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1. Kim EL, Wüstenberg R, Rübsam A, Schmitz-Salue C, Warnecke G, Bücker EM, Pettkus N, Speidel D, Rohde V, Schulz-Schaeffer W, Deppert W, Giese A: Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells. Neuro Oncol; 2010 Apr;12(4):389-400
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  • Glioblastoma is the most common malignant brain tumor in adults.
  • Induction of apoptosis is one of the mechanisms underlying the effects of chloroquine on suppressing glioma cell growth and viability. siRNA-mediated downregulation of p53 in wild-type but not mutant p53 glioblastoma cells substantially impaired chloroquine-induced apoptosis.
  • In addition to its p53-activating effects, chloroquine may also inhibit glioma cell growth via p53-independent mechanisms.
  • [MeSH-major] Antimalarials / pharmacology. Apoptosis / drug effects. Brain Neoplasms / pathology. Chloroquine / pharmacology. Glioma / pathology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation. Humans. Mice. Mice, Nude. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Tumor Cells, Cultured

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  • (PMID = 20308316.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimalarials; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 886U3H6UFF / Chloroquine
  • [Other-IDs] NLM/ PMC2940600
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2. Müller S, Kunkel P, Lamszus K, Ulbricht U, Lorente GA, Nelson AM, von Schack D, Chin DJ, Lohr SC, Westphal M, Melcher T: A role for receptor tyrosine phosphatase zeta in glioma cell migration. Oncogene; 2003 Oct 2;22(43):6661-8
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  • [Title] A role for receptor tyrosine phosphatase zeta in glioma cell migration.
  • Glioblastomas (GBM) are the most frequent and malignant human brain tumor type.
  • Typically striking in adulthood, tumor progression is rapid, relentless, and ultimately leads to the patient's death within a year of diagnosis.
  • The identification of transcriptionally regulated genes can lead to the discovery of targets for antibody or small-molecule-mediated therapy, as well as diagnostic markers.
  • We prepared cDNA arrays that are specifically enriched for genes expressed in human brain tumors and profiled gene expression patterns in 14 individual tumor samples.
  • Out of 25,000 clones arrayed, greater than 200 genes were found transcriptionally induced in glioblastomas compared to normal human brain tissue including the receptor tyrosine phosphatasezeta (RPTPzeta) and one of its ligands, pleiotrophin (Ptn).
  • We confirmed by Northern blot analysis and immunohistochemistry that RPTPzeta is enriched in tumor samples.
  • Knockdown of RPTPzeta by RNA interference studies established a functional role of RPTPzeta in cell migration.
  • Our results suggest a novel function for RPTPzeta in regulating glioblastoma cell motility and point to the therapeutic utility of RPTPzeta as a target for antibody-mediated therapy of brain tumors.
  • [MeSH-major] Brain Neoplasms / enzymology. Glioma / enzymology. Protein Tyrosine Phosphatases / metabolism. Protein Tyrosine Phosphatases / physiology
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Brain / metabolism. Cell Movement. DNA, Complementary / metabolism. Dose-Response Relationship, Drug. Gene Expression Regulation. Humans. Immunohistochemistry. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Protein Structure, Tertiary. RNA / metabolism. RNA Interference. RNA, Messenger / metabolism. Receptor-Like Protein Tyrosine Phosphatases, Class 5. Transcription, Genetic. Tumor Cells, Cultured

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  • (PMID = 14555979.001).
  • [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 / DNA, Complementary; 0 / RNA, Messenger; 63231-63-0 / RNA; EC 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
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3. Saito T, Hama S, Izumi H, Yamasaki F, Kajiwara Y, Matsuura S, Morishima K, Hidaka T, Shrestha P, Sugiyama K, Kurisu K: Centrosome amplification induced by survivin suppression enhances both chromosome instability and radiosensitivity in glioma cells. Br J Cancer; 2008 Jan 29;98(2):345-55
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  • In this study, we examined the effect of survivin suppression on radiosensitivity in malignant glioma cells, while focusing on centrosome aberration and chromosome instability (CIN).
  • We suppressed survivin by small interfering RNA transfection, and examined the radiosensitivity using a clonogenic assay and a trypan blue exclusion assay in U251MG (p53 mutant) and D54MG (p53 wild type) cells.
  • This cell death was accompanied by an increased degree of aneuploidy, suggesting mitotic cell death.
  • [MeSH-major] Centrosome / drug effects. Chromosomal Instability / drug effects. Glioma / pathology. Microtubule-Associated Proteins / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. RNA, Small Interfering / pharmacology. Radiation Tolerance / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Cycle / radiation effects. Cell Death / drug effects. Cell Death / radiation effects. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Down-Regulation / drug effects. Humans. Inhibitor of Apoptosis Proteins. Radiation-Sensitizing Agents / pharmacology. Transfection

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  • (PMID = 18195712.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / Radiation-Sensitizing Agents
  • [Other-IDs] NLM/ PMC2361434
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4. Berney DM, Shamash J, Gaffney J, Jordan S, Oliver RT: DNA topoisomerase I and II expression in drug resistant germ cell tumours. Br J Cancer; 2002 Sep 9;87(6):624-9
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  • [Title] DNA topoisomerase I and II expression in drug resistant germ cell tumours.
  • A small number of testicular germ cell tumours are refractory to current chemotherapy regimens.
  • DNA topoisomerase I is the target for several new drugs and a potential candidate treatment for chemorefractory germ cell tumours.
  • DNA topoisomerase II alpha is the target for etoposide, which is currently used regularly in germ cell tumour treatment.
  • The expression of DNA topoisomerase I and II alpha were therefore assessed immunohistochemically in a range of testicular tumours, especially those with persistent malignant elements on retroperitoneal lymph node dissection.
  • These results suggest that topoisomerase I inhibitors may be useful in chemorefractory germ cell tumours, especially yolk sac tumours and where there are unresectable residual teratoma, mature deposits.
  • [MeSH-major] Carcinoma, Embryonal / metabolism. DNA Topoisomerases, Type I / metabolism. DNA Topoisomerases, Type II / metabolism. Drug Resistance, Neoplasm. Seminoma / metabolism. Teratoma / metabolism. Testicular Neoplasms / metabolism

