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1. Park I, Tamai G, Lee MC, Chuang CF, Chang SM, Berger MS, Nelson SJ, Pirzkall A: Patterns of recurrence analysis in newly diagnosed glioblastoma multiforme after three-dimensional conformal radiation therapy with respect to pre-radiation therapy magnetic resonance spectroscopic findings. Int J Radiat Oncol Biol Phys; 2007 Oct 1;69(2):381-9
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  • [Title] Patterns of recurrence analysis in newly diagnosed glioblastoma multiforme after three-dimensional conformal radiation therapy with respect to pre-radiation therapy magnetic resonance spectroscopic findings.
  • METHODS AND MATERIALS: A total of 23 glioblastoma multiforme (GBM) patients underwent MRI and MRSI within 4 weeks after surgery but before the initiation of RT and at 2-month follow-up intervals thereafter.
  • The MRSI data were quantified on the basis of a Choline-to-NAA Index (CNI) as a measure of spectroscopic abnormality.
  • CONCLUSION: These data indicate that the definition of RT target volumes according to the combined morphologic and metabolic abnormality may be sufficient for RT targeting.

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  • (PMID = 17513061.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097257-010002; United States / NCI NIH HHS / CA / CA059880-09A1; United States / NCI NIH HHS / CA / R01 CA059880-09A1; United States / NCI NIH HHS / CA / P50 CA97297; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA-59880; United States / NCI NIH HHS / CA / R01 CA059880; United States / NCI NIH HHS / CA / P50 CA097257-010002
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS30938; NLM/ PMC2377157
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2. Candolfi M, Kroeger KM, Pluhar GE, Bergeron J, Puntel M, Curtin JF, McNiel EA, Freese AB, Ohlfest JR, Moore P, Lowenstein PR, Castro MG: Adenoviral-mediated gene transfer into the canine brain in vivo. Neurosurgery; 2007 Jan;60(1):167-77; discussion 178
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  • OBJECTIVE: Glioblastoma multiforme (GBM) is a devastating brain tumor for which there is no cure.
  • Adenoviral-mediated transfer of conditional cytotoxic (herpes simplex virus [HSV] 1-derived thymidine kinase [TK]) and immunostimulatory (Fms-like tyrosine kinase 3 ligand [Flt3L]) transgenes elicited immune-mediated long-term survival in a syngeneic intracranial GBM model in rodents.
  • However, the lack of a large GBM animal model makes it difficult to predict the outcome of therapies in humans.
  • Dogs develop spontaneous GBM that closely resemble the human disease; therefore, they constitute an excellent large animal model.
  • We assayed the transduction efficiency of adenoviral vectors (Ads) encoding beta-galactosidase (betaGal), TK, and Flt3L in J3T dog GBM cells in vitro and in the dog brain in vivo.
  • RESULTS: Adenoviral-mediated gene transfer of HSV1-TK, Flt3L, and betaGal was detected in dog glioma cells in vitro (45% transduction efficiency) and in the dog brain in vivo (10-mm area transduced surrounding each injection site).
  • CONCLUSION: We demonstrate effective adenoviral-mediated gene transfer into the brain of dogs in vivo and support the use of these vectors to develop an efficacy trial for canine GBM as a prelude to human trials.

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  • (PMID = 17228266.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / 1 R01 NS42893; United States / NINDS NIH HHS / NS / U54 NS045309-010005; United States / NINDS NIH HHS / NS / R21 NS047298; United States / NINDS NIH HHS / NS / R01 NS074387; United States / NINDS NIH HHS / NS / R01 NS044556; United States / NINDS NIH HHS / NS / 1R01 NS44556.01; United States / NINDS NIH HHS / NS / U54 NS045309; United States / NINDS NIH HHS / NS / U54 4 NS04-5309; United States / NINDS NIH HHS / NS / NS045309-010005; United States / NINDS NIH HHS / NS / R21 NS047298-01; United States / NINDS NIH HHS / NS / NS044556-01; United States / FIC NIH HHS / TW / 1 R03 TW006273-01; United States / NINDS NIH HHS / NS / NS047298-01; United States / FIC NIH HHS / TW / R03 TW006273-01A1; United States / NINDS NIH HHS / NS / R01 NS042893; United States / NINDS NIH HHS / NS / R01 NS044556-01; United States / NINDS NIH HHS / NS / NS042893-01A1; United States / FIC NIH HHS / TW / TW006273-01A1; United States / NINDS NIH HHS / NS / R01 NS042893-01A1; United States / FIC NIH HHS / TW / R03 TW006273; United States / NINDS NIH HHS / NS / R21 NS47298
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS28768; NLM/ PMC2095776
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3. Lin HY, Sun M, Tang HY, Lin C, Luidens MK, Mousa SA, Incerpi S, Drusano GL, Davis FB, Davis PJ: L-Thyroxine vs. 3,5,3'-triiodo-L-thyronine and cell proliferation: activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Am J Physiol Cell Physiol; 2009 May;296(5):C980-91
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  • 3,5,3'-Triiodo-l-thyronine (T(3)), but not l-thyroxine (T(4)), activated Src kinase and, downstream, phosphatidylinositol 3-kinase (PI3-kinase) by means of an alpha(v)beta(3) integrin receptor on human glioblastoma U-87 MG cells.
  • A model proposes that one site binds T(3) exclusively, activates PI3-kinase via Src kinase, and stimulates TRalpha trafficking and HIF-1alpha gene expression.
  • Tetrac and RGD peptide both inhibit T(3) action at this site.
  • The second site binds T(4) and T(3), and, via this receptor, the iodothyronines stimulate ERK1/2-dependent tumor cell proliferation.
  • [MeSH-minor] Cell Division / drug effects. Cell Division / physiology. Cell Line, Tumor. Cell Nucleus / metabolism. Cytoplasm / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Integrin alphaVbeta3 / metabolism. Mitogen-Activated Protein Kinase 1 / genetics. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / genetics. Mitogen-Activated Protein Kinase 3 / metabolism. Protein Transport / drug effects. Protein Transport / physiology. Thyroid Hormone Receptors alpha / metabolism. Transfection


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4. van Zaane F, Subbaiyan D, van der Ploeg-van den Heuvel A, de Bruijn HS, Balbas EM, Pandraud G, Sterenborg HJ, French PJ, Robinson DJ: A telemetric light delivery system for metronomic photodynamic therapy (mPDT) in rats. J Biophotonics; 2010 Jun;3(5-6):347-55
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  • Light delivery and monitoring during photodynamic therapy (PDT) is often limited by the need for a physical link between the light source, detectors and the treatment volume.
  • This paper reports on the first in vivo experiments performed with a fully implantable telemetric system, designed for a rat glioblastoma model.
  • [MeSH-minor] Animals. Biocompatible Materials. Brain Neoplasms / drug therapy. Disease Models, Animal. Equipment Design. Equipment Failure. Equipment Failure Analysis. Feasibility Studies. Glioblastoma / drug therapy. Male. Materials Testing. Rats. Rats, Wistar. Time Factors

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  • [Copyright] (c) 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 20217900.001).
  • [ISSN] 1864-0648
  • [Journal-full-title] Journal of biophotonics
  • [ISO-abbreviation] J Biophotonics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biocompatible Materials
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5. Badr G, Sayed D: Human melanoma cells release soluble and functional receptors. Egypt J Immunol; 2006;13(2):23-31
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  • However, it does not inhibit the growth of glioblastoma cells that express the IL-13R alpha 2 chain.

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  • (PMID = 18689268.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Interleukin-13; 0 / Interleukin-13 Receptor alpha1 Subunit; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Receptors, Interleukin-4; 207137-56-2 / Interleukin-4; EC 3.4.- / Metalloproteases
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6. Solly F, Fish R, Simard B, Bolle N, Kruithof E, Polack B, Pernod G: Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model. Cancer Gene Ther; 2008 Oct;15(10):685-92
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  • [Title] Tissue-type plasminogen activator has antiangiogenic properties without effect on tumor growth in a rat C6 glioma model.
  • Although the treatment of tPA+ tumor-bearing animals with the FSD captopril generated angiostatin in situ and reduced endothelial vascularization of the tumors, it had no effect on tumor growth.
  • Alternative mechanisms could account for this lack of effect and consequently have important implications for vascular the treatment of glioblastoma.
  • [MeSH-minor] Angiostatins / metabolism. Angiotensin-Converting Enzyme Inhibitors / pharmacology. Angiotensin-Converting Enzyme Inhibitors / therapeutic use. Animals. Antigens, CD31 / analysis. Blotting, Western. Captopril / pharmacology. Captopril / therapeutic use. Cell Line, Tumor. Combined Modality Therapy. Genetic Vectors / genetics. Immunohistochemistry. Lentivirus / genetics. Male. Mice. Mice, Nude. Rats. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 18535615.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antigens, CD31; 86090-08-6 / Angiostatins; 9G64RSX1XD / Captopril; EC 3.4.21.68 / Tissue Plasminogen Activator
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7. Kumar R, Kamdar D, Madden L, Hills C, Crooks D, O'Brien D, Greenman J: Th1/Th2 cytokine imbalance in meningioma, anaplastic astrocytoma and glioblastoma multiforme patients. Oncol Rep; 2006 Jun;15(6):1513-6
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  • [Title] Th1/Th2 cytokine imbalance in meningioma, anaplastic astrocytoma and glioblastoma multiforme patients.
  • Patients were divided into various groups depending on their histological diagnosis: meningioma (n=11), anaplastic astrocytoma (n=4) and glioblastoma multiforme (GBM; n=46).
  • Significant reduction in serum IL-12 was seen in all groups as compared with the controls: meningioma, p=0.03; anaplastic astrocytoma, p<0.001; and GBM, p<0.001.
  • Conversely, serum IL-10 was significantly increased in anaplastic astrocytoma, p=0.02, and GBM, p=0.03.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-10 / blood. Interleukin-12 / blood. Meningioma / immunology. Th1 Cells / immunology. Th2 Cells / immunology


8. Jaeckle KA, Ballman KV, Giannini C, Schomberg PJ, Ames MM, Reid JM, McGovern RM, Safgren SL, Galanis E, Uhm JH, Brown PD, Hammack JE, Arusell R, Nikcevich DA, Morton RF, Wender DB, Buckner JC: Phase II NCCTG trial of RT + irinotecan and adjuvant BCNU plus irinotecan for newly diagnosed GBM. J Neurooncol; 2010 Aug;99(1):73-80
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  • [Title] Phase II NCCTG trial of RT + irinotecan and adjuvant BCNU plus irinotecan for newly diagnosed GBM.
  • We performed a Phase II study of RT and irinotecan, followed by BCNU plus irinotecan in newly-diagnosed GBM.
  • Patients went off treatment due to adverse events (7%), refusal (11%), progressive disease (48%), death (9%), and other (9%); 16% completed protocol treatment.
  • Grade 3-4 toxicity was more common in non-EIAC patients with variant alleles.

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  • (PMID = 20063115.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA035113-24; United States / NCI NIH HHS / CA / U10 CA035267; United States / NCI NIH HHS / CA / CA035101-24; United States / NCI NIH HHS / CA / U10 CA052352; United States / NCI NIH HHS / CA / U10 CA037417; United States / NCI NIH HHS / CA / N01 CA035431; United States / NCI NIH HHS / CA / U10 CA035269; United States / NCI NIH HHS / CA / CA-37404; United States / NCI NIH HHS / CA / CA-35431; United States / NCI NIH HHS / CA / U10 CA035267-24; United States / NCI NIH HHS / CA / CA063848-16; United States / NCI NIH HHS / CA / U10 CA025224-24; United States / NCI NIH HHS / CA / CA-52352; United States / NCI NIH HHS / CA / U10 CA035113-24; United States / NCI NIH HHS / CA / U10 CA037404; United States / NCI NIH HHS / CA / CA037417-24; United States / NCI NIH HHS / CA / CA035431-24; United States / NCI NIH HHS / CA / U10 CA063848-16; United States / NCI NIH HHS / CA / CA052352-20; United States / NCI NIH HHS / CA / U10 CA063848; United States / NCI NIH HHS / CA / U10 CA037404-16; United States / NCI NIH HHS / CA / CA-35103; United States / NCI NIH HHS / CA / CA-25224; United States / NCI NIH HHS / CA / U10 CA035431-24; United States / NCI NIH HHS / CA / CA037404-16; United States / NCI NIH HHS / CA / CA035103-24; United States / NCI NIH HHS / CA / CA-35113; United States / NCI NIH HHS / CA / U10 CA035101; United States / NCI NIH HHS / CA / U10 CA035113; United States / NCI NIH HHS / CA / U10 CA035269-24; United States / NCI NIH HHS / CA / CA035267-24; United States / NCI NIH HHS / CA / CA025224-24; United States / NCI NIH HHS / CA / CA-63848; United States / NCI NIH HHS / CA / U10 CA037417-24; United States / NCI NIH HHS / CA / U10 CA035103-24; United States / NCI NIH HHS / CA / U10 CA035431; United States / NCI NIH HHS / CA / UG1 CA189808; United States / NCI NIH HHS / CA / CA-37417; United States / NCI NIH HHS / CA / CA-35269; United States / NCI NIH HHS / CA / CA035269-24; United States / NCI NIH HHS / CA / CA-35101; United States / NCI NIH HHS / CA / U10 CA025224; United States / NCI NIH HHS / CA / U10 CA035101-24; United States / NCI NIH HHS / CA / CA-35267; United States / NCI NIH HHS / CA / U10 CA052352-20; United States / NCI NIH HHS / CA / U10 CA035103
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7673326042 / irinotecan; U68WG3173Y / Carmustine; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ NIHMS197040; NLM/ PMC2897141
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9. Cottin S, Ghani K, Caruso M: Bystander effect in glioblastoma cells with a predominant cytoplasmic localization of connexin43. Cancer Gene Ther; 2008 Dec;15(12):823-31
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  • [Title] Bystander effect in glioblastoma cells with a predominant cytoplasmic localization of connexin43.
  • Herpes simplex virus thymidine kinase (TK) gene transfer followed by ganciclovir (GCV) administration is an approach investigated for glioblastoma treatment.
  • In this study, we investigated the level of expression, the localization and the functionality of connexin43 (Cx43) in three glioblastoma cell lines.
  • Our results indicate for the first time that the very limited numbers of gap junctions present in glioblastoma cells are highly functional.
  • We thus conclude that the TK/GCV strategy is still a valuable therapeutic option to be developed for the treatment of glioblastoma patients.
  • [MeSH-major] Bystander Effect / physiology. Connexin 43 / analysis. Connexin 43 / metabolism. Cytoplasm / metabolism. Glioblastoma / metabolism
  • [MeSH-minor] Cell Communication. Cell Line, Tumor. Ganciclovir / therapeutic use. Gap Junctions / metabolism. Genetic Therapy. HeLa Cells. Humans

