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1. Das B, Antoon R, Tsuchida R, Lotfi S, Morozova O, Farhat W, Malkin D, Koren G, Yeger H, Baruchel S: Squalene selectively protects mouse bone marrow progenitors against cisplatin and carboplatin-induced cytotoxicity in vivo without protecting tumor growth. Neoplasia; 2008 Oct;10(10):1105-19
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  • [Title] Squalene selectively protects mouse bone marrow progenitors against cisplatin and carboplatin-induced cytotoxicity in vivo without protecting tumor growth.
  • Squalene, an isoprenoid antioxidant is a potential cytoprotective agent against chemotherapy-induced toxicity.
  • Here, we developed an in vivo mouse model of cisplatin and cis-diammine (cyclobutane-1,1-dicarboxylato) platinum(II) (carboplatin)-induced toxicity to further investigate squalene-mediated LD-BM cytoprotection including the molecular mechanism behind selective cytoprotection.
  • Importantly, squalene did not protect neuroblastoma, small cell carcinoma, or medulloblastoma xenografts against cisplatin-induced toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Cells / drug effects. Carboplatin / adverse effects. Cisplatin / adverse effects. Cytoprotection / drug effects. Neoplasms / drug therapy. Squalene / pharmacology
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Cell Proliferation / drug effects. Cells, Cultured. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Organ Specificity / drug effects. Stem Cells / drug effects. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 18813359.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antioxidants; 7QWM220FJH / Squalene; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2546596
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2. Fogarty MP, Emmenegger BA, Grasfeder LL, Oliver TG, Wechsler-Reya RJ: Fibroblast growth factor blocks Sonic hedgehog signaling in neuronal precursors and tumor cells. Proc Natl Acad Sci U S A; 2007 Feb 20;104(8):2973-8
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  • Here, we examine the relationship between Shh and FGF signaling in granule cell precursors (GCPs), which are the most abundant neural progenitors in the cerebellum and the putative cell of origin for the childhood brain tumor medulloblastoma.
  • Finally, FGF promotes differentiation of GCPs in vitro and in vivo and halts proliferation of tumor cells from patched (ptc) mutant mice, a model for medulloblastoma.
  • These findings suggest that FGF is a potent inhibitor of Shh signaling and may be a useful therapy for tumors involving activation of the hedgehog pathway.

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  • (PMID = 17299056.001).
  • [ISSN] 0027-8424
  • [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 / NIMH NIH HHS / MH / MH067916-01A1; United States / NIMH NIH HHS / MH / MH067916-04; United States / NIMH NIH HHS / MH / R01 MH067916-05; United States / NIMH NIH HHS / MH / MH067916-05; United States / NIMH NIH HHS / MH / R01 MH067916-04; United States / NIMH NIH HHS / MH / MH067916-02; United States / NIMH NIH HHS / MH / R01 MH067916; United States / NIMH NIH HHS / MH / R01 MH067916-01A1; United States / NIMH NIH HHS / MH / R01 MH067916-02; United States / NIMH NIH HHS / MH / MH 067916-03; United States / NIMH NIH HHS / MH / MH067916-03; United States / NIMH NIH HHS / MH / R01 MH067916-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Mutant Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, Fibroblast Growth Factor; 0 / patched receptors; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1815291
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3. Robarge KD, Brunton SA, Castanedo GM, Cui Y, Dina MS, Goldsmith R, Gould SE, Guichert O, Gunzner JL, Halladay J, Jia W, Khojasteh C, Koehler MF, Kotkow K, La H, Lalonde RL, Lau K, Lee L, Marshall D, Marsters JC Jr, Murray LJ, Qian C, Rubin LL, Salphati L, Stanley MS, Stibbard JH, Sutherlin DP, Ubhayaker S, Wang S, Wong S, Xie M: GDC-0449-a potent inhibitor of the hedgehog pathway. Bioorg Med Chem Lett; 2009 Oct 1;19(19):5576-81
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  • The 2-pyridyl amides were optimized for potency, PK, and drug-like properties by modifications to the amide portion of the molecule resulting in 31 (GDC-0449).
  • Amide 31 produced complete tumor regression at doses as low as 12.5mg/kg BID in a medulloblastoma allograft mouse model that is wholly dependent on the Hh pathway for growth and is currently in human clinical trials, where it is initially being evaluated for the treatment of BCC.
  • [MeSH-minor] Animals. Benzimidazoles / chemistry. Carcinoma, Basal Cell / drug therapy. Cell Line. Cerebellar Neoplasms / drug therapy. Humans. Medulloblastoma / drug therapy. Mice. Mice, Nude. Signal Transduction. Structure-Activity Relationship. Xenograft Model Antitumor Assays

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  • [ErratumIn] Bioorg Med Chem Lett. 2010 Jan 15;20(2):771
  • (PMID = 19716296.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amides; 0 / Anilides; 0 / Benzimidazoles; 0 / Hedgehog Proteins; 0 / HhAntag691; 0 / Pyridines
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4. Taipale J, Chen JK, Cooper MK, Wang B, Mann RK, Milenkovic L, Scott MP, Beachy PA: Effects of oncogenic mutations in Smoothened and Patched can be reversed by cyclopamine. Nature; 2000 Aug 31;406(6799):1005-9
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  • Basal cell carcinoma, medulloblastoma, rhabdomyosarcoma and other human tumours are associated with mutations that activate the proto-oncogene Smoothened (SMO) or that inactivate the tumour suppressor Patched (PTCH).
  • Here we show that the plant-derived teratogen cyclopamine, which inhibits the Hh response, is a potential 'mechanism-based' therapeutic agent for treatment of these tumours.
  • We show that cyclopamine or synthetic derivatives with improved potency block activation of the Hh response pathway and abnormal cell growth associated with both types of oncogenic mutation.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Drosophila Proteins. Membrane Proteins / genetics. Proteins / antagonists & inhibitors. Receptors, Cell Surface / genetics. Receptors, G-Protein-Coupled. Signal Transduction / drug effects. Trans-Activators. Veratrum Alkaloids / pharmacology
  • [MeSH-minor] 3T3 Cells. Animals. Basal Cell Nevus Syndrome / drug therapy. Basal Cell Nevus Syndrome / genetics. Basal Cell Nevus Syndrome / metabolism. Cell Line. Cell Transformation, Neoplastic / drug effects. Cloning, Molecular. Drosophila. Gene Expression Regulation / drug effects. Hedgehog Proteins. Humans. Intracellular Signaling Peptides and Proteins. Mice. Mutation. Oncogenes. Patched Receptors. Patched-1 Receptor. Smoothened Receptor

