-206 [18602898.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 2008 Jul-Aug;44(7):280-9 [18594936.001]
  • [Cites] J Neurooncol. 2008 Oct;90(1):19-24 [18594766.001]
  • [Cites] Eur J Pharm Biopharm. 2008 Sep;70(1):66-74 [18555675.001]
  • [Cites] Cancer Gene Ther. 2008 Oct;15(10):685-92 [18535615.001]
  • [Cites] Neurol Res. 2008 Jun;30(5):511-7 [18953742.001]
  • [Cites] NMR Biomed. 2008 Nov;21(10):1043-56 [18615861.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2009 Feb 1;73(2):530-6 [19147017.001]
  • [Cites] Eur J Radiol. 2009 Apr;70(1):180-9 [18541399.001]
  • [Cites] J Neurosurg. 2000 Feb;92(2):326-33 [10659021.001]
  • [Cites] IEEE Trans Biomed Eng. 2000 Feb;47(2):259-65 [10721633.001]
  • [Cites] Clin Exp Metastasis. 1992 Sep;10(5):345-50 [1505124.001]
  • [Cites] J Neurooncol. 1991 Dec;11(3):185-97 [1823340.001]
  • [Cites] Int J Cancer. 1992 Sep 30;52(3):409-13 [1399117.001]
  • [Cites] Cancer Res. 1993 Jan 1;53(1):176-82 [8416743.001]
  • [Cites] Science. 1993 Jan 1;259(5091):94-7 [8418502.001]
  • [Cites] J Neurosurg. 1993 Nov;79(5):729-35 [8410252.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Mar 30;28(5):1067-77 [8175391.001]
  • [Cites] J Neurooncol. 1994;19(3):259-68 [7807177.001]
  • [Cites] J Neurooncol. 1994;22(3):191-200 [7760095.001]
  • [Cites] J Surg Oncol. 1995 Jun;59(2):105-9 [7776650.001]
  • [Cites] Br J Cancer. 1995 Sep;72(3):607-14 [7669569.001]
  • [Cites] Leukemia. 1995 Oct;9 Suppl 1:S106-12 [7475300.001]
  • [Cites] Int J Cancer. 1995 Sep 15;62(6):767-71 [7558428.001]
  • [Cites] Hum Gene Ther. 1995 Nov;6(11):1467-76 [8573619.001]
  • [Cites] Cancer Lett. 1997 May 1;115(1):81-90 [9097982.001]
  • [Cites] Invasion Metastasis. 1996;16(3):107-15 [9186546.001]
  • [Cites] Klin Padiatr. 1997 Jul-Aug;209(4):275-7 [9293462.001]
  • [Cites] J Neurooncol. 1998 Jan;36(1):91-102 [9525831.001]
  • [Cites] Cancer Res. 1998 May 1;58(9):2020-8 [9581848.001]
  • [Cites] Hum Gene Ther. 1999 Jan 1;10(1):95-101 [10022534.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3861-5 [10463570.001]
  • [Cites] Cancer Gene Ther. 2004 Nov;11(11):721-32 [15475879.001]
  • [Cites] Pathobiology. 1999 Jul-Aug;67(4):202-6 [10738182.001]
  • [Cites] Gene Ther. 2000 Jun;7(12):993-9 [10871746.001]
  • [Cites] Cancer Gene Ther. 2000 Jun;7(6):879-84 [10880018.001]
  • [Cites] Cancer Gene Ther. 2000 Jun;7(6):947-53 [10880027.001]
  • [Cites] J Neurooncol. 2000;46(3):231-40 [10902854.001]
  • [Cites] J Biol Chem. 2000 Jul 28;275(30):22695-703 [10801887.001]
  • [Cites] Neurosurgery. 2000 Oct;47(4):993-9; discussion 999-1000 [11014444.001]
  • [Cites] Cancer Gene Ther. 2001 Jan;8(1):3-8 [11219491.001]
  • [Cites] Neurol Res. 2001 Jun;23(4):359-66 [11428516.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):37-47 [11451201.001]
  • [Cites] Histol Histopathol. 2001 Jul;16(3):735-44 [11510963.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7056-9 [11585735.001]
  • [Cites] J Neurooncol. 2001 Jul;53(3):275-87 [11718260.001]
  • [Cites] J Neurooncol. 2002 Jan;56(1):1-12 [11949821.001]
  • [Cites] Gene Ther. 2002 May;9(9):584-91 [11973634.001]
  • [Cites] J Neurooncol. 2002 Jan;56(2):143-8 [11995815.001]
  • [Cites] J Pharmacol Exp Ther. 2002 Jun;301(3):838-51 [12023511.001]
  • [Cites] Med Oncol. 2002;19(1):1-9 [12025885.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Aug;61(8):725-35 [12152787.001]
  • [Cites] Gene Ther. 2002 Sep;9(17):1139-45 [12170377.001]
  • [Cites] Cancer Lett. 2003 Mar 20;192(1):97-107 [12637158.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1083-93 [12651601.001]
  • [Cites] Neoplasia. 2003 Jan-Feb;5(1):17-22 [12659666.001]
  • [Cites] J Neurooncol. 2003 Mar-Apr;62(1-2):61-74 [12749703.001]
  • [Cites] Cancer Res. 2003 Jun 15;63(12):3195-201 [12810648.001]
  • [Cites] J Neurooncol. 2003 May;63(1):1-7 [12814248.001]
  • [Cites] Ann Neurol. 2003 Sep;54(3):388-92 [12953273.001]
  • [Cites] Cell Immunol. 2003 Oct;225(2):113-21 [14698145.001]
  • [Cites] Gene Ther. 2004 Jan;11(2):161-9 [14712300.001]
  • [Cites] Gene Ther. 2004 Jan;11(2):214-23 [14712306.001]
  • [Cites] Mol Ther. 2004 Feb;9(2):282-91 [14759812.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2317-23 [15059878.001]
  • [Cites] Acta Neurochir (Wien). 2004 Jul;146(7):731-4 [15197617.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5187-201 [15297423.001]
  • [Cites] Science. 1968 Jul 26;161(3839):370-1 [4873531.001]
  • [Cites] J Cell Physiol. 1970 Jun;75(3):329-39 [4988781.001]
  • [Cites] J Neurosurg. 1971 Mar;34(3):310-23 [4323142.001]
  • [Cites] J Neurosurg. 1971 Mar;34(3):335-40 [5547317.001]
  • [Cites] Cancer Res. 1973 May;33(5):976-86 [4703128.001]
  • [Cites] J Med. 1975;6(3-4):249-59 [1059719.001]
  • [Cites] J Natl Cancer Inst. 1975 Nov;55(5):1177-87 [1206744.001]
  • [Cites] Am J Pathol. 1976 Apr;83(1):149-76 [179328.001]
  • [Cites] Can J Neurol Sci. 2006 Feb;33(1):86-91 [16583728.001]
  • [Cites] Neurosurg Focus. 2006;20(4):E25 [16709031.001]
  • [Cites] J Nucl Med. 2006 Jun;47(6):989-98 [16741309.001]
  • [Cites] J Neurosci. 2006 Jun 21;26(25):6781-90 [16793885.001]
  • [Cites] J Neurooncol. 2006 Aug;79(1):9-17 [16575532.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5288-97 [17000661.001]
  • [Cites] NMR Biomed. 2006 Dec;19(8):1035-42 [16894643.001]
  • [Cites] Childs Nerv Syst. 2006 Dec;22(12):1519-25 [17021732.001]
  • [Cites] J Neurooncol. 2007 Jan;81(2):149-62 [16941073.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1260-8 [17317838.001]
  • [Cites] J Magn Reson. 2007 May;186(1):150-5 [17303454.001]
  • [Cites] Clin Cancer Res. 2007 May 1;13(9):2728-37 [17473206.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4541-4 [17510377.001]
  • [Cites] Mol Ther. 2007 Jul;15(7):1373-81 [17457322.001]
  • [Cites] Stem Cells. 2007 Jul;25(7):1645-53 [17412894.001]
  • [Cites] Behav Brain Res. 2007 Aug 22;182(1):42-50 [17572515.001]
  • [Cites] Mol Cancer Ther. 2007 Aug;6(8):2290-302 [17699724.001]
  • [Cites] Neoplasia. 2007 Jul;9(7):546-55 [17710157.001]
  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5195-201 [17726137.001]
  • [Cites] Magn Reson Med. 2007 Sep;58(3):454-62 [17763344.001]
  • [Cites] Can J Neurol Sci. 2007 Aug;34(3):296-306 [17803026.001]
  • [Cites] J Neurooncol. 2007 Nov;85(2):191-202 [17557137.001]
  • (PMID = 19381449.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA150153; United States / NINDS NIH HHS / NS / R01 NS064607; United States / NINDS NIH HHS / NS / R21 NS056203; United States / NINDS NIH HHS / NS / K01 NS059575; United States / NINDS NIH HHS / NS / K01 NS059575-02; United States / NINDS NIH HHS / NS / R01 NS064607-01; United States / NINDS NIH HHS / NS / R21 NS056203-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 149
  • [Other-IDs] NLM/ NIHMS127810; NLM/ PMC2730996
  •  go-up   go-down