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  • (PMID = 18600256.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Connexin 43; P9G3CKZ4P5 / Ganciclovir
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10. Guo H, Gu F, Li W, Zhang B, Niu R, Fu L, Zhang N, Ma Y: Reduction of protein kinase C zeta inhibits migration and invasion of human glioblastoma cells. J Neurochem; 2009 Apr;109(1):203-13
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  • [Title] Reduction of protein kinase C zeta inhibits migration and invasion of human glioblastoma cells.
  • Glioblastomas are the most aggressive forms of primary brain tumors with their tendency to invade surrounding healthy brain tissues, rendering them largely incurable.
  • In this report, we used small-interference RNA technology to knock down the expression of protein kinase C (PKC) zeta, which resulted in specific and massive impairment of glioblastoma cell migration and invasion.
  • We also explained the fundamental molecular processes of glioblastoma migration and invasion in which PKCzeta is a participant.
  • These results indicate that PKCzeta is involved in the control of glioblastoma cell migration and invasion by regulating the cytoskeleton rearrangement, cell adhesion, and matrix metalloprotease-9 expression.
  • Collectively, these findings suggest that PKCzeta is a potential therapeutic target for glioblastoma infiltration.
  • [MeSH-major] Cell Movement / physiology. Glioblastoma / enzymology. Glioblastoma / pathology. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / physiology
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Regulation, Enzymologic / physiology. Gene Targeting. Humans. Neoplasm Invasiveness. RNA, Small Interfering / genetics

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  • (PMID = 19187446.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
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11. Choi JY, Lee SH, Na HB, An K, Hyeon T, Seo TS: In vitro cytotoxicity screening of water-dispersible metal oxide nanoparticles in human cell lines. Bioprocess Biosyst Eng; 2010 Jan;33(1):21-30
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  • In this study, we present in vitro cytotoxicity of iron oxide (Fe(3)O(4)) and manganese oxide (MnO) using live/dead cell assay, lactate dehydrogenase assay, and reactive oxygen species detection with variation of the concentration of nanoparticles (5-500 microg/ml), incubation time (18-96 h), and different human cell lines (lung adenocarcinoma, breast cancer cells, and glioblastoma cells).
  • The engineered MnO and Fe(3)O(4) exhibited excellent stability compared with Feridex for a prolonged incubation time.
  • [MeSH-minor] Cell Culture Techniques. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Time Factors

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  • (PMID = 19636592.001).
  • [ISSN] 1615-7605
  • [Journal-full-title] Bioprocess and biosystems engineering
  • [ISO-abbreviation] Bioprocess Biosyst Eng
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ferric Compounds; 0 / Manganese Compounds; 0 / Oxides; 1317-35-7 / manganese oxide; 1K09F3G675 / ferric oxide
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12. Fabi A, Russillo M, Metro G, Vidiri A, Di Giovanni S, Cognetti F: Pseudoprogression and MGMT status in glioblastoma patients: implications in clinical practice. Anticancer Res; 2009 Jul;29(7):2607-10
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  • [Title] Pseudoprogression and MGMT status in glioblastoma patients: implications in clinical practice.
  • In radiological imaging, it is shown as an increase in the size of the tumor lesion and contrast enhancement occurring within a few months from the completion of radio-chemotherapy without worsening of the neurological signs and symptoms.
  • In 12 glioblastoma patients treated with radio-chemotherapy, 4 cases of early radiological progression without discontinuation of temozolomide treatment are reported.
  • At the sunsequent tumor assessment, 2 cases (13%) were revealed to be PsPD.
  • The PsPD phenomenon opens the prospect of a new era for the management of glioblastoma patients undergoing radio-chemotherapy.
  • [MeSH-major] Brain Neoplasms / pathology. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Glioblastoma / pathology. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Disease Progression. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 19596935.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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13. Shaikh AJ, Masood N: Acute lymphoblastic leukemia subsequent to temozolomide use in a 26-year-old man: a case report. J Med Case Rep; 2010;4:274
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  • INTRODUCTION: We report the development of acute lymphoblastic leukemia in a patient in whom temozolomide was used for the treatment of a brain tumor.
  • CASE PRESENTATION: A 26-year-old Pakistani man who was treated for glioblastoma with temozolomide in an adjuvant setting was diagnosed to have acute lymphoblastic leukemia one year after stopping temozolomide.
  • CONCLUSION: Temozolomide is a highly active agent, used in the management of high-grade brain neoplasms.
  • This finding should be of interest to physicians in general and to medical oncologists in particular.

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  • (PMID = 20718954.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2931525
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14. Combs SE: Radiation therapy. Recent Results Cancer Res; 2009;171:125-40
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  • However, application of radiation has to be adapted to the distinct characteristics of the various glioma subtypes, with respect to dosing, time-point of irradiation, choice of treatment technique, and more recently, of radiation quality.Treatment of low-grade gliomas has been characterized by much controversy, which is still ongoing.
  • For glioblastomas, a change in treatment paradigm has taken place with the alkylating agent temozolomide, which could increase survival significantly for the first time in many centuries.

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  • (PMID = 19322541.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 96
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15. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Also, the first steps have been taken in refining classical histopathological diagnosis by use of molecular predictive markers, for example, MGMT promoter hypermethylation in glioblastomas.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • Novel animal models will provide us with the opportunity to comprehensively study this multilayered disease and explore novel therapeutic approaches in vivo.
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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16. Zhang M, Chakravarti A: Novel radiation-enhancing agents in malignant gliomas. Semin Radiat Oncol; 2006 Jan;16(1):29-37
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  • For many decades, significant improvements in clinical outcomes of newly diagnosed glioblastoma (GBM) patients have not been observed until recently.
  • A landmark European Organization for Research and Treatment of Cancer (EORTC) phase III study showed significant improvements in median and 2-year survivals in newly diagnosed GBM patients treated with a combination of radiation and temozolomide chemotherapy versus radiation alone.
  • [MeSH-major] Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Radiation-Sensitizing Agents

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  • (PMID = 16378904.001).
  • [ISSN] 1053-4296
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents
  • [Number-of-references] 45
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17. Boudreau CR, Yang I, Liau LM: Gliomas: advances in molecular analysis and characterization. Surg Neurol; 2005 Oct;64(4):286-94; discussion 294
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  • BACKGROUND: Gliomas represent the most common primary brain tumor.
  • This review will describe the technological advances being used to enrich the classification of gliomas, present specific studies that have successfully used the new technologies to identify molecular subtypes of glioblastoma, and discuss the implications of such enhanced classification and molecular characterizations for the prediction of therapeutic response and the design of future brain tumor therapies.
  • Alterations of several tumor suppressor genes and oncogenes have already been identified as being critical to glioma transformation and progression.
  • These approaches have led to the subclassification of glioblastoma multiforme into distinct subtypes based on the molecular signatures of the tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / diagnosis. Genetic Markers / genetics. Glioma / diagnosis
  • [MeSH-minor] Gene Expression Profiling / methods. Gene Expression Profiling / trends. Gene Expression Regulation, Neoplastic / genetics. Humans. Medical Oncology / methods. Medical Oncology / trends. Molecular Biology / methods. Molecular Biology / trends. Oligonucleotide Array Sequence Analysis / methods. Oligonucleotide Array Sequence Analysis / trends

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  • [CommentIn] Surg Neurol. 2005 Oct;64(4):285 [16181992.001]
  • (PMID = 16229087.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers
  • [Number-of-references] 50
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18. Ehtesham M, Mapara KY, Stevenson CB, Thompson RC: CXCR4 mediates the proliferation of glioblastoma progenitor cells. Cancer Lett; 2009 Feb 18;274(2):305-12
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  • [Title] CXCR4 mediates the proliferation of glioblastoma progenitor cells.
  • As such, in the context of glioblastoma multiforme (GBM), the development of treatment strategies specifically targeted towards CSC-like populations may hold significant therapeutic promise.
  • To this end, we now report that the cell surface chemokine receptor, CXCR4, a known mediator of cancer cell proliferation and invasion, is overexpressed in primary glioblastoma progenitor cells versus corresponding differentiated tumor cells.
  • Furthermore, administration of CXCL12, the only known ligand for CXCR4, stimulates a specific and significant proliferative response in progenitors but not differentiated tumor cells.
  • Taken together, these results implicate an important role for the CXCR4 signaling mechanism in glioma CSC biology and point to the therapeutic potential of targeting this pathway in patients with GBM.

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  • (PMID = 19008040.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS051557-03; United States / NINDS NIH HHS / NS / R01 NS051557-02; United States / NINDS NIH HHS / NS / NS051557; United States / NINDS NIH HHS / NS / NS051557-01A1; United States / NINDS NIH HHS / NS / NS051557-02; United States / NINDS NIH HHS / NS / R01 NS051557-01A1; United States / NINDS NIH HHS / NS / R01 NS051557; United States / NINDS NIH HHS / NS / NS051557-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / DNA Primers; 0 / Receptors, CXCR4
  • [Other-IDs] NLM/ NIHMS79681; NLM/ PMC2628453
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19. Paugh BS, Bryan L, Paugh SW, Wilczynska KM, Alvarez SM, Singh SK, Kapitonov D, Rokita H, Wright S, Griswold-Prenner I, Milstien S, Spiegel S, Kordula T: Interleukin-1 regulates the expression of sphingosine kinase 1 in glioblastoma cells. J Biol Chem; 2009 Feb 6;284(6):3408-17
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  • [Title] Interleukin-1 regulates the expression of sphingosine kinase 1 in glioblastoma cells.
  • In the brain, neuroinflammatory cytokines affect the growth and differentiation of both normal and malignant glial cells, with interleukin 1 (IL-1) shown to be secreted by the majority of glioblastoma cells.
  • Recently, elevated levels of sphingosine kinase 1 (SphK1), but not SphK2, were correlated with a shorter survival prognosis for patients with glioblastoma multiforme.
  • SphK1 is a lipid kinase that produces the pro-growth, anti-apoptotic sphingosine 1-phosphate, which can induce invasion of glioblastoma cells.
  • Here, we show that the expression of IL-1 correlates with the expression of SphK1 in glioblastoma cells, and neutralizing anti-IL-1 antibodies inhibit both the growth and invasion of glioblastoma cells.
  • Furthermore, IL-1 up-regulates SphK1 mRNA levels, protein expression, and activity in both primary human astrocytes and various glioblastoma cell lines; however, it does not affect SphK2 expression.
  • In summary, our results suggest that SphK1 expression is transcriptionally regulated by IL-1 in glioblastoma cells, and this pathway may be important in regulating survival and invasiveness of glioblastoma cells.

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  • (PMID = 19074142.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / F31NS060433; United States / NINDS NIH HHS / NS / R21NS063283
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Proto-Oncogene Proteins c-jun; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase; EC 2.7.12.2 / MAP Kinase Kinase 4
  • [Other-IDs] NLM/ PMC2635028
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20. Black KL, Yin D, Konda BM, Wang X, Hu J, Ko MK, Bayan JA, Sacapano MR, Espinoza AJ, Ong JM, Irvin D, Shu Y: Different effects of KCa and KATP agonists on brain tumor permeability between syngeneic and allogeneic rat models. Brain Res; 2008 Aug 28;1227:198-206
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  • [Title] Different effects of KCa and KATP agonists on brain tumor permeability between syngeneic and allogeneic rat models.
  • The blood-brain tumor barrier (BTB) significantly limits delivery of effective concentrations of chemotherapeutic drugs to brain tumors.
  • In this study, we studied the relationship of BTB permeability increase mediated by potassium channel agonists to channel expression in two rat brain tumor models.
  • Intravenous infusion of KCO912 (K(ATP) agonist), minoxidil sulfate (K(ATP) agonist) or NS1619 (K(Ca) agonist) increased tumor permeability more in the 9L allogeneic brain tumor model than in the syngeneic brain tumor model.
  • Furthermore, as a preliminary effort to understand clinical implication of potassium channels in brain tumor treatment, we determined the expression of K(ATP) in surgical specimens.
  • K(ATP) mRNA was detected in glioblastoma multiforme (GBM) from nineteen patients examined, with a wide range of expression levels.
  • Interestingly, in paired GBM tissues from seven patients before and after vaccination therapy, increased levels of K(ATP) were detected in five patients after vaccination that had positive response to chemotherapy after vaccination.
  • The expression of potassium channels in brain tumors is variable, which may be associated with different tumor permeability to therapeutic agents among patients.