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  • (PMID = 12237772.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 6PLQ3CP4P3 / Etoposide; EC 5.99.1.2 / DNA Topoisomerases, Type I; EC 5.99.1.3 / DNA Topoisomerases, Type II; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2364243
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5. Johansson G, Mahller YY, Collins MH, Kim MO, Nobukuni T, Perentesis J, Cripe TP, Lane HA, Kozma SC, Thomas G, Ratner N: Effective in vivo targeting of the mammalian target of rapamycin pathway in malignant peripheral nerve sheath tumors. Mol Cancer Ther; 2008 May;7(5):1237-45
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  • [Title] Effective in vivo targeting of the mammalian target of rapamycin pathway in malignant peripheral nerve sheath tumors.
  • Malignant peripheral nerve sheath tumors (MPNST) are chemoresistant sarcomas with poor 5-year survival that arise in patients with neurofibromatosis type 1 (NF1) or sporadically.
  • We tested three drugs for single and combinatorial effects on collected MPNST cell lines and in MPNST xenografts.
  • The mammalian target of rapamycin complex 1 inhibitor RAD001 (Everolimus) decreased growth 19% to 60% after 4 days of treatment in NF1 and sporadic-derived MPNST cell lines.
  • Treatment of subcutaneous sporadic MPNST cell xenografts with RAD001 significantly, but transiently, delayed tumor growth, and decreased vessel permeability within xenografts.
  • RAD001 combined with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib caused additional inhibitory effects on growth and apoptosis in vitro, and a small but significant additional inhibitory effect on MPNST growth in vivo that were larger than the effects of RAD001 with doxorubicin.
  • The preclinical tests described allow rapid screening strata for drugs that block MPNST growth, prior to tests in more complex models, and should be useful to identify drugs that synergize with RAD001.

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  • (PMID = 18483311.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS028840-09; United States / NINDS NIH HHS / NS / R01 NS028840; United States / NINDS NIH HHS / NS / R01 NS028840-09; United States / NINDS NIH HHS / NS / R01 NS28840-17
  • [Publication-type] Comparative Study; 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; 0 / Immunosuppressive Agents; 0 / Quinazolines; 9HW64Q8G6G / Everolimus; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.1 / ribosomal protein S6 kinase, 70kD, polypeptide 2; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS187346; NLM/ PMC2855168
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6. Carapancea M, Alexandru O, Fetea AS, Dragutescu L, Castro J, Georgescu A, Popa-Wagner A, Bäcklund ML, Lewensohn R, Dricu A: Growth factor receptors signaling in glioblastoma cells: therapeutic implications. J Neurooncol; 2009 Apr;92(2):137-47
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  • Our results demonstrated that appreciable levels of these proteins could be detected in the analysed GB cell lines, except for a low level of PDGFR and ERK1/2 expression in one GB cell line.
  • The small molecule inhibitors towards IGF-1R, PDGFR, PI3-K and ERK1/2 respectively, have only modest or no anti-tumour activity on GB cells and therefore their combination with other therapy modalities was analysed.
  • The interaction between small inhibitors and radiation was mostly additive or sub-additive; synergistic interaction was found in five of forty analysed combinations.
  • Our results showed that GB cells are in general resistant to treatment and illustrate the difficulties in predicting the treatment response in malignant gliomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Receptors, Growth Factor / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Proliferation / radiation effects. Flow Cytometry. Humans. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 1 / radiation effects. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Mitogen-Activated Protein Kinase 3 / radiation effects. Phosphatidylinositol 3-Kinases / drug effects. Phosphatidylinositol 3-Kinases / metabolism. Phosphatidylinositol 3-Kinases / radiation effects. Receptor, IGF Type 1 / drug effects. Receptor, IGF Type 1 / metabolism. Receptor, IGF Type 1 / radiation effects. Receptors, Platelet-Derived Growth Factor / drug effects. Receptors, Platelet-Derived Growth Factor / metabolism. Receptors, Platelet-Derived Growth Factor / radiation effects

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  • (PMID = 19043776.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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7. Turbyville TJ, Gürsel DB, Tuskan RG, Walrath JC, Lipschultz CA, Lockett SJ, Wiemer DF, Beutler JA, Reilly KM: Schweinfurthin A selectively inhibits proliferation and Rho signaling in glioma and neurofibromatosis type 1 tumor cells in a NF1-GRD-dependent manner. Mol Cancer Ther; 2010 May;9(5):1234-43
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  • [Title] Schweinfurthin A selectively inhibits proliferation and Rho signaling in glioma and neurofibromatosis type 1 tumor cells in a NF1-GRD-dependent manner.
  • Neurofibromatosis type 1 (NF1) is the most common genetic disease affecting the nervous system.
  • Natural products represent an opportunity to develop new therapies, as they have been evolutionarily selected to play targeted roles in organisms.
  • Schweinfurthin A is a prenylated stilbene natural product that has previously shown specific inhibitory activity against brain and hematopoietic tumor lines.
  • We show that patient-derived GBM and NF1 malignant peripheral nerve sheath tumor (MPNST) lines, as well as tumor lines derived from the Nf1-/+;Trp53-/+ (NPcis) mouse model of astrocytoma and MPNST are highly sensitive to inhibition by schweinfurthin A and its synthetic analogs.
  • In contrast, primary mouse astrocytes are resistant to the growth inhibitory effects of schweinfurthin A, suggesting that schweinfurthin A may act specifically on tumor cells.
  • In summary, we have identified a class of small molecules that specifically inhibit growth of cells from both central and peripheral nervous system tumors and seem to act on NF1-deficient cells through cytoskeletal reorganization correlating to changes in Rho signaling.

