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1. Morton CL, Iacono L, Hyatt JL, Taylor KR, Cheshire PJ, Houghton PJ, Danks MK, Stewart CF, Potter PM: Activation and antitumor activity of CPT-11 in plasma esterase-deficient mice. Cancer Chemother Pharmacol; 2005 Dec;56(6):629-36
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  • PURPOSE: To examine the antitumor activity and the pharmacokinetics of CPT-11 (irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) in a plasma esterase-deficient scid mouse model, bearing human tumor xenografts.
  • Hence, these mice may represent a more accurate model for antitumor studies with this drug and other agents metabolized by CEs.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacokinetics. Antineoplastic Agents, Phytogenic / pharmacology. Camptothecin / analogs & derivatives. Esterases / deficiency. Sarcoma, Experimental / drug therapy
  • [MeSH-minor] Animals. Body Weight / drug effects. Dose-Response Relationship, Drug. Gastrointestinal Tract / drug effects. Gastrointestinal Tract / enzymology. Humans. Mice. Mice, SCID. Neoplasm Transplantation. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / pathology

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  • (PMID = 15918039.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA76202; United States / NCI NIH HHS / CA / R25 CA023944; United States / NCI NIH HHS / CA / CA23099; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA79763
  • [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] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0H43101T0J / irinotecan; EC 3.1.- / Esterases; XT3Z54Z28A / Camptothecin
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2. Michaelis M, Rothweiler F, Klassert D, von Deimling A, Weber K, Fehse B, Kammerer B, Doerr HW, Cinatl J Jr: Reversal of P-glycoprotein-mediated multidrug resistance by the murine double minute 2 antagonist nutlin-3. Cancer Res; 2009 Jan 15;69(2):416-21
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  • Nutlin-3 is a MDM2 inhibitor under preclinical investigation as nongenotoxic activator of the p53 pathway for cancer therapy.
  • Here, nutlin-3 was evaluated for its activity alone or in combination with established chemotherapeutic drugs for antitumor action in chemosensitive and chemoresistant neuroblastoma and rhabdomyosarcoma cell lines.
  • Effects of nutlin-3 single treatment were much more pronounced in p53 wild-type cell lines (IC(50)s <3 micromol/L) than in p53-mutated cell lines (IC(50)s >17 micromol/L).
  • Examination of the nutlin-3 enantiomers nutlin-3a and nutlin-3b revealed that, in contrast to MDM2-inhibitory activity that is limited to nutlin-3a, both enantiomers similarly interfere with P-gp-mediated drug efflux.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Imidazoles / pharmacology. Neuroblastoma / drug therapy. P-Glycoprotein / antagonists & inhibitors. Piperazines / pharmacology. Rhabdomyosarcoma, Alveolar / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Drug Synergism. Humans. Mice. Mutation. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors. Rhodamine 123 / pharmacokinetics. Stereoisomerism. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics. Vincristine / administration & dosage

