[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 120
6. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


7. Korones DN, Smith A, Foreman N, Bouffet E: Temozolomide and oral VP-16 for children and young adults with recurrent or treatment-induced malignant gliomas. Pediatr Blood Cancer; 2006 Jul;47(1):37-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Diagnoses included recurrent brain stem glioma (2), recurrent anaplastic astrocytoma (2), and glioblastoma (7) (3 treatment-induced, 2 malignant transformations of lower grade tumors, 1 recurrence, and 1 second tumor arising 10 months after diagnosis of medulloblastoma).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Neoplasms, Second Primary / drug therapy
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Child. Child, Preschool. Dacarbazine / administration & dosage. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Retrospective Studies. Survival Analysis. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16047359.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


9. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [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


10. Blom T, Fox H, Angers-Loustau A, Peltonen K, Kerosuo L, Wartiovaara K, Linja M, Jänne OA, Kovanen P, Haapasalo H, Nupponen NN: KIT overexpression induces proliferation in astrocytes in an imatinib-responsive manner and associates with proliferation index in gliomas. Int J Cancer; 2008 Aug 15;123(4):793-800
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • KIT and its ligand stem cell factor are widely expressed in embryonic and adult mouse brain, and they play a role in many signal transduction pathways involved in cellular proliferation, differentiation and cancer cell metastasis.
  • However, the function of KIT in gliomagenesis or disease progression remains unresolved as well as its role in neural and brain tumor development.
  • [MeSH-major] Astrocytes / drug effects. Astrocytes / enzymology. Glioma / enzymology. Glioma / pathology. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / biosynthesis. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis / physiology. Benzamides. Cell Growth Processes. Enzyme Activation. Humans. Imatinib Mesylate. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mice. Neoplastic Stem Cells. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transfection

  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18506689.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


11. Hargrave DR, Hargrave UA, Bouffet E: Quality of health information on the Internet in pediatric neuro-oncology. Neuro Oncol; 2006 Apr;8(2):175-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Internet is now the single largest source of health information and is used by many patients and their families who are affected by childhood brain tumors.
  • To assess the quality of pediatric neuro-oncology information on the Internet, we used search engines to look for information on five common tumor types (brain stem glioma, craniopharyngioma, ependymoma, low-grade glioma, and medulloblastoma).
  • Few sites offered information in languages other than English, and readability statistics showed an average required reading level of U.S. grade 12+ (the suggested level being grades 6-8 for an adult audience).
  • [MeSH-major] Brain Neoplasms. Internet / standards. Medical Informatics / standards. Medical Oncology. Neurology


12. Lázaro BC, Landeiro JA: Tectal plate tumors. Arq Neuropsiquiatr; 2006 Jun;64(2B):432-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tectal plate is a rare location for a tumor.
  • Open surgery was performed in three cases (due to tumor enlargement or need for the exact diagnosis).
  • In our series, except in the metastatic tumor case and the cavernoma, the other types of lesion consisted of low grade gliomas.
  • These lesions represent a different type of brain stem tumor sharing a common good prognosis, with a benign behavior.
  • [MeSH-major] Brain Stem Neoplasms / diagnosis. Glioma / diagnosis. Tectum Mesencephali
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Time Factors. Tomography, X-Ray Computed. Treatment Outcome. Ventriculostomy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16917614.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  •  go-up   go-down


13. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


1
Advertisement
4. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


15. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [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


16. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression 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] ATP Binding Cassette Transporter, Sub-Family G, Member 2. 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.
  • MedlinePlus Health Information. consumer health - Childhood 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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Neoplasm Proteins
  •  go-up   go-down


17. Zagzag D, Esencay M, Mendez O, Yee H, Smirnova I, Huang Y, Chiriboga L, Lukyanov E, Liu M, Newcomb EW: Hypoxia- and vascular endothelial growth factor-induced stromal cell-derived factor-1alpha/CXCR4 expression in glioblastomas: one plausible explanation of Scherer's structures. Am J Pathol; 2008 Aug;173(2):545-60
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The morphological patterns of glioma cell invasion are known as the secondary structures of Scherer.
  • In contrast, the SDF-1alpha receptor, CXCR4, was highly expressed in invading glioma cells organized around neurons and blood vessels, in subpial regions, and along white matter tracts.
  • CXCR4-positive tumor cells migrated toward a SDF-1alpha gradient in vitro, whereas inhibition of CXCR4 expression decreased their migration.
  • Similarly, inhibition of CXCR4 decreased levels of SDF-1alpha-induced phosphorylation of FAK, AKT, and ERK1/2, suggesting CXCR4 involvement in glioma invasion signaling.
  • These studies offer one plausible molecular basis and explanation of the formation of Scherer's structures in glioma patients.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / metabolism. Chemokine CXCL12 / metabolism. Glioblastoma / metabolism. Receptors, CXCR4 / physiology. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Hypoxia. Cell Line, Tumor. Chemotaxis. Endothelial Cells / metabolism. Endothelium, Vascular / cytology. Female. Humans. Male. Mice. Middle Aged. Neurons / metabolism. Signal Transduction


18. Häyry V, Tynninen O, Haapasalo HK, Wölfer J, Paulus W, Hasselblatt M, Sariola H, Paetau A, Sarna S, Niemelä M, Wartiovaara K, Nupponen NN: Stem cell protein BMI-1 is an independent marker for poor prognosis in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2008 Oct;34(5):555-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell protein BMI-1 is an independent marker for poor prognosis in oligodendroglial tumours.
  • AIMS: The polycomb factor BMI-1 has recently been implicated in tumorigenesis of the central nervous system in several experimental animal models.
  • However, the significance of BMI-1 in human glioma has not been investigated.
  • Here we describe expression of the polycomb protein BMI-1 and its downstream targets p16(Ink4a) and MDM2 in both high- and low-grade human glioma.
  • METHODS: Tumour samples were collected from 305 adult patients treated for primary grades 2-4 gliomas between 1980 and 2006 in Finland and Germany.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Glioma / metabolism. Nuclear Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Female. Gene Expression. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Polycomb Repressive Complex 1. Proto-Oncogene Proteins c-mdm2 / biosynthesis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18346113.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Polycomb Repressive Complex 1; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  •  go-up   go-down


19. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Glioma.
  • [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


20. Panagiotakos G, Tabar V: Brain tumor stem cells. Curr Neurol Neurosci Rep; 2007 May;7(3):215-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [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


21. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • Zurich Open Access Repository and Archive. Full text from .
  • [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


22. Tabatabai G, Frank B, Möhle R, Weller M, Wick W: Irradiation and hypoxia promote homing of haematopoietic progenitor cells towards gliomas by TGF-beta-dependent HIF-1alpha-mediated induction of CXCL12. Brain; 2006 Sep;129(Pt 9):2426-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previously we defined a pathway of transforming growth factor beta (TGF-beta) and stromal cell-derived factor-1/CXC chemokine ligand 12 (SDF-1alpha/CXCL12) dependent migration of adult haematopoietic stem and progenitor cells (HPC) towards glioma cells in vitro and their homing to experimental gliomas in vivo.
  • To evaluate the therapeutic potential of HPC as vectors for a cell-based therapy of gliomas, we investigated the impact of hypoxia and irradiation on the attraction of HPC by glioma cells.
  • Supernatants of irradiated or hypoxic LNT-229 glioma cells promote HPC migration in vitro.
  • This delineates a novel stress signalling cascade in glioma cells involving TGF-beta, HIF-1alpha and CXCL12.
  • Cerebral irradiation of nude mice at 21 days after intracerebral implantation of LNT-229 glioma induces tumour satellite formation and enhances the glioma tropism of HPC to the tumour bulk and even to these satellites in vivo.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Cell Hypoxia / physiology. Chemokines, CXC / physiology. Glioma / radiotherapy. Hematopoietic Stem Cells / physiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Transforming Growth Factor beta / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Brain / pathology. Brain / radiation effects. Cell Line, Tumor. Cell Movement / radiation effects. Chemokine CXCL12. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Gamma Rays. Humans. Immunohistochemistry / methods. Mice. Mice, Nude. Neoplasm Proteins / physiology. Promoter Regions, Genetic / genetics. Signal Transduction / genetics. Transcription, Genetic