60. Moviglia GA, Carrizo AG, Varela G, Gaeta CA, Paes de Lima A, Farina P, Molina H: Preliminary report on tumor stem cell/B cell hybridoma vaccine for recurrent glioblastoma multiforme. Hematol Oncol Stem Cell Ther; 2008 Jan-Mar;1(1):3-13
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary report on tumor stem cell/B cell hybridoma vaccine for recurrent glioblastoma multiforme.
  • BACKGROUND: Glioblastoma multiforme (GBM), the most aggressive glioma, presents with a rapid evolution and relapse within the first year, which is attributed to the persistence of tumor stem cells (TSC) and the escape of immune surveillance.
  • Tumor B-cell hybridoma (TBH) vaccines have been shown to function as antigen-presenting cells.
  • RESULTS: Treatment with MLC had strong and rapid therapeutic effects, but was limited in duration and induced various degrees of brain inflammation.
  • Treatment with MLC+TBH acted synergistically, provoking a rapid, strong and lasting therapeutic response but also generating different degrees of brain inflammation.
  • A lasting therapeutic effect without generating high degrees of brain inflammation occurred in patients treated with TBH vaccine alone.
  • CONCLUSION: TSC vaccine consisting of TBH alone seems to have potent adjuvant reactions overcoming both persistence of tumor stem cells and immune escape of GBM without provoking an encephalitic reaction.
  • [MeSH-major] B-Lymphocytes / transplantation. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Glioblastoma / therapy. Hybridomas / transplantation. Neoplastic Stem Cells / transplantation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukocytes, Mononuclear / immunology. Leukocytes, Mononuclear / transplantation. Lymphocyte Culture Test, Mixed. Male. Middle Aged. Neoplasm Recurrence, Local / therapy

  • Genetic Alliance. consumer health - Glioblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20063522.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
  •  go-up   go-down


61. Riina HA, Knopman J, Greenfield JP, Fralin S, Gobin YP, Tsiouris AJ, Souweidane MM, Boockvar JA: Balloon-assisted superselective intra-arterial cerebral infusion of bevacizumab for malignant brainstem glioma. A technical note. Interv Neuroradiol; 2010 Mar;16(1):71-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Balloon-assisted superselective intra-arterial cerebral infusion of bevacizumab for malignant brainstem glioma. A technical note.
  • Malignant brainstem gliomas (BSG) are rare tumors in adults, associated with a grim prognosis and limited treatment options.
  • Intravenous (IV) administration of bevacizumab (Avastin, Genentech Pharmaceuticals) has been shown to be active in the treatment of some enhancing malignant brainstem gliomas.
  • In addition, the percentage of IV drug that reaches the tumor site is restricted by the blood brain barrier (BBB).Weill Cornell Brain Tumor Center, Department of Neurosurgery, Weill Cornell Medical College of Cornell University: New York, NY, USA.
  • This technical report describes our protocol in performing superselective intra-arterial cerebral infusion (SIACI) of bevacizumab using endovascular balloon-assistance in the top of the basilar artery in a patient with a recurrent malignant brainstem glioma.
  • This method of drug delivery may have important implications in the treatment of both adult and pediatric brainstem gliomas.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Brain Stem Neoplasms / diagnostic imaging. Brain Stem Neoplasms / drug therapy. Catheterization / methods. Glioma / diagnostic imaging. Glioma / drug therapy. Infusions, Intra-Arterial / methods
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / administration & dosage. Bevacizumab. Humans. Male. Radiography. Treatment Outcome

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Radiology. 2001 Mar;218(3):724-32 [11230646.001]
  • [Cites] J Exp Ther Oncol. 2009;8(2):145-50 [20192120.001]
  • [Cites] Neurosurgery. 1985 Sep;17(3):419-23 [3930991.001]
  • [Cites] Neurosurgery. 1986 Oct;19(4):573-82 [3097567.001]
  • [Cites] J Neurooncol. 1987;4(3):195-207 [3104548.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jan 15;40(2):265-71 [9457808.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):171-7 [9892099.001]
  • [Cites] Arch Neurol. 1999 Apr;56(4):421-5 [10199329.001]
  • [Cites] Neurology. 2006 Apr 25;66(8):1258-60 [16636248.001]
  • [Cites] J Neurooncol. 2006 May;77(3):279-84 [16314949.001]
  • [Cites] Pediatr Blood Cancer. 2006 Aug;47(2):174-82 [16086410.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4714-21 [17947718.001]
  • [Cites] J Neurol. 2008 Feb;255(2):171-7 [18293027.001]
  • [Cites] J Neurooncol. 2008 Jul;88(3):339-47 [18389177.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Aug 1;71(5):1372-80 [18355978.001]
  • [Cites] Neuro Oncol. 2008 Jun;10(3):355-60 [18436627.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Brain. 2001 Dec;124(Pt 12):2528-39 [11701605.001]
  • (PMID = 20377982.001).
  • [ISSN] 1591-0199
  • [Journal-full-title] Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences
  • [ISO-abbreviation] Interv Neuroradiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC3277958
  •  go-up   go-down


62. Hall WA, Doolittle ND, Daman M, Bruns PK, Muldoon L, Fortin D, Neuwelt EA: Osmotic blood-brain barrier disruption chemotherapy for diffuse pontine gliomas. J Neurooncol; 2006 May;77(3):279-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Osmotic blood-brain barrier disruption chemotherapy for diffuse pontine gliomas.
  • From 1984 to 1998, eight patients (4M/4F), median age 11 years, with DPG were treated with monthly osmotic blood-brain barrier disruption (BBBD) chemotherapy using intraarterial carboplatin or methotrexate and intravenous cytoxan and etoposide.
  • The median time to tumor progression was 15 months with the range from <1 to 40 months.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Blood-Brain Barrier / metabolism. Brain Stem Neoplasms / drug therapy. Drug Delivery Systems / methods. Glioma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Carboplatin / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Methotrexate / administration & dosage. Osmosis / drug effects. Retrospective Studies. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pharmacol Exp Ther. 1998 Jul;286(1):77-84 [9655844.001]
  • [Cites] Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30 [8133987.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):171-7 [9892099.001]
  • [Cites] Med Pediatr Oncol. 1998 Jan;30(1):28-33 [9371386.001]
  • [Cites] Cancer. 1996 Feb 1;77(3):555-62 [8630965.001]
  • [Cites] Neuro Oncol. 2003 Jan;5(1):8-13 [12626128.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Neurosurgery. 1995 Jul;37(1):17-27; discussion 27-8 [8587686.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Apr 1;55(5):1182-5 [12654425.001]
  • [Cites] Pediatr Neurosurg. 2001 Apr;34(4):206-14 [11359114.001]
  • [Cites] Pediatr Neurosurg. 1996;24(5):263-6 [8933570.001]
  • [Cites] Bull Cancer. 2004 Jun;91(6):E167-83 [15562562.001]
  • [Cites] Cancer. 2000 Feb 1;88(3):685-92 [10649264.001]
  • [Cites] Childs Nerv Syst. 2004 Mar;20(3):143-53 [14669023.001]
  • [Cites] Cancer. 2000 Feb 1;88(3):637-47 [10649259.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Mar 15;43(5):959-64 [10192340.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):493-500 [11297239.001]
  • [Cites] Cancer. 1999 Sep 15;86(6):1064-9 [10491535.001]
  • (PMID = 16314949.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS33618; United States / NINDS NIH HHS / NS / NS34608; United States / NINDS NIH HHS / NS / NS44687
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