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  • (PMID = 19147553.001).
  • [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 / Imidazoles; 0 / P-Glycoprotein; 0 / Piperazines; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; 1N3CZ14C5O / Rhodamine 123; 5J49Q6B70F / Vincristine; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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3. 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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4. Adepoju LJ, Geiger JD: Antitumor activity of polyuridylic acid in human soft tissue and bone sarcomas. J Surg Res; 2010 Nov;164(1):e107-14
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  • [Title] Antitumor activity of polyuridylic acid in human soft tissue and bone sarcomas.
  • MATERIALS AND METHODS: TLR8 mRNA and protein expression in soft tissue sarcoma (STS) and bone sarcoma (BS) cell lines were determined by PCR and flow cytometry, respectively.
  • RESULTS: We demonstrate that PolyU treatment resulted in a significant decrease in STS and BS cell count by inducing apoptosis and inhibition of cell proliferation.
  • Several apoptotic proteins including caspases were activated or increased in STS cells after treatment with PolyU.
  • Administration PolyU resulted in significant growth inhibition of STS without any observable adverse effects in mouse xenograft tumor models.
  • CONCLUSIONS: These results elucidate the effect of PolyU in STS and BS cells and demonstrate that PolyU may be a potential therapeutic agent for STS and BS.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bone Neoplasms / drug therapy. Fibrosarcoma / drug therapy. Poly U / pharmacology. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Humans. Male. Mice. Mice, SCID. Mitochondria / drug effects. Nerve Sheath Neoplasms / drug therapy. Nerve Sheath Neoplasms / metabolism. Nerve Sheath Neoplasms / pathology. Osteosarcoma / drug therapy. Osteosarcoma / metabolism. Osteosarcoma / pathology. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / metabolism. Rhabdomyosarcoma / pathology. Sarcoma, Clear Cell / drug therapy. Sarcoma, Clear Cell / metabolism. Sarcoma, Clear Cell / pathology. Toll-Like Receptor 8 / metabolism. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20828720.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [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 / TLR8 protein, human; 0 / Toll-Like Receptor 8; 27416-86-0 / Poly U; EC 3.4.22.- / Caspases
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5. 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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6. Liang H, Sha N: Modeling antitumor activity by using a non-linear mixed-effects model. Math Biosci; 2004 May;189(1):61-73
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  • The response of solid tumors to antitumor treatment generally declines markedly with treatment time.
  • Sometimes, a tumor regrows (rebounds) before the end of the treatment period.
  • Studies of the patterns of tumor response to treatment are important, because they may provide useful information for clinical decision-making.
  • We have investigated patterns of tumor response in mouse xenograft tumors by using data from a study conducted at St. Jude Children's Research Hospital.
  • We applied a biexponential non-linear mixed-effects model to an analysis of changes in tumor volume over a given period of treatment.
  • We addressed the relation between the baseline tumor volumes and the decay rates of the first and second stages of the tumor's response to treatment, and we applied sensitive analysis to determine the effect of using different imputed values for missing data.
  • We also proposed a novel approach to a comparison of the antitumor effects of three different treatments, and we used the data from a St. Jude study to demonstrate the potential of this comparison approach in cancer clinical decision-making.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Camptothecin / analogs & derivatives. Dacarbazine / analogs & derivatives. Neoplasms / drug therapy. Nonlinear Dynamics. Xenograft Model Antitumor Assays
  • [MeSH-minor] Algorithms. Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Computer Simulation. Data Interpretation, Statistical. Humans. Mice. Rhabdomyosarcoma / drug therapy. Treatment Outcome

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  • (PMID = 15051414.001).
  • [ISSN] 0025-5564
  • [Journal-full-title] Mathematical biosciences
  • [ISO-abbreviation] Math Biosci
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 2G12RR08124
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; XT3Z54Z28A / Camptothecin
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7. 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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8. Zeisberger SM, Odermatt B, Marty C, Zehnder-Fjällman AH, Ballmer-Hofer K, Schwendener RA: Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach. Br J Cancer; 2006 Aug 7;95(3):272-81
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  • [Title] Clodronate-liposome-mediated depletion of tumour-associated macrophages: a new and highly effective antiangiogenic therapy approach.
  • Treatment with clodronate encapsulated in liposomes (clodrolip) efficiently depleted these phagocytic cells in the murine F9 teratocarcinoma and human A673 rhabdomyosarcoma mouse tumour models resulting in significant inhibition of tumour growth ranging from 75 to >92%, depending on therapy and schedule.
  • Tumour inhibition was accompanied by a drastic reduction in blood vessel density in the tumour tissue.
  • The strongest effects were observed with the combination therapy of clodrolip and a VEGF-neutralising antibody, whereas free clodronate was not significantly active.
  • Blood vessel staining (CD31) and quantification of the vessels as well as TAMs and tumour-associated dendritic cells (TADCs) in the A673 model showed reduction rates of 85 to >94%, even 9 days after the end of therapy.
  • In addition, CD11c+ TADCs, which have been shown to potentially differentiate into endothelial-like cells upon stimulation by tumour released growth and differentiation factors, were similarly reduced by clodrolip or antibody treatment.
  • These results validate clodrolip therapy in combination with angiogenesis inhibitors as a promising novel strategy for an indirect cancer therapy aimed at the haematopoietic precursor cells that stimulate tumour growth and dissemination and as a tool to study the role of macrophages and dendritic cells in tumorigenesis.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Clodronic Acid / pharmacology. Macrophages / drug effects. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Immunohistochemistry. In Vitro Techniques. Liposomes. Mice. Mice, Nude. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 16832418.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Liposomes; 0 / Vascular Endothelial Growth Factor A; 0813BZ6866 / Clodronic Acid
  • [Other-IDs] NLM/ PMC2360657
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9. Wang Q, Fang WH, Krupinski J, Kumar S, Slevin M, Kumar P: Pax genes in embryogenesis and oncogenesis. J Cell Mol Med; 2008 Dec;12(6A):2281-94
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  • The Splotch phenotype in mouse exhibits defects in neural crest derivatives such as, pigment cells, sympathetic ganglia and cardiac neural crest-derived structures.
  • In particular, PAX3 is involved in rhabdomyosarcoma and tumours of neural crest origin, including melanoma and neuroblastoma.
  • [MeSH-minor] Alternative Splicing. Animals. Genetic Therapy. Humans. Melanocytes / cytology. Melanocytes / metabolism. Melanoma / etiology. Melanoma / genetics. Mice. Models, Genetic. Muscle Development / genetics. Neuroblastoma / etiology. Neuroblastoma / genetics. Neurogenesis / genetics. Oncogenes. Rhabdomyosarcoma / etiology. Rhabdomyosarcoma / genetics