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  • (PMID = 20442305.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / Intramural NIH HHS / / Z01 BC010541-06; United States / PHS HHS / / HHSN261200800001E
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / Stilbenes; 0 / schweinfurthin A; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS187633; NLM/ PMC3268685
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8. Inoue A, Takahashi H, Harada H, Kohno S, Ohue S, Kobayashi K, Yano H, Tanaka J, Ohnishi T: Cancer stem-like cells of glioblastoma characteristically express MMP-13 and display highly invasive activity. Int J Oncol; 2010 Nov;37(5):1121-31
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  • Glioblastoma is the most malignant type of primary brain tumor that has been shown to contain a small population of cancer stem cells.
  • Recent studies have suggested that cancer stem cells cause tumor recurrence based on their resistance to radiotherapy and chemotherapy.
  • In this study, we isolated tumor sphere-forming cells bearing cancer stem-like characteristics such as self-renewal, multipotency, drug-resistibility, and in vivo tumorigenicity, from the human glioblastoma cell line U251, under serum-free neural stem cell culture condition, and assessed their migratory and invasive ability.
  • These cells showed enhanced migratory and invasive ability on both Matrigel and organotypic brain slices compared to parental U251 cells.
  • The expression of matrix metalloproteinase (MMP)-13 was specifically expressed in tumor sphere-forming cells derived from U251 and primary human glioma cells.
  • [MeSH-major] Glioblastoma / enzymology. Glioblastoma / pathology. Matrix Metalloproteinase 13 / biosynthesis. Neoplasm Invasiveness / pathology. Neoplastic Stem Cells / enzymology
  • [MeSH-minor] Animals. Brain Neoplasms / enzymology. Brain Neoplasms / pathology. Cell Line, Tumor. Cell Movement / physiology. Cell Separation. Flow Cytometry. Gene Knockdown Techniques. Humans. Immunohistochemistry. Mice. Mice, Inbred BALB C. Neoplasms, Experimental / enzymology. Neoplasms, Experimental / pathology. Organ Culture Techniques. Rats. Transplantation, Heterologous

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  • (PMID = 20878060.001).
  • [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] EC 3.4.24.- / Matrix Metalloproteinase 13
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9. Yue X, Lan F, Yang W, Yang Y, Han L, Zhang A, Liu J, Zeng H, Jiang T, Pu P, Kang C: Interruption of β-catenin suppresses the EGFR pathway by blocking multiple oncogenic targets in human glioma cells. Brain Res; 2010 Dec 17;1366:27-37
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  • Malignant gliomas are the most common type of intrinsic central nervous system (CNS) tumors with high mortality and morbidity.
  • β-catenin is overexpressed in human glioblastoma and knockdown of β-catenin inhibits glioblastoma cell proliferation and invasive ability, and induces apoptotic cell death.
  • Furthermore, treating the nude mice carrying established subcutaneous LN229 gliomas with siRNA targeting β-catenin intratumorally also delayed the tumor growth.
  • We utilized text-mining of MEDLINE abstracts with natural language processing to establish the β-catenin biologic association network, and identified several interactions of this network with the EGFR pathway.
  • These results suggest that the Wnt/β-catenin pathway regulates glioma cell proliferation and invasion, in part via the EGFR pathway.
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Down-Regulation / drug effects. Down-Regulation / genetics. Flow Cytometry / methods. Humans. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. STAT3 Transcription Factor / genetics. STAT3 Transcription Factor / metabolism

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20969832.001).
  • [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 / Carcinogens; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / beta Catenin; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.24.24 / Matrix Metalloproteinase 2
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10. Batista LF, Roos WP, Christmann M, Menck CF, Kaina B: Differential sensitivity of malignant glioma cells to methylating and chloroethylating anticancer drugs: p53 determines the switch by regulating xpc, ddb2, and DNA double-strand breaks. Cancer Res; 2007 Dec 15;67(24):11886-95
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  • [Title] Differential sensitivity of malignant glioma cells to methylating and chloroethylating anticancer drugs: p53 determines the switch by regulating xpc, ddb2, and DNA double-strand breaks.
  • Glioblastoma multiforme is the most severe form of brain cancer.
  • First line therapy includes the methylating agent temozolomide and/or the chloroethylating nitrosoureas [1-(2-chloroethyl)-1-nitrosourea; CNU] nimustine [1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea; ACNU], carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], or lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU].
  • The mechanism of cell death after CNU treatment is largely unknown.
  • Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.
  • However, contrary to what we observed previously for temozolomide, chloroethylating drugs are more toxic for p53-mutated glioma cells and induce both apoptosis and necrosis.
  • Expression analysis revealed an up-regulation of xpc and ddb2 mRNA in response to ACNU in U87MG but not U138MG cells, indicating p53 regulates a pathway that involves these DNA repair proteins.
  • The data suggest that p53 has opposing effects in gliomas treated with methylating or chloroethylating agents and, therefore, the p53 status should be taken into account when deciding which therapeutic drug to use.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Damage / genetics. DNA, Neoplasm / genetics. DNA-Binding Proteins / genetics. Glioblastoma / drug therapy. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Cell Line, Tumor. DNA Methylation. Humans. RNA, Neoplasm / genetics. RNA, Small Interfering / genetics

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  • (PMID = 18089819.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DDB2 protein, human; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 156533-34-5 / XPC protein, human
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11. Tran TT, Uhl M, Ma JY, Janssen L, Sriram V, Aulwurm S, Kerr I, Lam A, Webb HK, Kapoun AM, Kizer DE, McEnroe G, Hart B, Axon J, Murphy A, Chakravarty S, Dugar S, Protter AA, Higgins LS, Wick W, Weller M, Wong DH: Inhibiting TGF-beta signaling restores immune surveillance in the SMA-560 glioma model. Neuro Oncol; 2007 Jul;9(3):259-70
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  • Transforming growth factor-beta (TGF-beta) is a proinvasive and immunosuppressive cytokine that plays a major role in the malignant phenotype of gliomas.
  • SX-007, an orally active, small-molecule TGF-betaRI kinase inhibitor, was evaluated for its therapeutic potential in cell culture and in an in vivo glioma model.
  • SX-007 dosed at 20 mg/kg p.o. once daily (q.d.) modulated TGF-beta signaling in the tumor and improved the median survival.
  • Strikingly, approximately 25% of the treated animals were disease-free at the end of the study.
  • Survival benefit is due to reduced tumor invasion and reversal of TGF-beta-mediated immune suppression, allowing for rejection of the tumor.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioma / drug therapy. Immunologic Surveillance / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Receptors, Transforming Growth Factor beta / antagonists & inhibitors. Signal Transduction / drug effects. Transforming Growth Factor beta / drug effects
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoblotting. Immunohistochemistry. Mice. Reverse Transcriptase Polymerase Chain Reaction. Xenograft Model Antitumor Assays