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  • (PMID = 18602898.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS046388; United States / NINDS NIH HHS / NS / NS032103-12; United States / NINDS NIH HHS / NS / NS032103; United States / NINDS NIH HHS / NS / NS046388-04; United States / NINDS NIH HHS / NS / R37 NS032103-12; United States / NINDS NIH HHS / NS / R01 NS032103; United States / NINDS NIH HHS / NS / R01 NS046388; United States / NINDS NIH HHS / NS / R01 NS046388-04; United States / NINDS NIH HHS / NS / R37 NS032103
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzimidazoles; 0 / KATP Channels; 0 / Potassium Channels, Calcium-Activated; 0 / RNA, Messenger; 153587-01-0 / NS 1619; 5965120SH1 / Minoxidil; 83701-22-8 / minoxidil sulfate ester
  • [Other-IDs] NLM/ NIHMS69612; NLM/ PMC2605468
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21. Jensen RL: Hypoxia in the tumorigenesis of gliomas and as a potential target for therapeutic measures. Neurosurg Focus; 2006;20(4):E24
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  • Tumor hypoxia predicts the likelihood of metastases, tumor recurrence, resistance to chemotherapy and radiation therapy, invasive potential, and decreased patient survival for many human malignancies.
  • Various methods of measurement of tumor hypoxia are discussed, including direct measurement and imaging methods.
  • The progression of a low-grade astrocytoma to a glioblastoma multiforme may be mediated by hypoxia-induced phenotypic changes and subsequent clonal selection of cells that overexpress hypoxia-responsive molecules, such as HIF-1.
  • In this model, intratumoral hypoxia causes genetic changes that produce a microenvironment that selects for cells of a more aggressive phenotype.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Hypoxia / drug effects. Drug Design. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic. Humans. Neovascularization, Pathologic

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  • (PMID = 16709030.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
  • [Number-of-references] 166
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22. Terasaki M, Abe T, Miyagi N, Ogo E, Shigemori M: Feasibility and response to 1-(4-amino-2-methyl-5-pyrimidynyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride chemotherapy with pre-treated procarbazine for elderly patients with newly diagnosed glioblastoma. J Neurooncol; 2007 Feb;81(3):265-9
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  • [Title] Feasibility and response to 1-(4-amino-2-methyl-5-pyrimidynyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride chemotherapy with pre-treated procarbazine for elderly patients with newly diagnosed glioblastoma.
  • PURPOSE: To evaluate the feasibility of 1-(4-amino- 2-methyl-5-pyrimidynyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) of pre-treated procarbazine for elderly patients with newly diagnosed glioblastomas.
  • PATIENTS AND METHODS: From January 2004 to March 2005, 7 patients with glioblastoma were enrolled.
  • Among the 7 patients enrolled, there were 6 patients were died, and one was still alive with disease at 13 months.
  • CONCLUSION: The chemotherapy regimen is active but too toxic for elderly patients with newly diagnosed glioblastoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Nimustine / therapeutic use
  • [MeSH-minor] Aged. Alkaloids / therapeutic use. Benzylisoquinolines. Disease-Free Survival. Feasibility Studies. Female. Humans. Male. Middle Aged. Neutropenia / chemically induced. Procarbazine / therapeutic use. Survival Analysis. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 16937011.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Benzylisoquinolines; 0S726V972K / Nimustine; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7592YJ0J6T / cepharanthine
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23. Homma T, Fukushima T, Vaccarella S, Yonekawa Y, Di Patre PL, Franceschi S, Ohgaki H: Correlation among pathology, genotype, and patient outcomes in glioblastoma. J Neuropathol Exp Neurol; 2006 Sep;65(9):846-54
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  • [Title] Correlation among pathology, genotype, and patient outcomes in glioblastoma.
  • Glioblastomas are histologically and genetically heterogeneous.
  • Key histologic characteristics, including major cell types (small cell, nonsmall cell), other components such as oligodendroglial components, gemistocytes, multinucleated giant cells, as well as necrosis and microvascular proliferation, of 420 cases of glioblastoma within a population-based study (1) were reassessed and correlated with patients' clinical outcome and key genetic alterations.
  • EGFR amplification and p16 homozygous deletion were significantly more frequent in small cell glioblastomas than in nonsmall cell glioblastomas (EGFR, 46% vs 26%, p = 0.0002; p16 39% vs 25%, p = 0.0167).
  • Multivariate analyses with adjustment for age and gender showed that small cell glioblastomas had frequent EGFR amplification and p16 deletion but infrequent PTEN mutations.
  • An oligodendroglial component was detected in 20% of glioblastomas; these patients were significantly younger (54.4 +/- 13.6 vs 59.2 +/- 13.8 years; p = 0.0049) and survived longer (10.3 +/- 8.3 vs 8.2 +/- 8.4 months; p = 0.0647).
  • After adjustment for age and gender, LOH 1p was associated with longer survival (hazard ratio, 0.7; 95% confidence interval [CI], 0.5-1.0), whereas LOH 10q was associated with shorter survival (hazard ratio, 1.4; 95% CI, 1.0-1.8) of patients with glioblastoma.
  • Glioblastomas containing >or=5% multinucleated giant cells showed more frequent TP53 mutation and infrequent EGFR amplification than those containing <5% multinucleated giant cells (TP53, 45% vs 24%, p = 0.0001; EGFR, 24% vs 42%, p = 0.0005).
  • Vascular proliferation was observed in all glioblastomas, whereas large ischemic and/or pseudopalisading necrosis was observed in 366 of 420 (87%) cases.
  • Glioblastomas with necrosis were associated with older age (59.2 +/- 13.3 vs 51.6 +/- 15.3 years; p = 0.0001) and shorter survival (7.9 +/- 6.8 vs 12.9 +/- 14.2 months; p = 0.0017).
  • These results suggest that some histologic features in glioblastomas are associated with specific genetic alterations and with clinical outcome.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Glioblastoma / genetics. Glioblastoma / pathology
  • [MeSH-minor] Adult. Age Factors. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Community Health Planning. Female. Genes, erbB-1 / genetics. Genotype. Humans. Loss of Heterozygosity. Male. Middle Aged. Multivariate Analysis. Necrosis. PTEN Phosphohydrolase / genetics. Sex Factors. Statistics as Topic. Switzerland / epidemiology. Tumor Suppressor Protein p53 / genetics


24. Adamson DC, Rasheed BA, McLendon RE, Bigner DD: Central nervous system. Cancer Biomark; 2010;9(1-6):193-210
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  • The prognoses for these tumors are related to several factors, such as the age of the patient and the location and histology of the tumor.
  • Arising from glial cells, gliomas represent over 36% of all primary CNS tumors and consist of astrocytomas, oligodendrogliomas, ependymomas, mixed gliomas, and neuroepithelial tumors.
  • The most common gliomas are astrocytomas, and these tumors are typically classified by the World Health Organization (WHO) as Grades I through IV.
  • Grade IV, the most malignant grade of astrocytoma, includes glioblastoma multiforme (GBM), the most common malignant primary CNS glioma in adults, which represents 51% of all CNS gliomas.
  • GBM is unfortunately the most challenging to effectively treat and has the worst patient survival.
  • We also review the importance of glioma stem cell biology and tumor immunology in early gliomagenesis.

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  • (PMID = 22112477.001).
  • [ISSN] 1875-8592
  • [Journal-full-title] Cancer biomarkers : section A of Disease markers
  • [ISO-abbreviation] Cancer Biomark
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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25. Han L, Yang Y, Yue X, Huang K, Liu X, Pu P, Jiang H, Yan W, Jiang T, Kang C: Inactivation of PI3K/AKT signaling inhibits glioma cell growth through modulation of β-catenin-mediated transcription. Brain Res; 2010 Dec 17;1366:9-17
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  • In the present study, we report decreased cell proliferation and invasive ability upon the LY294002-induced inhibition of PI3K in both U251 and LN229 human glioblastoma cells in vitro.
  • Similar results were observed in vivo, as intratumoral injection of LY294002 downregulated the expression of the components of the β-catenin pathway and delayed tumor growth in nude mice harboring subcutaneous LN229 xenografts.
  • [MeSH-minor] Animals. Cell Cycle / genetics. Cell Cycle / physiology. Cell Line, Tumor. Chromones / pharmacology. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation / drug effects. Gene Expression Regulation / genetics. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Morpholines / pharmacology. Serine / metabolism. Time Factors. Transfection / methods

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20888802.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / beta Catenin; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 452VLY9402 / Serine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
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26. Klein O, Grignon Y, Civit T, Auque J, Marchal JC: [Methylation status of RARbeta gene promoter in low and high grade cerebral glioma. Comparison with normal tissue. Immuno-histochemical study of nuclear RARbeta expression in low and high grade cerebral glioma cells. Comparison with normal cells. 48 tumors]. Neurochirurgie; 2005 Sep;51(3-4 Pt 1):147-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Methylation status of RARbeta gene promoter in low and high grade cerebral glioma. Comparison with normal tissue. Immuno-histochemical study of nuclear RARbeta expression in low and high grade cerebral glioma cells. Comparison with normal cells. 48 tumors].
  • [Transliterated title] Statut de méthylation du promoteur du gène RARB dans les tumeurs cérébrales gliales de bas et de haut grade. Comparaison avec le tissu sain. Etude immuno-histochimique du marquage au RARbeta des noyaux des cellules tumorales dans les gliomes de bas et de haut grade. Comparaison avec les cellules saines, à propos de 48 tumeurs.
  • An immunohistochemical study was conducted to examine the level of expression of this receptor in the nucleus of glial cell tumors (low and high grade glioma) as well as a study of the methylation status of the gene promoter coding this receptor on the same tumor samples.
  • 48 tumors were eligible for the study (15 glioblastomas, 20 grade III oligodendrogliomas and 13 grade II oligodendrogliomas).
  • A constant decrease of RARbeta expression was found by comparison with normal tissue whatever the histological grade of the tumor, suggesting a deregulation of RARbeta gene expression.
  • Methylation of RARbeta promoter gene was a rare event (12.5% of all cases), except for grade III oligodendrogliomas (20%), and is thus not a major event of this gene deregulation.
  • [MeSH-minor] Brain / physiology. Brain Neoplasms / genetics. Chromosomes, Human, Pair 3. DNA Methylation. DNA, Neoplasm / genetics. Humans. Immunohistochemistry. Loss of Heterozygosity. Reference Values

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  • (PMID = 16389900.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta
  • [Number-of-references] 31
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27. Loizos N, Xu Y, Huber J, Liu M, Lu D, Finnerty B, Rolser R, Malikzay A, Persaud A, Corcoran E, Deevi DS, Balderes P, Bassi R, Jimenez X, Joynes CJ, Mangalampalli VR, Steiner P, Tonra JR, Wu Y, Pereira DS, Zhu Z, Ludwig DL, Hicklin DJ, Bohlen P, Witte L, Kussie P: Targeting the platelet-derived growth factor receptor alpha with a neutralizing human monoclonal antibody inhibits the growth of tumor xenografts: implications as a potential therapeutic target. Mol Cancer Ther; 2005 Mar;4(3):369-79
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  • [Title] Targeting the platelet-derived growth factor receptor alpha with a neutralizing human monoclonal antibody inhibits the growth of tumor xenografts: implications as a potential therapeutic target.
  • Platelet-derived growth factor receptor alpha (PDGFRalpha) is a type III receptor tyrosine kinase that is expressed on a variety of tumor types.
  • This inhibition was seen in both transfected and tumor cell lines expressing PDGFRalpha.
  • The in vivo antitumor activity of 3G3 was tested in human glioblastoma (U118) and leiomyosarcoma (SKLMS-1) xenograft tumor models in athymic nude mice.
  • [MeSH-minor] Animals. Biological Assay. Cell Line, Tumor. Dose-Response Relationship, Immunologic. Flow Cytometry. Humans. Kinetics. Ligands. MAP Kinase Signaling System. Mice. Mice, Nude. Mice, Transgenic. Neoplasm Transplantation. Phosphorylation. Platelet-Derived Growth Factor / chemistry. Protein Binding. Protein Structure, Tertiary. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Proto-Oncogene Proteins c-sis. Time Factors. Transfection

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  • (PMID = 15767546.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Ligands; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-sis; 0 / platelet-derived growth factor A; 0 / platelet-derived growth factor BB; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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28. Servotte S, Camby I, Debeir O, Deroanne C, Lambert CA, Lapière CM, Kiss R, Nusgens B, Decaestecker C: The in vitro influences of neurotensin on the motility characteristics of human U373 glioblastoma cells. Neuropathol Appl Neurobiol; 2006 Dec;32(6):575-84
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  • [Title] The in vitro influences of neurotensin on the motility characteristics of human U373 glioblastoma cells.
  • Astrocytic tumours are associated with dismal prognoses due to their pronounced ability to diffusely invade the brain parenchyma.
  • While neurotensin has been shown to influence the proliferation of glioma cells and the migratory ability of a large set of other cell types, its role in glioma cell migration has never been investigated.
  • Neurotensin-induced modifications to the motility features of human U373 glioblastoma cells therefore constitute the topic of the present study.
  • We evidenced that three subtypes of neurotensin receptors (NTR1, NTR2 and NTR3) are expressed in U373 glioblastoma cells, at least as far as their mRNAs are concerned.
  • In addition, quantitative phase-contrast videomicroscopy analyses showed that neurotensin decreases the motility levels of U373 glioblastoma cells when these cells are cultured on plastic.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioblastoma / metabolism. Neoplasm Invasiveness. Neurotensin / metabolism
  • [MeSH-minor] Actins / metabolism. Cell Line, Tumor. Cytoskeleton / metabolism. Enzyme Activation / physiology. Humans. In Vitro Techniques. Microscopy, Phase-Contrast. Microscopy, Video. RNA, Messenger / analysis. Receptors, Neurotensin / biosynthesis. cdc42 GTP-Binding Protein / metabolism. rac1 GTP-Binding Protein / metabolism. rhoA GTP-Binding Protein / metabolism

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  • (PMID = 17083472.001).
  • [ISSN] 0305-1846
  • [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 / Actins; 0 / RNA, Messenger; 0 / Receptors, Neurotensin; 39379-15-2 / Neurotensin; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / rhoA GTP-Binding Protein
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29. Shin SY, Choi BH, Ko J, Kim SH, Kim YS, Lee YH: Clozapine, a neuroleptic agent, inhibits Akt by counteracting Ca2+/calmodulin in PTEN-negative U-87MG human glioblastoma cells. Cell Signal; 2006 Nov;18(11):1876-86
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  • [Title] Clozapine, a neuroleptic agent, inhibits Akt by counteracting Ca2+/calmodulin in PTEN-negative U-87MG human glioblastoma cells.
  • This study investigated the effect of CZP on the modulation of the PI3K/Akt/GSK-3beta pathway in PTEN-negative U-87MG glioblastoma cells.
  • These results suggest that the antipsychotic drug CZP modulates the PI3K/Akt/GSK-3beta pathway by counteracting Ca(2+)/CaM in PTEN-negative U-87MG glioblastoma cells.
  • [MeSH-major] Calcium / metabolism. Calmodulin / metabolism. Clozapine / pharmacology. Glioblastoma / metabolism. Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • [MeSH-minor] Antipsychotic Agents / pharmacology. Cell Line, Tumor. Cytoskeletal Proteins / metabolism. Gene Deletion. Humans. Nuclear Proteins / metabolism. PTEN Phosphohydrolase / genetics. Phosphorylation. Signal Transduction. Tumor Cells, Cultured