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  • (PMID = 18627422.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Paired Box Transcription Factors
  • [Number-of-references] 138
  • [Other-IDs] NLM/ PMC4514106
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10. Collingridge DR, Rockwell S: Pentoxifylline improves the oxygenation and radiation response of BA1112 rat rhabdomyosarcomas and EMT6 mouse mammary carcinomas. Int J Cancer; 2000 Oct 20;90(5):256-64
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  • [Title] Pentoxifylline improves the oxygenation and radiation response of BA1112 rat rhabdomyosarcomas and EMT6 mouse mammary carcinomas.
  • Tumor hypoxia can significantly impact the efficacy of cancer therapy.
  • Pentoxifylline, a methylxanthine derivative, can improve oxygen delivery to tissues and is widely used in the treatment of peripheral vascular disease and various cerebrovascular disorders.
  • Our findings confirm that preirradiation administration of pentoxifylline can improve radiation efficacy, but suggest that its role as a postirradiation modifier of treatment response, reported by others, may be tumor-specific.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / radiotherapy. Mammary Neoplasms, Animal / drug therapy. Mammary Neoplasms, Animal / radiotherapy. Oxygen / metabolism. Pentoxifylline / therapeutic use. Radiation-Protective Agents / therapeutic use. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / radiotherapy
  • [MeSH-minor] Animals. Anoxia. Cell Survival. Combined Modality Therapy. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Pressure. Radiation-Sensitizing Agents / therapeutic use. Rats. Tumor Cells, Cultured

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  • (PMID = 11091349.001).
  • [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 / Radiation-Protective Agents; 0 / Radiation-Sensitizing Agents; S88TT14065 / Oxygen; SD6QCT3TSU / Pentoxifylline
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11. Wan X, Helman LJ: Effect of insulin-like growth factor II on protecting myoblast cells against cisplatin-induced apoptosis through p70 S6 kinase pathway. Neoplasia; 2002 Sep-Oct;4(5):400-8
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  • Cisplatin treatment of C2C12 mouse myoblasts led to cell death associated with an inhibition of p70 S6K activity.
  • Furthermore, treatment of IGF-II-overexpressing Rh30 and CTR rhabdomyosarcoma cells with rapamycin restored sensitivity to cisplatin-induced apoptosis.
  • Thus, inhibition of the p70 S6 pathway may enhance chemotherapy-induced apoptosis in the treatment of IGF-II-overexpressing tumors.
  • [MeSH-major] Antineoplastic Agents / toxicity. Apoptosis / drug effects. Cisplatin / toxicity. Insulin-Like Growth Factor II / pharmacology. Myoblasts / drug effects. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Antibiotics, Antineoplastic / pharmacology. Blotting, Western. Carrier Proteins / antagonists & inhibitors. Cell Division. Cell Line. Cytoprotection. Drug Resistance, Neoplasm. Flow Cytometry. Humans. Mice. Phosphoproteins / antagonists & inhibitors. Phosphorylation. Rhabdomyosarcoma / drug therapy. Sirolimus / pharmacology. Transfection. Up-Regulation