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  • (PMID = 17522330.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC1907409
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12. Thomas CR Jr, Berkey BA, Minsky BD, Gaspar LE, Herskovic A, Rich TA, Gunderson LL: Recursive partitioning analysis of pretreatment variables of 416 patients with locoregional esophageal cancer treated with definitive concomitant chemoradiotherapy on Intergroup and Radiation Therapy Oncology Group trials. Int J Radiat Oncol Biol Phys; 2004 Apr 1;58(5):1405-10
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  • PURPOSE: To analyze the relative contributions of uniformly collected pretreatment patient- and tumor-related variables to survival and to identify the terminal nodes via recursive partitioning analysis (RPA) that could be used as a stratification variable for future Phase III trials.
  • The following pretreatment factors were evaluated: histologic type, age, weight loss, Karnofsky performance status, gender, race, T stage, tumor location, tumor size, N stage, and degree of dysphagia.
  • CONCLUSION: Unlike our experience with malignant glioma, brain metastases, and locally advanced non-small-cell lung cancer, RPA failed to identify novel prognostic information that could be incorporated into the stratification scheme of future chemoradiotherapy trials for esophageal cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Cisplatin / administration & dosage. Clinical Trials, Phase III as Topic. Combined Modality Therapy. Female. Fluorouracil / administration & dosage. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 15050316.001).
  • [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 / U10 CA21661; United States / NCI NIH HHS / CA / U10 CA32115; United States / NCI NIH HHS / CA / U10 CA37422
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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13. Roth P, Kissel M, Herrmann C, Eisele G, Leban J, Weller M, Schmidt F: SC68896, a novel small molecule proteasome inhibitor, exerts antiglioma activity in vitro and in vivo. Clin Cancer Res; 2009 Nov 1;15(21):6609-18
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  • [Title] SC68896, a novel small molecule proteasome inhibitor, exerts antiglioma activity in vitro and in vivo.
  • Here, we characterized the antitumor properties of SC68896, a novel small molecule proteasome inhibitor.
  • EXPERIMENTAL DESIGN: Different tumor cell lines were tested by crystal violet staining for sensitivity to SC68896, given alone or in combination with death ligands.
  • The molecular mechanisms mediating SC68896-induced cell death and changes in cell cycle progression were assessed by immunoblot and flow cytometry.
  • RESULTS: SC68896 inhibits the proliferation of cell lines of different types of cancer, including malignant glioma.
  • Exposure of LNT-229 glioma cells to SC68896 results in a concentration- and time-dependent inhibition of the proteasome, with a consequent accumulation of p21 and p27 proteins, cell cycle arrest, caspase cleavage, and induction of apoptosis.
  • Using RNA interference, we show that the effect of SC68896 on glioma cells is facilitated by wild-type p53.
  • SC68896 sensitizes glioma cells to tumor necrosis factor-related apoptosis-inducing ligand and CD95 ligand and up-regulates the cell surface expression of the tumor necrosis factor-related apoptosis-inducing ligand receptor cell death receptors 4 and 5, which may contribute to this sensitization.
  • It may represent a novel prototype agent for the treatment of malignant gliomas and warrants clinical evaluation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Proteasome Inhibitors. Semicarbazones / therapeutic use
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Fas Ligand Protein / metabolism. Humans. Mice. Mice, Nude. TNF-Related Apoptosis-Inducing Ligand / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19825946.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fas Ligand Protein; 0 / Proteasome Inhibitors; 0 / SC 68896; 0 / Semicarbazones; 0 / TNF-Related Apoptosis-Inducing Ligand
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14. Dey N, Crosswell HE, De P, Parsons R, Peng Q, Su JD, Durden DL: The protein phosphatase activity of PTEN regulates SRC family kinases and controls glioma migration. Cancer Res; 2008 Mar 15;68(6):1862-71
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  • Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is mutated or lost in 60% to 70% of advanced gliomas and is associated with malignant phenotypic changes such as migration, which contribute to the morbidity and mortality of this disease.
  • Most of the tumor suppressor function of PTEN has been attributed to its ability to dephosphorylate the second messenger, phosphatidylinositol 3,4,5-triphosphate, resulting in the biological control of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway.
  • Despite recent work suggesting that the protein phosphatase activity of PTEN controls glioma cell migration, the mechanisms by which this occurs are unclear.
  • Herein, we show using glioma cell lines (U87MG and U373MG) stably transfected with wild-type PTEN or catalytically altered mutants of PTEN that PTEN controls integrin-directed migration in a lipid phosphatase, PI3K/AKT-independent manner.
  • Furthermore, studying vitronectin-directed migration using (a) Fyn small interfering RNA and (b) astrocytes from Fyn heterozygous (+/-) mice, Pten heterozygous (+/-) mice, Pten and Fyn double heterozygous (+/-) mice, or Fyn knockout (-/-) mice confirmed a role of FYN in alpha(v) integrin-mediated haptotaxis in glial cells.
  • [MeSH-major] Brain Neoplasms / enzymology. Brain Neoplasms / pathology. Cell Movement / physiology. Glioma / enzymology. Glioma / pathology. PTEN Phosphohydrolase / metabolism. src-Family Kinases / metabolism
  • [MeSH-minor] Animals. Astrocytes / drug effects. Astrocytes / enzymology. Cell Line, Tumor. Humans. Integrin alphaVbeta3 / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-fyn / metabolism. Vitronectin / pharmacology. rac1 GTP-Binding Protein / metabolism