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16835250.001).
  • [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 / Antineoplastic Agents, Alkylating; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Transforming Growth Factor beta; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  •  go-up   go-down


23. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • The Lens. Cited by Patents in .
  • [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


24. Miki T, Nakajima N, Akimoto J, Wada J, Haraoka J: Neuroendoscopic trans-third ventricle approach for lesions of the ventral brainstem surface. Minim Invasive Neurosurg; 2008 Dec;51(6):313-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendoscopic trans-third ventricle approach for lesions of the ventral brainstem surface.
  • Due to the establishment in recent years of neuroendoscopic third ventriculostomy (ETV), it has become possible during ETV to observe the ventral brainstem surface--particularly the prepontine cistern--in a minimally invasive manner via the third ventricular base with a neuroendoscope.
  • As an adaptation of that technique in this study, we investigated a neuroendoscopic trans-third ventricle approach (ETTVA), which accesses lesions of the ventral brainstem surface with a neuroendoscope inserted via the stoma of the third ventricular floor.
  • Our study included 6 cases, including one case each of neurenteric cyst, chordoma, pontine glioma (astrocytoma), ecchordosis physaliphora, endodermal cyst, and cystic schwannoma.
  • Surgical operations performed by ETTVA included 3 cases of tumor resection, 2 cases of tumor biopsy, and 1 case of cyst puncture and aspiration.
  • [MeSH-major] Astrocytoma / surgery. Brain Stem Neoplasms / surgery. Chordoma / surgery. Minimally Invasive Surgical Procedures / methods. Neuroendoscopy / methods. Third Ventricle / surgery. Ventriculostomy / methods
  • [MeSH-minor] Adult. Aged. Child. Female. Humans. Male. Middle Aged. Neurosurgical Procedures / methods. Retrospective Studies. Treatment Outcome. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19061139.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


25. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer 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


26. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


27. Ueoka DI, Nogueira J, Campos JC, Maranhão Filho P, Ferman S, Lima MA: Brainstem gliomas--retrospective analysis of 86 patients. J Neurol Sci; 2009 Jun 15;281(1-2):20-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brainstem gliomas--retrospective analysis of 86 patients.
  • Brainstem gliomas constitute 10% of brain tumors in children and less than 2% in adults.
  • Since therapeutic options are limited and brainstem gliomas are associated with a high morbidity and mortality, we sought to analyze the prognostic factors associated with a better outcome.
  • We reviewed the records of 86 patients with brainstem gliomas treated between 1996 and 2006.
  • Of 86 patients with brainstem gliomas, 55.8% were females.
  • A short duration of symptoms, which may imply a more aggressive tumor, was associated with a worst prognosis in patients with brainstem gliomas.
  • [MeSH-major] Brain Stem Neoplasms / diagnosis. Glioma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Age of Onset. Brain Stem / pathology. Child. Child, Preschool. Disease Progression. Female. Humans. Infant. Kaplan-Meier Estimate. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Treatment Outcome. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19345380.001).
  • [ISSN] 1878-5883
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


28. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Glioma.
  • [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


29. Kesari S, Kim RS, Markos V, Drappatz J, Wen PY, Pruitt AA: Prognostic factors in adult brainstem gliomas: a multicenter, retrospective analysis of 101 cases. J Neurooncol; 2008 Jun;88(2):175-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in adult brainstem gliomas: a multicenter, retrospective analysis of 101 cases.
  • BACKGROUND: Adult brainstem gliomas (BSG) are uncommon and poorly understood with respect to prognostic factors.
  • Out of 24 candidate prognosis factors, we selected seven covariates for proportional hazards model by Lasso procedure: age of diagnosis, ethnicity, need for corticosteroids, tumor grade, dysphagia, tumor location, and karnofsky performance status (KPS).
  • Multivariate analysis showed that four covariates significantly increased hazard for survival: ethnicity, tumor location, age of diagnosis, and tumor grade.
  • [MeSH-major] Brain Stem Neoplasms / diagnosis. Glioma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Algorithms. Disease Progression. Female. Follow-Up Studies. Health Surveys. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Multivariate Analysis. Prognosis. Retrospective Studies. Survival Analysis

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurol Med Chir (Tokyo). 1993 Sep;33(9):625-9 [7505402.001]
  • [Cites] AJNR Am J Neuroradiol. 1985 Mar-Apr;6(2):159-63 [3920875.001]
  • [Cites] J Clin Neurosci. 2006 May;13(4):431-7 [16678721.001]
  • [Cites] Neurosurgery. 1993 Dec;33(6):1026-9; discussion 1029-30 [8133987.001]
  • [Cites] Indian J Cancer. 1999 Jun-Dec;36(2-4):99-108 [10921213.001]
  • [Cites] Brain. 2001 Dec;124(Pt 12):2528-39 [11701605.001]
  • [Cites] Pediatr Neurosurg. 1996 Jul;25(1):45-53 [9055335.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1993 Jan 15;25(2):235-41 [8420871.001]
  • [Cites] Ethn Dis. 2004 Summer;14(3):360-71 [15328937.001]
  • [Cites] J Clin Oncol. 2006 Mar 10;24(8):1266-72 [16525181.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;24(4):599-610 [1429081.001]
  • [Cites] J Neurosurg. 1989 Dec;71(6):826-36 [2585073.001]
  • [Cites] Cancer. 1980 Jun 1;45(11):2787-92 [7379009.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):751-5 [3772472.001]
  • [Cites] Acta Neurochir (Wien). 1999;141(7):721-6; discussion 726-7 [10481783.001]
  • [Cites] Pediatr Neurosurg. 2001 Apr;34(4):206-14 [11359114.001]
  • [Cites] Pediatr Neurosurg. 1996 Jul;25(1):41-4 [9055334.001]
  • [Cites] J Proteome Res. 2007 Feb;6(2):559-70 [17269713.001]
  • [Cites] J Neurosurg. 1984 Oct;61(4):665-73 [6470776.001]
  • [Cites] Neurology. 1986 May;36(5):602-5 [3703258.001]
  • [Cites] Pediatr Neurosurg. 1990-1991;16(2):73-83 [2132928.001]
  • [Cites] Neurology. 1998 Oct;51(4):1136-9 [9781543.001]
  • [Cites] Acta Neurochir (Wien). 1986;79(2-4):67-73 [3962745.001]
  • [Cites] Neurology. 1985 Mar;35(3):397-401 [3974898.001]
  • [Cites] Childs Nerv Syst. 2004 Mar;20(3):143-53 [14669023.001]
  • [Cites] Stat Med. 1997 Feb 28;16(4):385-95 [9044528.001]
  • [Cites] J Neurosurg. 1993 Jun;78(6):859-63 [8487066.001]
  • [Cites] Neurosurgery. 1983 Mar;12 (3):298-302 [6302553.001]
  • [Cites] Am J Dis Child. 1970 Jun;119(6):465-72 [4315314.001]
  • [Cites] Cancer. 1989 Jun 1;63(11):2124-9 [2720563.001]
  • [Cites] Cancer Treat Res. 1995;75:95-112 [7640169.001]
  • [Cites] Surg Neurol. 1995 Jun;43(6):563-7; discussion 567-8 [7482235.001]
  • [Cites] Cancer. 1982 Mar 15;49(6):1294-6 [6277461.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Apr;20(4):757-60 [2004952.001]
  • [Cites] Pediatr Neurosurg. 1996;24(4):185-92 [8873160.001]
  • [Cites] Neurosurgery. 1980 Sep;7(3):243-8 [7207742.001]
  • (PMID = 18365144.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  •  go-up   go-down