63. Schichor C, Birnbaum T, Etminan N, Schnell O, Grau S, Miebach S, Aboody K, Padovan C, Straube A, Tonn JC, Goldbrunner R: Vascular endothelial growth factor A contributes to glioma-induced migration of human marrow stromal cells (hMSC). Exp Neurol; 2006 Jun;199(2):301-10
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial growth factor A contributes to glioma-induced migration of human marrow stromal cells (hMSC).
  • OBJECTIVE: It has been demonstrated that murine neural stem cells (mNSCs) and human mesenchymal stroma cells migrate toward experimental gliomas, making stem cells a candidate for cellular carrier systems of anti-glioma therapy.
  • However, few data are available on the factors involved in regulating stem cell migration.
  • The aim of our study was to characterize the migratory and invasive behavior of adult human marrow stromal cells (hMSC) that interact with glioma cells, especially focusing on vascular endothelial growth factor A (VEGF-A)-mediated effects.
  • The chemokinetic activity of hMSC in response to glioma-conditioned medium as well as VEGF-A was analyzed using a modified Boyden chamber assay.
  • Invasion of hMSC and glioma spheroids was investigated using confrontational cultures.
  • To provide analogous data from a well-described system, invasion of murine C17.2 neural stem cells was assessed.
  • RESULTS: Human MSC showed an extensive invasion into glioma spheroids.
  • Glioma-conditioned medium significantly increased hMSC migration and also invasion, driven by chemotaxis.
  • VEGF-A also showed significant pro-migratory and pro-invasive effects on hMSC, but in a reduced fashion compared to glioma-conditioned medium.
  • CONCLUSIONS: Human MSC show intensive migratory and invasive behavior in the presence of glioma cells and glioma-conditioned medium.
  • Among others, VEGF-A seems to be one important factor in enhancing and directing stem cell motility.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioma / metabolism. Hematopoietic Stem Cells / physiology. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Animals. Cell Communication / physiology. Cell Line, Tumor. Cells, Cultured. Chemokines / metabolism. Culture Media, Conditioned / pharmacology. Enzyme-Linked Immunosorbent Assay / methods. Flow Cytometry / methods. Gene Expression / drug effects. Gene Expression / physiology. Green Fluorescent Proteins / metabolism. Humans. Immunohistochemistry / methods. Mice. Spheroids, Cellular. Time Factors. Transfection / methods

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16574102.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines; 0 / Culture Media, Conditioned; 0 / Vascular Endothelial Growth Factor A; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


64. Ricci-Vitiani L, Pallini R, Larocca LM, Lombardi DG, Signore M, Pierconti F, Petrucci G, Montano N, Maira G, De Maria R: Mesenchymal differentiation of glioblastoma stem cells. Cell Death Differ; 2008 Sep;15(9):1491-8
MedlinePlus Health Information. consumer health - Brain Tumors.

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

  • Genetic Alliance. consumer health - Glioblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18497759.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


65. Panosyan EH, Laks DR, Masterman-Smith M, Mottahedeh J, Yong WH, Cloughesy TF, Lazareff JA, Mischel PS, Moore TB, Kornblum HI: Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formation. Pediatr Blood Cancer; 2010 Oct;55(4):644-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formation.
  • BACKGROUND: Cultured brain tumors can form neurospheres harboring tumorigenic cells with self renewal and differentiation capacities.
  • Renewable neurosphere formation has clinical predictive value in adult malignant gliomas, yet its prognostic role for pediatric brain tumors is unknown.
  • CONCLUSIONS: Neurosphere formation is more predictive of pediatric brain tumor progression than semi-quantitative Ki67 staining.
  • Pediatric brain tumor derived neurospheres may provide a predictive model for preclinical explorations.

  • 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
  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4572-8 [14673044.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Pediatr Blood Cancer. 2007 Dec;49(7):888-93 [17554787.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8205-12 [19088037.001]
  • [Cites] Stem Cells. 2009 Apr;27(4):980-7 [19353526.001]
  • [Cites] J Neurosurg Pediatr. 2009 Jun;3(6):461-6 [19485728.001]
  • [Cites] Neurotherapeutics. 2009 Jul;6(3):570-86 [19560746.001]
  • [Cites] Pediatr Blood Cancer. 2009 Sep;53(3):312-7 [19434732.001]
  • [Cites] Curr Stem Cell Res Ther. 2009 Dec;4(4):298-305 [19500067.001]
  • [Cites] Cancer. 2009 Dec 15;115(24):5761-70 [19813274.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Neurosurgery. 2002 Jun;50(6):1238-44; discussion 1244-5 [12015841.001]
  • [Cites] Clin Neuropathol. 2002 Nov-Dec;21(6):252-7 [12489673.001]
  • [Cites] Am J Surg Pathol. 2004 Jul;28(7):914-20 [15223962.001]
  • (PMID = 20589659.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS052563; United States / NCI NIH HHS / CA / T32 CA009056; United States / NCI NIH HHS / CA / U54 CA119347; United States / NINDS NIH HHS / NS / R01NS052563
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS572199; NLM/ PMC4017922
  •  go-up   go-down


66. Fischer I, Cunliffe CH, Bollo RJ, Raza S, Monoky D, Chiriboga L, Parker EC, Golfinos JG, Kelly PJ, Knopp EA, Gruber ML, Zagzag D, Narayana A: High-grade glioma before and after treatment with radiation and Avastin: initial observations. Neuro Oncol; 2008 Oct;10(5):700-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-grade glioma before and after treatment with radiation and Avastin: initial observations.
  • We evaluate the effects of adjuvant treatment with the angiogenesis inhibitor Avastin (bevacizumab) on pathological tissue specimens of high-grade glioma.
  • Tissue from five patients before and after treatment with Avastin was subjected to histological evaluation and compared to four control cases of glioma before and after similar treatment protocols not including bevacizumab.
  • Histological analysis focused on microvessel density and vascular morphology, and expression patterns of vascular endothelial growth factor-A (VEGF-A) and the hematopoietic stem cell, mesenchymal, and cell motility markers CD34, smooth muscle actin, D2-40, and fascin.
  • VEGF-A expression in tumor cells was increased in two cases and decreased in three and did not correlate with treatment response.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy
  • [MeSH-minor] Actins / drug effects. Actins / radiation effects. Adult. Antibodies, Monoclonal, Humanized. Antigens, CD34 / drug effects. Antigens, CD34 / radiation effects. Bevacizumab. Carrier Proteins / drug effects. Carrier Proteins / radiation effects. Combined Modality Therapy. Female. Humans. Magnetic Resonance Imaging. Male. Microfilament Proteins / drug effects. Microfilament Proteins / radiation effects. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Retrospective Studies. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / radiation effects