15. Lui VC, Lung SS, Pu JK, Hung KN, Leung GK: Invasion of human glioma cells is regulated by multiple chloride channels including ClC-3. Anticancer Res; 2010 Nov;30(11):4515-24
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  • BACKGROUND: Glioblastoma is a type of highly malignant primary brain tumour.
  • MATERIALS AND METHODS: The expression of chloride channels (ClCs) and metalloproteinase-2 (MMP-2) was studied in two human glioma cell lines (STTG1 and U251-MG).
  • Glioma cell invasion was markedly but not completely inhibited by ClC-3 and MMP-2 siRNA knockdown, and by chlorotoxin treatment.
  • CONCLUSION: ClCs are crucial in glioma cell migration and invasion.
  • Blockade of a single ClC, however, is not sufficient to achieve complete inhibition of glioma cell invasion, suggesting that any future therapy should be targeted at pharmacological blockade of multiple ClCs.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Movement / drug effects. Chloride Channels / physiology. Glioma / pathology. Matrix Metalloproteinase 2 / physiology
  • [MeSH-minor] Blotting, Western. Cell Adhesion / drug effects. Cell Proliferation / drug effects. Fluorescent Antibody Technique. Gene Silencing / physiology. Humans. Immunoenzyme Techniques. Neoplasm Invasiveness. Neurotoxins / pharmacology. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Scorpion Venoms / pharmacology. Tumor Cells, Cultured

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  • (PMID = 21115901.001).
  • [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 / Chloride Channels; 0 / Chlorotoxin; 0 / ClC-3 channel; 0 / Neurotoxins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Scorpion Venoms; EC 3.4.24.24 / Matrix Metalloproteinase 2
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16. Shingu T, Fujiwara K, Bögler O, Akiyama Y, Moritake K, Shinojima N, Tamada Y, Yokoyama T, Kondo S: Inhibition of autophagy at a late stage enhances imatinib-induced cytotoxicity in human malignant glioma cells. Int J Cancer; 2009 Mar 1;124(5):1060-71
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  • [Title] Inhibition of autophagy at a late stage enhances imatinib-induced cytotoxicity in human malignant glioma cells.
  • Malignant gliomas are common primary tumors of the central nervous system.
  • The prognosis of patients with malignant glioma is poor in spite of current intensive therapy and thus novel therapeutic modalities are necessary.
  • Imatinib mesylate, a tyrosine kinase inhibitor, is effective in the therapy of tumors including leukemias but not as a monotherapy for malignant glioma.
  • The outcome of autophagy manipulation, however, seems to depend on the autophagy initiator, the combined stimuli, the extent of cellular damage and the type of cells, and it is not yet fully understood how we should modulate autophagy to augment efficacy of each anticancer therapy.
  • In this study, we examined the effect of imatinib with or without different types of autophagy inhibitors on human malignant glioma cells.
  • Imatinib inhibited the viability of U87-MG and U373-MG cells in a dose dependent manner and caused nonapoptotic autophagic cell death.
  • Suppression of imatinib-induced autophagy by 3-methyladenine or small interfering RNA against Atg5, which inhibit autophagy at an early stage, attenuated the imatinib-induced cytotoxicity.
  • Our findings suggest that therapeutic efficiency of imatinib for malignant glioma may be augmented by inhibition of autophagy at a late stage, and that appropriate modulation of autophagy may sensitize tumor cells to anticancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Autophagy / drug effects. Bicyclo Compounds, Heterocyclic / pharmacology. Brain Neoplasms / drug therapy. Glioma / drug therapy. Macrolides / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Adenine / analogs & derivatives. Adenine / pharmacology. Benzamides. Cell Line, Tumor. Cisplatin / pharmacology. Extracellular Signal-Regulated MAP Kinases / physiology. Humans. Imatinib Mesylate. MAP Kinase Signaling System / drug effects. Membrane Potential, Mitochondrial / drug effects. Microtubule-Associated Proteins / antagonists & inhibitors. Paclitaxel / pharmacology

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  • (PMID = 19048625.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATG5 protein, human; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Bicyclo Compounds, Heterocyclic; 0 / Macrolides; 0 / Microtubule-Associated Proteins; 0 / Piperazines; 0 / Pyrimidines; 0 / RTA 203; 5142-23-4 / 3-methyladenine; 88899-55-2 / bafilomycin A1; 8A1O1M485B / Imatinib Mesylate; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; JAC85A2161 / Adenine; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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17. Wesolowska A, Kwiatkowska A, Slomnicki L, Dembinski M, Master A, Sliwa M, Franciszkiewicz K, Chouaib S, Kaminska B: Microglia-derived TGF-beta as an important regulator of glioblastoma invasion--an inhibition of TGF-beta-dependent effects by shRNA against human TGF-beta type II receptor. Oncogene; 2008 Feb 7;27(7):918-30
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  • [Title] Microglia-derived TGF-beta as an important regulator of glioblastoma invasion--an inhibition of TGF-beta-dependent effects by shRNA against human TGF-beta type II receptor.
  • The invasion of tumor cells into brain tissue is a pathologic hallmark of malignant gliomas and contributes to treatment failures.
  • Transforming growth factor-beta (TGF-beta) can enhance tumor growth, invasion, angiogenesis and immunosuppression.
  • Antagonizing TGF-beta activity has been shown to inhibit tumor invasion in vitro and tumorigenicity, but a systemic inhibition or lack of TGF-beta signaling results in acute inflammation and disruption of immune system homeostasis.
  • We developed plasmid-transcribed small hairpin RNAs (shRNAs) to downregulate the TGF-beta type II receptor (TbetaIIR) expression, which effectively inhibited cytokine-induced signaling pathways and transcriptional responses in transiently transfected human glioblastoma cells.
  • Microglia strongly enhanced glioma invasiveness in the co-culture system, but this invasion-promoting activity was lost in glioma cells stably expressing shTbetaRII, indicating a crucial role of microglia-derived TGF-beta in tumor-host interactions.
  • [MeSH-major] Cell Movement / physiology. Gene Silencing / physiology. Glioma / pathology. Microglia / metabolism. Protein-Serine-Threonine Kinases / genetics. Receptors, Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Coculture Techniques. Collagen / metabolism. Drug Combinations. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Laminin / metabolism. Male. Mice. Mice, Nude. Neoplasm Invasiveness. Proteoglycans / metabolism. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Tumor Cells, Cultured

