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1. Urbanska K, Pannizzo P, Grabacka M, Croul S, Del Valle L, Khalili K, Reiss K: Activation of PPARalpha inhibits IGF-I-mediated growth and survival responses in medulloblastoma cell lines. Int J Cancer; 2008 Sep 1;123(5):1015-24
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  • [Title] Activation of PPARalpha inhibits IGF-I-mediated growth and survival responses in medulloblastoma cell lines.
  • Recent studies suggest a potential role of lipid lowering drugs, fibrates and statins, in anticancer treatment.
  • Our results demonstrate elevated expression of PPARalpha in the nuclei of neoplatic cells in 12 out of 13 cases of medulloblastoma, and of PPARgamma in six out of 13 cases.
  • Further analysis demonstrated that aggressive mouse medulloblastoma cells, BsB8, express PPARalpha in the absence PPARgamma, and human medulloblastoma cells, D384 and Daoy, express both PPARalpha and PPARgamma.
  • Mouse and human cells responded to fenofibrate by a significant increase of PPAR-mediated transcriptional activity, and by a gradual accumulation of cells in G1 and G2/M phase of the cell cycle, leading to the inhibition of cell proliferation and elevated apoptosis.
  • These results indicate a strong supportive role of fenofibrate in chemoprevention against IGF-I-induced growth responses in medulloblastoma.

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  • (PMID = 18546270.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095518; United States / NINDS NIH HHS / NS / P01 NS036466; United States / NCI NIH HHS / CA / R01 CA095518-08; United States / NCI NIH HHS / CA / R01CA095518-01; United States / NCI NIH HHS / CA / CA095518-07; United States / NCI NIH HHS / CA / CA095518-08; United States / NCI NIH HHS / CA / R01 CA095518-07; United States / NINDS NIH HHS / NS / P01 NS36466-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PPAR alpha; 67763-96-6 / Insulin-Like Growth Factor I; U202363UOS / Fenofibrate
  • [Other-IDs] NLM/ NIHMS277965; NLM/ PMC3222922
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2. Heine VM, Priller M, Ling J, Rowitch DH, Schüller U: Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma. Cancer Res; 2010 Jul 01;70(13):5220-5
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  • [Title] Dexamethasone destabilizes Nmyc to inhibit the growth of hedgehog-associated medulloblastoma.
  • Mouse studies indicate that the synthetic glucocorticoid dexamethasone (Dex) impairs the proliferation of granule neuron precursors in the cerebellum, which are transformed to medulloblastoma by activation of Sonic hedgehog (Shh) signaling.
  • Here, we show that Dex treatment also inhibits Shh-induced tumor growth, enhancing the survival of tumor-prone transgenic mice.
  • Together, our findings show that Dex antagonizes Shh signaling downstream of Smoothened in medulloblastoma.
  • [MeSH-major] Brain Neoplasms / drug therapy. Dexamethasone / pharmacology. Hedgehog Proteins / metabolism. Medulloblastoma / drug therapy. Proto-Oncogene Proteins c-myc / antagonists & inhibitors

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20530674.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / / ; United States / NINDS NIH HHS / NS / R01 NS047527; United States / NINDS NIH HHS / NS / NS047527
  • [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 / Proto-Oncogene Proteins c-myc; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.1 / Gsk3b protein, mouse; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ HHMIMS207553; NLM/ PMC2896447
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3. Romer J, Curran T: Targeting medulloblastoma: small-molecule inhibitors of the Sonic Hedgehog pathway as potential cancer therapeutics. Cancer Res; 2005 Jun 15;65(12):4975-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting medulloblastoma: small-molecule inhibitors of the Sonic Hedgehog pathway as potential cancer therapeutics.
  • Medulloblastoma is the most common malignant pediatric brain tumor for which no satisfactory treatments exist.
  • Here we review our recent demonstration that a small-molecule inhibitor of this pathway can regress tumors that arise in a transgenic mouse model of medulloblastoma.
  • [MeSH-major] Brain Neoplasms / drug therapy. Medulloblastoma / drug therapy. Trans-Activators / antagonists & inhibitors
  • [MeSH-minor] Animals. Benzimidazoles / pharmacology. Disease Models, Animal. Hedgehog Proteins. Humans. Mice. Mice, Transgenic. Signal Transduction / drug effects