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  • [CommentIn] Nature. 2000 Aug 31;406(6799):944-5 [10984033.001]
  • (PMID = 10984056.001).
  • [ISSN] 0028-0836
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drosophila Proteins; 0 / Hedgehog Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / PTCH protein, human; 0 / Patched Receptors; 0 / Patched-1 Receptor; 0 / Proteins; 0 / Ptch1 protein, mouse; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Smo protein, mouse; 0 / Smoothened Receptor; 0 / Trans-Activators; 0 / Veratrum Alkaloids; 0 / smoothened protein, Drosophila; ZH658AJ192 / cyclopamine
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5. Kim J, Tang JY, Gong R, Kim J, Lee JJ, Clemons KV, Chong CR, Chang KS, Fereshteh M, Gardner D, Reya T, Liu JO, Epstein EH, Stevens DA, Beachy PA: Itraconazole, a commonly used antifungal that inhibits Hedgehog pathway activity and cancer growth. Cancer Cell; 2010 Apr 13;17(4):388-99
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  • In a screen of drugs previously tested in humans we identified itraconazole, a systemic antifungal, as a potent antagonist of the Hedgehog (Hh) signaling pathway that acts by a mechanism distinct from its inhibitory effect on fungal sterol biosynthesis.
  • Systemically administered itraconazole, like other Hh pathway antagonists, can suppress Hh pathway activity and the growth of medulloblastoma in a mouse allograft model and does so at serum levels comparable to those in patients undergoing antifungal therapy.

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  • (PMID = 20385363.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD039306; United States / NCI NIH HHS / CA / R21 CA158640; United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Cyclodextrins; 0 / Hedgehog Proteins; 0 / Lipoproteins, LDL; 304NUG5GF4 / Itraconazole
  • [Other-IDs] NLM/ NIHMS199097; NLM/ PMC4039177
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6. Garzia L, Andolfo I, Cusanelli E, Marino N, Petrosino G, De Martino D, Esposito V, Galeone A, Navas L, Esposito S, Gargiulo S, Fattet S, Donofrio V, Cinalli G, Brunetti A, Vecchio LD, Northcott PA, Delattre O, Taylor MD, Iolascon A, Zollo M: MicroRNA-199b-5p impairs cancer stem cells through negative regulation of HES1 in medulloblastoma. PLoS One; 2009;4(3):e4998
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  • [Title] MicroRNA-199b-5p impairs cancer stem cells through negative regulation of HES1 in medulloblastoma.
  • BACKGROUND: Through negative regulation of gene expression, microRNAs (miRNAs) can function in cancers as oncosuppressors, and they can show altered expression in various tumor types.
  • Here we have investigated medulloblastoma tumors (MBs), which arise from an early impairment of developmental processes in the cerebellum, where Notch signaling is involved in many cell-fate-determining stages.
  • On the basis of this evidence, we hypothesized that miRNAs targeting the Notch pathway can regulated these phenomena, and can be used in anti-cancer therapies.
  • Furthermore, two cell lines (Med8a and UW228) showed significant up-regulation of miR-199b-5p upon treatment.
  • Infection with MB cells in an induced xenograft model in the mouse cerebellum and the use of an adenovirus carrying miR-199b-5p indicate a clinical benefit through this negative influence of miR-199b-5p on tumor growth and on the subset of MB stem-cell-like cells, providing further proof of concept.
  • CONCLUSIONS/SIGNIFICANCE: Despite advances in our understanding of the pathogenesis of MB, one-third of these patients remain incurable and current treatments can significantly damage long-term survivors.
  • We further show that in a xenograft model, MB tumor burden can be reduced, indicating the use of miR199b-5p as an adjuvant therapy after surgery, in combination with radiation and chemotherapy, for the improvement of anti-cancer MB therapies and patient quality of life.
  • To date, this is the first report that expression of a miRNA can deplete the tumor stem cells, indicating an interesting therapeutic approach for the targeting of these cells in brain tumors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Down-Regulation / genetics. Homeodomain Proteins / genetics. Medulloblastoma / pathology. Medulloblastoma / therapy. MicroRNAs / physiology. Neoplastic Stem Cells / pathology

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  • (PMID = 19308264.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / MicroRNAs; 0 / Receptors, Notch; 0 / mirn199 microRNA, human; 149348-15-2 / HES1 protein, human
  • [Other-IDs] NLM/ PMC2656623
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7. Chiou SH, Kao CL, Lin HT, Tseng WS, Liu RS, Chung CF, Ku HH, Lin CP, Wong TT: Monitoring the growth effect of xenotransplanted human medulloblastoma in an immunocompromised mouse model using in vitro and ex vivo green fluorescent protein imaging. Childs Nerv Syst; 2006 May;22(5):475-80
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  • [Title] Monitoring the growth effect of xenotransplanted human medulloblastoma in an immunocompromised mouse model using in vitro and ex vivo green fluorescent protein imaging.
  • INTRODUCTION: Medulloblastoma (MB) is one of the most common malignant brain tumors in children.
  • CASE REPORT: In this study, we established xenotransplanted human MB (hMB) cells - isochromosome 17q - in a severe combined immunodeficiency (SCID) mouse model.
  • Because MB is sensitive to radiation and also response to chemotherapy, this SCID mouse model will be helpful for preclinical studies in the future.
  • [MeSH-major] Green Fluorescent Proteins / metabolism. Medulloblastoma / metabolism. Medulloblastoma / physiopathology
  • [MeSH-minor] Animals. Cell Proliferation. Diagnostic Imaging. Disease Models, Animal. Glial Fibrillary Acidic Protein / metabolism. Humans. In Vitro Techniques. Mice. Mice, SCID. Neoplasm Transplantation / methods. Time Factors