30. Glantz M, Kesari S, Recht L, Fleischhack G, Van Horn A: Understanding the origins of gliomas and developing novel therapies: cerebrospinal fluid and subventricular zone interplay. Semin Oncol; 2009 Aug;36(4 Suppl 2):S17-24
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glioblastoma multiforme (GBM), the most common malignant primary brain tumor in adults, carries a poor prognosis, with median survival generally less than 1 year.
  • Although initial therapy often eradicates the bulk of the tumor, disease recurrence, usually within 2 cm of the original tumor, is almost inevitable.
  • An increasing body of preclinical data suggests that these cells may correspond to stem cells derived from the subventricular zone (SVZ), which migrate to tumor sites and contribute to glioma growth and recurrence.
  • Therapeutic targeting of SVZ stem cell populations via cerebrospinal fluid (CSF)-directed therapy may provide a means for limiting tumor recurrence.
  • This approach has proved successful in the treatment of medulloblastoma, another brain tumor thought to be derived from stem cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant / methods. Humans. Injections, Spinal. Neoplastic Stem Cells. Research Design

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19660679.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


31. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [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


32. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [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


33. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


34. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


35. Kang SK, Park JB, Cha SH: Multipotent, dedifferentiated cancer stem-like cells from brain gliomas. Stem Cells Dev; 2006 Jun;15(3):423-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


36. Jiang ZL, Wang ZC, Jiang T: [Surgical outcomes of different approaches for mesial temporal lobe gliomas]. Zhonghua Yi Xue Za Zhi; 2005 Sep 7;85(34):2428-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Microsurgery was performed via trans-sylvian, trans-temporal, or subtemporal approaches on 62 patients with mesial temporal lobe gliomas, 33 with localized tumors within the mesial temporal structures (type A), 19 in anterior portion (type A1), and 14 extending to posterior portion (type A2); 19 patients with multicompartmental tumors involving the mesial temporal lobe, insular lobe, and posterior frontorbital gurus (type B); 14 patients with tumors involving the temporal pole and lateral areas of the temporal horn (type C); and 6 patients with tumors infiltrating the brain stem, basal nuclei and thalamus (type D).
  • RESULTS: Trans-sylvian approach was performed in 25 cases of which total tumor removal was achieved in 14 cases, subtotal removal in 6 cases, and gross removal in 5 cases.
  • Trans-temporal approach was used in 23 cases of which total tumor resection was achieved in 15 cases, subtotal resection in 5 cases, and gross resection in 3 cases.
  • Subtemporal approach was used in 14 cases of which total tumor removal was achieved in 10 cases, and subtotal removal in 4 cases.
  • [MeSH-major] Brain Neoplasms / surgery. Glioma / surgery. Neurosurgical Procedures / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Temporal Lobe / pathology. Treatment Outcome. Young Adult

  • 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 = 16321253.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


37. Oh MC, Lim DA: Novel treatment strategies for malignant gliomas using neural stem cells. Neurotherapeutics; 2009 Jul;6(3):458-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


38. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


39. Terrile M, Appolloni I, Calzolari F, Perris R, Tutucci E, Malatesta P: PDGF-B-driven gliomagenesis can occur in the absence of the proteoglycan NG2. BMC Cancer; 2010;10:550
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: In the last years, the transmembrane proteoglycan NG2 has gained interest as a therapeutic target for the treatment of diverse tumor types, including gliomas, because increases of its expression correlate with dismal prognosis.
  • We have recently generated a glioma model based on the overexpression of PDGF-B in neural progenitors and here we investigated the possible relevance of NG2 during PDGF-driven gliomagenesis.
  • The characteristics of tumors induced in NG2-KO were compared to those of tumors induced in wild type mice by immunostaining for different cell lineage markers and by transplantation assays in adult mice.
  • RESULTS: We showed that the lack of NG2 does not appreciably affect any of the characterized steps of PDGF-driven brain tumorigenesis, such as oligodendrocyte progenitor cells (OPC) induction, the recruitment of bystander OPCs and the progression to full malignancy, which take place as in wild type animals.
  • On the basis of the data obtained, we therefore suggest that the role of NG2 as a target molecule for glioma treatment should be carefully reconsidered.
  • [MeSH-major] Antigens / physiology. Brain Neoplasms / pathology. Glioma / pathology. Proteoglycans / physiology. Receptor, Platelet-Derived Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Gene Expression Regulation, Developmental. Gene Expression Regulation, Neoplastic. Gene Silencing. Ligands. Mice. Mice, Inbred C57BL. Mice, Knockout. MicroRNAs / metabolism. Oligodendroglia / cytology. Retroviridae. Stem Cells

  • 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 Dev Neurosci. 1999 Aug-Oct;17(5-6):421-35 [10571405.001]
  • [Cites] Cancer Cell. 2010 Jan 19;17(1):98-110 [20129251.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Genes Dev. 2001 Aug 1;15(15):1913-25 [11485986.001]
  • [Cites] FASEB J. 2002 Apr;16(6):586-8 [11919162.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5551-8 [12359767.001]
  • [Cites] Neuropathol Appl Neurobiol. 2002 Oct;28(5):367-80 [12366818.001]
  • [Cites] J Neurocytol. 2002 Jul-Aug;31(6-7):507-21 [14501220.001]
  • [Cites] Mol Biol Cell. 2004 Aug;15(8):3580-90 [15181153.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Jan;76(1):514-7 [284369.001]
  • [Cites] Cancer Res. 1988 Jul 15;48(14):3910-8 [2454731.001]
  • [Cites] Cancer Res. 1991 Sep 15;51(18):4986-93 [1893386.001]
  • [Cites] Cancer Res. 1992 Jun 1;52(11):3213-9 [1317261.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8392-6 [7690960.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2177-85 [7743521.001]
  • [Cites] Exp Cell Res. 1995 Nov;221(1):231-40 [7589250.001]
  • [Cites] J Neurosci Res. 1996 Feb 1;43(3):315-30 [8714520.001]
  • [Cites] Neurosurgery. 1998 Feb;42(2):341-6 [9482185.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5275-9 [9850047.001]
  • [Cites] J Cell Sci. 1999 Mar;112 ( Pt 6):905-15 [10036240.001]
  • [Cites] J Biol Chem. 1999 Jun 11;274(24):16831-7 [10358027.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10361-6 [10468613.001]
  • [Cites] Neoplasia. 2005 Apr;7(4):397-406 [15967117.001]
  • [Cites] Neuroimage. 2006 Feb 1;29(3):965-76 [16253523.001]
  • [Cites] J Neurosci. 2006 Jun 21;26(25):6781-90 [16793885.001]
  • [Cites] Neuron. 2006 Jul 20;51(2):187-99 [16846854.001]
  • [Cites] Methods Mol Biol. 2007;361:93-117 [17172708.001]
  • [Cites] J Cell Biol. 2007 Jul 2;178(1):155-65 [17591920.001]
  • [Cites] Brain Cell Biol. 2006 Jun;35(2-3):159-72 [17957481.001]
  • [Cites] Oncogene. 2008 Sep 4;27(39):5182-94 [18469852.001]
  • [Cites] Neoplasia. 2008 Dec;10(12):1373-82, following 1382 [19048116.001]
  • [Cites] Cell Adh Migr. 2008 Jul-Sep;2(3):192-201 [19262111.001]
  • [Cites] Int J Cancer. 2009 May 15;124(10):2251-9 [19165863.001]
  • [Cites] Glia. 2009 Dec;57(16):1835-47 [19533602.001]
  • [Cites] PLoS One. 2009;4(11):e7752 [19915670.001]
  • [Cites] Neuroscience. 2010 Mar 10;166(1):185-94 [20006679.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):398-406 [10652433.001]
  • (PMID = 20939912.001).
  • [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 / Antigens; 0 / Ligands; 0 / MicroRNAs; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2964636
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • The Lens. Cited by Patents in .
  • [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. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