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  • (PMID = 15958535.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzimidazoles; 0 / Hedgehog Proteins; 0 / SHH protein, human; 0 / Trans-Activators
  • [Number-of-references] 23
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4. Samano AK, Ohshima-Hosoyama S, Whitney TG, Prajapati SI, Kilcoyne A, Taniguchi E, Morgan WW, Nelon LD, Lin AL, Togao O, Jung I, Rubin BP, Nowak BM, Duong TQ, Keller C: Functional evaluation of therapeutic response for a mouse model of medulloblastoma. Transgenic Res; 2010 Oct;19(5):829-40
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  • [Title] Functional evaluation of therapeutic response for a mouse model of medulloblastoma.
  • Medulloblastoma is an aggressive childhood cerebellar tumor.
  • We recently reported a mouse model with conditional deletion of Patched1 gene that recapitulates many characteristics of the human medulloblastoma.
  • Qualitative symptoms observed in the mouse model include irregular stride length, impaired cranial nerve function and decreased motor coordination and performance.
  • In our current study, several quantitative behavioral assays including a mouse rotarod, a forced air challenge, a screen inversion test, a horizontal wire test, and stride length analysis were evaluated to determine the most sensitive and cost-effective functional assay for impaired neuromotor behavior associated with disease progression.
  • Magnetic resonance imaging (MRI) was used to confirm and monitor tumor growth and as an anatomical biomarker for therapeutic response.
  • Wild type mice or medulloblastoma-prone, conditional Patched1 knockout mice were observed by behavioral assays and MRI from postnatal weeks 3-6.
  • Bortezomib treatment was administered during this period and therapeutic response was assessed using cerebellar volumes at the end of treatment.
  • Of the behavioral tests assessed in this study, stride length analysis was best able to detect differences between tumor-prone mice and wild type mice as early as postnatal day 37 (P=0.003).
  • Cerebellar volumes measured by MRI at the end of treatment validated the therapeutic effects seen by behavioral tests (P=0.03).
  • These findings suggest that stride length analysis may serve as one of the more sensitive and cost-effective method for assessing new therapeutic compounds in this and other preclinical model of brain tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ataxia / etiology. Boronic Acids / therapeutic use. Cerebellar Neoplasms / drug therapy. Medulloblastoma / drug therapy. Protease Inhibitors / therapeutic use. Psychomotor Performance. Pyrazines / therapeutic use. Receptors, Cell Surface / deficiency
  • [MeSH-minor] Animals. Bortezomib. Disease Models, Animal. Disease Progression. Drug Screening Assays, Antitumor / economics. Drug Screening Assays, Antitumor / methods. Gait Disorders, Neurologic / etiology. Lameness, Animal / etiology. Magnetic Resonance Imaging. Mice. Mice, Knockout

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  • (PMID = 20107895.001).
  • [ISSN] 1573-9368
  • [Journal-full-title] Transgenic research
  • [ISO-abbreviation] Transgenic Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS045879
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / Receptors, Cell Surface; 0 / patched receptors; 69G8BD63PP / Bortezomib
  • [Other-IDs] NLM/ NIHMS759162; NLM/ PMC4770905
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5. 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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6. 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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7. 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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8. 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
BindingDB. BindingDB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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9. Ohshima-Hosoyama S, Hosoyama T, Nelon LD, Keller C: IGF-1 receptor inhibition by picropodophyllin in medulloblastoma. Biochem Biophys Res Commun; 2010 Sep 3;399(4):727-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IGF-1 receptor inhibition by picropodophyllin in medulloblastoma.
  • Increased IGF pathway activity has been reported in human and murine medulloblastoma.
  • Tumors from our genetically-engineered medulloblastoma mouse model over-express Igf1r, and thus this mouse model is a good platform with which to study the role of Igf1r in tumor progression.
  • We hypothesize that inhibition of IGF pathway in medulloblastoma can slow or inhibit tumor growth and metastasis.
  • To test our hypothesis, we tested the role of IGF in tumor growth in vitro by treatment with the tyrosine kinase small molecule inhibitor, picropodophyllin (PPP), which strongly inhibits the IGF pathway.
  • Our results demonstrate that PPP-mediated downregulation of the IGF pathway inhibits mouse tumor cell growth and induces apoptotic cell death in vitro in primary medulloblastoma cultures that are most reflective of tumor cell behavior in vivo.
  • [MeSH-major] Cerebellar Neoplasms / drug therapy. Medulloblastoma / drug therapy. Podophyllotoxin / analogs & derivatives. Receptor, IGF Type 1 / antagonists & inhibitors
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Cell Proliferation / drug effects. Disease Models, Animal. Gene Knockdown Techniques. Humans. Mice