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  • (PMID = 16541296.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 147336-22-9 / Green Fluorescent Proteins
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8. Cheng CL, Johnson SP, Keir ST, Quinn JA, Ali-Osman F, Szabo C, Li H, Salzman AL, Dolan ME, Modrich P, Bigner DD, Friedman HS: Poly(ADP-ribose) polymerase-1 inhibition reverses temozolomide resistance in a DNA mismatch repair-deficient malignant glioma xenograft. Mol Cancer Ther; 2005 Sep;4(9):1364-8
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  • Temozolomide is a DNA-methylating agent used in the treatment of malignant gliomas.
  • In two separate experiments, the combination therapy increased the growth delay by 21.6 and 9.7 days with partial regressions observed in four of eight and three of nine mice, respectively.
  • When the temozolomide treatment was in combination with 200 mg/kg INO-1001, there was an increase in growth delay to 48.9 and 45.7 days, respectively.
  • These results suggest that inhibition of PARP may increase the efficacy of temozolomide in the treatment of malignant gliomas, particularly in tumors deficient in DNA mismatch repair.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Base Pair Mismatch. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / drug effects. Indoles / pharmacology. Medulloblastoma / drug therapy. Poly(ADP-ribose) Polymerase Inhibitors

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  • (PMID = 16170028.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS30245
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / INO 1001; 0 / Indoles; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.4.2.30 / Parp1 protein, mouse
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9. Saito R, Mizuno M, Nakahara N, Tsuno T, Kumabe T, Yoshimoto T, Yoshida J: Vaccination with tumor cell lysate-pulsed dendritic cells augments the effect of IFN-beta gene therapy for malignant glioma in an experimental mouse intracranial glioma. Int J Cancer; 2004 Sep 20;111(5):777-82
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  • [Title] Vaccination with tumor cell lysate-pulsed dendritic cells augments the effect of IFN-beta gene therapy for malignant glioma in an experimental mouse intracranial glioma.
  • Interferon-beta (IFN-beta) has been used as an antitumor drug against human glioma, melanoma and medulloblastoma since the 1980s.
  • Recently, we developed a new gene therapy using the IFN-beta gene against malignant gliomas and then began clinical trials in 2000.
  • Since stimulation of immune system was one mechanism of antitumor effect induced by IFN-beta gene therapy, we hypothesized that combination of IFN-beta gene therapy with immunotherapy might increase its effectiveness.
  • In the present study, we tested whether combination therapy with IFN-beta gene therapy and immunotherapy using tumor cell lysate-pulsed dendritic cells (DCs) would increase the efficacy of IFN-beta gene therapy.
  • In an experimental mouse intracranial glioma (GL261), which cannot be cured by either IFN-beta gene therapy or DC immunotherapy alone, IFN-beta gene therapy following DC immunotherapy resulted in a significant prolongation in survival of the mice.
  • Considering these results, this combination therapy may be one promising candidate for glioma therapy in the near future.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / genetics. Brain Neoplasms / therapy. Cancer Vaccines. Dendritic Cells / immunology. Genetic Therapy. Glioma / genetics. Glioma / therapy. Interferon-beta / genetics. Interferon-beta / pharmacology
  • [MeSH-minor] Animals. Combined Modality Therapy. Female. Immunotherapy. Lipids. Mice. Mice, Inbred C57BL. Neoplasms, Experimental. Plasmids. Tumor Cells, Cultured

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15252850.001).
  • [ISSN] 0020-7136
  • [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 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Lipids; 77238-31-4 / Interferon-beta
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10. Lucas BS, Aaron W, An S, Austin RJ, Brown M, Chan H, Chong A, Hungate R, Huang T, Jiang B, Johnson MG, Kaizerman JA, Lee G, McMinn DL, Orf J, Powers JP, Rong M, Toteva MM, Uyeda C, Wickramasinghe D, Xu G, Ye Q, Zhong W: Design of 1-piperazinyl-4-arylphthalazines as potent Smoothened antagonists. Bioorg Med Chem Lett; 2010 Jun 15;20(12):3618-22
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  • The Hedgehog (Hh) signaling pathway regulates cell proliferation and differentiation in developing tissues, and abnormal activation of the Hh pathway has been linked to several tumor subsets.
  • A series of 1-amino-4-arylphthalazines was developed as potent and orally bioavailable inhibitors of Smo.
  • A representative compound from this class demonstrated significant tumor volume reduction in a mouse medulloblastoma model.
  • [MeSH-minor] Administration, Oral. Animals. Biological Availability. Cell Line, Tumor. Cytochrome P-450 Enzyme System / drug effects. Drug Design. Hedgehog Proteins. Humans. Medulloblastoma / drug therapy. Medulloblastoma / pathology. Mice. Signal Transduction