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  • (PMID = 17684491.001).
  • [ISSN] 1476-5594
  • [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 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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18. Iwamaru A, Kondo Y, Iwado E, Aoki H, Fujiwara K, Yokoyama T, Mills GB, Kondo S: Silencing mammalian target of rapamycin signaling by small interfering RNA enhances rapamycin-induced autophagy in malignant glioma cells. Oncogene; 2007 Mar 22;26(13):1840-51
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  • [Title] Silencing mammalian target of rapamycin signaling by small interfering RNA enhances rapamycin-induced autophagy in malignant glioma cells.
  • The mammalian target of rapamycin (mTOR) plays a central role in regulating the proliferation of malignant glioma cells, and mTOR-specific inhibitors such as rapamycin analogs are considered as promising therapy for malignant gliomas.
  • However, the efficacy of mTOR inhibitors alone in the treatment of patients with malignant gliomas is only modest, potentially because these agents rather than acting as mTOR kinase inhibitors instead interfere with the function of only mTOR/raptor (regulatory-associated protein of mTOR) complex and thus do not perturb all mTOR functions.
  • The purpose of this study was to determine whether global inhibition of the mTOR molecule enhances the antitumor effect of rapamycin on malignant glioma cells.
  • We showed that rapamycin induced autophagy and that inhibition of autophagy by small interfering RNA (siRNA) directed against autophagy-related gene Beclin 1 attenuated the cytotoxicity of rapamycin in rapamycin-sensitive tumor cells, indicating that the autophagy was a primary mediator of rapamycin's antitumor effect rather than a protective response.
  • Moreover, silencing of mTOR with siRNA augmented the inhibitory effect of rapamycin on tumor cell viability by stimulating autophagy.
  • Importantly, not only rapamycin-sensitive malignant glioma cells with PTEN mutations but also rapamycin-resistant malignant glioma cells with wild-type PTEN were sensitized to rapamycin by mTOR siRNA.
  • These results indicate that rapamycin-induced autophagy is one of the agent's antitumor effects and that silencing or inhibiting mTOR kinase activity could enhance the effectiveness of rapamycin.
  • [MeSH-major] Autophagy / drug effects. Brain Neoplasms / epidemiology. Gene Silencing. Glioma / genetics. Protein Kinases / genetics. RNA, Small Interfering. Sirolimus / pharmacology
  • [MeSH-minor] Base Sequence. Catalysis. Cell Line, Tumor. Humans. Microscopy, Electron. PTEN Phosphohydrolase / metabolism. TOR Serine-Threonine Kinases


19. Amos S, Redpath GT, Dipierro CG, Carpenter JE, Hussaini IM: Epidermal growth factor receptor-mediated regulation of urokinase plasminogen activator expression and glioblastoma invasion via C-SRC/MAPK/AP-1 signaling pathways. J Neuropathol Exp Neurol; 2010 Jun;69(6):582-92
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  • One of the major pathophysiological features of malignant astrocytomas is their ability to infiltrate surrounding brain tissue.
  • The epidermal growth factor receptor (EGFR) and proteases are known to be overexpressed in glioblastomas (GBMs), but the interaction between the activation of the EGFR and urokinase plasminogen activator (uPA) in promoting astrocytic tumor invasion has not been fully elucidated.
  • We show that EGFR activation and constitutively active EGFR vIII in GBM cell lines upregulate uPA expression.
  • Small-molecule inhibitors of mitogen-activated protein kinase, tyrosine kinase, and small interfering RNA targeting c-Src blocked uPA upregulation.
  • Treatment of GBM cells with EGF increased in vitro cell invasion, and the invasive phenotype was attenuated by gene silencing of uPA using small interfering RNA and short hairpin RNA.


20. Tran NL, McDonough WS, Savitch BA, Sawyer TF, Winkles JA, Berens ME: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expression. J Biol Chem; 2005 Feb 4;280(5):3483-92
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  • [Title] The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expression.
  • The Fn14 gene encodes a type Ia transmembrane protein that belongs to the tumor necrosis factor receptor superfamily.
  • To determine the biological role of Fn14 in brain cancer progression, we examined the activity of Fn14 as a potential mediator of cell survival.
  • Tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-stimulated glioma cells had increased cellular resistance to cytotoxic therapy-induced apoptosis.
  • Additionally small interfering RNA-mediated depletion of either BCL-XL or BCL-W antagonized the TWEAK protective effect on glioma cells.
  • We propose that the Fn14 protein functions, in part, through the NFkappaB signaling pathway to up-regulate BCL-XL and BCL-W expression to foster malignant glioblastoma cell survival.
  • [MeSH-major] Astrocytoma. Brain Neoplasms. Carrier Proteins / metabolism. NF-kappa B / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Receptors, Tumor Necrosis Factor / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Apoptosis Regulatory Proteins. Cell Line. Cell Survival / physiology. Cytotoxins / pharmacology. Gene Expression Regulation, Neoplastic. Humans. I-kappa B Proteins / metabolism. Ligands. Phosphorylation. Proteins. RNA, Small Interfering. Signal Transduction / physiology. Tumor Necrosis Factors. bcl-X Protein