  • Genetic Alliance. consumer health - Glioma.
  • 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
  • [Cites] Nat Med. 2001 Nov;7(11):1194-201 [11689883.001]
  • [Cites] Acta Neuropathol. 2003 Apr;105(4):358-64 [12624789.001]
  • [Cites] J Hematother Stem Cell Res. 2003 Feb;12(1):23-32 [12662433.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):133-43 [12744467.001]
  • [Cites] Oncogene. 2003 Jun 5;22(23):3616-23 [12789270.001]
  • [Cites] Brain Tumor Pathol. 2003;20(2):53-8 [14756441.001]
  • [Cites] Nat Rev Drug Discov. 2004 May;3(5):391-400 [15136787.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):35-52 [15215160.001]
  • [Cites] Endocr Rev. 2004 Aug;25(4):581-611 [15294883.001]
  • [Cites] Curr Opin Cell Biol. 2004 Oct;16(5):590-6 [15363811.001]
  • [Cites] Am J Clin Pathol. 1991 Jul;96(1):32-45 [1712542.001]
  • [Cites] J Neuropathol Exp Neurol. 1992 Sep;51(5):493-8 [1381414.001]
  • [Cites] J Neuropathol Exp Neurol. 1995 May;54(3):304-10 [7745429.001]
  • [Cites] Ann Oncol. 1996 Feb;7(2):205-7 [8777179.001]
  • [Cites] Acta Neuropathol. 1999 May;97(5):481-90 [10334485.001]
  • [Cites] Microsc Res Tech. 1999 Jul 1;46(1):53-8 [10402272.001]
  • [Cites] APMIS. 2004 Jul-Aug;112(7-8):450-62 [15563309.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 29;333(2):328-35 [15961063.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Nov 11;337(1):355-62 [16185662.001]
  • [Cites] Oncology. 2005;69 Suppl 3:11-6 [16301831.001]
  • [Cites] Ann Diagn Pathol. 2005 Dec;9(6):307-11 [16308158.001]
  • [Cites] Brain Pathol. 2005 Oct;15(4):297-310 [16389942.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):217-27 [16365183.001]
  • [Cites] J Clin Oncol. 2006 Feb 10;24(5):769-77 [16391297.001]
  • [Cites] Virchows Arch. 2006 Apr;448(4):493-9 [16411134.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):261-72 [16616332.001]
  • [Cites] Acta Neuropathol. 2006 May;111(5):483-8 [16596424.001]
  • [Cites] J Cell Biol. 2006 Sep 11;174(6):863-75 [16966425.001]
  • [Cites] Histol Histopathol. 2006 Dec;21(12):1287-93 [16977579.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2610-21 [17016557.001]
  • [Cites] J Cell Sci. 2006 Nov 1;119(Pt 21):4541-53 [17046996.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Nov;28(11):703-10 [17114955.001]
  • [Cites] Arch Pathol Lab Med. 2007 Feb;131(2):234-41 [17284108.001]
  • [Cites] Am J Surg Pathol. 2007 Mar;31(3):351-62 [17325476.001]
  • [Cites] Mod Pathol. 2007 May;20(5):552-61 [17396145.001]
  • [Cites] Dis Markers. 2007;23(3):153-60 [17473384.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1310-2 [17330095.001]
  • [Cites] Nat Rev Neurosci. 2007 Aug;8(8):610-22 [17643088.001]
  • [Cites] Circ Res. 2007 Aug 3;101(3):286-94 [17569886.001]
  • [CommentIn] Neuro Oncol. 2008 Oct;10(5):647 [18776128.001]
  • (PMID = 18697955.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD34; 0 / Carrier Proteins; 0 / Microfilament Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 146808-54-0 / fascin; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2666246
  •  go-up   go-down


67. Kumar AJ, Leeds NE, Kumar VA, Fuller GN, Lang FF, Milas Z, Weinberg JS, Ater JL, Sawaya R: Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas. J Comput Assist Tomogr; 2010 Jul;34(4):601-11
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas.
  • METHODS: One hundred patients referred to the cancer center with brain tumors histologically proven to be PA were retrospectively reviewed (95 by magnetic resonance imaging and 5 by computed tomographic imaging) and analyzed.
  • Tumor locations consisted of the following: optic chiasm (22), lateral ventricle (3), thalamus (12), basal ganglia (1), cerebral hemisphere (10), corpus callosum (2), brain stem (26), fourth ventricle (1), and cerebellum (23).
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Glioma / diagnosis. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Brain / pathology. Brain / radiography. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies. Tomography, X-Ray Computed / methods. Young Adult

  • Genetic Alliance. consumer health - Pilocytic astrocytoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20657231.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


68. Sharma MK, Mansur DB, Reifenberger G, Perry A, Leonard JR, Aldape KD, Albin MG, Emnett RJ, Loeser S, Watson MA, Nagarajan R, Gutmann DH: Distinct genetic signatures among pilocytic astrocytomas relate to their brain region origin. Cancer Res; 2007 Feb 1;67(3):890-900
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct genetic signatures among pilocytic astrocytomas relate to their brain region origin.
  • Pilocytic astrocytomas (PAs) are the most common glioma in children.
  • Whereas many PAs are slow-growing or clinically indolent, others exhibit more aggressive features with tumor recurrence and death.
  • Lastly, we also identified a gene expression pattern common to PAs and normal mouse astrocytes and neural stem cells from these distinct brain regions as well as a gene expression pattern shared between PAs and another human glial tumor (ependymoma) arising supratentorially compared with those originating in the posterior fossa.
  • These results suggest that glial tumors share an intrinsic, lineage-specific molecular signature that reflects the brain region in which their nonmalignant predecessors originated.
  • [MeSH-minor] Adolescent. Adult. Algorithms. Child. Child, Preschool. Cluster Analysis. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neurofibromatosis 1 / genetics. Neurofibromatosis 1 / metabolism. Neurofibromatosis 1 / pathology. Oligonucleotide Array Sequence Analysis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17283119.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE5582/ GSE5675
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 91842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


69. Kansal R, Mahore A, Goel A: Cerebrospinal fluid rhinorrhea after ventriculoperitoneal shunt in a patient with tectal plate glioma. J Clin Neurosci; 2010 Apr;17(4):532-3
Genetic Alliance. consumer health - Glioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebrospinal fluid rhinorrhea after ventriculoperitoneal shunt in a patient with tectal plate glioma.
  • Cerebrospinal fluid (CSF) rhinorrhea due to a remote tumor is a rare but increasingly reported condition, where it is usually a presenting complaint.
  • CSF rhinorrhea occurring after tumor decompression has also been reported.
  • We report a patient with tectal plate glioma that caused CSF rhinorrhea following insertion of ventriculoperitoneal shunt.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Cerebrospinal Fluid Rhinorrhea / etiology. Glioma / pathology. Ventriculoperitoneal Shunt / adverse effects
  • [MeSH-minor] Humans. Hydrocephalus / etiology. Hydrocephalus / surgery. Magnetic Resonance Imaging. Male. Tectum Mesencephali / pathology. Tectum Mesencephali / surgery. Tomography, X-Ray Computed. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20096589.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  •  go-up   go-down


70. Tamura K, Aoyagi M, Wakimoto H, Ando N, Nariai T, Yamamoto M, Ohno K: Accumulation of CD133-positive glioma cells after high-dose irradiation by Gamma Knife surgery plus external beam radiation. J Neurosurg; 2010 Aug;113(2):310-8
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accumulation of CD133-positive glioma cells after high-dose irradiation by Gamma Knife surgery plus external beam radiation.
  • OBJECT: Recent evidence suggests that a glioma stem cell subpopulation might contribute to radioresistance in malignant gliomas.
  • Histological sections were subjected to immunohistochemistry for MIB-1, factor VIII, and stem cell markers, nestin and CD133.
  • Histopathological examination after GKS and EBRT showed variable mixtures of viable tumor tissues and necrosis.
  • Viable tumor tissues exhibited high MIB-1 indices but reduced numbers of tumor blood vessels.
  • There was marked accumulation of CD133-positive glioma cells, particularly in remnant tumors within the necrotic areas, in sections obtained after GKS plus EBRT, whereas CD133-positive cells appeared very infrequently in primary sections prior to adjuvant treatment.
  • CONCLUSIONS: The results indicate that CD133-positive glioma stemlike cells can survive high-dose irradiation, leading to recurrence, despite prolonged damage to tumor blood vessels.
  • [MeSH-major] Antigens, CD / metabolism. Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Glioblastoma / radiotherapy. Glioblastoma / surgery. Glycoproteins / metabolism. Peptides / metabolism
  • [MeSH-minor] Adult. Aged. Biomarkers / metabolism. Biopsy. Blood Vessels / radiation effects. Combined Modality Therapy. Disease Progression. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Positron-Emission Tomography. Radiation Tolerance. Radiosurgery. Radiotherapy. Young Adult