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20493695.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Phthalazines; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Smo protein, mouse; 9035-51-2 / Cytochrome P-450 Enzyme System
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11. Romer JT, Kimura H, Magdaleno S, Sasai K, Fuller C, Baines H, Connelly M, Stewart CF, Gould S, Rubin LL, Curran T: Suppression of the Shh pathway using a small molecule inhibitor eliminates medulloblastoma in Ptc1(+/-)p53(-/-) mice. Cancer Cell; 2004 Sep;6(3):229-40
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  • [Title] Suppression of the Shh pathway using a small molecule inhibitor eliminates medulloblastoma in Ptc1(+/-)p53(-/-) mice.
  • Medulloblastoma is the most common malignant pediatric brain tumor.
  • Current treatment is associated with major long-term side effects; therefore, new nontoxic therapies, targeting specific molecular defects in this cancer, need to be developed.
  • We use a mouse model of medulloblastoma to show that inhibition of the Sonic Hedgehog (Shh) pathway provides a novel therapy for medulloblastoma.
  • A small molecule inhibitor of the Shh pathway, HhAntag, blocked the function of Smoothened in mice with medulloblastoma.
  • This resulted in suppression of several genes highly expressed in medulloblastoma, inhibition of cell proliferation, increase in cell death and, at the highest dose, complete eradication of tumors.
  • Long-term treatment with HhAntag prolonged medulloblastoma-free survival.
  • These findings support the development of Shh antagonists for the treatment of medulloblastoma.
  • [MeSH-major] Brain Neoplasms / metabolism. Medulloblastoma / metabolism. Trans-Activators / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Division. Disease-Free Survival. Dose-Response Relationship, Drug. Hedgehog Proteins. Kruppel-Like Transcription Factors. Mice. Mice, Transgenic. Receptors, G-Protein-Coupled / metabolism. Signal Transduction. Transcription Factors / metabolism. Tumor Cells, Cultured


12. Ecke I, Rosenberger A, Obenauer S, Dullin C, Aberger F, Kimmina S, Schweyer S, Hahn H: Cyclopamine treatment of full-blown Hh/Ptch-associated RMS partially inhibits Hh/Ptch signaling, but not tumor growth. Mol Carcinog; 2008 May;47(5):361-72
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  • [Title] Cyclopamine treatment of full-blown Hh/Ptch-associated RMS partially inhibits Hh/Ptch signaling, but not tumor growth.
  • However, the evidence that treatment with cyclopamine is an effective anti-cancer therapy against full-blown tumors is sparse.
  • Here, we have investigated the responsiveness of full-blown Hh/Ptch-associated rhabdomyosarcoma (RMS) to this drug.
  • Hh signaling was also partially suppressed by the drug in RMS in vivo, but cyclopamine treatment did not result in stable disease or tumor regression.
  • This was in contrast to anti-proliferative effects on tumor growth caused by doxorubicin, an anthracycline routinely used in therapy of human RMS.
  • [MeSH-major] Hedgehog Proteins / physiology. Medulloblastoma / pathology. Receptors, Cell Surface / physiology. Rhabdomyosarcoma / pathology. Signal Transduction / drug effects. Veratrum Alkaloids / therapeutic use
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Blotting, Western. Cell Proliferation / drug effects. Doxorubicin / therapeutic use. Gene Expression Profiling. Humans. Insulin-Like Growth Factor II / genetics. Insulin-Like Growth Factor II / metabolism. Kruppel-Like Transcription Factors / genetics. Kruppel-Like Transcription Factors / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. NIH 3T3 Cells. Patched Receptors. Patched-1 Receptor. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Zinc Finger Protein GLI1

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17963245.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 16518
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Gli protein, mouse; 0 / Hedgehog Proteins; 0 / IGF2 protein, mouse; 0 / Kruppel-Like Transcription Factors; 0 / PTCH protein, human; 0 / Patched Receptors; 0 / Patched-1 Receptor; 0 / Ptch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Veratrum Alkaloids; 0 / Zinc Finger Protein GLI1; 67763-97-7 / Insulin-Like Growth Factor II; 80168379AG / Doxorubicin; ZH658AJ192 / cyclopamine
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13. Rubin JB, Kung AL, Klein RS, Chan JA, Sun Y, Schmidt K, Kieran MW, Luster AD, Segal RA: A small-molecule antagonist of CXCR4 inhibits intracranial growth of primary brain tumors. Proc Natl Acad Sci U S A; 2003 Nov 11;100(23):13513-8
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  • Systemic administration of CXCR4 antagonist AMD 3100 inhibits growth of intracranial glioblastoma and medulloblastoma xenografts by increasing apoptosis and decreasing the proliferation of tumor cells.
  • [MeSH-major] Brain Neoplasms / drug therapy. Protein-Serine-Threonine Kinases. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Animals. Anti-HIV Agents / pharmacology. Apoptosis. Cell Division. Cell Line, Tumor. Chemokine CXCL12. Chemokines, CXC / biosynthesis. Chemotaxis. Glioblastoma / drug therapy. Heterocyclic Compounds / pharmacology. Humans. In Situ Nick-End Labeling. Luciferases / metabolism. Magnetic Resonance Imaging. Medulloblastoma / drug therapy. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Neoplasm Transplantation. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Time Factors


14. De Smaele E, Ferretti E, Gulino A: Vismodegib, a small-molecule inhibitor of the hedgehog pathway for the treatment of advanced cancers. Curr Opin Investig Drugs; 2010 Jun;11(6):707-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vismodegib, a small-molecule inhibitor of the hedgehog pathway for the treatment of advanced cancers.
  • Vismodegib inhibits the Hedgehog (Hh) pathway, which is involved in tumorigenesis, thus providing a strong rationale for its use in the treatment of a variety of cancers.
  • Preclinical studies demonstrated the antitumor activity of vismodegib in mouse models of medulloblastoma (MB) and in xenograft models of colorectal and pancreatic cancer.
  • Vismodegib is currently undergoing phase II clinical trials for the treatment of advanced BCC, metastatic colorectal cancer, ovarian cancer, MB and other solid tumors.
  • Because of its low toxicity and specificity for the Hh pathway, this drug has potential advantages compared with conventional chemotherapy, and may also be used in combination treatments.
  • Clinical trials with other Hh inhibitors are also ongoing and their therapeutic potential will need to be compared with vismodegib.
  • [MeSH-major] Anilides / therapeutic use. Molecular Targeted Therapy. Neoplasms / drug therapy. Pyridines / therapeutic use. Receptors, G-Protein-Coupled / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Humans