42. Zhai DZ, Huang Q, Zhu Q, Huo HM, Dong J, Qian ZY, Wang AD, Lan Q: [Expression of cyclin-dependent kinase CDC2 and its significance in malignant progression of gliomas]. Zhonghua Bing Li Xue Za Zhi; 2007 Mar;36(3):196-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Brain Neoplasms / metabolism. CDC2 Protein Kinase / metabolism. Glioma / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Bone Marrow / metabolism. Brain / metabolism. Cell Line, Tumor. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Mice, Nude. Middle Aged. Neoplasm Transplantation. Neoplastic Stem Cells / metabolism. Young Adult

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17535689.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.11.22 / CDC2 Protein Kinase
  •  go-up   go-down


43. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • The Lens. Cited by Patents in .
  • [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


44. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [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


45. Tanaka K, Sasayama T, Kawamura A, Kondoh T, Kanomata N, Kohmura E: Isolated oculomotor nerve paresis in anaplastic astrocytoma with exophytic invasion. Neurol Med Chir (Tokyo); 2006 Apr;46(4):198-201
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 30-year-old man presented with a supratentorial malignant glioma manifesting as isolated progressive left oculomotor nerve paresis.
  • Computed tomography and magnetic resonance imaging showed an intra-axial tumor in the left temporal lobe, extending to the basal and prepontine cisterns, and compressing the brainstem.
  • The tumor was removed subtotally.
  • Malignant glioma with exophytic growth in the temporal lobe should be considered in the differential diagnosis of isolated oculomotor nerve paresis.
  • [MeSH-minor] Adult. Astrocytes / pathology. Biomarkers, Tumor / analysis. Brain Stem / pathology. Cerebral Arteries / pathology. Cisterna Magna / pathology. Dominance, Cerebral / physiology. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Nerve Compression Syndromes / diagnosis. Nerve Compression Syndromes / etiology. Nerve Compression Syndromes / pathology. Nerve Compression Syndromes / surgery. Neuronavigation. Oculomotor Nerve / pathology. Oculomotor Nerve / surgery. Pons / pathology

  • Genetic Alliance. consumer health - Anaplastic Astrocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16636512.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


46. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [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


47. Greenfield JP, Jin DK, Young LM, Christos PJ, Abrey L, Rafii S, Gutin PH: Surrogate markers predict angiogenic potential and survival in patients with glioblastoma multiforme. Neurosurgery; 2009 May;64(5):819-26; discussion 826-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The neovascularization of malignant brain tumors is a poorly understood phenomenon.
  • However, a quantitative noninvasive assay to assess glioma vascularity and associated clinical aggressiveness has not been developed.
  • Circulating endothelial progenitor cells are unique vascular precursors recruited from the bone marrow through the circulation to form new tumor blood vessels.
  • We hypothesized that this might reflect the extent of tumor vascularity, predict prognosis, or be useful as an assay to assess response to antiangiogenesis therapies.
  • In addition, we report on a novel in vitro assay to assess the proangiogenic activity within the plasma samples obtained from glioma patients.
  • In addition, all patients with GBM had measurable numbers of bone marrow-derived endothelial precursor cells coexpressing CD133 and vascular endothelial growth factor receptor 2 in their peripheral circulation at the time of tumor resection.
  • CONCLUSION: These studies suggest that plasma and circulating CD133+ vascular endothelial growth factor receptor 2+ proangiogenic cells are present in the peripheral blood of patients with glioma and can be used as a surrogate biomarker to measure tumor angiogenicity.
  • These assays can be used to predict tumor aggressiveness.
  • Also promising is their potential to identify patients with increased angiogenic activity who might respond maximally to antiangiogenesis therapies or to assess tumor response in patients using those therapies as the use of these adjuvant molecular modalities becomes more prevalent in neuro-oncology.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / blood. Glioblastoma / blood. Neovascularization, Pathologic / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / metabolism. Biological Assay / methods. Endothelial Cells / metabolism. Endothelial Cells / pathology. Enzyme-Linked Immunosorbent Assay / methods. Female. Flow Cytometry. Follow-Up Studies. Glycoproteins / metabolism. Humans. Male. Middle Aged. Peptides / metabolism. Stem Cells / metabolism. Stem Cells / pathology. Umbilical Veins / pathology. Vascular Endothelial Growth Factor Receptor-2 / metabolism


48. Perry A, Miller CR, Gujrati M, Scheithauer BW, Zambrano SC, Jost SC, Raghavan R, Qian J, Cochran EJ, Huse JT, Holland EC, Burger PC, Rosenblum MK: Malignant gliomas with primitive neuroectodermal tumor-like components: a clinicopathologic and genetic study of 53 cases. Brain Pathol; 2009 Jan;19(1):81-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant gliomas with primitive neuroectodermal tumor-like components: a clinicopathologic and genetic study of 53 cases.
  • Central nervous system neoplasms with combined features of malignant glioma and primitive neuroectodermal tumor (MG-PNET) are rare, poorly characterized, and pose diagnostic as well as treatment dilemmas.
  • In contrast, glioma-associated alterations involved both components, 10q loss (50%) being most common.
  • (ii) may represent a metaplastic process or expansion of a tumor stem/progenitor cell clone;.
  • [MeSH-major] Glioma / pathology. Neuroectodermal Tumors, Primitive / pathology. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy. Combined Modality Therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Follow-Up Studies. Genes, myc / genetics. Humans. In Situ Hybridization, Fluorescence. Medulloblastoma / genetics. Medulloblastoma / pathology. Medulloblastoma / therapy. Neoplasm Metastasis. Neoplasms, Multiple Primary / genetics. Neoplasms, Multiple Primary / pathology. Neoplasms, Multiple Primary / therapy. Prognosis. Radiotherapy / methods. Treatment Outcome. Young Adult

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18452568.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Proto-Oncogene Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  •  go-up   go-down


49. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [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]
  • [Cites] Cancer Lett. 2007 Sep 8;254(2):255-64 [17467167.001]
  • [Cites] Mol Ther. 2009 Oct;17(10):1667-76 [19690519.001]
  • [Cites] FEMS Microbiol Rev. 2000 Apr;24(2):123-33 [10717311.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12846-51 [11070094.001]
  • [Cites] Tissue Eng. 2001 Apr;7(2):211-28 [11304456.001]
  • [Cites] Curr Opin Oncol. 2001 May;13(3):160-6 [11307058.001]
  • [Cites] J Natl Cancer Inst. 2001 Jun 20;93(12):903-12 [11416111.001]
  • [Cites] Viral Immunol. 2002;15(2):229-46 [12081009.001]
  • [Cites] Hum Gene Ther. 2003 Jan 1;14(1):59-66 [12573059.001]
  • [Cites] J Neurooncol. 2003 Dec;65(3):203-26 [14682372.001]
  • [Cites] Semin Oncol. 2003 Dec;30(6 Suppl 19):10-4 [14765378.001]
  • [Cites] Drug Discov Today. 2004 Sep 1;9(17):759-68 [15450242.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):151-60 [9892097.001]
  • [Cites] J Natl Cancer Inst. 2004 Nov 3;96(21):1593-603 [15523088.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 16;97(6):414-6 [15770001.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3307-18 [15833864.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9982-90 [16267023.001]
  • [Cites] Oncogene. 2005 Nov 21;24(52):7802-16 [16299539.001]
  • [Cites] Stem Cells. 2007 Apr;25(4):818-27 [17420225.001]
  • (PMID = 19904233.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA012197; United States / NCI NIH HHS / CA / CA-12197
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2839314
  •  go-up   go-down


50. Murat A, Migliavacca E, Gorlia T, Lambiv WL, Shay T, Hamou MF, de Tribolet N, Regli L, Wick W, Kouwenhoven MC, Hainfellner JA, Heppner FL, Dietrich PY, Zimmer Y, Cairncross JG, Janzer RC, Domany E, Delorenzi M, Stupp R, Hegi ME: Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. J Clin Oncol; 2008 Jun 20;26(18):3015-24
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma.
  • PURPOSE: Glioblastomas are notorious for resistance to therapy, which has been attributed to DNA-repair proficiency, a multitude of deregulated molecular pathways, and, more recently, to the particular biologic behavior of tumor stem-like cells.
  • Better outcome was associated with gene clusters characterizing features of tumor-host interaction including tumor vascularization and cell adhesion, and innate immune response.
  • CONCLUSION: This study provides first clinical evidence for the implication of a "glioma stem cell" or "self-renewal" phenotype in treatment resistance of glioblastoma.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Brain Neoplasms / therapy. Glioblastoma / pathology. Glioblastoma / therapy. Receptor, Epidermal Growth Factor / biosynthesis
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Alkylating / therapeutic use. Combined Modality Therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Drug Resistance, Neoplasm. Gene Expression Profiling. Genes, Homeobox. Humans. Middle Aged. Multigene Family. Radiation Tolerance

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18565887.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


51. Boer K, Troost D, Timmermans W, Gorter JA, Spliet WG, Nellist M, Jansen F, Aronica E: Cellular localization of metabotropic glutamate receptors in cortical tubers and subependymal giant cell tumors of tuberous sclerosis complex. Neuroscience; 2008 Sep 22;156(1):203-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Expression of metabotropic glutamate receptor (mGluR) subtypes is developmentally regulated and several studies suggest an involvement of mGluR-mediated glutamate signaling in the regulation of proliferation and survival of neural stem-progenitor cells, as well as in the control of tumor growth.
  • Strong group I mGluR immunoreactivity (IR) was observed in the large majority of TSC specimens in dysplastic neurons and in giant cells within cortical tubers, as well as in tumor cells within SGCTs.
  • Group II and particularly group III mGluR IR was less frequently observed than group I mGluRs in dysplastic neurons and giant cells of tubers and tumor cells of SGCTs.
  • These findings expand our knowledge concerning the cellular phenotype in cortical tubers and in SGCTs and highlight the role of group I mGluRs as important mediators of glutamate signaling in TSC brain lesions.
  • Individual mGluR subtypes may represent potential pharmacological targets for the treatment of the neurological manifestations associated with TSC brain lesions.
  • [MeSH-major] Brain Neoplasms / metabolism. Cerebral Cortex / metabolism. Giant Cells / metabolism. Glioma, Subependymal / metabolism. Receptors, Metabotropic Glutamate / metabolism. Tuberous Sclerosis / metabolism
  • [MeSH-minor] Adolescent. Adult. Astrocytes / metabolism. Astrocytes / pathology. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Female. Glutamic Acid / metabolism. Humans. Immunohistochemistry. Infant. Male. Neurons / metabolism. Neurons / pathology. Protein Kinases / metabolism. Receptor, Metabotropic Glutamate 5. TOR Serine-Threonine Kinases. Young Adult


52. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Glioma.
  • [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


53. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


54. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [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


56. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [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 .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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


57. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


58. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [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


59. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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) .
  • The Lens. Cited by Patents in .
  • [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


60. Squatrito M, Brennan CW, Helmy K, Huse JT, Petrini JH, Holland EC: Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas. Cancer Cell; 2010 Dec 14;18(6):619-29
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas.
  • Maintenance of genomic integrity is essential for adult tissue homeostasis and defects in the DNA-damage response (DDR) machinery are linked to numerous pathologies including cancer.
  • Here, we present evidence that the DDR exerts tumor suppressor activity in gliomas.
  • We show that genes encoding components of the DDR pathway are frequently altered in human gliomas and that loss of elements of the ATM/Chk2/p53 cascade accelerates tumor formation in a glioma mouse model.
  • We demonstrate that Chk2 is required for glioma response to ionizing radiation in vivo and is necessary for DNA-damage checkpoints in the neuronal stem cell compartment.