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  • (PMID = 15611130.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-39727; United States / NINDS NIH HHS / NS / NS-42262
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL2L1 protein, human; 0 / BCL2L2 protein, human; 0 / Carrier Proteins; 0 / Cytotoxins; 0 / I-kappa B Proteins; 0 / Ligands; 0 / NF-kappa B; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFSF12 protein, human; 0 / TWEAK receptor; 0 / Tumor Necrosis Factors; 0 / bcl-X Protein; 139874-52-5 / NF-kappaB inhibitor alpha
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21. Villeneuve J, Tremblay P, Vallières L: Tumor necrosis factor reduces brain tumor growth by enhancing macrophage recruitment and microcyst formation. Cancer Res; 2005 May 1;65(9):3928-36
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  • [Title] Tumor necrosis factor reduces brain tumor growth by enhancing macrophage recruitment and microcyst formation.
  • Recent findings implicate macrophages and some of their secreted products, especially tumor necrosis factor (TNF), as tumor promoters.
  • Inhibitors of these inflammatory components are currently regarded as potential therapeutic tools to block tumor progression.
  • Here, we show that infiltrating macrophages represented a significant population of nonneoplastic cells within malignant gliomas, in which they were the exclusive producers of TNF.
  • Contrary to the reported pro-oncogenic effects of TNF in other types of solid tumors, glioma-bearing mice deficient in TNF developed larger tumors and had reduced survival compared with their wild-type controls.
  • Histologic examinations revealed that glioma volume was negatively correlated with the number of macrophages and small cavities called microcysts.
  • Overall, our results support the concept that macrophages alter brain tumor development through a TNF-dependent process that culminates in the formation of microcysts.
  • This raises the question of whether anti-inflammatory drugs, such as those commonly administrated to patients with brain cancer, could interfere with antitumor mechanisms.
  • [MeSH-major] Brain Neoplasms / immunology. Glioma / immunology. Macrophages / immunology. Tumor Necrosis Factor-alpha / deficiency. Tumor Necrosis Factor-alpha / immunology
  • [MeSH-minor] Animals. Cell Growth Processes / immunology. Chickens. Mice. Mice, Inbred C57BL. Mice, Transgenic. Recombinant Proteins / pharmacology

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  • (PMID = 15867393.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
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22. Miyashita K, Kawakami K, Nakada M, Mai W, Shakoori A, Fujisawa H, Hayashi Y, Hamada J, Minamoto T: Potential therapeutic effect of glycogen synthase kinase 3beta inhibition against human glioblastoma. Clin Cancer Res; 2009 Feb 1;15(3):887-97
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  • PURPOSE: Glioblastoma represents the malignant brain tumor that is most refractory to treatment and in which the identification of molecular target(s) is urgently required.
  • EXPERIMENTAL DESIGN: The active fraction of GSK3beta that is phosphorylated at the tyrosine 216 residue (pGSK3betaY216) was identified in glioblastoma cell lines.
  • RESULTS: Higher expression levels of GSK3beta and pGSK3betaY216 were frequently detected in glioblastomas compared with nonneoplastic brain tissues.
  • Inhibition of GSK3beta activity by escalating doses of a small-molecule inhibitor (AR-A014418) or inhibition of its expression by RNA interference induced the apoptosis and attenuated the survival and proliferation of glioblastoma cells in vitro.
  • Inhibition of GSK3beta was associated with increased expression of p53 and p21 in glioblastoma cells with wild-type p53 and with decreased Rb phosphorylation and expression of cyclin-dependent kinase 6 in all glioblastoma cell lines.
  • Administration of AR-A014418 at a low dose significantly sensitized glioblastoma cells to temozolomide and 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea, chemotherapeutic agents used in the clinical setting, as well as to ionizing radiation.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Thiazoles / pharmacology. Urea / analogs & derivatives
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Drug Evaluation, Preclinical. Humans. RNA Interference. Radiation-Sensitizing Agents / pharmacology


23. Schally AV, Varga JL, Engel JB: Antagonists of growth-hormone-releasing hormone: an emerging new therapy for cancer. Nat Clin Pract Endocrinol Metab; 2008 Jan;4(1):33-43
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  • This article reviews the potential clinical uses of antagonists of growth-hormone-releasing hormone (GHRH) for tumor therapy.
  • GHRH antagonists suppress the growth of various human cancer lines xenografted into nude mice; such tumors include breast, ovarian, endometrial and prostate cancers, lung cancers (small-cell lung carcinomas and non-small-cell lung carcinomas), renal, pancreatic, gastric and colorectal carcinomas, brain tumors (malignant gliomas), osteogenic sarcomas and non-Hodgkin's lymphomas.
  • Pituitary-type GHRH receptors and their splice variants are also found in many human cancers.
  • Antagonists of GHRH can also suppress cancer growth by blocking production of IGF-I and/or IGF-II by the tumor.
  • Further development of GHRH antagonists that are still-more potent should lead to potential therapeutic agents for various cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Growth Hormone-Releasing Hormone / antagonists & inhibitors. Receptors, Neuropeptide / antagonists & inhibitors. Receptors, Pituitary Hormone-Regulating Hormone / antagonists & inhibitors
  • [MeSH-minor] Amino Acid Sequence. Animals. Humans. Mice. Mice, Nude. Molecular Sequence Data. Neoplasms / drug therapy. Xenograft Model Antitumor Assays

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  • (PMID = 18084344.001).
  • [ISSN] 1745-8374
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor; 9034-39-3 / Growth Hormone-Releasing Hormone
  • [Number-of-references] 81
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24. Irvin DK, Jouanneau E, Duvall G, Zhang XX, Zhai Y, Sarayba D, Seksenyan A, Panwar A, Black KL, Wheeler CJ: T cells enhance stem-like properties and conditional malignancy in gliomas. PLoS One; 2010 Jun 07;5(6):e10974
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  • BACKGROUND: Small populations of highly tumorigenic stem-like cells (cancer stem cells;.
  • CSCs) can exist within, and uniquely regenerate cancers including malignant brain tumors (gliomas).
  • METHODS: We found gene expression similarity superiorly defined glioma "stemness", and revealed that GSC similarity increased with lower tumor grade.
  • Using this method, we examined stemness in human grade IV gliomas (GBM) before and after dendritic cell (DC) vaccine therapy.
  • This was followed by gene expression, phenotypic and functional analysis of murine GL26 tumors recovered from nude, wild-type, or DC-vaccinated host brains.
  • RESULTS: GSC similarity was specifically increased in post-vaccine GBMs, and correlated best to vaccine-altered gene expression and endogenous anti-tumor T cell activity.
  • GL26 analysis confirmed immune alterations, specific acquisition of stem cell markers, specifically enhanced sensitivity to anti-stem drug (cyclopamine), and enhanced tumorigenicity in wild-type hosts, in tumors in proportion to anti-tumor T cell activity.
  • Nevertheless, vaccine-exposed GL26 cells were no more tumorigenic than parental GL26 in T cell-deficient hosts, though they otherwise appeared similar to GSCs enriched by chemotherapy.
  • Finally, vaccine-exposed GBM and GL26 exhibited relatively homogeneous expression of genes expressed in progenitor cells and/or differentiation.
  • CONCLUSIONS: T cell activity represents an inducible physiological process capable of proportionally enriching GSCs in human and mouse gliomas.
  • Stem-like gliomas enriched by strong T cell activity, however, may differ from other GSCs in that their stem-like properties may be disassociated from increased tumor malignancy and heterogeneity under specific host immune conditions.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Neoplastic Stem Cells / cytology. T-Lymphocytes, Cytotoxic / cytology
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Flow Cytometry. Fluorescent Antibody Technique. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction