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20692232.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0F35AOI227 / picropodophyllin; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.4.22.- / Caspase 3; L36H50F353 / Podophyllotoxin
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10. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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11. Yauch RL, Dijkgraaf GJ, Alicke B, Januario T, Ahn CP, Holcomb T, Pujara K, Stinson J, Callahan CA, Tang T, Bazan JF, Kan Z, Seshagiri S, Hann CL, Gould SE, Low JA, Rudin CM, de Sauvage FJ: Smoothened mutation confers resistance to a Hedgehog pathway inhibitor in medulloblastoma. Science; 2009 Oct 23;326(5952):572-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Smoothened mutation confers resistance to a Hedgehog pathway inhibitor in medulloblastoma.
  • The Hedgehog (Hh) signaling pathway is inappropriately activated in certain human cancers, including medulloblastoma, an aggressive brain tumor.
  • GDC-0449, a drug that inhibits Hh signaling by targeting the serpentine receptor Smoothened (SMO), has produced promising anti-tumor responses in early clinical studies of cancers driven by mutations in this pathway.
  • To evaluate the mechanism of resistance in a medulloblastoma patient who had relapsed after an initial response to GDC-0449, we determined the mutational status of Hh signaling genes in the tumor after disease progression.
  • A mutation altering the same amino acid also arose in a GDC-0449-resistant mouse model of medulloblastoma.
  • These findings show that acquired mutations in a serpentine receptor with features of a G protein-coupled receptor can serve as a mechanism of drug resistance in human cancer.
  • [MeSH-major] Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Hedgehog Proteins / metabolism. Medulloblastoma / drug therapy. Medulloblastoma / genetics. Pyridines / therapeutic use. Receptors, G-Protein-Coupled / genetics
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution. Animals. Cell Line, Tumor. Cinnamates / pharmacology. Drug Resistance, Neoplasm. Humans. Mice. Molecular Sequence Data. Mutant Proteins / antagonists & inhibitors. Mutant Proteins / chemistry. Mutant Proteins / metabolism. Mutation, Missense. Neoplasm Metastasis. Patched Receptors. Protein Conformation. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Signal Transduction. Smoothened Receptor. Veratrum Alkaloids / pharmacology


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


13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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15. 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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16. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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17. Rossi A, Schenone S, Angelucci A, Cozzi M, Caracciolo V, Pentimalli F, Puca A, Pucci B, La Montagna R, Bologna M, Botta M, Giordano A: New pyrazolo-[3,4-d]-pyrimidine derivative Src kinase inhibitors lead to cell cycle arrest and tumor growth reduction of human medulloblastoma cells. FASEB J; 2010 Aug;24(8):2881-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New pyrazolo-[3,4-d]-pyrimidine derivative Src kinase inhibitors lead to cell cycle arrest and tumor growth reduction of human medulloblastoma cells.
  • Medulloblastoma is the most common malignant brain tumor in children, and despite improvements in the overall survival rate, it still lacks an effective treatment.
  • Src plays an important role in cancer, and recently high Src activity was documented in medulloblastoma.
  • In this report, we examined the effects of novel pyrazolo-[3,4-d]-pyrimidine derivative Src inhibitors in medulloblastoma.
  • By MTS assay, we showed that the pyrimidine derivatives indicated as S7, S29, and SI163 greatly reduce the growth rate of medulloblastoma cells by inhibiting Src phosphorylation, compared with HT22 non-neoplastic nerve cells.
  • Moreover, the exposure to pyrimidine derivatives induces apoptosis, assayed by the supravital propidium iodide assay, through modulation of the apoptotic proteins Bax and Bcl2, and inhibits tumor growth in vivo in a mouse model.
  • Notably, S7, S29, and SI163 show major inhibitory effects on medulloblastoma cell growth compared with the chemotherapeutic agents cisplatin and etoposide.
  • In conclusion, our results suggest that S7, S29, and SI163 could be novel attractive candidates for the treatment of medulloblastoma or tumors characterized by high Src activity.
  • [MeSH-major] Cell Cycle / drug effects. Cell Proliferation / drug effects. Medulloblastoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / chemistry. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Humans