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20205512.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers; 0 / Glycoproteins; 0 / Peptides
  •  go-up   go-down


71. Oh MC, Lim DA: Novel treatment strategies for malignant gliomas using neural stem cells. Neurotherapeutics; 2009 Jul;6(3):458-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment strategies for malignant gliomas using neural stem cells.
  • Recent studies in stem cell biology have refined our understanding of the origin and progression of cancer.
  • Identification and characterization of endogenous neural stem cells (NSCs), especially those in the adult human brain, have inspired new ideas for selectively targeting and destroying malignant gliomas.
  • Gliomas consist of a heterogeneous population of cells, and some of these cells have characteristics of cancer stem cells.
  • These brain tumor stem cells (BTSCs) share certain characteristics with normal NSCs.
  • Nonetheless, the cellular and molecular similarities between BTSCs and normal NSCs suggest a common research landscape underlying both normal and cancer stem cell biology, wherein findings of one field are relevant to the other.
  • Furthermore, the natural tropism of NSCs to gliomas has generated the idea that modified NSCs can deliver modified genes to selectively destroy malignant brain tumor cells, and even BTSCs, while leaving healthy surrounding neurons intact.
  • [MeSH-major] Brain / physiology. Brain Neoplasms / therapy. Glioma / therapy. Neurons / physiology. Stem Cells / physiology
  • [MeSH-minor] Adult Stem Cells / physiology. Animals. Genetic Therapy. Humans. Stem Cell Transplantation. Tropism / physiology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 = 19560736.001).
  • [ISSN] 1933-7213
  • [Journal-full-title] Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
  • [ISO-abbreviation] Neurotherapeutics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 66
  •  go-up   go-down


72. Patru C, Romao L, Varlet P, Coulombel L, Raponi E, Cadusseau J, Renault-Mihara F, Thirant C, Leonard N, Berhneim A, Mihalescu-Maingot M, Haiech J, Bièche I, Moura-Neto V, Daumas-Duport C, Junier MP, Chneiweiss H: CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors. BMC Cancer; 2010;10:66
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors.
  • BACKGROUND: Tumor initiating cells (TICs) provide a new paradigm for developing original therapeutic strategies.
  • METHODS: We screened for TICs in 47 human adult brain malignant tumors.
  • Cells forming floating spheres in culture, and endowed with all of the features expected from tumor cells with stem-like properties were obtained from glioblastomas, medulloblastoma but not oligodendrogliomas.
  • Xenografts of fewer than 500 cells in Nude mouse brains induced a progressively growing tumor.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD15 / biosynthesis. Antigens, CD34 / biosynthesis. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Glycoproteins / biosynthesis. Neoplastic Stem Cells / cytology. Neurons / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Peptides. Proteomics / methods

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Acta Neuropathol. 2006 Jan;111(1):29-38 [16320026.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):761-5 [17151667.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Stem Cells. 2007 Apr;25(4):961-73 [17204602.001]
  • [Cites] Oncogene. 2007 Apr 26;26(19):2695-706 [17057735.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4010-5 [17483311.001]
  • [Cites] Clin Cancer Res. 2007 May 15;13(10):2897-904 [17504989.001]
  • [Cites] PLoS One. 2008;3(11):e3655 [18985161.001]
  • [Cites] Cell Stem Cell. 2009 May 8;4(5):440-52 [19427293.001]
  • [Cites] Stem Cells. 2009 Oct;27(10):2373-82 [19544474.001]
  • [Cites] Prog Neurobiol. 2000 Dec;62(5):443-73 [10869779.001]
  • [Cites] Ann Pathol. 2000 Oct;20(5):413-28 [11084409.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1652-8 [11245479.001]
  • [Cites] Nat Rev Genet. 2001 Feb;2(2):120-9 [11253051.001]
  • [Cites] J Neurooncol. 2001 Jul;53(3):289-96 [11718261.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Neuron. 2002 Aug 29;35(5):865-75 [12372282.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1589-95 [12670909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Trends Neurosci. 2004 Mar;27(3):148-54 [15036880.001]
  • [Cites] Nature. 2004 Jul 15;430(6997):350-6 [15254537.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Neurosurgery. 2004 Dec;55(6):1377-91: discussion 1391-2 [15574220.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9392-400 [15558011.001]
  • [Cites] Oncogene. 2006 Mar 16;25(12):1696-708 [16449977.001]
  • (PMID = 20181261.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides
  • [Other-IDs] NLM/ PMC2841664
  •  go-up   go-down


73. Pollack IF, Jakacki RI, Blaney SM, Hancock ML, Kieran MW, Phillips P, Kun LE, Friedman H, Packer R, Banerjee A, Geyer JR, Goldman S, Poussaint TY, Krasin MJ, Wang Y, Hayes M, Murgo A, Weiner S, Boyett JM: Phase I trial of imatinib in children with newly diagnosed brainstem and recurrent malignant gliomas: a Pediatric Brain Tumor Consortium report. Neuro Oncol; 2007 Apr;9(2):145-60
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of imatinib in children with newly diagnosed brainstem and recurrent malignant gliomas: a Pediatric Brain Tumor Consortium report.
  • This study estimated the maximum tolerated dose (MTD) of imatinib with irradiation in children with newly diagnosed brainstem gliomas, and those with recurrent malignant intracranial gliomas, stratified according to use of enzyme-inducing anticonvulsant drugs (EIACDs).
  • In the brainstem glioma stratum, imatinib was initially administered twice daily during irradiation, but because of possible association with intratumoral hemorrhage (ITH) was subsequently started two weeks after irradiation.
  • Twenty-four evaluable patients received therapy before the amendment, and three of six with a brainstem tumor experienced dose-limiting toxicity (DLT): one had asymptomatic ITH, one had grade 4 neutropenia and, one had renal insufficiency.
  • None of 18 patients with recurrent glioma experienced DLT.
  • After protocol amendment, 3 of 16 patients with brainstem glioma and 2 of 11 patients with recurrent glioma who were not receiving EIACDs experienced ITH DLTs, with three patients being symptomatic.
  • The recommended phase II dose for brainstem gliomas was 265 mg/m(2).
  • Three of 27 patients with brainstem gliomas with imaging before and after irradiation, prior to receiving imatinib, had new hemorrhage, excluding their receiving imatinib.
  • In summary, recommended phase II imatinib doses were determined for children with newly diagnosed brainstem glioma and recurrent high-grade glioma who were not receiving EIACDs.
  • Imatinib may increase the risk of ITH, although the incidence of spontaneous hemorrhages in brainstem glioma is sufficiently high that this should be considered in studies of agents in which hemorrhage is a concern.