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  • (PMID = 20496266.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents; 0 / HhAntag691; 0 / Pyridines; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human
  • [Number-of-references] 105
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15. Huse JT, Holland EC: Genetically engineered mouse models of brain cancer and the promise of preclinical testing. Brain Pathol; 2009 Jan;19(1):132-43
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  • [Title] Genetically engineered mouse models of brain cancer and the promise of preclinical testing.
  • Recent improvements in the understanding of brain tumor biology have opened the door to a number of rational therapeutic strategies targeting distinct oncogenic pathways.
  • The successful translation of such "designer drugs" to clinical application depends heavily on effective and expeditious screening methods in relevant disease models.
  • By recapitulating both the underlying genetics and the characteristic tumor-stroma microenvironment of brain cancer, genetically engineered mouse models (GEMMs) may offer distinct advantages over cell culture and xenograft systems in the preclinical testing of promising therapies.
  • This review focuses on recently developed GEMMs for both glioma and medulloblastoma, and discusses their potential use in preclinical trials.
  • Examples showcasing the use of GEMMs in the testing of molecularly targeted therapeutics are given, and relevant topics, such as stem cell biology, in vivo imaging technology and radiotherapy, are also addressed.
  • [MeSH-major] Brain Neoplasms / pathology. Disease Models, Animal. Drug Evaluation, Preclinical / methods. Genetic Engineering / methods
  • [MeSH-minor] Animals. Glioma / drug therapy. Glioma / genetics. Glioma / pathology. Humans. Medulloblastoma / drug therapy. Medulloblastoma / genetics. Medulloblastoma / pathology. Mice. Mice, Transgenic

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  • (PMID = 19076778.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA141502
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 98
  • [Other-IDs] NLM/ PMC2659383
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16. Spiller SE, Ditzler SH, Pullar BJ, Olson JM: Response of preclinical medulloblastoma models to combination therapy with 13-cis retinoic acid and suberoylanilide hydroxamic acid (SAHA). J Neurooncol; 2008 Apr;87(2):133-41
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  • [Title] Response of preclinical medulloblastoma models to combination therapy with 13-cis retinoic acid and suberoylanilide hydroxamic acid (SAHA).
  • PURPOSE: Current medulloblastoma therapy, surgery, radiation, and chemotherapy, is unacceptably toxic.
  • However, 13-cis retinoic acid (RA) and SAHA, a histone deacetylase inhibitor, have each been shown to induce apoptosis in medulloblastoma cultures and mouse models.
  • Both drugs cross the blood brain barrier, have been given safely to children, and achieve brain concentrations that are at or near therapeutic levels.
  • We tested the hypothesis that these drugs additively induce BMP-2 transcription and apoptosis.
  • EXPERIMENTAL DESIGN: RA + SAHA induction of BMP-2 transcription and apoptosis in medulloblastoma cultures was evaluated.
  • Subsequently the response of mouse medulloblastomas to these two agents in the presence and absence of cisplatin was evaluated.
  • Flank D283 tumors in athymic mice had slower growth in the RA + SAHA arm than single drug or control arms.
  • CONCLUSIONS: RA + SAHA additively induce BMP-2 transcription and medulloblastoma apoptosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cerebellar Neoplasms / drug therapy. Hydroxamic Acids / administration & dosage. Isotretinoin / administration & dosage. Medulloblastoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bone Morphogenetic Protein 2. Bone Morphogenetic Proteins / drug effects. Cell Line, Tumor. Cisplatin / administration & dosage. Mice. Mice, Transgenic. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / drug effects. Transforming Growth Factor beta / drug effects

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  • (PMID = 18060600.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 112350-02; United States / NCI NIH HHS / CA / R01 CA 114567-01A1; United States / NCI NIH HHS / CA / U01 CA 814547-07
  • [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 / Bmp2 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / Hydroxamic Acids; 0 / Transforming Growth Factor beta; 58IFB293JI / vorinostat; EH28UP18IF / Isotretinoin; Q20Q21Q62J / Cisplatin
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17. Ecke I, Petry F, Rosenberger A, Tauber S, Mönkemeyer S, Hess I, Dullin C, Kimmina S, Pirngruber J, Johnsen SA, Uhmann A, Nitzki F, Wojnowski L, Schulz-Schaeffer W, Witt O, Hahn H: Antitumor effects of a combined 5-aza-2'deoxycytidine and valproic acid treatment on rhabdomyosarcoma and medulloblastoma in Ptch mutant mice. Cancer Res; 2009 Feb 1;69(3):887-95
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  • [Title] Antitumor effects of a combined 5-aza-2'deoxycytidine and valproic acid treatment on rhabdomyosarcoma and medulloblastoma in Ptch mutant mice.
  • Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors.
  • Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers.
  • A combined treatment with the Dnmt inhibitor 5-aza-2'deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prevented MB and RMS formation, whereas monotherapies with either drug were less effective.
  • Wild-type Ptch expression was efficiently reactivated in tumors by 5-aza-dC/VPA combination therapy.
  • However, the treatment was not effective in clinically overt, advanced stage tumors.
  • The results suggest a novel clinical strategy for consolidation therapy of corresponding tumors in humans after completion of conventional treatment.
  • Our data also suggest that epigenetic therapy may be less effective in treating advanced stages of tumors, at least in this tumor model.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Medulloblastoma / drug therapy. Receptors, Cell Surface / genetics. Rhabdomyosarcoma / drug therapy
  • [MeSH-minor] Acetylation. Animals. Azacitidine / administration & dosage. Azacitidine / analogs & derivatives. DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. DNA (Cytosine-5-)-Methyltransferase / metabolism. DNA Methylation. Gene Expression / drug effects. Gene Silencing. Histone Deacetylase Inhibitors. Histone Deacetylases / metabolism. Histones / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Muscle, Skeletal / drug effects. Muscle, Skeletal / metabolism. Valproic Acid / administration & dosage