31. Yuan L, Choi K, Khosla C, Zheng X, Higashikubo R, Chicoine MR, Rich KM: Tissue transglutaminase 2 inhibition promotes cell death and chemosensitivity in glioblastomas. Mol Cancer Ther; 2005 Sep;4(9):1293-302
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  • [Title] Tissue transglutaminase 2 inhibition promotes cell death and chemosensitivity in glioblastomas.
  • We have identified the novel finding that treatment of glioblastoma cells with transglutaminase 2 inhibitors promotes cell death and enhances sensitivity to chemotherapy.
  • Treatment with either the competitive transglutaminase 2 inhibitor, monodansylcadaverine, or with highly specific small-molecule transglutaminase 2 inhibitors, KCA075 or KCC009, results in induction of apoptosis in glioblastoma cells.
  • In vivo studies with s.c. murine DBT glioblastoma tumors treated with transglutaminase 2 inhibitors combined with the chemotherapeutic agent, N-N'-bis (2-chloroethyl)-N-nitrosourea (BCNU), decreased tumor size based on weight by 50% compared with those treated with BCNU alone.
  • These studies identify inhibition of transglutaminase 2 as a potential target to enhance cell death and chemosensitivity in glioblastomas.
  • [MeSH-major] Cell Death / drug effects. Enzyme Inhibitors / pharmacology. GTP-Binding Proteins / antagonists & inhibitors. Glioblastoma / pathology. Transglutaminases / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Azo Compounds / chemical synthesis. Azo Compounds / pharmacology. Brain Neoplasms / enzymology. Brain Neoplasms / pathology. Cadaverine / analogs & derivatives. Cadaverine / pharmacology. Carmustine / pharmacology. Drug Resistance, Neoplasm. Glycogen Synthase Kinase 3 / metabolism. Inhibitor of Apoptosis Proteins. Membrane Proteins / metabolism. Mice. Mice, Inbred BALB C. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Phosphorylation. Proto-Oncogene Proteins / metabolism. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 16170020.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01 63158; United States / NINDS NIH HHS / NS / R01 NS29477
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Azo Compounds; 0 / BIRC5 protein, human; 0 / Bcl-2-like protein 11; 0 / Enzyme Inhibitors; 0 / Inhibitor of Apoptosis Proteins; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; EC 2.3.2.- / transglutaminase 2; EC 2.3.2.13 / Transglutaminases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.1.- / GTP-Binding Proteins; I9N81SC5HD / monodansylcadaverine; L90BEN6OLL / Cadaverine; U68WG3173Y / Carmustine
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32. Pellegatta S, Finocchiaro G: Cell therapies in neuro-oncology. Neurol Sci; 2005 May;26 Suppl 1:S43-5
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  • [Title] Cell therapies in neuro-oncology.
  • We show that vaccination with DC pulsed with a tumour lysate considerably increases survival in mice bearing intracranial glioblastomas.
  • These results support the development of DC-based clinical trials for patients with glioblastomas that do not respond to standard therapies.

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  • (PMID = 15883693.001).
  • [ISSN] 1590-1874
  • [Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
  • [ISO-abbreviation] Neurol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cancer Vaccines
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33. Li GH, Wei H, Lv SQ, Ji H, Wang DL: Knockdown of STAT3 expression by RNAi suppresses growth and induces apoptosis and differentiation in glioblastoma stem cells. Int J Oncol; 2010 Jul;37(1):103-10
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  • [Title] Knockdown of STAT3 expression by RNAi suppresses growth and induces apoptosis and differentiation in glioblastoma stem cells.
  • Glioblastoma is a highly lethal brain tumor of the human primary nervous system tumors.
  • Previous studies demonstrated that glioblastoma stem cells were able to initiate and reform the original cancer.
  • In this study, we found that there were expression and activation of STAT3, a key signal transduction factor and oncoprotein, in human glioblastoma stem cells (GSCs).
  • Inhibition of STAT3 expression is associated not only with decreasing of CD133+ cell proportion and increasing of GFAP and MBP expression, but also with decrease of the capacity to initiate a tumor in human primary GSCs.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / drug effects. RNA, Small Interfering / pharmacology. STAT3 Transcription Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Proliferation / drug effects. Down-Regulation / drug effects. Gene Knockdown Techniques. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. Up-Regulation / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 20514402.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human
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34. Bralten LB, Gravendeel AM, Kloosterhof NK, Sacchetti A, Vrijenhoek T, Veltman JA, van den Bent MJ, Kros JM, Hoogenraad CC, Sillevis Smitt PA, French PJ: The CASPR2 cell adhesion molecule functions as a tumor suppressor gene in glioma. Oncogene; 2010 Nov 18;29(46):6138-48
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  • [Title] The CASPR2 cell adhesion molecule functions as a tumor suppressor gene in glioma.
  • In a set of 25 glioblastomas and 22 oligodendrogliomas, mutation analysis identified two additional samples with genetic alterations in the CASPR2 gene and all three identified genetic alterations are likely to reduce CASPR2 protein expression levels.
  • These results indicate that CASPR2 acts as a tumor suppressor gene in glioma.
  • [MeSH-major] Brain Neoplasms / genetics. Genes, Tumor Suppressor. Glioma / genetics. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Cell Movement. Cell Proliferation. DNA Methylation. Humans. Mutation. Neoplasm Invasiveness. Nuclear Receptor Coactivator 1 / physiology. RNA, Messenger / analysis

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  • (PMID = 20711234.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CNTNAP2 protein, human; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1
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35. Motaln H, Schichor C, Lah TT: Human mesenchymal stem cells and their use in cell-based therapies. Cancer; 2010 Jun 1;116(11):2519-30
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  • The human population is increasingly facing various diseases, including types of cancer, that cannot be cured with conventional drugs.
  • Advanced drug targeting of tumor cells is also often impossible when treating highly invasive and infiltrative tumors such as glioblastoma or pulmonary cancer, because of tumor cells' high migration and invasiveness.
  • Pluripotent human mesenchymal stem cells (hMSCs) have been extensively studied, and strategies are being proposed for treating "incurable" cancers and injury/disease-affected organs.
  • Their unprecedented use has been shadowed, however, by their spontaneous transformation, which links them to cancer-initiating cells during tumor development.

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  • [Copyright] (c) 2010 American Cancer Society.
  • (PMID = 20301117.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 90
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36. Salvati M, D'Elia A, Formichella AI, Frati A: Insights into pharmacotherapy of malignant glioma in adults. Expert Opin Pharmacother; 2009 Oct;10(14):2279-90
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  • The standard care for glioblastoma is surgery and concomitant radio- and chemotherapy with temozolomide (TMZ), followed by adjuvant treatment with TMZ.
  • [MeSH-minor] Adult. Aged. Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Bevacizumab. Chemotherapy, Adjuvant. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Erlotinib Hydrochloride. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Quinazolines / therapeutic use

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  • (PMID = 19663635.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Quinazolines; 2S9ZZM9Q9V / Bevacizumab; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; DA87705X9K / Erlotinib Hydrochloride
  • [Number-of-references] 115
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37. Monami G, Gonzalez EM, Hellman M, Gomella LG, Baffa R, Iozzo RV, Morrione A: Proepithelin promotes migration and invasion of 5637 bladder cancer cells through the activation of ERK1/2 and the formation of a paxillin/FAK/ERK complex. Cancer Res; 2006 Jul 15;66(14):7103-10
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  • [Title] Proepithelin promotes migration and invasion of 5637 bladder cancer cells through the activation of ERK1/2 and the formation of a paxillin/FAK/ERK complex.
  • Proepithelin is overexpressed in a great variety of cancer cell lines and clinical specimens of breast, ovarian, and renal cancer as well as glioblastomas.
  • Our results provide the first evidence for a role of proepithelin in stimulating migration and invasion of bladder cancer cells, and support the hypothesis that this growth factor may play a critical role in the establishment of the invasive phenotype.
  • [MeSH-minor] Enzyme Activation. Humans. MAP Kinase Signaling System. Neoplasm Invasiveness. Protein Precursors / metabolism. Protein Precursors / pharmacology. Recombinant Proteins / pharmacology

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  • (PMID = 16849556.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA07282; United States / NCI NIH HHS / CA / R01 CA39481; United States / NIDDK NIH HHS / DK / R01 DK 068419
  • [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 / GRN protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Paxillin; 0 / Protein Precursors; 0 / Recombinant Proteins; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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38. Ranger A, Szymczak A, Hammond RR, Zelcer S: Pediatric thalamic glioblastoma associated with Ollier disease (multiple enchondromatosis): a rare case of concurrence. J Neurosurg Pediatr; 2009 Oct;4(4):363-7
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  • [Title] Pediatric thalamic glioblastoma associated with Ollier disease (multiple enchondromatosis): a rare case of concurrence.
  • Ollier disease and Maffucci syndrome are rare syndromes in which there is deforming dysplasia of cartilage, primarily but not exclusively involving the metaphyses and diaphyses of long bones.
  • Little has been written about the association between Ollier disease and intracranial tumors, and these papers have largely consisted of case reports in adults.
  • The authors present the case of a 6-year-old girl with left arm osseous changes consistent with Ollier disease and a biopsy-proven thalamic glioblastoma multiforme.
  • They then examine the co-occurrence of brain tumors in conjunction with a dyschondroplasia syndrome in children and adolescents to assess the presentation, treatment offered, and disease course of similar cases.
  • Eight other such cases were identified, 6 in patients with Ollier disease (ranging in age from 7 to 18 years), and 2 with Maffucci syndrome (both in late adolescence).
  • [MeSH-major] Brain Neoplasms / complications. Enchondromatosis / complications. Glioblastoma / complications. Thalamic Diseases / complications


39. Thiessen B, Stewart C, Tsao M, Kamel-Reid S, Schaiquevich P, Mason W, Easaw J, Belanger K, Forsyth P, McIntosh L, Eisenhauer E: A phase I/II trial of GW572016 (lapatinib) in recurrent glioblastoma multiforme: clinical outcomes, pharmacokinetics and molecular correlation. Cancer Chemother Pharmacol; 2010 Jan;65(2):353-61
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  • [Title] A phase I/II trial of GW572016 (lapatinib) in recurrent glioblastoma multiforme: clinical outcomes, pharmacokinetics and molecular correlation.
  • PURPOSE: We undertook a phase I/II study of the EGFR/erbB2 inhibitor lapatinib in patients with recurrent glioblastoma multiforme (GBM) to determine response rate, pharmacokinetics (PK) and recommended dose in patients taking enzyme-inducing anti-epileptic drugs (EIAEDs) and to explore relationships of molecular genetics to outcome.
  • METHODS: Recurrent GBM patients taking EIAEDs were enrolled on the phase I portion (starting dose of lapatinib 1,000 mg po bid).
  • Immunohistochemical and quantitative RT PCR studies were performed on tumor to determine PTEN and EGFRvIII status, respectively.
  • RESULTS: Phase II: Of 17 patients, 4 had stable disease and 13 progressed.
  • In this small sample, EGFRvIII expression and PTEN loss did not predict a favorable subtype.
  • Overall, lapatinib did not show significant activity in GBM patients.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Quinazolines / pharmacokinetics. Quinazolines / therapeutic use
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family B. ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette, Sub-Family B, Member 1 / genetics. Adult. Aged. Anticonvulsants / therapeutic use. Cytochrome P-450 CYP3A / genetics. Enzyme Induction. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. PTEN Phosphohydrolase / biosynthesis. Polymorphism, Single Nucleotide. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / antagonists & inhibitors

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  • (PMID = 19499221.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Quinazolines; 0VUA21238F / lapatinib; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.1.3.67 / PTEN Phosphohydrolase
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40. Lu J, Kovach JS, Johnson F, Chiang J, Hodes R, Lonser R, Zhuang Z: Inhibition of serine/threonine phosphatase PP2A enhances cancer chemotherapy by blocking DNA damage induced defense mechanisms. Proc Natl Acad Sci U S A; 2009 Jul 14;106(28):11697-702
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  • We demonstrate that a small molecule inhibitor, LB-1.2, of protein phosphatase 2A (PP2A) activates Plk-1 and Akt-1 and decreases p53 abundance in tumor cells.
  • Combined with temozolomide (TMZ; a DNA-methylating chemotherapeutic drug), LB-1.2 causes complete regression of glioblastoma multiforme (GBM) xenografts without recurrence in 50% of animals (up to 28 weeks) and complete inhibition of growth of neuroblastoma (NB) xenografts.
  • Combined with another widely used anticancer drug, Doxorubicin (DOX, a DNA intercalating agent), LB-1.2 also causes marked GBM xenograft regression, whereas DOX alone only slows growth.
  • [MeSH-major] DNA Damage. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Enzymologic / drug effects. Glioblastoma / drug therapy. Neuroblastoma / drug therapy. Protein Phosphatase 2 / antagonists & inhibitors