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):398-406 [10652433.001]
  • [Cites] Dig Dis Sci. 2005 Jan;50(1):65-9 [15712639.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5143-50 [11016641.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2929-34 [11306470.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Mar 5;768(2):325-40 [11888061.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3729-35 [12097282.001]
  • [Cites] J Clin Oncol. 2002 Aug 15;20(16):3431-7 [12177103.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):481-7 [12181402.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7377-83 [14612536.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):935-42 [14990650.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1364-71 [16463390.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):313-23 [14658008.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2655-60 [15231574.001]
  • [Cites] Cancer. 1988 Mar 1;61(5):896-902 [3338054.001]
  • [Cites] Cancer Lett. 1988 Jan;38(3):283-96 [3258178.001]
  • [Cites] J Neurooncol. 1990 Feb;8(1):1-12 [2156959.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):131-40 [2164040.001]
  • [Cites] Neuroradiology. 1990;32(4):265-71 [2234384.001]
  • [Cites] J Neurosurg. 1991 Aug;75(2):284-93 [1649272.001]
  • [Cites] J Biol Chem. 1991 Sep 5;266(25):16755-63 [1653246.001]
  • [Cites] Science. 1991 Nov 22;254(5035):1146-53 [1659742.001]
  • [Cites] Childs Nerv Syst. 1991 Dec;7(8):432-6 [1665101.001]
  • [Cites] Cancer Res. 1992 Jun 1;52(11):3213-9 [1317261.001]
  • [Cites] Cancer. 1993 Aug 15;72(4):1414-21 [8339232.001]
  • [Cites] J Cell Physiol. 1994 Feb;158(2):381-9 [8106574.001]
  • [Cites] Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30 [8133987.001]
  • [Cites] Neurosurgery. 1994 Feb;34(2):309-14; discussion 314-5 [8177392.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6106-14 [7954456.001]
  • [Cites] N Engl J Med. 1994 Dec 1;331(22):1500-7 [7969301.001]
  • [Cites] Stat Med. 1995 Jun 15;14(11):1149-61 [7667557.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] J Clin Oncol. 1996 Sep;14(9):2495-503 [8823328.001]
  • [Cites] J Neurooncol. 1996 May-Jun;28(2-3):207-22 [8832463.001]
  • [Cites] Pediatr Neurosurg. 1996;24(4):185-92 [8873160.001]
  • [Cites] Eur J Cancer. 1996 Dec;32A(13):2236-41 [9038604.001]
  • [Cites] Surg Neurol. 1998 Feb;49(2):189-95; discussion 196 [9457270.001]
  • [Cites] Pediatr Neurosurg. 1998 Nov;29(5):228-44 [9917540.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1464-72 [10197615.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):249-57 [11001068.001]
  • (PMID = 17293590.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01 CA081457; United States / NCRR NIH HHS / RR / M01 RR00188-37; United States / NCI NIH HHS / CA / U01 CA81457
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1871662
  •  go-up   go-down


74. Walton NM, Snyder GE, Park D, Kobeissy F, Scheffler B, Steindler DA: Gliotypic neural stem cells transiently adopt tumorigenic properties during normal differentiation. Stem Cells; 2009 Feb;27(2):280-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gliotypic neural stem cells transiently adopt tumorigenic properties during normal differentiation.
  • An increasing body of evidence suggests that astrocytic gliomas of the central nervous system may be derived from gliotypic neural stem cells.
  • To date, the study of these tumors, particularly the identification of originating cellular population(s), has been frustrated by technical difficulties in accessing the native niche of stem cells.
  • To identify any hallmark signs of cancer in neural stem cells or their progeny, we cultured subventricular zone-derived tissue in a unique in vitro model that temporally and phenotypically recapitulates adult neurogenesis.
  • Contrary to some reports, we found undifferentiated neural stem cells possess few characteristics, suggesting prototumorigenic potential.
  • 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.
  • As tumorigenic characteristics in progenitor cells normally disappear with the generation of mature progeny, this suggests that developmentally intermediate progenitor cells, rather than neural stem cells, may be the origin of so-called "stem cell-derived" tumors.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [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
  •  go-up   go-down


75. Qiu J, Ai L, Ramachandran C, Yao B, Gopalakrishnan S, Fields CR, Delmas AL, Dyer LM, Melnick SJ, Yachnis AT, Schwartz PH, Fine HA, Brown KD, Robertson KD: Invasion suppressor cystatin E/M (CST6): high-level cell type-specific expression in normal brain and epigenetic silencing in gliomas. Lab Invest; 2008 Sep;88(9):910-25
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Invasion suppressor cystatin E/M (CST6): high-level cell type-specific expression in normal brain and epigenetic silencing in gliomas.
  • Malignant gliomas are the most common primary brain tumors in adults and the second most common tumor in children.
  • Morbidity and mortality are high in glioma patients because tumors are resistant to treatment and are highly invasive into surrounding brain tissue rendering complete surgical resection impossible.
  • In our previous studies we identified cystatin E/M (CST6) as a frequent target of epigenetic silencing in glioma.
  • Cystatin E/M is a potent inhibitor of cathepsin B, which is frequently overexpressed in glioma.
  • Here, we study the expression of cystatin E/M in normal brain and show that it is highly and moderately expressed in oligodendrocytes and astrocytes, respectively, but not in neurons.
  • In contrast, 78% of 28 primary brain tumors demonstrated reduced/absent cystatin E/M expression using a tissue microarray and this reduced expression correlated with CST6 promoter hypermethylation.
  • Interestingly, CST6 was expressed in neural stem cells (NSC) and markedly induced upon differentiation, whereas a glioma tumor initiating cell (TIC) line was completely blocked for CST6 expression by promoter methylation.
  • Analysis of primary pediatric brain tumor-derived lines also showed CST6 downregulation and methylation in nearly 100% of 12 cases.
  • Finally, ectopic expression of cystatin E/M in glioma lines reduced cell motility and invasion.
  • These results demonstrate that epigenetic silencing of CST6 is frequent in adult and pediatric brain tumors and occurs in TICs, which are thought to give rise to the tumor.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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] Cancer Lett. 2006 Apr 28;235(2):159-76 [15893421.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] J Biol Chem. 2006 Jun 9;281(23):15893-9 [16565075.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):132-8 [10655057.001]
  • [Cites] Neuron. 2000 Nov;28(2):385-97 [11144350.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):687-92 [11257100.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] Oncogene. 2001 Jun 21;20(28):3665-73 [11439329.001]
  • [Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]
  • [Cites] J Neurochem. 2002 Jun;81(5):922-34 [12065604.001]
  • [Cites] J Neurooncol. 2002 May;58(1):21-32 [12160137.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7899-909 [16912163.001]
  • [Cites] Biol Chem. 2006 Oct-Nov;387(10-11):1429-39 [17081116.001]
  • [Cites] Lab Invest. 2006 Dec;86(12):1233-42 [17043665.001]
  • [Cites] Carcinogenesis. 2006 Dec;27(12):2409-23 [16952911.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Oncogene. 2007 Apr 19;26(18):2621-34 [17043644.001]
  • [Cites] Oncogene. 2007 May 10;26(21):3089-94 [17099723.001]
  • [Cites] Stem Cells Dev. 2007 Jun;16(3):447-60 [17610375.001]
  • [Cites] Nat Protoc. 2007;2(9):2265-75 [17853883.001]
  • [Cites] Biochim Biophys Acta. 2007 Dec;1776(2):125-37 [17868999.001]
  • [Cites] Cancer Cell. 2008 Jan;13(1):69-80 [18167341.001]
  • [Cites] Mol Cancer Res. 2008 Jan;6(1):21-30 [18184972.001]
  • [Cites] Int J Mol Med. 2003 May;11(5):655-60 [12684707.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):203-15 [15674478.001]
  • [Cites] Acta Neuropathol. 2005 Jan;109(1):93-108 [15685439.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Feb 3;340(1):175-82 [16356477.001]
  • [Cites] Life Sci. 2006 Jan 18;78(8):898-907 [16150465.001]
  • [Cites] Nat Rev Genet. 2002 Sep;3(9):662-73 [12209141.001]
  • [Cites] Brain Tumor Pathol. 2002;19(1):15-22 [12455884.001]
  • [Cites] Oncogene. 2002 Dec 12;21(57):8705-12 [12483523.001]
  • [Cites] J Natl Cancer Inst. 2003 Feb 19;95(4):327-30 [12591989.001]
  • [Cites] Nat Rev Cancer. 2003 Apr;3(4):253-66 [12671664.001]
  • [Cites] Science. 2003 Apr 18;300(5618):455 [12702868.001]
  • [Cites] J Pediatr Nurs. 2003 Apr;18(2):96-102 [12720206.001]
  • [Cites] Nat Rev Cancer. 2003 Jul;3(7):489-501 [12835669.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 15;144(2):134-42 [12850376.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):1911-9 [14578190.001]
  • [Cites] Biochem Soc Symp. 2003;(70):179-99 [14587292.001]
  • [Cites] J Neurosci Res. 2003 Dec 15;74(6):838-51 [14648588.001]
  • [Cites] Neurol Clin. 2003 Nov;21(4):897-913 [14743655.001]
  • [Cites] Oncogene. 2004 Mar 18;23(12):2206-15 [14676833.001]
  • [Cites] Oncogene. 2004 Mar 18;23(12):2224-30 [14730346.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Jun;36(6):1046-69 [15094120.001]
  • [Cites] Mol Cell. 2004 Apr 23;14(2):207-19 [15099520.001]
  • [Cites] Oncogene. 2004 Jun 10;23(27):4681-9 [15122332.001]
  • [Cites] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):118-31 [15313584.001]
  • [Cites] Curr Opin Cell Biol. 2004 Oct;16(5):558-64 [15363807.001]
  • [Cites] Nat Rev Neurosci. 2004 Oct;5(10):782-92 [15378038.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6957-64 [15466187.001]
  • [Cites] Development. 1989 Feb;105(2):387-400 [2680425.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1827-31 [1542678.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6027-31 [7954439.001]
  • [Cites] Clin Exp Metastasis. 1995 Jan;13(1):49-56 [7820956.001]
  • [Cites] J Neurosurg. 1995 Aug;83(2):285-90 [7542317.001]
  • [Cites] Neurosci Lett. 1996 Apr 26;208(3):171-4 [8733297.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Clin Exp Metastasis. 1996 Sep;14(4):344-50 [8878408.001]
  • [Cites] J Biol Chem. 1997 Apr 18;272(16):10853-8 [9099741.001]
  • [Cites] Nat Med. 1998 Jul;4(7):844-7 [9662379.001]
  • [Cites] Nature. 1998 Sep 3;395(6697):89-93 [9738504.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):798-802 [10029065.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6665-74 [16818640.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7490-501 [16885346.001]
  • [Cites] Cancer Lett. 2006 Sep 28;241(2):159-73 [16442709.001]
  • (PMID = 18607344.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114229-04; United States / NCI NIH HHS / CA / R01 CA114229-03; United States / NCI NIH HHS / CA / R01 CA114229; United States / NCI NIH HHS / CA / CA114229-03; United States / NCI NIH HHS / CA / R01CA102289; United States / NCI NIH HHS / CA / R01 CA102289; United States / NCI NIH HHS / CA / CA114229-04; United States / NCI NIH HHS / CA / R01CA114229
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CST6 protein, human; 0 / Cystatin M; 0 / Cystatins; 0 / DNA Primers
  • [Other-IDs] NLM/ NIHMS59304; NLM/ PMC2574902
  •  go-up   go-down