  • 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
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Oncogene. 2010 Sep 9;29(36):5095-102 [20581868.001]
  • [Cites] Cell Stem Cell. 2010 Feb 5;6(2):141-52 [20144787.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1824-7 [10710310.001]
  • [Cites] Neurogenetics. 2000 Sep;3(1):45-6 [11085597.001]
  • [Cites] Curr Opin Cell Biol. 2001 Apr;13(2):225-31 [11248557.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5843-9 [11479224.001]
  • [Cites] Genes Dev. 2001 Aug 1;15(15):1913-25 [11485986.001]
  • [Cites] J Biol Chem. 2001 Dec 21;276(51):47759-62 [11673449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9825-9 [12097646.001]
  • [Cites] Mol Cell Biol. 2002 Sep;22(18):6521-32 [12192050.001]
  • [Cites] EMBO J. 2002 Oct 1;21(19):5195-205 [12356735.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):155-68 [12612651.001]
  • [Cites] J Biol Chem. 2003 Apr 4;278(14):12207-13 [12519769.001]
  • [Cites] Cancer Cell. 2003 May;3(5):421-9 [12781359.001]
  • [Cites] Nat Genet. 2004 Jan;36(1):63-8 [14702042.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):920-7 [14871821.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2390-6 [15059890.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4783-9 [15256447.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Am J Hum Genet. 2004 Dec;75(6):1131-5 [15492928.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7491-5 [1323840.001]
  • [Cites] Acta Neurochir (Wien). 1995;135(1-2):87-92 [8748798.001]
  • [Cites] Genes Dev. 1996 Oct 1;10(19):2401-10 [8843193.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1218-23 [9448312.001]
  • [Cites] Science. 1998 Dec 4;282(5395):1893-7 [9836640.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3675-85 [9851974.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):864-70 [15829956.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):907-13 [15829965.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4861-9 [15930307.001]
  • [Cites] J Neurooncol. 2005 Aug;74(1):93-5 [16078115.001]
  • [Cites] Mol Cell Biol. 2005 Nov;25(22):10079-86 [16260621.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10734-41 [16322218.001]
  • [Cites] Mol Cell Biol. 2006 Mar;26(5):1598-609 [16478982.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Methods Enzymol. 2006;409:251-84 [16793406.001]
  • [Cites] Radiat Res. 2006 Oct;166(4):646-51 [17007555.001]
  • [Cites] Nature. 2006 Nov 30;444(7119):633-7 [17136093.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Nature. 2007 May 10;447(7141):218-21 [17429352.001]
  • [Cites] Carcinogenesis. 2007 Oct;28(10):2082-8 [17522062.001]
  • [Cites] Nat Rev Cancer. 2007 Dec;7(12):925-36 [18004398.001]
  • [Cites] Oncogene. 2007 Dec 10;26(56):7773-9 [18066090.001]
  • [Cites] Nat Rev Cancer. 2008 Mar;8(3):180-92 [18273037.001]
  • [Cites] Neurosurg Focus. 2008;24(3-4):E28 [18341405.001]
  • [Cites] Mol Cell. 2008 Jul 11;31(1):21-32 [18614044.001]
  • [Cites] Stem Cell Rev. 2008 Sep;4(3):203-10 [18595010.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Oct;9(10):759-69 [18813293.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] Brain Pathol. 2009 Jan;19(1):132-43 [19076778.001]
  • [Cites] Mol Cell Biol. 2009 Jan;29(2):526-37 [18981219.001]
  • [Cites] Cell Stem Cell. 2009 Mar 6;4(3):226-35 [19265662.001]
  • [Cites] DNA Repair (Amst). 2009 Sep 2;8(9):1047-54 [19473886.001]
  • [Cites] Nature. 2009 Oct 22;461(7267):1071-8 [19847258.001]
  • [Cites] PLoS One. 2009;4(11):e7752 [19915670.001]
  • [Cites] Life Sci. 2010 Jan 30;86(5-6):185-91 [19969004.001]
  • [Cites] Cancer Cell. 2010 Jan 19;17(1):98-110 [20129251.001]
  • [Cites] Oncogene. 2007 Nov 22;26(53):7414-22 [17546051.001]
  • (PMID = 21156285.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141502; United States / NIGMS NIH HHS / GM / R37 GM059413; United States / NCI NIH HHS / CA / U01 CA105492; United States / NCI NIH HHS / CA / R01 CA100688; United States / NCI NIH HHS / CA / U54 CA163167; United States / Howard Hughes Medical Institute / /
  • [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 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Chek2 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS250143; NLM/ PMC3818087
  •  go-up   go-down


61. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • COS Scholar Universe. author profiles.
  • [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


62. Yen CP, Sheehan J, Steiner M, Patterson G, Steiner L: Gamma knife surgery for focal brainstem gliomas. J Neurosurg; 2007 Jan;106(1):8-17
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gamma knife surgery for focal brainstem gliomas.
  • OBJECT: Focal tumors, a distinct subgroup of which is composed of brainstem gliomas, may have an indolent clinical course.
  • In the present study the authors assess clinical and imaging results in 20 patients who harbored focal brainstem gliomas treated with GKS between 1990 and 2001.
  • The mean tumor volume at the time of GKS was 2.5 cm3.
  • In 10 cases a tumor specimen was obtained either by open surgery or stereotactic biopsy, securing the diagnosis of pilocytic astrocytoma in five patients and nonpilocytic astrocytoma in five others.
  • Another patient whose tumor disappeared 3 years following GKS died of stroke 8 years postoperatively.
  • Tumor progression occurred in four patients; of these four, one patient developed hydrocephalus requiring a ventriculoperitoneal shunt, two showed neurological deterioration, and one 4-year-old boy died of tumor progression.
  • CONCLUSIONS: Gamma Knife surgery may be an effective primary treatment or adjunct to open surgery for focal brainstem gliomas.
  • [MeSH-major] Brain Stem Neoplasms / surgery. Glioma / surgery. Radiosurgery
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Male. Middle Aged. Radiotherapy Dosage. Retrospective Studies. Treatment Outcome. Tumor Burden

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Neurosurg. 2007 Sep;107(3):708; author reply 708-9 [17886574.001]
  • [CommentIn] J Neurosurg. 2007 Jan;106(1):6-7 [17262931.001]
  • (PMID = 17236482.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


63. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Childhood 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


64. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [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


65. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • 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] 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. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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 .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 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


68. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression 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 .
  • The Lens. Cited by Patents in .
  • [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


69. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


70. De Sio L, Milano GM, Castellano A, Jenkner A, Fidani P, Dominici C, Donfrancesco A: Temozolomide in resistant or relapsed pediatric solid tumors. Pediatr Blood Cancer; 2006 Jul;47(1):30-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor types were: neuroblastoma (NB; n = 17), medulloblastoma (MB; 8), brain stem glioma (BSG; 8), extraosseous Ewing's sarcoma/peripheral neuroectodermal tumor (EOES; 4), Ewing's sarcoma (ES; 4), anaplastic astrocytoma (AA; 3), rhabdomyosarcoma (RMS; 2), ependymoma (EP; 2), cerebral primitive neuroectodermal tumor (cPNET; 2), hepatocarcinoma (HC; 1), and osteosarcoma (OS; 1).
  • CONCLUSION: Oral TMZ was well tolerated in children with resistant or relapsed solid tumors and showed activity in NB and CNS tumours refractory to standard chemotherapy.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm. Neoplasm Recurrence, Local / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Male. Survival Analysis

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Cancer in Children.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • [ErratumIn] Pediatr Blood Cancer. 2006 Oct 15;47(5):647-8
  • (PMID = 16047361.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  •  go-up   go-down


76. Li KW, Roonprapunt C, Lawson HC, Abbott IR, Wisoff J, Epstein F, Jallo GI: Endoscopic third ventriculostomy for hydrocephalus associated with tectal gliomas. Neurosurg Focus; 2005 Jun 15;18(6A):E2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECT: Tectal gliomas are a distinct form of pediatric brainstem tumor that present in patients with symptoms related to increased intracranial pressure due to obstructive hydrocephalus.
  • [MeSH-major] Brain Stem Neoplasms / surgery. Endoscopy / methods. Glioma / surgery. Hydrocephalus / surgery. Ventriculostomy / methods
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Magnetic Resonance Imaging / methods. Male. Tomography, X-Ray Computed / methods. Treatment Outcome

  • Genetic Alliance. consumer health - Hydrocephalus.
  • MedlinePlus Health Information. consumer health - Endoscopy.
  • MedlinePlus Health Information. consumer health - Hydrocephalus.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16048288.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


77. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


78. Reynolds BA, Vescovi AL: Brain cancer stem cells: Think twice before going flat. Cell Stem Cell; 2009 Nov 6;5(5):466-7; author reply 468-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brain cancer stem cells: Think twice before going flat.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Culture Techniques. Glioblastoma / pathology. Glioma / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adult. Animals. Apoptosis. Cell Adhesion. Cell Differentiation. Cell Line, Tumor. Humans. Mice. Neoplasm Transplantation. Reproducibility of Results