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  • [ErratumIn] Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14734
  • (PMID = 19564615.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 NS003052-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.7.11.1 / Akt1 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / polo-like kinase 1; EC 3.1.3.16 / Protein Phosphatase 2
  • [Other-IDs] NLM/ PMC2710674
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41. Su J, Liu ZH, Zeng CH, Wei-Gong, Chen HP, Li LS: Quantitative analysis of type IV collagen subchains in the glomerular basement membrane of patients with Alport syndrome with confocal microscopy. Nephrol Dial Transplant; 2006 Jul;21(7):1838-47
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  • [Title] Quantitative analysis of type IV collagen subchains in the glomerular basement membrane of patients with Alport syndrome with confocal microscopy.
  • BACKGROUND: Alport syndrome (AS) is an inherited nephropathy characterized by glomerular basement membrane (GBM) abnormalities due to mutations in the type IV collagen genes.
  • Through immunofluorescence analysis, the absence of alpha3(IV), alpha4(IV) and alpha5(IV) chains within the GBM has been shown in the majority of AS cases.
  • In some atypical AS cases, however, staining of the GBM with antibodies against the alpha3(IV), alpha4(IV) and alpha5(IV) chains appeared normal.
  • In this study, we studied these atypical AS cases by quantitative analysis of the expression of type IV collagen subchains in GBM.
  • METHODS: Twelve patients diagnosed with AS, yet having normal staining for alpha3(IV) and alpha5(IV) chains in the GBM, were recruited.
  • Quantitative analysis of type IV collagen subchains in the GBM was performed using confocal microscopy and immunofluorescence double label techniques.
  • RESULTS: The absolute amounts of alpha3(IV), alpha4(IV) and alpha5(IV) were significantly lower in AS patients than that in normal subjects, associated with up-regulated expression of type IV collagen in GBM.
  • It was found that eight cases had decreased ratios of alpha3(IV)/IV, alpha4(IV)/IV and alpha5(IV)/IV in the GBM simultaneously; one had reduced levels of alpha3(IV)/IV and alpha5(IV)/IV but had a normal level of alpha4(IV)/IV, and one had reduced alpha3(IV)/IV with normal alpha4(IV)/IV and alpha5(IV)/IV levels.
  • The remaining two patients had normal ratios of alpha3(IV)/IV, alpha4(IV)/IV and alpha5(IV)/IV.
  • CONCLUSIONS: Confocal analysis demonstrated for the first time that the ratios of alpha3(IV)/IV, alpha4(IV)/IV and alpha5(IV)/IV in the GBM decreased in patients with AS, even though routine immunofluorescence staining for alpha(IV) chains appeared normal.
  • [MeSH-major] Collagen Type IV / chemistry. Glomerular Basement Membrane / metabolism. Kidney Glomerulus / pathology. Microscopy, Confocal / methods. Nephritis, Hereditary / diagnosis. Nephritis, Hereditary / embryology

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  • (PMID = 16574687.001).
  • [ISSN] 0931-0509
  • [Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • [ISO-abbreviation] Nephrol. Dial. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Collagen Type IV
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42. Avital I, Moreira AL, Klimstra DS, Leversha M, Papadopoulos EB, Brennan M, Downey RJ: Donor-derived human bone marrow cells contribute to solid organ cancers developing after bone marrow transplantation. Stem Cells; 2007 Nov;25(11):2903-9
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  • We identified four male patients who developed solid organ cancers (lung adenocarcinoma, laryngeal squamous cell carcinoma, glioblastoma, and Kaposi sarcoma) after myeloablation, total body irradiation, and ABMT from female donors.
  • Donor-derived malignant cells comprised 2.5%-6% of the tumor cellularity The presence of donor-derived malignant cells in solid organ cancers suggests that human bone marrow-derived stem cells have a role in solid organ cancer's carcinogenesis.


43. Wu HS, Dikman S: Segmentation and thickness measurement of glomerular basement membranes from electron microscopy images. J Electron Microsc (Tokyo); 2010;59(5):409-18
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  • An algorithm for segmentation and thickness measurement of the glomerular basement membranes (GBM) in electron microscopy kidney images is presented.
  • Differences in intensities and variations between GBM and other components in the image are employed.
  • Areas of sharp edges are either at the GBM borders or unrelated to GBM regions.
  • These non-GBM sharp edges, along with the pre-excluded regions, are used as barriers limiting the size of the fitting circles centered at a location in the image domain to form a two-dimensional function, proportional to the radius of the largest fitting circle, at the location.
  • After removing the unwanted branches, a centerline of the GBM is produced.
  • The segmentation of the GBM is then straightforward from expanding each point in the centerline to a circle of radius defined by the radius function.
  • The average of the diameters of the circles gives the average GBM thickness.
  • Results of the real GBM images are provided.
  • Visual comparisons from the superimposed GBM boundaries show that the algorithm provides accurate GBM segmentation.
  • The evaluations of the average GBM thicknesses are also compared to those from the manual tracing method.
  • [MeSH-major] Glomerular Basement Membrane / pathology. Kidney Diseases / diagnosis. Kidney Glomerulus / pathology. Kidney Transplantation / adverse effects. Microscopy, Electron, Transmission / methods

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  • (PMID = 20675608.001).
  • [ISSN] 1477-9986
  • [Journal-full-title] Journal of electron microscopy
  • [ISO-abbreviation] J Electron Microsc (Tokyo)
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Japan
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44. Del Valle L, Khalili K: Detection of human polyomavirus proteins, T-antigen and agnoprotein, in human tumor tissue arrays. J Med Virol; 2010 May;82(5):806-11
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  • [Title] Detection of human polyomavirus proteins, T-antigen and agnoprotein, in human tumor tissue arrays.
  • The viral proteins, T-antigen and Agnoprotein, contribute to the oncogenesis of JCV by associating with several tumor suppressor proteins and dysregulating signaling pathways, which results in uncontrolled cell proliferation.
  • Most notably, more than 40% of human glioblastomas and greater than 30% of colon adenocarcinomas express viral proteins.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (PMID = 20336718.001).
  • [ISSN] 1096-9071
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS055644-04; United States / NINDS NIH HHS / NS / R01 NS055644; United States / NINDS NIH HHS / NS / R01 NS055644-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Capsid Proteins; 0 / Viral Regulatory and Accessory Proteins; 0 / agnoprotein, polyomavirus
  • [Other-IDs] NLM/ NIHMS197323; NLM/ PMC2861297
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45. Sánchez-Guadarrama O, López-Sandoval H, Sánchez-Bartéz F, Gracia-Mora I, Höpfl H, Barba-Behrens N: Cytotoxic activity, X-ray crystal structures and spectroscopic characterization of cobalt(II), copper(II) and zinc(II) coordination compounds with 2-substituted benzimidazoles. J Inorg Biochem; 2009 Sep;103(9):1204-13
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  • Their cytotoxic activity was evaluated using human cancer cell lines, PC3 (prostate), MCF-7 (breast), HCT-15 (colon), HeLa (cervic-uterine), SKLU-1 (lung) and U373 (glioblastoma), showing that the zinc(II) and copper(II) compounds [Zn(2mbz)(2)Cl(2)].0.5H(2)O, [Zn(2cmbz)(2)Cl(2)].EtOH, [Cu(2cmbz)Br(2)].0.7H(2)O and [Cu(2gbz)Br(2)] had significant cytotoxic activity.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Crystallography, X-Ray. Drug Design. Drug Screening Assays, Antitumor. HeLa Cells. Humans. Inhibitory Concentration 50. Ligands. Magnetic Resonance Spectroscopy. Models, Molecular. Molecular Structure. Spectrophotometry. Spectroscopy, Near-Infrared. Structure-Activity Relationship

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  • (PMID = 19628280.001).
  • [ISSN] 1873-3344
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Chelating Agents; 0 / Growth Inhibitors; 0 / Ligands; 0 / Organometallic Compounds; 3G0H8C9362 / Cobalt; 789U1901C5 / Copper; J41CSQ7QDS / Zinc
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46. He H, Nilsson CL, Emmett MR, Ji Y, Marshall AG, Kroes RA, Moskal JR, Colman H, Lang FF, Conrad CA: Polar lipid remodeling and increased sulfatide expression are associated with the glioma therapeutic candidates, wild type p53 elevation and the topoisomerase-1 inhibitor, irinotecan. Glycoconj J; 2010 Jan;27(1):27-38
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  • We report changes in gene and polar lipid expression induced by adenovirus-delivered wild-type (wt) p53 gene and chemotherapy of U87 MG glioblastoma cells, a treatment known to trigger apoptosis and cell cycle arrest.
  • [MeSH-major] Camptothecin / analogs & derivatives. Glioma / drug therapy. Glioma / metabolism. Lipids / chemistry. Sulfoglycosphingolipids / metabolism. Topoisomerase I Inhibitors. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Gangliosides / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Genes, Neoplasm. Glycomics. Humans. Mice. Phosphatidylglycerols / metabolism

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  • (PMID = 19557511.001).
  • [ISSN] 1573-4986
  • [Journal-full-title] Glycoconjugate journal
  • [ISO-abbreviation] Glycoconj. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gangliosides; 0 / Lipids; 0 / Phosphatidylglycerols; 0 / Sulfoglycosphingolipids; 0 / Topoisomerase I Inhibitors; 0 / Tumor Suppressor Protein p53; 0H43101T0J / irinotecan; XT3Z54Z28A / Camptothecin
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47. Bubik A, Sedmak B, Novinec M, Lenarcic B, Lah TT: Cytotoxic and peptidase inhibitory activities of selected non-hepatotoxic cyclic peptides from cyanobacteria. Biol Chem; 2008 Oct;389(10):1339-46
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  • All three tested cyanopeptides show no short-term cytotoxicity in concentrations of up to 10 mum, but impair the metabolic activity of normal human astrocytes after prolonged exposure (48-96 h), whereas glioblastoma cells, tumour cells of the same type, are resistant.
  • Strong inhibition and relative selectivity of the tested cyanopeptides suggests that they are potential candidates for application in inflammatory diseases and possibly some types of cancers.
  • [MeSH-minor] Astrocytes / drug effects. Cell Line. Cell Line, Tumor. Humans. Kinetics. Leukocytes / drug effects

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  • (PMID = 18713022.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Peptides, Cyclic; 0 / Protease Inhibitors; EC 3.4.- / Peptide Hydrolases
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48. Wolańczyk M, Hułas-Bigoszewska K, Witusik-Perkowska M, Papierz W, Jaskólski D, Liberski PP, Rieske P: Imperfect oligodendrocytic and neuronal differentiation of glioblastoma cells. Folia Neuropathol; 2010;48(1):27-34
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  • [Title] Imperfect oligodendrocytic and neuronal differentiation of glioblastoma cells.
  • Previously, we have reported that glioblastoma (GBM) cells can be differentiated into cells showing neuronal, glial and non-neural (mesenchymal) phenotypes.
  • Before the differentiation the GBM cells co-expressed GFAP, CD44, Beta III tubulin, MAP2, Vimentin, Nestin and SOX-2, whereas during the exposure to a neural differentiation medium the differentiation process was arrested at the early stages and the GBM cells presented features of four phenotypes: multi-lineage, non-neural (mesenchymal), intermediate of neuronal cells and glial cells.
  • Currently, we decided to check if changes in expression of: TH (tyrosine hydroxylase, marker of catecholaminergic cells) and GABA (neurotransmitter of GABAergic neurons) and markers of oligodendrocytic cells (O4, CNP) occur during the exposure of GBM cells to the differentiation medium.
  • Our work confirmed that the neuronal differentiation of GBM was inhibited at the stage of the neuronal intermediate phenotype.
  • Moreover, we showed that the oligodendrocytic differentiation of GBM cells is very inefficient.

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  • (PMID = 20383808.001).
  • [ISSN] 1509-572X
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Culture Media; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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49. Debinski W: Drug cocktails for effective treatment of glioblastoma multiforme. Expert Rev Neurother; 2008 Apr;8(4):515-7
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  • [Title] Drug cocktails for effective treatment of glioblastoma multiforme.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Drug Delivery Systems / methods. Glioblastoma / drug therapy. Glioblastoma / metabolism

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  • (PMID = 18416653.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Number-of-references] 20
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50. Seltzer MJ, Bennett BD, Joshi AD, Gao P, Thomas AG, Ferraris DV, Tsukamoto T, Rojas CJ, Slusher BS, Rabinowitz JD, Dang CV, Riggins GJ: Inhibition of glutaminase preferentially slows growth of glioma cells with mutant IDH1. Cancer Res; 2010 Nov 15;70(22):8981-7
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  • Therefore, we inhibited glutaminase with siRNA or the small molecule inhibitor bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) and found slowed growth of glioblastoma cells expressing mutant IDH1 compared with those expressing wild-type IDH1.

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  • [Copyright] Copyright © 2010 AACR.
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  • (PMID = 21045145.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057341-20; United States / NINDS NIH HHS / NS / R01 NS052507-04; United States / NINDS NIH HHS / NS / NS052507-04; United States / NCI NIH HHS / CA / R01 CA057341; United States / NCI NIH HHS / CA / R01CA57341; United States / NCI NIH HHS / CA / CA051497-17; United States / NINDS NIH HHS / NS / R01 NS052507; United States / NCI NIH HHS / CA / R01 CA051497; United States / NCI NIH HHS / CA / R37 CA051497-17; United States / NCI NIH HHS / CA / CA057341-20; United States / NINDS NIH HHS / NS / R01NS052507; United States / NCI NIH HHS / CA / R37 CA051497; United States / NCI NIH HHS / CA / R01CA051497
  • [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 / Glutarates; 0 / Ketoglutaric Acids; 0 / Sulfides; 0 / Thiadiazoles; 0 / bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide; 2889-31-8 / alpha-hydroxyglutarate; 328-50-7 / alpha-ketoglutaric acid; 3KX376GY7L / Glutamic Acid; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.5.1.2 / Glutaminase
  • [Other-IDs] NLM/ NIHMS240941; NLM/ PMC3058858
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51. Facoetti A, Pasi F, Nano R: Some considerations for the study of TGFbeta in medium of irradiated T98G cells: activation, release and consumption. Anticancer Res; 2010 Sep;30(9):3341-4
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  • AIM: To assess the influence that the presence of latent TGFβ in the medium may have on the modulation of TGFβ1 release and on its receptor (TGFβR2) expression after irradiation of glioblastoma cells or after treatment with medium collected from γ-irradiated cells.
  • [MeSH-major] Bystander Effect / radiation effects. Culture Media, Conditioned / radiation effects. Glioblastoma / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Gamma Rays. Humans. Immunohistochemistry

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  • (PMID = 20944106.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Transforming Growth Factor beta
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52. Ji H, Wang J, Nika H, Hawke D, Keezer S, Ge Q, Fang B, Fang X, Fang D, Litchfield DW, Aldape K, Lu Z: EGF-induced ERK activation promotes CK2-mediated disassociation of alpha-Catenin from beta-Catenin and transactivation of beta-Catenin. Mol Cell; 2009 Nov 25;36(4):547-59
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  • In addition, levels of alpha-catenin S641 phosphorylation correlate with levels of ERK1/2 activity in human glioblastoma specimens and with grades of glioma malignancy.
  • This EGFR-ERK-CK2-mediated phosphorylation of alpha-catenin promotes beta-catenin transactivation and tumor cell invasion.
  • These findings highlight the importance of the crosstalk between EGFR and Wnt pathways in tumor development.