76. Günther HS, Schmidt NO, Phillips HS, Kemming D, Kharbanda S, Soriano R, Modrusan Z, Meissner H, Westphal M, Lamszus K: Glioblastoma-derived stem cell-enriched cultures form distinct subgroups according to molecular and phenotypic criteria. Oncogene; 2008 May 1;27(20):2897-909
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma-derived stem cell-enriched cultures form distinct subgroups according to molecular and phenotypic criteria.
  • Tumor cells with stem cell-like properties can be cultured from human glioblastomas by using conditions that select for the expansion of neural stem cells.
  • We generated cell lines from glioblastoma specimens with the goal to obtain model systems for glioma stem cell biology.
  • Unsupervised analysis of the expression profiles of nine cell lines established under neural stem cell conditions yielded two distinct clusters.
  • Our findings show that stable, multipotent glioblastoma cell lines with a full stem-like phenotype express neurodevelopmental genes as a distinctive feature, which may offer therapeutic targeting opportunities.
  • The generation of another distinct cluster of cell lines showing similarly homogeneous profiling but restricted stem cell properties suggests that different phenotypes exist, each of which may lead to the typical appearance of glioblastoma.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Neoplastic Stem Cells / classification. Neoplastic Stem Cells / metabolism. Phenotype
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Culture Techniques. Cell Line, Tumor. Female. Gene Expression Profiling. Humans. Male. Mice. Mice, Nude. Middle Aged. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18037961.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


77. Kang SK, Cha SH, Jeon HG: Curcumin-induced histone hypoacetylation enhances caspase-3-dependent glioma cell death and neurogenesis of neural progenitor cells. Stem Cells Dev; 2006 Apr;15(2):165-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Curcumin-induced histone hypoacetylation enhances caspase-3-dependent glioma cell death and neurogenesis of neural progenitor cells.
  • Our studies first proved that curcumin induces histone hypoacetylation in brain cancer cells and finally induces apoptotic cell death through a (PARP)- and caspase 3-mediated manner.
  • In addition, curcumin induces recontrolling of neural stem cell fates.
  • It induces effective neurogenesis, synaptogenesis, and migration of neural progenitor cells in vitro in brain-derived adult neural stem cells.
  • We suggest that histone hypoacetylation plays an important role in determine stem cell fate through controlling the simultaneous expression of many genes.
  • Thus, the present finding that curcumin, a nontoxic dietary compound, is a histone acetyltransferase inhibitor would supply a new window to understand further the molecular mechanism of histone acetylase inhibitors (HAI) in cancer and neural stem cells and provide a new target molecule for treating central nervous system disorders.
  • [MeSH-major] Apoptosis / drug effects. Caspases / metabolism. Curcumin / pharmacology. Histones / metabolism. Neurons / metabolism. Stem Cells / metabolism
  • [MeSH-minor] Acetylation / drug effects. Animals. Astrocytes / cytology. Astrocytes / drug effects. Astrocytes / metabolism. Brain / cytology. Brain / drug effects. Brain / metabolism. Caspase 3. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Cell Survival / drug effects. Cells, Cultured. Collagen Type XI / metabolism. Dentate Gyrus / cytology. Dentate Gyrus / drug effects. Dentate Gyrus / metabolism. Glioma / metabolism. Glioma / pathology. Histone Acetyltransferases / antagonists & inhibitors. Humans. Mice. Mice, Inbred ICR. bcl-2-Associated X Protein / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. CURCUMIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16646663.001).
  • [ISSN] 1547-3287
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COL11A2 protein, human; 0 / Collagen Type XI; 0 / Histones; 0 / bcl-2-Associated X Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; IT942ZTH98 / Curcumin
  •  go-up   go-down


78. Yamaguchi S, Terasaka S, Kobayashi H, Shiga T, Usui R, Hirata K, Kubota K, Murata J, Iwasaki Y: Indolent dorsal midbrain tumor: new findings based on positron emission tomography. J Neurosurg Pediatr; 2009 Apr;3(4):270-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Indolent dorsal midbrain tumor: new findings based on positron emission tomography.
  • Gliosis or glial proliferation was diagnosed in 1 patient, and possible low-grade glioma in 2 patients.
  • On the other hand, the PET features of these lesions were almost identical, and the scans did not show a high uptake of FDG and MET compared with the cortical uptake in a normal brain.
  • The mean tumor tissue/normal tissue ratio of FDG uptake was 0.65, and that of MET was 0.99.
  • [MeSH-major] Brain Stem Neoplasms / radionuclide imaging. Glioma / radionuclide imaging. Gliosis / radionuclide imaging. Positron-Emission Tomography
  • [MeSH-minor] Adolescent. Aged. Child. Female. Humans. Magnetic Resonance Imaging. Male. Young Adult

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19338404.001).
  • [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
  •  go-up   go-down