79. Ruivo J, Antunes JL: Maffucci syndrome associated with a pituitary adenoma and a probable brainstem tumor. J Neurosurg; 2009 Feb;110(2):363-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maffucci syndrome associated with a pituitary adenoma and a probable brainstem tumor.
  • Malignancies are a common feature of Maffucci syndrome, with chondrosarcomas being the most common tumor type.
  • The authors present the first case of Maffucci syndrome associated with a pituitary adenoma and a probable brainstem glioma and review the literature concerning intracranial tumors related to this disease.
  • Neuroimaging revealed a pituitary macroadenoma and a suspected brainstem tumor.
  • To the authors' knowledge, including the present case, only 7 cases of Maffucci syndrome associated with glioma and 7 cases associated with pituitary adenoma have been reported in the literature.
  • [MeSH-major] Brain Stem Neoplasms / complications. Enchondromatosis / complications. Magnetic Resonance Imaging. Neoplasms, Multiple Primary / complications. Pituitary Neoplasms / complications. Pons
  • [MeSH-minor] Adult. Decompression, Surgical. Female. Humans. Nerve Compression Syndromes / diagnosis. Nerve Compression Syndromes / surgery. Optic Chiasm / pathology. Optic Nerve Diseases / diagnosis. Optic Nerve Diseases / surgery. Vision Disorders / diagnosis. Vision Disorders / etiology. Vision Disorders / surgery

  • Genetic Alliance. consumer health - Maffucci syndrome.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18976063.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
  •  go-up   go-down


80. Magrassi L, Conti L, Lanterna A, Zuccato C, Marchionni M, Cassini P, Arienta C, Cattaneo E: Shc3 affects human high-grade astrocytomas survival. Oncogene; 2005 Aug 4;24(33):5198-206
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous studies showed that in the embryo, Shc1 is maximally expressed in dividing CNS stem cells while it is silenced in mature neurons, where it is replaced by Shc3.
  • Our data indicate that Shc3 is maximally expressed, together with Shc1, in glioblastoma, a highly proliferative tumor with little, if any, indication of neuronal differentiation.
  • In primary cultures of glioblastoma, tumor cells maintain Shc1 expression but downregulate Shc3.
  • Analysis of the phosphorylation status of Shc3 in human glioblastoma tumor samples in vivo indicates that it is tyrosine phosphorylated.
  • Finally, we found that the expression of truncated variants of Shc3 with dominant-negative effects in human high-grade glioma cells that maintain Shc3 expression in vitro leads to a decreased Akt posphorylation and increased apoptosis, thus resulting in impaired survival of the transfected cells.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Glioblastoma / genetics. Glioblastoma / pathology. Neuropeptides / physiology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / biosynthesis. Adaptor Proteins, Signal Transducing / physiology. Adult. Apoptosis. Blotting, Western. Cell Differentiation. Cell Line. Cell Proliferation. Cell Survival. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Phosphorylation. Shc Signaling Adaptor Proteins. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15870690.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Neuropeptides; 0 / SHC1 protein, human; 0 / SHC3 protein, human; 0 / Shc Signaling Adaptor Proteins
  •  go-up   go-down


81. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial 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 .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [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


82. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [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


83. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [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


84. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


85. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


86. Li DM, Wu XH, Zhu XX: [Impact of MRI-CT image registration on target delineation of postoperative radiotherapy for gliomas]. Ai Zheng; 2008 May;27(5):544-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND & OBJECTIVE: Magnetic resonance imaging (MRI) can well distinguish soft tissue, but its usage in radiotherapy for brain tumors was limited by its image distortion and lack of electron density for dosage calculation.
  • METHODS: Nine glioma patients were examined by MRI and CT after operation.
  • RESULTS: The registration accuracy by the method of artificial landmarks was less than 1.5 mm, which reached the error requirement for brain tumors.
  • The change of central position of CTV was the largest [(8.74+/-6.60) mm], those of 2 eyes were the next [(5.25+/-2.38) mm for the left eyeû (5.65+/-2.56) mm for the right eye], and that of the brain stem was the least [(1.83+/-1.06) mm].
  • MRI-CT registration can reduce the uncertainty of CTV delineation in radiation treatment planning for glioma patients after operation.
  • [MeSH-major] Brain Neoplasms / radiography. Glioma / radiography. Magnetic Resonance Imaging / methods. Radiotherapy Planning, Computer-Assisted. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Radiotherapy, Intensity-Modulated. Tumor Burden

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18479608.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


87. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [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


88. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


89. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • The Lens. Cited by Patents in .
  • [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


90. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


91. Laigle-Donadey F, Doz F, Delattre JY: Brainstem gliomas in children and adults. Curr Opin Oncol; 2008 Nov;20(6):662-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Brainstem gliomas in children and adults.
  • PURPOSE OF REVIEW: The purpose of this review is to determine if recent advances in diagnostic and treatment modalities result in improvement in the pattern of care of brainstem gliomas.
  • RECENT FINDINGS: New MRI techniques may contribute to differential diagnosis and aid neurosurgeons in removing resectable brainstem tumors.
  • However, biopsy remains indicated in many contrast enhancing brainstem masses in adults because of the great variety of differential diagnosis.
  • SUMMARY: Diffuse brainstem glioma is the most common subtype of brainstem tumor and remains a devastating malignancy in children.
  • Given the lack of efficacy of conventional drugs, a better understanding of the biology of this tumor is the key to more targeted therapy.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Stem / pathology. Glioma / drug therapy
  • [MeSH-minor] Adult. Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Biopsy. Child. Drug Delivery Systems. Humans. Magnetic Resonance Imaging / methods. Medical Oncology / methods. Neoplasm Metastasis. Neurofibromatosis 1 / drug therapy. Neurofibromatosis 1 / pathology. Signal Transduction

  • 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 = 18841048.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents
  • [Number-of-references] 57
  •  go-up   go-down


92. Lavon I, Zrihan D, Granit A, Einstein O, Fainstein N, Cohen MA, Cohen MA, Zelikovitch B, Shoshan Y, Spektor S, Reubinoff BE, Felig Y, Gerlitz O, Ben-Hur T, Smith Y, Siegal T: Gliomas display a microRNA expression profile reminiscent of neural precursor cells. Neuro Oncol; 2010 May;12(5):422-33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gliomas express many genes that play a role in neural precursor cells (NPCs), but no direct comparison between glioma and stem cell (SC) gene expression profiles has been performed.
  • To investigate the similarities and differences between gliomas and SCs, we compared the microRNA (miRNA) expression signatures of glial tumors, embryonic SCs (ESCs), NPCs, and normal adult brains from both human and mouse tissues.
  • We demonstrated that both human gliomas (regardless of their grade) and methylcholanthrene-induced mouse glioma shared an miRNA expression profile that is reminiscent of NPCs.
  • The bipartite cluster of 7 + 46 miRNAs on chromosome 14q32.31, which might represent the largest tumor suppressor miRNA cluster, was downregulated in the shared expression profile.
  • Our finding showed that all gliomas displayed NPC-like miRNA signatures, which may have implications for studies of glioma origins.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression Profiling. Glioma / genetics. Neurons / metabolism. RNA, Messenger / analysis. Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Loss of Heterozygosity. Mice. Mice, Inbred C57BL