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  • (PMID = 19155313.001).
  • [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 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Receptors, Cell Surface; 0 / patched receptors; 614OI1Z5WI / Valproic Acid; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
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18. Coon V, Laukert T, Pedone CA, Laterra J, Kim KJ, Fults DW: Molecular therapy targeting Sonic hedgehog and hepatocyte growth factor signaling in a mouse model of medulloblastoma. Mol Cancer Ther; 2010 Sep;9(9):2627-36
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  • [Title] Molecular therapy targeting Sonic hedgehog and hepatocyte growth factor signaling in a mouse model of medulloblastoma.
  • The use of genetically engineered mice has provided insights into the molecular pathogenesis of the pediatric brain tumor medulloblastoma and revealed promising therapeutic targets.
  • To determine whether Shh + HGF-driven medulloblastomas were responsive to Shh signaling blockade and whether treatment response could be enhanced by combination therapy targeting both HGF and Shh signaling pathways, we carried out a survival study in mice.
  • We report that monotherapy targeting either HGF signaling or Shh signaling prolonged survival and that anti-HGF therapy had a more durable response than Shh-targeted therapy.
  • The effect of L2G7 + 5E1 combination therapy on cumulative survival was equivalent to that of L2G7 monotherapy and that of L2G7 + cyclopamine therapy was worse.
  • The principal mechanism by which Shh- and HGF-targeted therapies inhibited tumor growth was a potent apoptotic death response in tumor cells, supplemented by a weaker suppressive effect on proliferation.
  • Our observation that combination therapy either failed to improve or even reduced survival in mice bearing Shh + HGF-induced medulloblastomas compared with monotherapy underscores the importance of preclinical testing of molecular-targeted therapies in animal models of tumors in which the targeted pathways are known to be active.

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  • (PMID = 20807782.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108622-05; United States / NCI NIH HHS / CA / CA108622; United States / NINDS NIH HHS / NS / R01 NS043987; United States / NCI NIH HHS / CA / CA129192; United States / NCI NIH HHS / CA / R01 CA108622; United States / NCI NIH HHS / CA / R01 CA108622-05; United States / NINDS NIH HHS / NS / NS43987; United States / NCI NIH HHS / CA / R01 CA129192
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Veratrum Alkaloids; 67256-21-7 / Hepatocyte Growth Factor; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ NIHMS231530; NLM/ PMC2937075
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19. Lun XQ, Zhou H, Alain T, Sun B, Wang L, Barrett JW, Stanford MM, McFadden G, Bell J, Senger DL, Forsyth PA: Targeting human medulloblastoma: oncolytic virotherapy with myxoma virus is enhanced by rapamycin. Cancer Res; 2007 Sep 15;67(18):8818-27
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  • [Title] Targeting human medulloblastoma: oncolytic virotherapy with myxoma virus is enhanced by rapamycin.
  • Here, we show that myxoma virus used alone or in combination with rapamycin is effective and safe when used in experimental models of medulloblastoma in vitro and in vivo.
  • Nine of 10 medulloblastoma cell lines tested were susceptible to lethal myxoma virus infection, and pretreatment of cells with rapamycin increased the extent of in vitro oncolysis.
  • Intratumoral injection of live myxoma virus when compared with control inactivated virus prolonged survival in D341 and Daoy orthotopic human medulloblastoma xenograft mouse models [D341 median survival: 21 versus 12.5 days; P = 0.0008; Daoy median survival: not reached (three of five mice apparently "cured" after 223 days) versus 75 days; P = 0.0021].
  • These observations suggest that myxoma virus may be an effective oncolytic agent against medulloblastoma and that combination therapy with signaling inhibitors that modulate activity of the phosphatidylinositol 3-kinase/Akt pathway will further enhance the oncolytic potential of myxoma virus.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Medulloblastoma / therapy. Myxoma virus / physiology. Oncolytic Virotherapy / methods. Sirolimus / pharmacology
  • [MeSH-minor] Animals. Combined Modality Therapy. Enzyme Activation / drug effects. Humans. Injections, Intralesional. Mice. Mice, Nude. NIH 3T3 Cells. Neoplasm Metastasis. Oncogene Protein v-akt / metabolism. Virus Replication / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 17875723.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138541
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; EC 2.7.11.1 / Oncogene Protein v-akt; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS673031; NLM/ PMC4380180
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20. Spiller SE, Ravanpay AC, Hahn AW, Olson JM: Suberoylanilide hydroxamic acid is effective in preclinical studies of medulloblastoma. J Neurooncol; 2006 Sep;79(3):259-70
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  • [Title] Suberoylanilide hydroxamic acid is effective in preclinical studies of medulloblastoma.
  • However, little information has been reported on the effects of SAHA on central nervous system (CNS) tumors including medulloblastoma, the most common malignant brain tumor in children.
  • We investigated SAHA in preclinical medulloblastoma models to determine its anti-cancer efficacy as well as its ability to affect intracranial lesions when administered systemically.
  • EXPERIMENTAL DESIGN AND RESULTS: Tissue culture studies were performed treating primary human fibroblasts, established medulloblastoma cell lines, and primary human medulloblastoma tumors with SAHA.
  • At 10 microM concentration, SAHA had little effect on normal fibroblasts but caused >90% apoptosis in cultured medulloblastoma cells.
  • In athymic mice with medulloblastoma xenograft tumors, oral SAHA resulted in apoptosis of tumor tissue and significantly slowed tumor growth.
  • In the ND2:Smo transgenic mouse medulloblastoma model, SAHA treatment caused significant apoptosis in these cerebellar tumors.
  • CONCLUSIONS: SAHA effectively induces cell death in established medulloblastoma cell lines, human patient primary tumor cultures, medulloblastoma xenografts and intracranial spontaneous medulloblastomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cerebellar Neoplasms / drug therapy. Hydroxamic Acids / pharmacology. Medulloblastoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cells, Cultured. Child. Fibroblasts / drug effects. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy

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  • (PMID = 16645722.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA112350-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxamic Acids; 58IFB293JI / vorinostat
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21. Yang L, Jackson E, Woerner BM, Perry A, Piwnica-Worms D, Rubin JB: Blocking CXCR4-mediated cyclic AMP suppression inhibits brain tumor growth in vivo. Cancer Res; 2007 Jan 15;67(2):651-8
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  • To develop such a therapeutic approach, we investigated the signaling pathways critical for CXCL12 function in normal and malignant cells.
  • Consistent with these findings, we show that pharmacologic elevation of cAMP with the phosphodiesterase inhibitor Rolipram suppresses tumor cell growth in vitro and, upon oral administration, inhibits intracranial growth in xenograft models of malignant brain tumors with comparable efficacy to AMD 3465.
  • These data indicate that the clinical evaluation of phosphodiesterase inhibitors in the treatment of patients with brain tumors is warranted.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Cyclic AMP / antagonists & inhibitors. Pyridines / pharmacology. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Chemokine CXCL12. Chemokines, CXC. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Medulloblastoma / drug therapy. Medulloblastoma / metabolism. Medulloblastoma / pathology. Mice. Mice, Inbred BALB C. Phosphorylation. Rolipram / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 17234775.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA94056
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / N-(1,4,8,11- tetraazacyclotetradecanyl-1,4-phenylenebis(methylene))-2-(aminomethyl)- pyridine; 0 / Pyridines; 0 / Receptors, CXCR4; E0399OZS9N / Cyclic AMP; K676NL63N7 / Rolipram
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22. Gershon TR, Becher OJ: Medulloblastoma: therapy and biologic considerations. Curr Neurol Neurosci Rep; 2006 May;6(3):200-6
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  • [Title] Medulloblastoma: therapy and biologic considerations.
  • Tremendous strides have been made in both the treatment and the biologic understanding of medulloblastoma.
  • Present optimal treatment can cure most medulloblastoma patients.
  • Recent studies have demonstrated that the success of treatment is not simply a matter of chance, but rather can be predicted based on specific biologic markers.
  • Molecular biologic investigation, including replication of tumorigenesis in transgenic mice, has further elucidated the complex biology of medulloblastoma.
  • Current standard and investigational treatments, however, do not yet make use of biologic markers that predict risk of recurrence.
  • Practical limitations have slowed the pace at which treatment paradigms can be revised to incorporate biologic insights.
  • Mouse medulloblastoma models may provide an important bridge between biologic investigation and the development of new therapeutic approaches.
  • [MeSH-major] Medulloblastoma
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Evaluation, Preclinical. Humans. Risk Factors

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  • (PMID = 16635428.001).
  • [ISSN] 1528-4042
  • [Journal-full-title] Current neurology and neuroscience reports
  • [ISO-abbreviation] Curr Neurol Neurosci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
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23. Wick W, Wick A, Schulz JB, Dichgans J, Rodemann HP, Weller M: Prevention of irradiation-induced glioma cell invasion by temozolomide involves caspase 3 activity and cleavage of focal adhesion kinase. Cancer Res; 2002 Mar 15;62(6):1915-9
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  • In contrast, DAOY medulloblastoma cells, which respond with caspase activation to irradiation alone, do not show enhanced invasiveness when irradiated.
  • [MeSH-minor] 3T3 Cells. Animals. Caspase 3. Combined Modality Therapy. Focal Adhesion Kinase 1. Focal Adhesion Protein-Tyrosine Kinases. Humans. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase Inhibitors. Matrix Metalloproteinases, Membrane-Associated. Metalloendopeptidases / antagonists & inhibitors. Metalloendopeptidases / biosynthesis. Mice. Neoplasm Invasiveness. Rats. Receptors, Vitronectin / antagonists & inhibitors. Receptors, Vitronectin / biosynthesis. Tumor Cells, Cultured. Up-Regulation / drug effects

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  • (PMID = 11912174.001).
  • [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 / Antineoplastic Agents, Alkylating; 0 / Matrix Metalloproteinase Inhibitors; 0 / Receptors, Vitronectin; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / PTK2 protein, human; EC 2.7.10.2 / Ptk2 protein, mouse; EC 2.7.10.2 / Ptk2 protein, rat; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.24.- / Matrix Metalloproteinases, Membrane-Associated; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.24 / Matrix Metalloproteinase 2
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24. Saran A: Medulloblastoma: role of developmental pathways, DNA repair signaling, and other players. Curr Mol Med; 2009 Dec;9(9):1046-57
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  • [Title] Medulloblastoma: role of developmental pathways, DNA repair signaling, and other players.
  • Medulloblastoma is a cerebellar tumor affecting children and young adults, and accounts for approximately one fifth of all pediatric brain tumors.
  • Despite multimodal therapy that includes surgery, radiotherapy and chemotherapy, recurrence is frequent and overall mortality rate remains relatively high.
  • Moreover, radiation therapy results in severe effects on intellect, and younger age of treatment correlates with larger deficits.
  • Improvements in therapy of this childhood tumor will focus increasingly on the clarification of the exact cellular origin and the genetic mechanisms contributing to tumor formation, and on new targeted therapeutic options.
  • Aberrant activation of the Hedgehog (Hh) and Wnt developmental pathways is associated with medulloblastoma, but deregulation of other molecular pathways, including insulin-like growth factor (IGF) signaling, has also been implicated in the pathogenesis of the tumor.
  • Recent observations in mouse models have demonstrated the importance of genome surveillance, as defects in DNA repair pathways in animals can lead to genomic instability in neural progenitor cells, resulting in medulloblastoma.
  • The current review will focus on the most recent findings on the molecular pathology of medulloblastoma and discuss their potential contribution to treatments directed by the molecular alterations.
  • [MeSH-major] Cerebellar Neoplasms / metabolism. DNA Repair / physiology. Medulloblastoma / metabolism. Signal Transduction / physiology