79. Cui JG, Zhao Y, Sethi P, Li YY, Mahta A, Culicchia F, Lukiw WJ: Micro-RNA-128 (miRNA-128) down-regulation in glioblastoma targets ARP5 (ANGPTL6), Bmi-1 and E2F-3a, key regulators of brain cell proliferation. J Neurooncol; 2010 Jul;98(3):297-304
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Micro-RNA-128 (miRNA-128) down-regulation in glioblastoma targets ARP5 (ANGPTL6), Bmi-1 and E2F-3a, key regulators of brain cell proliferation.
  • High density micro-RNA (miRNA) arrays, fluorescent-reporter miRNA assay and Northern miRNA dot-blot analysis show that a brain-enriched miRNA-128 is significantly down-regulated in glioblastoma multiforme (GBM) and in GBM cell lines when compared to age-matched controls.
  • The down-regulation of miRNA-128 was found to inversely correlate with WHO tumor grade.
  • Three bioinformatics-verified miRNA-128 targets, angiopoietin-related growth factor protein 5 (ARP5; ANGPTL6), a transcription suppressor that promotes stem cell renewal and inhibits the expression of known tumor suppressor genes involved in senescence and differentiation, Bmi-1, and a transcription factor critical for the control of cell-cycle progression, E2F-3a, were found to be up-regulated.
  • Our data suggests that down-regulation of miRNA-128 may contribute to glioma and GBM, in part, by coordinately up-regulating ARP5 (ANGPTL6), Bmi-1 and E2F-3a, resulting in the proliferation of undifferentiated GBM cells.
  • [MeSH-major] Angiopoietins / metabolism. Brain / pathology. Brain Neoplasms / pathology. Cell Proliferation. Down-Regulation / physiology. E2F3 Transcription Factor / metabolism. Glioblastoma / pathology. MicroRNAs / metabolism. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Adult. Computational Biology / methods. Female. Humans. Male. Middle Aged. Polycomb Repressive Complex 1. RNA, Messenger / metabolism. Transfection / methods

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurooncol. 2009 Jan;91(1):27-32 [18759060.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 9;334(4):1351-8 [16039986.001]
  • [Cites] Mol Pharmacol. 2009 Feb;75(2):259-64 [19004981.001]
  • [Cites] Genes Dev. 2009 Mar 1;23 (5):561-74 [19270157.001]
  • [Cites] Genes Dev. 2001 Feb 15;15(4):386-91 [11230146.001]
  • [Cites] PLoS One. 2008;3(11):e3652 [18987751.001]
  • [Cites] Cancer Res. 2008 Nov 15;68(22):9125-30 [19010882.001]
  • [Cites] Biochemistry (Mosc). 2007 May;72(5):578-82 [17573714.001]
  • [Cites] Oncogene. 2004 Feb 26;23(8):1627-30 [14716298.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):159-67 [16397228.001]
  • [Cites] Mol Cell Biol. 2009 Jan;29(2):414-24 [19015245.001]
  • [Cites] J Neurooncol. 2009 Jul;93(3):325-32 [19159078.001]
  • [Cites] Methods Mol Biol. 2007;377:187-202 [17634618.001]
  • [Cites] J Mol Med (Berl). 2009 Jan;87(1):43-51 [18810376.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3415-23 [18202223.001]
  • [Cites] Annu Rev Pathol. 2006;1:97-117 [18039109.001]
  • [Cites] Biochem Biophys Res Commun. 2009 Aug 14;386(1):1-5 [19523920.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9494-9 [12871997.001]
  • [Cites] Neuroreport. 2007 Feb 12;18(3):297-300 [17314675.001]
  • [Cites] Neuroreport. 2008 Jun 11;19(9):981-5 [18521005.001]
  • [Cites] J Inorg Biochem. 2007 Sep;101(9):1265-9 [17629564.001]
  • [Cites] J Biol Chem. 2008 Nov 14;283(46):31315-22 [18801740.001]
  • [Cites] J Biomed Biotechnol. 2009;2009:871313 [19707536.001]
  • [Cites] Nat Genet. 2007 May;39(5):673-7 [17401365.001]
  • [Cites] Acta Neuropathol. 2009 Jun;117(6):599-611 [19343354.001]
  • [Cites] Neurosci Lett. 2009 Aug 7;459(2):100-4 [19406203.001]
  • (PMID = 19941032.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPTL6 protein, human; 0 / Angiopoietins; 0 / BMI1 protein, human; 0 / E2F3 Transcription Factor; 0 / MIRN128 microRNA, human; 0 / MicroRNAs; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; EC 2.3.2.27 / Polycomb Repressive Complex 1
  •  go-up   go-down


80. Assanah M, Lochhead R, Ogden A, Bruce J, Goldman J, Canoll P: Glial progenitors in adult white matter are driven to form malignant gliomas by platelet-derived growth factor-expressing retroviruses. J Neurosci; 2006 Jun 21;26(25):6781-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glial progenitors in adult white matter are driven to form malignant gliomas by platelet-derived growth factor-expressing retroviruses.
  • To test the gliomagenic potential of adult glial progenitors, we infected adult rat white matter with a retrovirus that expresses high levels of PDGF and green fluorescent protein (GFP).
  • The vast majority of both GFP+ and GFP- tumor cells expressed markers of glial progenitors.
  • Thus, the tumors arose from the massive expansion of both infected and uninfected glial progenitors, suggesting that PDGF was driving tumor formation via autocrine and paracrine stimulation of glial progenitor cells.
  • The resulting tumors contained a mixture of red cells (PDGF-expressing/tumor-initiating cells) and green cells (recruited progenitors).
  • Together, these results reveal that adult white matter progenitors not only have the capacity to give rise to gliomas, but resident progenitors are recruited to proliferate within the mitogenic environment of the tumor and in this way contribute significantly to the heterogeneous mass of cells that compose a malignant glioma.
  • [MeSH-major] Brain Neoplasms / genetics. Cell Transformation, Neoplastic. Glioma / genetics. Neuroglia / physiology. Platelet-Derived Growth Factor / metabolism. Stem Cells / physiology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16793885.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS045070; United States / NINDS NIH HHS / NS / NS17125
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / Platelet-Derived Growth Factor; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


81. Josiah DT, Zhu D, Dreher F, Olson J, McFadden G, Caldas H: Adipose-derived stem cells as therapeutic delivery vehicles of an oncolytic virus for glioblastoma. Mol Ther; 2010 Feb;18(2):377-85
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adipose-derived stem cells as therapeutic delivery vehicles of an oncolytic virus for glioblastoma.
  • Glioblastoma multiforme (GBM) accounts for the majority of primary malignant brain tumors and remains virtually incurable despite extensive surgical resection, radiotherapy, and chemotherapy.
  • Treatment difficulty is due to its exceptional infiltrative nature and proclivity to integrate into normal brain tissue.
  • Use of adult stem cells as cellular delivery vehicles for anticancer agents is a novel attractive therapeutic strategy.
  • We hypothesized that adipose-derived stem cells (ADSCs) possess the ability to home and deliver myxoma virus to glioma cells and experimental gliomas.
  • In vivo orthotopic studies injected with vMyxgfp-ADSCs intracranially away from the tumor demonstrated that myxoma virus was delivered by ADSCs resulting in significant survival increase.
  • Our data suggest that ADSCs are promising new carriers of oncolytic viruses, specifically myxoma virus, to brain tumors.
  • [MeSH-major] Adipose Tissue / cytology. Glioblastoma / therapy. Oncolytic Viruses / physiology. Stem Cells / cytology. Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Female. Fluorometry. Humans. Magnetic Resonance Imaging. Mice. Mice, Nude. Myxoma virus / genetics. Myxoma virus / physiology. Oncolytic Virotherapy / methods

  • Genetic Alliance. consumer health - Glioblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Ther. 2007 Apr;15(4):660-5 [17264852.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4640-5 [16537421.001]
  • [Cites] Cancer Lett. 2007 Sep 8;254(2):178-216 [17383089.001]
  • <