53. Tikhmyanova N, Little JL, Golemis EA: CAS proteins in normal and pathological cell growth control. Cell Mol Life Sci; 2010 Apr;67(7):1025-48
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  • Reflecting these complex functions, over-expression of CAS proteins has now been strongly linked to poor prognosis and increased metastasis in cancer, as well as resistance to first-line chemotherapeutics in multiple tumor types including breast and lung cancers, glioblastoma, and melanoma.
  • Further, CAS proteins have also been linked to additional pathological conditions including inflammatory disorders, Alzheimer's and Parkinson's disease, as well as developmental defects.

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  • (PMID = 19937461.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA06927; United States / NCI NIH HHS / CA / NIH R01 CA63366; United States / NCI NIH HHS / CA / T32 CA009035-34; United States / NCI NIH HHS / CA / CA063366-15; United States / NCI NIH HHS / CA / R01 CA113342-03; United States / NCI NIH HHS / CA / R01 CA063366; United States / NCI NIH HHS / CA / R01 CA113342; United States / NCI NIH HHS / CA / CA009035-34; United States / NCI NIH HHS / CA / R01 CA063366-15; United States / NCI NIH HHS / CA / P30 CA006927-38; United States / NCI NIH HHS / CA / CA113342-03; United States / NCI NIH HHS / CA / NIH T32 CA009035; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA006927-38; United States / NCI NIH HHS / CA / T32 CA009035
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCAR1 protein, human; 0 / Crk-Associated Substrate Protein; 0 / NEDD9 protein, human; 0 / Phosphoproteins
  • [Number-of-references] 248
  • [Other-IDs] NLM/ NIHMS164651; NLM/ PMC2836406
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54. Wiesner SM, Decker SA, Larson JD, Ericson K, Forster C, Gallardo JL, Long C, Demorest ZL, Zamora EA, Low WC, SantaCruz K, Largaespada DA, Ohlfest JR: De novo induction of genetically engineered brain tumors in mice using plasmid DNA. Cancer Res; 2009 Jan 15;69(2):431-9
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  • [Title] De novo induction of genetically engineered brain tumors in mice using plasmid DNA.
  • Spontaneous mouse models of cancer show promise to more accurately recapitulate human disease and predict clinical efficacy.
  • Transgenic mice or viral vectors have been required to generate spontaneous models of glioma, a lethal brain tumor, because nonviral gene transfer is typically transient.
  • The phenotype of tumors was influenced by the combination of oncogenes delivered, resembling human astrocytoma or glioblastoma in the majority of cases.
  • At least five different genes can be cotransfected simultaneously including reporters, allowing measurement of tumor viability by in vivo imaging.
  • This model can accelerate brain tumor research in a variety of ways such as generation of "humanized" models for high throughput drug screening and candidate gene validation with exceptional speed and flexibility.

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  • (PMID = 19147555.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R21 NS055738; United States / NINDS NIH HHS / NS / NS055738-01A2; United States / NCI NIH HHS / CA / R01CA113636-01A1; United States / NIDA NIH HHS / DA / T32 DA022616; United States / NINDS NIH HHS / NS / 1R21-NS055738-01A2; United States / NIDA NIH HHS / DA / T32DA022616; United States / NCI NIH HHS / CA / R01 CA160782; United States / NINDS NIH HHS / NS / R21 NS055738-01A2; United States / NCI NIH HHS / CA / R01 CA113636
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-98-6 / Polyethyleneimine; 9007-49-2 / DNA
  • [Other-IDs] NLM/ NIHMS79445; NLM/ PMC2701484
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55. Stupp R, Pica A, Mirimanoff RO, Michielin O: [A practical guide for the management of gliomas]. Bull Cancer; 2007 Sep;94(9):817-22
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  • Important progress has been made during the last years with the introduction of a combined treatment associating standard radiotherapy with concomitant chemotherapy using temozolomide, a novel alkylating agent.
  • In this "Practical Guide", we describe the daily practice and aim at answering some common questions in the management of patients suffering from glioblastoma, astrocytoma, oligodendroglioma and low grade glioma.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Disease Management. Glioma / therapy

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  • (PMID = 17878102.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 51
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56. Chen JH, Bian XW, Yao XH, Yang SX, Xu CR, Zhou XD, Ping YF: [Effect of nordy on FPR function of malignant human glioma cell line U87]. Yao Xue Xue Bao; 2007 Mar;42(3):257-62
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  • To investigate the effects of nordy (25 - 100 micromol x L(-1)) on the function of formylpeptide receptor (FPR) of malignant human glioma cells, human glioblastoma cell line U87 was used to detect its proliferation, migration, calcium mobilization, vascular endothelial growth factor (VEGF) mRNA and protein levels after activation of FPR by its agonist N-formyl-methionyl-leucyl-phenylalanine (fMLF).
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Calcium / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. N-Formylmethionine Leucyl-Phenylalanine / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Spectrophotometry / methods. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 17520823.001).
  • [ISSN] 0513-4870
  • [Journal-full-title] Yao xue xue bao = Acta pharmaceutica Sinica
  • [ISO-abbreviation] Yao Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Formyl Peptide; 0 / Vascular Endothelial Growth Factor A; 0 / nordy; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; 7BO8G1BYQU / Masoprocol; SY7Q814VUP / Calcium
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57. Bandyopadhyay S, Huang X, Cho H, Greig NH, Youdim MB, Rogers JT: Metal specificity of an iron-responsive element in Alzheimer's APP mRNA 5'untranslated region, tolerance of SH-SY5Y and H4 neural cells to desferrioxamine, clioquinol, VK-28, and a piperazine chelator. J Neural Transm Suppl; 2006;(71):237-47
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  • Desferrioxamine (high affinity Fe3+ chelator), (ii) clioquinol (low affinity Fe/Cu/Zn chelator), (iii) piperazine-1 (oral Fe chelator), (iv) VK-28 (oral Fe chelator), were tested for their relative modulation of APP 5' UTR directed translation of a luciferase reporter gene.
  • Iron chelation based therapeutic strategies for slowing the progression of Alzheimer's disease (and other neurological disorders that manifest iron imbalance) are discussed with regard to the relative neural toxic action of each chelator in SH-SY5Y cells and in H4 glioblastoma cells.
  • [MeSH-minor] Cell Line, Tumor. Clioquinol / pharmacology. Deferoxamine / pharmacology. Dose-Response Relationship, Drug. Glioblastoma. Humans. Models, Molecular. Neuroblastoma. Transfection / methods

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  • (PMID = 17447434.001).
  • [ISSN] 0303-6995
  • [Journal-full-title] Journal of neural transmission. Supplementum
  • [ISO-abbreviation] J. Neural Transm. Suppl.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / 5K01MH002001; United States / NIA NIH HHS / AG / AG18884; United States / NIA NIH HHS / AG / AG21081
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Iron Chelating Agents; 0 / Iron-Regulatory Proteins; 0 / RNA, Messenger; 0 / Untranslated Regions; 7BHQ856EJ5 / Clioquinol; J06Y7MXW4D / Deferoxamine
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58. Enam S, Gan DD, White MK, Del Valle L, Khalili K: Regulation of human neurotropic JCV in colon cancer cells. Anticancer Res; 2006 Mar-Apr;26(2A):833-41
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  • MATERIALS AND METHODS: Regulation of JCV was investigated in a human colon cancer cell line (SW480) and compared to a human glioblastoma cell line (U87-MG) that is permissive for JCV replication.
  • [MeSH-minor] Antigens, Viral, Tumor / genetics. Antigens, Viral, Tumor / metabolism. Antigens, Viral, Tumor / physiology. Cell Line, Tumor. DNA, Viral / genetics. DNA, Viral / metabolism. Glioblastoma / genetics. Glioblastoma / virology. Humans. Promoter Regions, Genetic. Signal Transduction. TCF Transcription Factors / genetics. TCF Transcription Factors / physiology. Transcription, Genetic. Transfection. Virus Replication. Wnt Proteins / genetics. Wnt Proteins / physiology

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  • (PMID = 16619477.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral; 0 / TCF Transcription Factors; 0 / Wnt Proteins
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59. Yao CJ, Lai GM, Chan CF, Cheng AL, Yang YY, Chuang SE: Dramatic synergistic anticancer effect of clinically achievable doses of lovastatin and troglitazone. Int J Cancer; 2006 Feb 1;118(3):773-9
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  • This synergism was found in far majority of cell lines tested including DBTRG 05 MG (glioblastoma) and CL1-0 (lung).
  • [MeSH-minor] Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Chromans / administration & dosage. Cyclin A / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Dose-Response Relationship, Drug. E2F1 Transcription Factor / metabolism. Glioblastoma / drug therapy. Glioblastoma / metabolism. HeLa Cells. Humans. Lovastatin / administration & dosage. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Male. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Phosphorylation / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Retinoblastoma Protein / metabolism. Thiazolidinediones / administration & dosage. Tumor Cells, Cultured / drug effects

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16094629.001).
  • [ISSN] 0020-7136
  • [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 / Chromans; 0 / Cyclin A; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Retinoblastoma Protein; 0 / Thiazolidinediones; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9LHU78OQFD / Lovastatin; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; I66ZZ0ZN0E / troglitazone
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60. Berger Y, Dehmlow H, Blum-Kaelin D, Kitas EA, Löffler BM, Aebi JD, Juillerat-Jeanneret L: Endothelin-converting enzyme-1 inhibition and growth of human glioblastoma cells. J Med Chem; 2005 Jan 27;48(2):483-98
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  • [Title] Endothelin-converting enzyme-1 inhibition and growth of human glioblastoma cells.
  • To evaluate this potential, we synthesized and characterized a series of low nanomolar nonpeptidic thiol-containing ECE-1 inhibitors, and evaluated their effect, as well as the effect of inhibitors for the related metalloproteases neprilysin (NEP; EC 3.4.24.11) and angiotensin-converting enzyme (ACE; EC 3.4.15.1), on human glioblastoma cell growth.
  • Only ECE-1 inhibitors inhibited DNA synthesis by human glioblastoma cells.
  • Exogenous addition of ET-1 or bigET-1 to glioblastoma cells did not counterbalance the growth inhibition elicited by ECE-1 inhibitors, suggesting that ECE-1 inhibitors block the proliferation of human glioblastoma cells most likely via a mechanism not involving extracellular production of ET-1.
  • [MeSH-minor] Carbamates / chemical synthesis. Carbamates / chemistry. Cell Line, Tumor. Cell Proliferation / drug effects. Central Nervous System Neoplasms. Drug Screening Assays, Antitumor. Endothelin-1 / pharmacology. Glioblastoma. Humans. Hydrazines / chemical synthesis. Hydrazines / chemistry. Metalloendopeptidases. Proline / analogs & derivatives. Proline / chemical synthesis. Proline / chemistry. Pyrimidines / chemical synthesis. Pyrimidines / chemistry. Pyrrolidines / chemical synthesis. Pyrrolidines / chemistry. Structure-Activity Relationship

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  • (PMID = 15658862.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / Endothelin-1; 0 / Hydrazines; 0 / Pyrimidines; 0 / Pyrrolidines; 0 / Sulfhydryl Compounds; 9DLQ4CIU6V / Proline; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.71 / endothelin-converting enzyme
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61. Hegi ME, Liu L, Herman JG, Stupp R, Wick W, Weller M, Mehta MP, Gilbert MR: Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity. J Clin Oncol; 2008 Sep 1;26(25):4189-99
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  • [Title] Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity.
  • The relative expression of MGMT in the tumor may determine response to alkylating agents, and epigenetic silencing of the MGMT gene by promoter methylation plays an important role in regulating MGMT expression in gliomas.
  • Another strategy is to deplete MGMT activity in tumor tissue using a dose-dense temozolomide schedule.
  • These alternative schedules are well tolerated; however, it remains unclear whether they are more effective than the standard dosing regimen or whether they effectively deplete MGMT activity in tumor tissue.
  • Of note, not all patients with glioblastoma having MGMT promoter methylation respond to alkylating agents, and even those who respond will inevitably experience relapse.
  • [MeSH-major] Brain Neoplasms / genetics. DNA Methylation. Glioblastoma / genetics. Glioma / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Antineoplastic Agents, Alkylating / pharmacology. CpG Islands. Gene Silencing. Humans. Maximum Tolerated Dose. Medical Oncology / methods. Models, Chemical. RNA Interference. Treatment Outcome

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  • (PMID = 18757334.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  • [Number-of-references] 86
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62. Arjona D, Bello MJ, Rey JA: EGFR intragenic loss and gene amplification in astrocytic gliomas. Cancer Genet Cytogenet; 2006 Jan 1;164(1):39-43
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  • [Title] EGFR intragenic loss and gene amplification in astrocytic gliomas.
  • We have studied EGFR gene amplification and allelic status of chromosome 7 in 68 tumors consisting of 34 WHO grade IV glioblastomas (26 primary and 8 secondary), 14 WHO grade III anaplastic astrocytomas, and 20 WHO grade II astrocytomas, by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP), quantitative PCR, and microsatellite analysis.
  • [MeSH-major] Astrocytoma / genetics. Gene Amplification. Genes, erbB-1. Loss of Heterozygosity