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  • (PMID = 20539758.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS048959; United States / NINDS NIH HHS / NS / NS054162-01; United States / NINDS NIH HHS / NS / R56 NS048959; United States / NINDS NIH HHS / NS / NS048959-01S1; United States / NINDS NIH HHS / NS / R21 NS054162
  • [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 / DNA Primers
  • [Other-IDs] NLM/ PMC2881867
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25. Yi L, Zhou ZH, Ping YF, Chen JH, Yao XH, Feng H, Lu JY, Wang JM, Bian XW: Isolation and characterization of stem cell-like precursor cells from primary human anaplastic oligoastrocytoma. Mod Pathol; 2007 Oct;20(10):1061-8
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  • [Title] Isolation and characterization of stem cell-like precursor cells from primary human anaplastic oligoastrocytoma.
  • A small population of stem cell-like precursors in solid tumors are linked to histological composition, progression, angiogenesis, metastasis, recurrence and drug resistance of a variety of malignant tumors.
  • Oligoastrocytoma is the most common brain mixed glioma composed of mixed cells of oligodendroglial and astrocytic phenotypes.
  • Identification and characterization of stem cell-like precursors in oligoastrocytoma may shed light on the oncogenesis of this unique type of tumor and assist in the design of novel therapeutic strategy.
  • Here, tumor stem cell-like precursors were identified from primary human anaplastic oligoastrocytomas by labeling of the tumor sections with nestin and CD133.
  • Tumor cells were cultured in vitro in stem cell medium with growth factors and the capacity of the surviving stem cell-like precursors to form tumor spheres was tested.
  • The tumor spheres were further injected subcutaneously into nude mice to observe the contribution of stem cell-like precursors to histological composition and tumor progression.
  • We found that primary human oligoastrocytoma tissues contained nestin+/CD133+ stem cell-like precursors.
  • These cells differentiated into tumor cells with both oligodendroglial and astrocytic characteristics and formed tumor spheres in vitro, which upon implantation in nude mice, grew into tumor nodules containing nestin+/CD133+ cells at levels higher than in the primary tumor tissues.
  • This study revealed for the first time that anaplastic human oligoastrocytomas contained stem cell-like precursors, which exhibit neural stem cell properties with tumorigenicity.
  • These stem cell-like precursors may be responsible for the oligodendroglial and astrocytic components of human oligoastrocytoma and should be considered as therapeutic targets.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Brain / pathology. Fluorescent Antibody Technique, Indirect. Glycoproteins / analysis. Humans. Intermediate Filament Proteins / analysis. Magnetic Resonance Imaging. Mice. Mice, Nude. Neoplasm Transplantation. Nerve Tissue Proteins / analysis. Nestin. Peptides / analysis. Spheroids, Cellular / chemistry. Spheroids, Cellular / pathology. Tumor Cells, Cultured

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  • (PMID = 17660801.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Peptides
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26. Arcaro A, Doepfner KT, Boller D, Guerreiro AS, Shalaby T, Jackson SP, Schoenwaelder SM, Delattre O, Grotzer MA, Fischer B: Novel role for insulin as an autocrine growth factor for malignant brain tumour cells. Biochem J; 2007 Aug 15;406(1):57-66
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  • [Title] Novel role for insulin as an autocrine growth factor for malignant brain tumour cells.
  • We characterized a panel of human AT/RT and MRT (malignant rhabdoid tumour) cell lines for expression of RTKs (receptor tyrosine kinases) and their involvement in tumour growth and survival.
  • When compared with normal brain tissue, AT/RT cell lines overexpressed the IR (insulin receptor) and the IGFIR (insulin-like growth factor-I receptor).
  • Pharmacological inhibitors, neutralizing antibodies, or RNAi (RNA interference) targeting the IR impaired the growth of AT/RT cell lines and induced apoptosis.
  • Inhibitors of the PI3K (phosphoinositide 3-kinase)/Akt pathway also impaired basal and insulin-stimulated AT/RT cell proliferation.
  • Experiments using RNAi and isoform-specific pharmacological inhibitors established a key role for the class I(A) PI3K p110alpha isoform in AT/RT cell growth and insulin signalling.
  • Taken together, our results reveal a novel role for autocrine signalling by insulin and the IR in growth and survival of malignant human CNS tumour cells via the PI3K/Akt pathway.
  • [MeSH-major] Autocrine Communication. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Growth Substances / metabolism. Insulin / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Child, Preschool. Chromosomal Proteins, Non-Histone / metabolism. Culture Media, Serum-Free. DNA-Binding Proteins / metabolism. Down-Regulation / drug effects. Down-Regulation / genetics. Enzyme Activation / drug effects. Female. Humans. Infant. Isoenzymes / metabolism. Male. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptor, IGF Type 1 / metabolism. Receptor, Insulin / genetics. Receptor, Insulin / metabolism. Signal Transduction / drug effects. Transcription Factors / metabolism

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  • (PMID = 17506723.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Culture Media, Serum-Free; 0 / DNA-Binding Proteins; 0 / Growth Substances; 0 / Insulin; 0 / Isoenzymes; 0 / RNA, Small Interfering; 0 / SMARCB1 protein, human; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1948991
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