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mamm Genome. 2006 Aug;17(8):833-40 [16897339.001]
  • [Cites] Int J Cancer. 2009 Sep 15;125(6):1407-13 [19536818.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Oct 13;349(1):59-68 [16934749.001]
  • [Cites] Neuropathol Appl Neurobiol. 2006 Oct;32(5):517-24 [16972885.001]
  • [Cites] Int J Cancer. 2007 Mar 1;120(5):1046-54 [17149698.001]
  • [Cites] Stem Cells. 2007 Feb;25(2):437-46 [17284651.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jun;175(2):159-65 [17556073.001]
  • [Cites] Mamm Genome. 2007 May;18(5):316-27 [17610011.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2059-66 [17671640.001]
  • [Cites] J Cell Sci. 2007 Oct 1;120(Pt 19):3327-35 [17881494.001]
  • [Cites] Nat Biotechnol. 2000 Apr;18(4):399-404 [10748519.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Chin Med J (Engl). 2002 Aug;115(8):1201-4 [12215292.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jan;36(1):57-69 [12461750.001]
  • [Cites] Dev Cell. 2003 Aug;5(2):351-8 [12919684.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):895-902 [14737120.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3087-95 [15126345.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):488-98 [15183728.001]
  • [Cites] Genome Res. 2004 Sep;14(9):1741-8 [15310658.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7267-73 [15378086.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Jul;43(3):284-93 [15834943.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]
  • [Cites] Genomics. 2006 Feb;87(2):225-35 [16309881.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1169-81 [16564011.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9136-41 [16754881.001]
  • [Cites] Stem Cells Dev. 2007 Dec;16(6):1003-16 [18004940.001]
  • [Cites] Curr Protoc Cell Biol. 2007 Sep;Chapter 23:Unit 23.7 [18228508.001]
  • [Cites] Nat Cell Biol. 2008 Feb;10(2):202-10 [18193036.001]
  • [Cites] Cell. 2008 Mar 7;132(5):860-74 [18329371.001]
  • [Cites] Cell. 2008 Mar 7;132(5):875-86 [18329372.001]
  • [Cites] Nat Immunol. 2008 Apr;9(4):405-14 [18327259.001]
  • [Cites] Genes Dev. 2008 Apr 1;22(7):894-907 [18381893.001]
  • [Cites] Cell. 2008 Apr 18;133(2):217-22 [18423194.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2690-5 [18451233.001]
  • [Cites] Nat Cell Biol. 2008 May;10(5):593-601 [18376396.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 13;105(19):7004-9 [18458333.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1268-72 [17989713.001]
  • [Cites] Stem Cells. 2008 Jun;26(6):1506-16 [18403753.001]
  • [Cites] BMC Med. 2008;6:14 [18577219.001]
  • [Cites] Am J Clin Pathol. 2008 Aug;130(2):178-85 [18628085.001]
  • [Cites] Cancer Res. 2008 Jul 15;68(14):5795-802 [18632633.001]
  • [Cites] Cancer Res. 2008 Aug 1;68(15):6162-70 [18676839.001]
  • [Cites] Mol Cell Biol. 2008 Sep;28(17):5369-80 [18591254.001]
  • [Cites] Cancer Res. 2008 Nov 15;68(22):9125-30 [19010882.001]
  • [Cites] Int J Cancer. 2009 Feb 1;124(3):568-77 [18973228.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2812-7 [19196975.001]
  • [Cites] Mol Cancer. 2006;5:29 [16854228.001]
  • (PMID = 20406893.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2940621
  •  go-up   go-down


93. Stockhausen MT, Kristoffersen K, Poulsen HS: The functional role of Notch signaling in human gliomas. Neuro Oncol; 2010 Feb;12(2):199-211
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gliomas are among the most devastating adult tumors for which there is currently no cure.
  • The tumors are derived from brain glial tissue and comprise several diverse tumor forms and grades.
  • These cells have been referred to as brain cancer stem cells (bCSC), as they share similarities to normal neural stem cells in the brain.
  • The Notch signaling pathway is involved in cell fate decisions throughout normal development and in stem cell proliferation and maintenance.
  • In this review, we explore the role of the Notch signaling pathway in gliomas with emphasis on its role in normal brain development and its interplay with pathways and processes that are characteristic of malignant gliomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioma / metabolism. Neoplastic Stem Cells / metabolism. Receptors, Notch / metabolism. Signal Transduction / physiology

  • 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] Genes Dev. 2000 Jun 1;14(11):1313-8 [10837024.001]
  • [Cites] Cell. 2000 May 26;101(5):499-510 [10850492.001]
  • [Cites] J Comp Neurol. 2000 Jul 31;423(3):359-72 [10870078.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Oncogene. 2000 Aug 31;19(37):4191-8 [10980592.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5879-86 [11059786.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14720-5 [11121071.001]
  • [Cites] EMBO J. 2001 Jul 2;20(13):3427-36 [11432830.001]
  • [Cites] J Comp Neurol. 2001 Jul 23;436(2):167-81 [11438922.001]
  • [Cites] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031.001]
  • [Cites] Neuron. 2001 Aug 30;31(4):557-68 [11545715.001]
  • [Cites] EMBO J. 2002 Jan 15;21(1-2):93-102 [11782429.001]
  • [Cites] Differentiation. 2001 Dec;69(2-3):135-44 [11798067.001]
  • [Cites] Curr Biol. 2002 Jan 22;12(2):R74-8 [11818085.001]
  • [Cites] Annu Rev Neurosci. 2002;25:471-90 [12052917.001]
  • [Cites] J Neurosci Methods. 2002 Jun 30;117(2):111-21 [12100976.001]
  • [Cites] Mech Dev. 2002 Jun;114(1-2):153-9 [12175503.001]
  • [Cites] Curr Opin Genet Dev. 2002 Oct;12(5):524-33 [12200157.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] J Neurosci Res. 2002 Sep 15;69(6):848-60 [12205678.001]
  • [Cites] Nat Med. 2002 Sep;8(9):979-86 [12185362.001]
  • [Cites] Nat Neurosci. 2002 Dec;5(12):1265-9 [12447381.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):14-25 [12482957.001]
  • [Cites] J Cell Physiol. 2003 Mar;194(3):237-55 [12548545.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):416-21 [12590261.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):203-5 [12676578.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Mol Cell. 2003 Oct;12(4):889-901 [14580340.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12876-82 [14709552.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Oncogene. 1990 Dec;5(12):1839-42 [2284103.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] EMBO J. 1991 Oct;10(10):2975-83 [1717258.001]
  • [Cites] J Biol Chem. 1993 Feb 25;268(6):3817-20 [8095043.001]
  • [Cites] Development. 1994 Sep;120(9):2421-30 [7956822.001]
  • [Cites] Cell. 1995 Mar 24;80(6):909-17 [7697721.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] Dev Biol. 1996 Apr 10;175(1):1-13 [8608856.001]
  • [Cites] Cell. 1997 Jul 25;90(2):281-91 [9244302.001]
  • [Cites] Development. 1997 Aug;124(16):3065-76 [9272948.001]
  • [Cites] Mol Cell Biol. 1997 Oct;17(10):6057-67 [9315665.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):303-14 [9440027.001]
  • [Cites] Oncogene. 1998 Feb 26;16(8):1009-19 [9519875.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8108-12 [9653148.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Jul;57(7):684-9 [9690672.001]
  • [Cites] Neuron. 1998 Jul;21(1):63-75 [9697852.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2269-77 [9694793.001]
  • [Cites] J Neurosci Res. 1998 Oct 15;54(2):125-36 [9788272.001]
  • [Cites] J Neurosci Methods. 1998 Dec 1;85(2):141-52 [9874150.001]
  • [Cites] Am J Pathol. 1999 Mar;154(3):785-94 [10079256.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):518-22 [10206645.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Exp Neurol. 1999 Apr;156(2):333-44 [10328940.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7787-93 [15520184.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):15949-54 [15520367.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9392-400 [15558011.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Trends Cell Biol. 2006 Jun;16(6):293-300 [16697642.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15