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  • (PMID = 16364761.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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63. Shnaper S, Desbaillets I, Brown DA, Murat A, Migliavacca E, Schluep M, Ostermann S, Hamou MF, Stupp R, Breit SN, de Tribolet N, Hegi ME: Elevated levels of MIC-1/GDF15 in the cerebrospinal fluid of patients are associated with glioblastoma and worse outcome. Int J Cancer; 2009 Dec 1;125(11):2624-30
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  • [Title] Elevated levels of MIC-1/GDF15 in the cerebrospinal fluid of patients are associated with glioblastoma and worse outcome.
  • Determination of MIC-1/GDF15 protein levels by ELISA in the CSF of a cohort of 94 patients with intracranial tumors including gliomas, meningioma and metastasis revealed significantly increased concentrations in glioblastoma patients (median, 229 pg/ml) when compared with control cohort of patients treated for non-neoplastic diseases (median below limit of detection of 156 pg/ml, p < 0.0001, Mann-Whitney test).
  • Most interestingly, patients with glioblastoma and increased CSF MIC-1/GDF15 had a shorter survival (p = 0.007, log-rank test).
  • [MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Glioblastoma / cerebrospinal fluid. Growth Differentiation Factor 15 / cerebrospinal fluid

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  • (PMID = 19521960.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GDF15 protein, human; 0 / Growth Differentiation Factor 15; 0 / RNA, Messenger
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64. Courtenay-Quirk C, Pals SL, Colfax G, McKirnan D, Gooden L, Eroğlu D: Factors associated with sexual risk behavior among persons living with HIV: gender and sexual identity group differences. AIDS Behav; 2008 Sep;12(5):685-94
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  • Sexually active participants were categorized as gay or bisexual men (GBM) (n = 545), heterosexual men (HSM, n = 223), or women (n = 214).
  • SDUAV was associated with multiple (2 or more) partners, using poppers, and lower safer sex self-efficacy among GBM.
  • These findings are consistent with prior research and facilitate our ability to target those who may be most at risk for transmitting HIV among HIV-positive GBM.

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  • (PMID = 17592764.001).
  • [ISSN] 1573-3254
  • [Journal-full-title] AIDS and behavior
  • [ISO-abbreviation] AIDS Behav
  • [Language] eng
  • [Grant] United States / PHS HHS / / PA 01190
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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65. Le Mercier M, Mathieu V, Haibe-Kains B, Bontempi G, Mijatovic T, Decaestecker C, Kiss R, Lefranc F: Knocking down galectin 1 in human hs683 glioblastoma cells impairs both angiogenesis and endoplasmic reticulum stress responses. J Neuropathol Exp Neurol; 2008 May;67(5):456-69
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  • [Title] Knocking down galectin 1 in human hs683 glioblastoma cells impairs both angiogenesis and endoplasmic reticulum stress responses.
  • Galectin (Gal) 1 is a hypoxia-regulated proangiogenic factor that also directly participates in glioblastoma cell migration.
  • To determine how Gal-1 exerts its proangiogenic effects, we investigated Gal-1 signaling in the human Hs683 glioblastoma cell line.
  • These results suggest that decreasing Gal-1 expression (e.g. through brain delivery of nonviral infusions of anti-Gal-1 siRNA in patients) can represent an additional therapeutic strategy for glioblastoma.
  • [MeSH-major] Brain Neoplasms / genetics. Endoplasmic Reticulum / genetics. Galectin 1 / genetics. Glioblastoma / genetics. Neovascularization, Pathologic / genetics. Oxidative Stress / genetics. RNA Interference / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Cell Line, Tumor. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Down-Regulation / drug effects. Down-Regulation / genetics. Endoribonucleases / drug effects. Endoribonucleases / genetics. Endoribonucleases / metabolism. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Gene Silencing / physiology. Genetic Therapy / methods. HSP40 Heat-Shock Proteins / drug effects. HSP40 Heat-Shock Proteins / genetics. HSP40 Heat-Shock Proteins / metabolism. HSP70 Heat-Shock Proteins. Humans. Membrane Proteins / drug effects. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Molecular Chaperones / drug effects. Molecular Chaperones / genetics. Molecular Chaperones / metabolism. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. Proteins / drug effects. Proteins / genetics. Proteins / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Signal Transduction / genetics. Transplantation, Heterologous

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  • (PMID = 18431251.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNAJB9 protein, human; 0 / Galectin 1; 0 / HSP40 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Membrane Proteins; 0 / Molecular Chaperones; 0 / Proteins; 0 / RNA, Small Interfering; 0 / oxygen-regulated proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.7.1.- / ERN2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.- / Endoribonucleases
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66. Baldwin RM, Garratt-Lalonde M, Parolin DA, Krzyzanowski PM, Andrade MA, Lorimer IA: Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling. Oncogene; 2006 May 11;25(20):2909-19
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  • [Title] Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling.
  • Glioblastoma multiforme is an aggressive form of brain cancer that responds poorly to chemotherapy and is generally incurable.
  • To assess the role of atypical PKC in glioblastoma cell chemoresistance, RNA interference was used to deplete human glioblastoma cells of PKCiota.
  • To screen for possible mechanisms for PKCiota-mediated chemoresistance, microarray analysis of gene expression was performed on RNA from glioblastoma cells that were either untreated or depleted of PKCiota.
  • These data show that PKCiota can confer partial resistance to cisplatin in glioblastoma cells by suppressing GMFbeta-mediated enhancement of p38 MAP kinase signaling.
  • [MeSH-major] Antineoplastic Agents / toxicity. Cell Proliferation / drug effects. Cisplatin / toxicity. Glioblastoma / drug therapy. Isoenzymes / metabolism. Protein Kinase C / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Cytoprotection. Gene Expression Profiling. Glia Maturation Factor / metabolism. Humans. Microarray Analysis. NF-kappa B / genetics. NF-kappa B / metabolism. Signal Transduction. Transfection. Tumor Cells, Cultured

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  • (PMID = 16331246.001).
  • [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 / Antineoplastic Agents; 0 / Glia Maturation Factor; 0 / Isoenzymes; 0 / NF-kappa B; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / protein kinase C lambda; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; Q20Q21Q62J / Cisplatin
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67. Tuettenberg J, Grobholz R, Seiz M, Brockmann MA, Lohr F, Wenz F, Vajkoczy P: Recurrence pattern in glioblastoma multiforme patients treated with anti-angiogenic chemotherapy. J Cancer Res Clin Oncol; 2009 Sep;135(9):1239-44
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  • [Title] Recurrence pattern in glioblastoma multiforme patients treated with anti-angiogenic chemotherapy.
  • PURPOSE: Glioblastoma multiforme is the prototype of an angiogenic tumour.
  • Here we report on the pattern of tumour recurrence in glioblastoma patients treated with an anti-angiogenic chemotherapy.
  • PATIENTS AND METHODS: A total of 32 patients with glioblastoma multiforme and a residual tumour mass after operation were treated with a continuous low-dose chemotherapy with temozolomide and a COX-II inhibitor, a presumably anti-angiogenic therapy.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 19277712.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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68. Park DM, Li J, Okamoto H, Akeju O, Kim SH, Lubensky I, Vortmeyer A, Dambrosia J, Weil RJ, Oldfield EH, Park JK, Zhuang Z: N-CoR pathway targeting induces glioblastoma derived cancer stem cell differentiation. Cell Cycle; 2007 Feb 15;6(4):467-70
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  • [Title] N-CoR pathway targeting induces glioblastoma derived cancer stem cell differentiation.
  • Nuclear localization of N-CoR is a feature of undifferentiated neural stem cells and cytoplasmic translocation of N-CoR leads to astrocytic differentiation.
  • Comparative proteomic analysis of microdissected glioblastoma multiforme (GBM) specimens and matched normal glial tissue reveals increased expression of N-CoR in GBM.
  • In GBM primary cell cultures, tumor cells with nuclear localization of N-CoR demonstrate an undifferentiated phenotype, but are subject to astroglial differentiation upon exposure to agents promoting phosphorylation of N-CoR and its subsequent translocation to the cytoplasm.
  • The identification of N-CoR in GBM provides insights into the tumorigenesis process and supports the development of differentiation-based therapeutic strategies.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / pathology. Nuclear Proteins / physiology. Repressor Proteins / physiology
  • [MeSH-minor] Biomarkers / analysis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Drug Synergism. Humans. Nuclear Receptor Co-Repressor 1. Okadaic Acid / administration & dosage. Okadaic Acid / pharmacology. Phosphorylation. Protein Transport. Signal Transduction / drug effects. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 17312396.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / NCOR1 protein, human; 0 / Nuclear Proteins; 0 / Nuclear Receptor Co-Repressor 1; 0 / Repressor Proteins; 1W21G5Q4N2 / Okadaic Acid; 5688UTC01R / Tretinoin
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69. Salunke P, Badhe P, Sharma A: Cerebellar glioblastoma multiforme with non-contiguous grade 2 astrocytoma of the temporal lobe in the same individual. Neurol India; 2010 Jul-Aug;58(4):651-3
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  • [Title] Cerebellar glioblastoma multiforme with non-contiguous grade 2 astrocytoma of the temporal lobe in the same individual.
  • Histopathology revealed grade II astrocytoma in the temporal lobe and glioblastoma multiforme in the cerebellum.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Glioblastoma / complications. Temporal Lobe / pathology

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  • (PMID = 20739816.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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70. Nakagawa T, Ido K, Sakuma T, Takeuchi H, Sato K, Kubota T: Prognostic significance of the immunohistochemical expression of O6-methylguanine-DNA methyltransferase, P-glycoprotein, and multidrug resistance protein-1 in glioblastomas. Neuropathology; 2009 Aug;29(4):379-88
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  • [Title] Prognostic significance of the immunohistochemical expression of O6-methylguanine-DNA methyltransferase, P-glycoprotein, and multidrug resistance protein-1 in glioblastomas.
  • We studied the expression of O(6)-methylguanine-DNA methyltransferase (O(6)-MGMT), P-glycoprotein (Pgp), and multidrug resistance protein-1 (MRP-1) in 23 glioblastomas using RT-PCR, methylation-specific PCR, and immunohistochemistry, and analyzed their association with overall patient survival.
  • Univariate analysis of collected data demonstrated that the expressions of O(6)-MGMT and MRP-1 detected by immunohistochemistry, in addition to the consistent factors, including preoperative Karnofsky performance scale (KPS), radical surgery, and tumor location and extension, were significant prognostic factors for the overall survival (OS) of patients with glioblastoma, who received nimustine (ACNU)-based chemotherapy in association with surgery and radiotherapy.
  • Among them, following multivariate analysis, preoperative KPS, radical surgery, tumor location, and the expression of O(6)-MGMT remained as significant prognostic factors.
  • These findings suggest that immunohistochemical analysis of O(6)-MGMT in patients with glioblastoma can be a useful method to predict the effects of chemotherapy and identify alternative chemotherapeutic regimens for O(6)-MGMT-positive patients.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. O(6)-Methylguanine-DNA Methyltransferase / biosynthesis. P-Glycoprotein / biosynthesis

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  • (PMID = 19019175.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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71. García-Morales P, Carrasco-García E, Ruiz-Rico P, Martínez-Mira R, Menéndez-Gutiérrez MP, Ferragut JA, Saceda M, Martínez-Lacaci I: Inhibition of Hsp90 function by ansamycins causes downregulation of cdc2 and cdc25c and G(2)/M arrest in glioblastoma cell lines. Oncogene; 2007 Nov 8;26(51):7185-93
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  • [Title] Inhibition of Hsp90 function by ansamycins causes downregulation of cdc2 and cdc25c and G(2)/M arrest in glioblastoma cell lines.
  • We wanted to study the effect of geldanamycin (GA) and its derivative 17-allylamino-17-demethoxygeldanamycin (17-AAG) on glioblastoma cell lines.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. CDC2-CDC28 Kinases / metabolism. Cell Division. Down-Regulation / drug effects. G2 Phase. Glioblastoma / metabolism. Glioblastoma / pathology. HSP90 Heat-Shock Proteins / physiology. Rifabutin / pharmacology. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Calpain / antagonists & inhibitors. Cell Line, Tumor. Humans

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  • (PMID = 17525741.001).
  • [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 / HSP90 Heat-Shock Proteins; 1W306TDA6S / Rifabutin; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 3.1.3.48 / CDC25C protein, human; EC 3.1.3.48 / cdc25 Phosphatases; EC 3.4.22.- / Calpain
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72. Huang J, Chen K, Gong W, Zhou Y, Le Y, Bian X, Wang JM: Receptor "hijacking" by malignant glioma cells: a tactic for tumor progression. Cancer Lett; 2008 Aug 28;267(2):254-61
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  • [Title] Receptor "hijacking" by malignant glioma cells: a tactic for tumor progression.
  • In the course of studying the role of chemoattractant receptors in tumor growth and metastasis, we discovered that highly malignant human glioblastoma and anaplastic astrocytoma specimens were stained positively for the formylpeptide receptor (FPR), which is normally expressed in myeloid cells and accounts for their chemotaxis and activation induced by bacterial peptides.
  • FPR expressed in glioblastoma cell lines mediates cell chemotaxis, proliferation and production of an angiogenic factor, vascular endothelial growth factor (VEGF), in response to agonists released by necrotic tumor cells.
  • Furthermore, FPR in glioblastoma cells activates the receptor for epidermal growth factor (EGFR) by increasing the phosphorylation of a selected tyrosine residue in the intracellular tail of EGFR.
  • Thus, FPR hijacked by human glioblastoma cells exploits the function of EGFR to promote rapid tumor progression.