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  • (PMID = 19747111.001).
  • [ISSN] 1875-5666
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 169
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25. Miller-Moslin K, Peukert S, Jain RK, McEwan MA, Karki R, Llamas L, Yusuff N, He F, Li Y, Sun Y, Dai M, Perez L, Michael W, Sheng T, Lei H, Zhang R, Williams J, Bourret A, Ramamurthy A, Yuan J, Guo R, Matsumoto M, Vattay A, Maniara W, Amaral A, Dorsch M, Kelleher JF 3rd: 1-amino-4-benzylphthalazines as orally bioavailable smoothened antagonists with antitumor activity. J Med Chem; 2009 Jul 9;52(13):3954-68
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  • Abnormal activation of the Hedgehog (Hh) signaling pathway has been linked to several types of human cancers, and the development of small-molecule inhibitors of this pathway represents a promising route toward novel anticancer therapeutics.
  • This compound displayed a good pharmacokinetic profile and also afforded tumor regression in a genetic mouse model of medulloblastoma.
  • [MeSH-minor] Administration, Oral. Animals. Hedgehog Proteins / metabolism. Humans. Medulloblastoma / drug therapy. Mice. Neoplasms, Experimental / drug therapy. Signal Transduction / drug effects. Structure-Activity Relationship

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  • (PMID = 19469545.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Phthalazines; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Smo protein, mouse
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26. Kimura H, Ng JM, Curran T: Transient inhibition of the Hedgehog pathway in young mice causes permanent defects in bone structure. Cancer Cell; 2008 Mar;13(3):249-60
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  • Although pathway activity was restored 2 days after drug removal, brief inhibition caused permanent defects in bone growth.
  • After drug removal, osteoblasts invaded the cartilage plate, mineralization occurred, and there was premature fusion of the growth plate resulting in permanent disruption of bone epiphyses.
  • [MeSH-major] Antineoplastic Agents / toxicity. Bone and Bones / drug effects. Chondrocytes / drug effects. Hedgehog Proteins. Receptors, G-Protein-Coupled / antagonists & inhibitors. Signal Transduction / drug effects
  • [MeSH-minor] Administration, Oral. Aging / metabolism. Animals. Animals, Newborn. Bone Remodeling / drug effects. Calcification, Physiologic / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Cerebellar Neoplasms / drug therapy. Dose-Response Relationship, Drug. Growth Plate / drug effects. Growth Plate / pathology. Kruppel-Like Transcription Factors / genetics. Kruppel-Like Transcription Factors / metabolism. Luciferases / genetics. Luciferases / metabolism. Medulloblastoma / drug therapy. Mice. Mice, Transgenic. Microscopy, Fluorescence. Microscopy, Video. Osteogenesis / drug effects. Recombinant Fusion Proteins / metabolism. Time Factors

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  • (PMID = 18328428.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA096832
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gli protein, mouse; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Fusion Proteins; 0 / Smo protein, mouse; EC 1.13.12.- / Luciferases
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27. Bai R, Siu IM, Tyler BM, Staedtke V, Gallia GL, Riggins GJ: Evaluation of retinoic acid therapy for OTX2-positive medulloblastomas. Neuro Oncol; 2010 Jul;12(7):655-63
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  • [Title] Evaluation of retinoic acid therapy for OTX2-positive medulloblastomas.
  • Treatment with 9-cis RA reduced the growth of D425 flank xenograft tumors in mice.
  • In an intracranial model, however, MB tumors showed resistance to 9-cis RA treatment, and we implicated fibroblast growth factor (FGF) as a potential mediator of resistance to RA therapy.
  • These findings suggest a mechanism for RA-mediated anti-tumor effect on OTX2-positive MB cells and indicate that therapeutic targeting of OTX2 might be effective if FGF pathway-mediated resistance can be overcome.

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  • (PMID = 20511190.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS052507
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Otx Transcription Factors; 0 / Otx2 protein, mouse; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC2940451
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28. Reifenberger J, Schön MP: [Cutaneous epithelial tumors. Molecular biology and pathogenesis-based therapy]. Hautarzt; 2003 Dec;54(12):1164-70
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  • [Title] [Cutaneous epithelial tumors. Molecular biology and pathogenesis-based therapy].
  • [Transliterated title] Molekulare Grundlagen und pathogeneseorientierte Therapie epithelialer Tumoren der Haut.
  • The development of novel, pathogenesis-based therapies requires a better knowledge of the molecular mechanisms leading to the development of these tumors.
  • Recently, specific inhibitors of the SHH-signaling pathway have been developed and shown promising results in preclinical studies on experimental basal cell carcinomas.
  • However, the clinical significance of such targeted molecular therapy remains to be evaluated.
  • Another successful pathogenesis-based therapy, which is already in clinical use, is the administration of topic immune response modifier imiquimod.
  • This drug can eradicate non-melanoma skin cancers by different mechanisms, including cytokine-mediated stimulation of the anti-tumor immune response, as well as the induction of tumor cell apoptosis.
  • [MeSH-major] Carcinoma, Basal Cell / genetics. Carcinoma, Basal Cell / therapy. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / therapy. Mutation. Skin Neoplasms / genetics. Skin Neoplasms / therapy
  • [MeSH-minor] Adjuvants, Immunologic / therapeutic use. Alleles. Aminoquinolines / therapeutic use. Animals. Antineoplastic Agents / therapeutic use. Apoptosis. Cerebellar Neoplasms / drug therapy. Disease Models, Animal. Genes, Tumor Suppressor. Hedgehog Proteins. Humans. Medulloblastoma / drug therapy. Membrane Proteins / genetics. Mice. Patched Receptors. Patched-1 Receptor. Receptors, Cell Surface. Signal Transduction / genetics. Trans-Activators. Transcription Factors / genetics. Tumor Cells, Cultured. Veratrum Alkaloids / therapeutic use

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  • (PMID = 14634745.001).
  • [ISSN] 0017-8470
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Membrane Proteins; 0 / PTCH protein, human; 0 / Patched Receptors; 0 / Patched-1 Receptor; 0 / Ptch1 protein, mouse; 0 / Receptors, Cell Surface; 0 / SHH protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Veratrum Alkaloids; P1QW714R7M / imiquimod; ZH658AJ192 / cyclopamine
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