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  • (PMID = 20354138.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [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 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ PMC2909284
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18. Fomchenko EI, Holland EC: Mouse models of brain tumors and their applications in preclinical trials. Clin Cancer Res; 2006 Sep 15;12(18):5288-97
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse models of brain tumors and their applications in preclinical trials.
  • Accurate recapitulation of these genetic alterations using genetically engineered mouse models allows for in vivo modeling of brain tumors with similar histopathology, etiology, and biology.
  • These mouse models, in turn, increase our understanding of brain tumor initiation, formation, progression, and metastasis, providing an experimental system to discover novel therapeutic targets and test various therapeutic agents.
  • [MeSH-major] Brain Neoplasms / drug therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Drug Design. Drug Evaluation, Preclinical / methods. Glioma / classification. Glioma / radiography. Humans. Magnetic Resonance Imaging. Medulloblastoma / classification. Medulloblastoma / radiography. Mice. Mice, Transgenic. Models, Biological

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  • [CommentIn] Clin Cancer Res. 2006 Sep 15;12(18):5274-6 [17000659.001]
  • (PMID = 17000661.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100688
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 73
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19. 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
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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20. 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
Hazardous Substances Data Bank. CARBOPLATIN .

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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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  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
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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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21. 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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22. 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
The Lens. Cited by Patents in .

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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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23. 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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24. 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


25. Shalaby T, Hiyama E, Grotzer MA: Telomere maintenance as therapeutic target in embryonal tumours. Anticancer Agents Med Chem; 2010 Mar;10(3):196-212
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomere maintenance as therapeutic target in embryonal tumours.
  • Knowledge of these tumours' genetics has already impacted on their clinical management and further knowledge of their cellular immortalization will hopefully result in novel therapies.
  • Telomere maintenance is evident in virtually all types of malignant cells, including embryonal tumours, where either a telomerase-dependent or alternative lengthening of telomeres (ALT) mechanism is employed in order to ensure their limitless replicative potential.
  • In this review, we are giving an overview about telomere maintenance in childhood tumours and discussing its potential as a new therapeutic target.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms, Germ Cell and Embryonal / drug therapy. Telomerase / physiology. Telomere / metabolism
  • [MeSH-minor] Animals. Child. Embryo, Mammalian / enzymology. G-Quadruplexes / drug effects. Hepatoblastoma / genetics. Humans. Medulloblastoma / genetics. Mice. Neuroblastoma / genetics. Rhabdomyosarcoma / genetics. Sarcoma, Ewing / genetics. Wilms Tumor / genetics

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  • (PMID = 20017721.001).
  • [ISSN] 1875-5992
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 2.7.7.49 / Tert protein, mouse
  • [Number-of-references] 250
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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. 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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28. 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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29. 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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30. 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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31. 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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32. 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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33. 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
eagle-i research resources. PMID 10984056 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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34. 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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35. Maris JM, Morton CL, Gorlick R, Kolb EA, Lock R, Carol H, Keir ST, Reynolds CP, Kang MH, Wu J, Smith MA, Houghton PJ: Initial testing of the aurora kinase A inhibitor MLN8237 by the Pediatric Preclinical Testing Program (PPTP). Pediatr Blood Cancer; 2010 Jul 15;55(1):26-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment duration was 6 weeks for solid tumor xenografts and 3 weeks for ALL xenografts.
  • Maintained CRs were observed among single xenografts in other panels, including the Wilms tumor, rhabdoid tumor, rhabdomyosarcoma, Ewing sarcoma, osteosarcoma, and medulloblastoma.

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  • (PMID = 20108338.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NCI NIH HHS / CA / CA108786; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CM / N01 CM042216; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CM / N01-CM-42216; United States / NCI NIH HHS / CA / N01CM42216
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Azepines; 0 / MLN 8237; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS165147; NLM/ PMC2874079
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36. Wildasin K: New therapy for medulloblastoma tested in mice. Lancet Neurol; 2004 Nov;3(11):640
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New therapy for medulloblastoma tested in mice.
  • [MeSH-major] Cerebellar Neoplasms / drug therapy. Growth Inhibitors / therapeutic use. Medulloblastoma / therapy. Trans-Activators / antagonists & inhibitors

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  • (PMID = 15515241.001).
  • [ISSN] 1474-4422
  • [Journal-full-title] The Lancet. Neurology
  • [ISO-abbreviation] Lancet Neurol
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Hedgehog Proteins; 0 / Shh protein, mouse; 0 / Trans-Activators
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