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  • (PMID = 18433988.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / Z01 BC010015-12; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, Formyl Peptide; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS69649; NLM/ PMC4191659
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73. Il'yasova D, Marcello JE, McCoy L, Rice T, Wrensch M: Total dietary antioxidant index and survival in patients with glioblastoma multiforme. Cancer Causes Control; 2009 Oct;20(8):1255-60
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  • [Title] Total dietary antioxidant index and survival in patients with glioblastoma multiforme.
  • METHODS: The study population includes 814 glioblastoma multiforme cases that were newly diagnosed, histologically confirmed, aged 20 or older, and residing in the San Francisco Bay Area at diagnosis.
  • CONCLUSIONS: Although it is possible that this is a chance finding, the association between dietary antioxidants and survival in the most recently recruited patients warrants further investigations.

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  • (PMID = 19363672.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NCI NIH HHS / CA / CA52689; United States / NCI NIH HHS / CA / CA108786-04; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants
  • [Other-IDs] NLM/ NIHMS465445; NLM/ PMC3660721
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74. Jain N, Mirakhur M, Flynn P, Choudhari KA: Cutaneous metastasis from glioblastoma. Br J Neurosurg; 2005 Feb;19(1):65-8
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  • [Title] Cutaneous metastasis from glioblastoma.
  • A rare case of glioblastoma with isolated cutaneous metastasis adjacent to the scar site is described.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / secondary. Head and Neck Neoplasms / secondary. Scalp. Skin Neoplasms / secondary


75. Seiz M, Nölte I, Pechlivanis I, Freyschlag CF, Schmieder K, Vajkoczy P, Tuettenberg J: Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib. Neurosurg Rev; 2010 Jul;33(3):375-81; discussion 381
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  • [Title] Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib.
  • Glioblastoma multiforme is the most common and most malignant primary brain tumour.
  • Here, we describe extreme far-distant metastases along the neural axis of glioblastoma multiforme in four patients receiving metronomic antiangiogenic chemotherapy and review the literature to discuss possible mechanisms.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / pathology. Central Nervous System Neoplasms / secondary. Cerebrospinal Fluid. Dacarbazine / analogs & derivatives. Glioblastoma / pathology. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 20306105.001).
  • [ISSN] 1437-2320
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Pyrazoles; 0 / Sulfonamides; 7GR28W0FJI / Dacarbazine; JCX84Q7J1L / Celecoxib; YF1K15M17Y / temozolomide
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76. Kondo N, Takahashi A, Mori E, Ohnishi K, McKinnon PJ, Sakaki T, Nakase H, Ohnishi T: DNA ligase IV as a new molecular target for temozolomide. Biochem Biophys Res Commun; 2009 Oct 2;387(4):656-60
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  • [Title] DNA ligase IV as a new molecular target for temozolomide.
  • Temozolomide (TMZ) is a methylating agent used in chemotherapy against glioblastoma.
  • Cultured mouse embryonic fibroblasts were used which were deficient in DSB repair genes such as homologous recombination repair-related genes X-ray repair cross-complementing group 2 (XRCC2)and radiation sensitive mutant54 (Rad54), non-homologous end joining repair-related gene DNAligase IV (Lig4).
  • In addition, it was found that small interference RNAs (siRNA) for Lig4 efficiently enhanced cell lethality induced by TMZ in human glioblastoma A172 cells.

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  • (PMID = 19615340.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA096832-06A18121; United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / P01 CA096832-06A18121
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Enzyme Inhibitors; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 6.5.1.- / DNA Ligases; EC 6.5.1.1 / DNA ligase (ATP)
  • [Other-IDs] NLM/ NIHMS173878; NLM/ PMC2831288
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77. Pipas JM, Meyer LP, Rhodes CH, Cromwell LD, McDonnell CE, Kingman LS, Rigas JR, Fadul CE: A Phase II trial of paclitaxel and topotecan with filgrastim in patients with recurrent or refractory glioblastoma multiforme or anaplastic astrocytoma. J Neurooncol; 2005 Feb;71(3):301-5
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  • [Title] A Phase II trial of paclitaxel and topotecan with filgrastim in patients with recurrent or refractory glioblastoma multiforme or anaplastic astrocytoma.
  • PURPOSE: Therapy for high-grade gliomas remains unsatisfactory.
  • We conducted a Phase II trial of these agents in combination with filgrastim (G-CSF) in patients with recurrent or refractory glioblastoma multiforme or anaplastic astrocytoma.
  • PATIENTS AND METHODS: Adult patients with radiographic evidence of recurrent or progressive tumor following primary therapy were eligible for study.
  • Patients received paclitaxel 175 mg/m2 IV over 3 h on day 1 and topotecan 1.0 mg/m2 IV over 30 min on days 1-5.
  • Two patients (12/%) exhibited partial remission and seven patients (41/%) exhibited stable disease in response to therapy.
  • Hematologic toxicity was common with 25 /% of patients experiencing grade III or IV leukopenia despite G-CSF support.
  • CONCLUSION: Paclitaxel and topotecan with G-CSF support exhibits modest activity in adults with recurrent or refractory glioblastoma and anaplastic astrocytoma.
  • The significant hematotoxicity encountered, however, cannot justify further investigation of this combination in patients with high grade brain tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Anemia / chemically induced. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Female. Filgrastim. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Leukopenia / chemically induced. Male. Middle Aged. Paclitaxel / administration & dosage. Recombinant Proteins. Thrombocytopenia / chemically induced. Topotecan / administration & dosage. Treatment Outcome

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  • (PMID = 15735921.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 7M7YKX2N15 / Topotecan; P88XT4IS4D / Paclitaxel; PVI5M0M1GW / Filgrastim
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78. Ducray F, Dutertre G, Ricard D, Gontier E, Idbaih A, Massard C: [Advances in adults' gliomas biology, imaging and treatment]. Bull Cancer; 2010 Jan;97(1):17-36
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  • [Transliterated title] Actualités dans la biologie, l'imagerie et le traitement des gliomes de l'adulte.
  • A better understanding of gliomas biology is now leading to a combined histo-molecular classification of these tumors.
  • In anaplastic gliomas ongoing studies depend on 1p/19q codeletion status and in glioblastomas on MGMT methylation status.
  • Advanced brain tumor imaging elicits a better identification of gliomas evolutive potential of.
  • In low-grade gliomas, the importance of maximal resection and the role of chemotherapy are being increasingly recognized.
  • In glioblastomas concomitant chemoradiotherapy is the standard.
  • [MeSH-minor] Adult. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / therapy. Combined Modality Therapy / methods. Diagnostic Imaging / methods. Humans. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics. Oligodendroglioma / therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors

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  • (PMID = 20028650.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 166
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79. Patel M, Siddiqui F, Jin JY, Mikkelsen T, Rosenblum M, Movsas B, Ryu S: Salvage reirradiation for recurrent glioblastoma with radiosurgery: radiographic response and improved survival. J Neurooncol; 2009 Apr;92(2):185-91
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  • [Title] Salvage reirradiation for recurrent glioblastoma with radiosurgery: radiographic response and improved survival.
  • PURPOSE: To determine the radiographic and clinical efficacy of stereotactic single dose radiosurgery (SRS) and fractionated stereotactic radiotherapy (FSRT) as salvage therapy for glioblastoma (GBM) at recurrence.
  • METHODS: Thirty-six patients with pathologically proven recurrent GBM were treated with salvage reirradiation by either SRS or FSRT between March of 2001 and August of 2006.
  • Thirty-one patients had an initial diagnosis of GBM.
  • Of 26 patients treated with SRS, radiographic tumor response or stable disease was observed in eight (35%) patients and tumor progression was seen in 18 (65%) patients.
  • Of 10 patients treated by FSRT, radiographic tumor response or stable disease was observed in four (40%) patients and tumor progression was observed in four (40%) patients (two lost to follow-up).
  • CONCLUSION: Salvage reirradiation with SRS or FSRT for recurrent GBM results in radiographic response in a proportion of patients.
  • Survival was significantly improved among patients who either responded or had stable disease after salvage reirradiation, compared to non-responders.
  • Further study is warranted to investigate the method and time of reirradiation for recurrent GBM.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery. Neoplasm Recurrence, Local / surgery. Radiosurgery / methods. Salvage Therapy / methods

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  • (PMID = 19066727.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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80. Roth J, Constantini S, Blumenthal DT, Ram Z: The value of ventriculo-peritoneal shunting in patients with glioblastoma multiforme and ventriculomegaly. Acta Neurochir (Wien); 2008 Jan;150(1):41-6; discussion 46-7
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  • [Title] The value of ventriculo-peritoneal shunting in patients with glioblastoma multiforme and ventriculomegaly.
  • BACKGROUND: Patients with an advanced-stage glioblastoma multiforme (GBM) often show general motor, gait, and cognitive deterioration.
  • Distinction between tumour patients who have dilated fluid spaces as a consequence of tissue loss from surgery or treatment, and those who have a symptomatic hydrocephalic process, one who may gain benefit from insertion of a ventriculo-peritoneal shunt, is an important clinical challenge.
  • METHODS: From a series of 530 GBM patients treated by a single surgeon (ZR), we retrospectively reviewed 16 patients with advanced-stage GBM who had presented with non-obstructive ventriculomegaly and clinical deterioration not explained by progressive disease.
  • Each had been treated by insertion of a ventriculo- peritoneal shunt (VPS).
  • CONCLUSIONS: Insertion of a ventriculo-peritoneal shunt can improve cognitive and motor function in a small subset of patients with advanced-stage glioblastoma multiforme and ventriculomegaly.
  • [MeSH-major] Glioblastoma / surgery. Ventriculoperitoneal Shunt / methods

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  • (PMID = 18180865.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
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81. Chen KT, Lin JD, Liou MJ, Weng HF, Chang CA, Chan EC: An aberrant autocrine activation of the platelet-derived growth factor alpha-receptor in follicular and papillary thyroid carcinoma cell lines. Cancer Lett; 2006 Jan 18;231(2):192-205
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  • Platelet-derived growth factor receptor (PDGFR) can bind to its ligand and consequently possess a kinase activity, and which is associated with the carcinogenesis of different cell types, including astrocytomas, oligodendrogliomas, and glioblastoma.
  • [MeSH-minor] Blotting, Western. Cell Proliferation / drug effects. DNA, Complementary. Enzyme Activation. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Phosphorylation. Platelet-Derived Growth Factor / genetics. Platelet-Derived Growth Factor / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured. Tyrosine / metabolism. Tyrphostins / pharmacology


82. Struck RF, Waud WR: Thiolo-, thiono- and dithiocarbonate and thiocarbamate derivatives of demethylpenclomedine as novel anticancer agents. Cancer Chemother Pharmacol; 2006 Jan;57(2):180-4
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  • PURPOSE: The purpose of this investigation was to synthesize a series of thiolo-, thiono- and dithiocarbonate and thiocarbamate derivatives of 4-demethylpenclomedine (DM-PEN), the major plasma metabolite of penclomedine (PEN) in patients observed subsequently to be an active antitumor agent and non-neurotoxic in a rat model, in order to compare their antitumor activity with that of DM-PEN.
  • METHODS: Derivatives were prepared from DM-PEN and evaluated in vivo against human MX-1 breast tumor xenografts implanted in the mammary fat pad, several of which were also evaluated against human brain tumor xenografts.
  • RESULTS: Thiolocarbonate and thiocarbamate derivatives were found to be superior to DM-PEN against MX-1 tumor and modestly active against glioblastoma.
  • CONCLUSION: The activity of the thiolocarbonates and thiocarbamates against human tumor xenografts in vivo suggests consideration of these two series of derivatives of DM-PEN for clinical development.

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  • (PMID = 16096790.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA34200
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / Carbonates; 0 / Picolines; 108030-77-9 / penclomedine
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83. Wolf A, Agnihotri S, Guha A: Targeting metabolic remodeling in glioblastoma multiforme. Oncotarget; 2010 Nov;1(7):552-62
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  • [Title] Targeting metabolic remodeling in glioblastoma multiforme.
  • A key aberrant biological difference between tumor cells and normal differentiated cells is altered metabolism, whereby cancer cells acquire a number of stable genetic and epigenetic alterations to retain proliferation, survive under unfavorable microenvironments and invade into surrounding tissues.
  • This review discusses the role of key metabolic enzymes and their association with aerobic glycolysis in Glioblastoma Multiforme (GBM), an aggressive, highly glycolytic and deadly brain tumor.
  • Targeting key metabolic enzymes involved in modulating the "Warburg Effect" may provide a novel therapeutic approach either singularly or in combination with existing therapies in GBMs.

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  • (PMID = 21317451.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] ENG
  • [Grant] None / None / / 83392; Canada / Canadian Institutes of Health Research / / 84294; Canada / Canadian Institutes of Health Research / / 83392; None / None / / 84294; Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Enzymes
  • [Keywords] NOTNLM ; cancer / drug discovery / oncotarget / stem cells / wnt
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84. Pellettieri L, H-Stenstam B, Rezaei A, Giusti V, Sköld K: An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme. Acta Neurol Scand; 2008 Mar;117(3):191-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme.
  • Objectives - To explore the use of boron neutron capture therapy (BNCT) for patients with glioblastoma multiforme (GBM), recurring after surgery and conventional radiotherapy (photon radiotherapy).
  • Materials and Methods - Boron uptake in recurrent GBM was measured for four patients.
  • BNCT was well tolerated and quality of life remained stable until tumor progression for all 12 patients.
  • No correlation was found between survival times and minimum tumor dose and number of radiation fields.
  • Conclusions - Boron neutron capture therapy, with the prolonged procedure for infusion, is at least as effective as other radiation therapies for recurrent GBM and is delivered in one treatment session, with low radiation dose to the healthy brain.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Adult. Aged. Body Weight. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Radiotherapy Dosage. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • (PMID = 18297764.001).
  • [ISSN] 1600-0404
  • [Journal-full-title] Acta neurologica Scandinavica
  • [ISO-abbreviation] Acta Neurol. Scand.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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85. Harris DA, Pellikka R, Gasser O, Blaeuenstein P, Waibel R, Schubiger PA, King SW, Parseghian MH: In-line radiolabeling: a novel continuous-flow system for commercial-scale protein labeling. J Nucl Med; 2009 Jul;50(7):1178-86
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