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  • (PMID = 12192598.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / EIF4EBP1 protein, human; 0 / Eif4ebp1 protein, mouse; 0 / Phosphoproteins; 67763-97-7 / Insulin-Like Growth Factor II; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1564119
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12. Ohnuma-Ishikawa K, Morio T, Yamada T, Sugawara Y, Ono M, Nagasawa M, Yasuda A, Morimoto C, Ohnuma K, Dang NH, Hosoi H, Verdin E, Mizutani S: Knockdown of XAB2 enhances all-trans retinoic acid-induced cellular differentiation in all-trans retinoic acid-sensitive and -resistant cancer cells. Cancer Res; 2007 Feb 1;67(3):1019-29
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  • In vitro and in vivo studies showed that XAB2 is involved in pre-mRNA splicing, transcription, and transcription-coupled DNA repair, leading to preimplantation lethality, and is essential for mouse embryogenesis.
  • Retinoids are effective for the treatment of preneoplastic diseases including xeroderma pigmentosum and other dermatologic diseases such as photoaging.
  • We therefore focused on defining the effect of XAB2 on cellular differentiation in the presence of ATRA treatment.
  • In the present study, we showed that overexpression of XAB2 inhibited ATRA-induced cellular differentiation in human rhabdomyosarcoma cell line, and that knockdown of XAB2 by small interfering RNA (siRNA) increased ATRA-sensitive cellular differentiation in the human promyelocytic leukemia cell line HL60 at both physiologic (10(-9)-10(-8) mol/L) and therapeutic (10(-7) mol/L) concentrations of ATRA.
  • Finally, using siRNA against XAB2, we showed that the ATRA-resistant neuroblastoma cell line IMR-32 underwent cellular differentiation induced by ATRA at a therapeutic concentration (10(-6) mol/L).
  • These results strongly suggest that XAB2 is a component of the RAR corepressor complex with an inhibitory effect on ATRA-induced cellular differentiation and that XAB2 plays a role in ATRA-mediated cellular differentiation as an important aspect of cancer therapy.
  • [MeSH-major] Cell Differentiation / drug effects. Neuroblastoma / drug therapy. Rhabdomyosarcoma / drug therapy. Transcription Factors / deficiency. Tretinoin / pharmacology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Drug Resistance, Neoplasm. HL-60 Cells. Histone Deacetylases / metabolism. Humans. RNA, Small Interfering / genetics. Receptors, Retinoic Acid / metabolism. Transcriptional Activation / drug effects

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  • (PMID = 17283134.001).
  • [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; 0 / RNA, Small Interfering; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / XAB2 protein, human; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
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13. Petricoin EF 3rd, Espina V, Araujo RP, Midura B, Yeung C, Wan X, Eichler GS, Johann DJ Jr, Qualman S, Tsokos M, Krishnan K, Helman LJ, Liotta LA: Phosphoprotein pathway mapping: Akt/mammalian target of rapamycin activation is negatively associated with childhood rhabdomyosarcoma survival. Cancer Res; 2007 Apr 1;67(7):3431-40
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  • [Title] Phosphoprotein pathway mapping: Akt/mammalian target of rapamycin activation is negatively associated with childhood rhabdomyosarcoma survival.
  • Mapping of protein signaling networks within tumors can identify new targets for therapy and provide a means to stratify patients for individualized therapy.
  • Despite advances in combination chemotherapy, the overall survival for childhood rhabdomyosarcoma remains approximately 60%.
  • A critical goal is to identify functionally important protein signaling defects associated with treatment failure for the 40% nonresponder cohort.
  • Specimens (n = 59) were obtained from the Children's Oncology Group Intergroup Rhabdomyosarcoma Study (IRS) IV, D9502 and D9803, with 12-year follow-up.
  • The functional significance of this pathway was tested using CCI-779 in a mouse xenograft model.
  • CCI-779 suppressed phosphorylation of mTOR downstream proteins and greatly reduced the growth of two different rhabdomyosarcoma (RD embryonal P = 0.00008; Rh30 alveolar P = 0.0002) cell lines compared with controls.
  • These results suggest that phosphoprotein mapping of the Akt/mTOR pathway should be studied further as a means to select patients to receive mTOR/IRS pathway inhibitors before administration of chemotherapy.
  • [MeSH-major] Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Rhabdomyosarcoma / metabolism
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Insulin Receptor Substrate Proteins. Male. Mice. Mice, SCID. Phosphoproteins / metabolism. Phosphorylation. Signal Transduction. Survival Rate. TOR Serine-Threonine Kinases. Xenograft Model Antitumor Assays


14. Chowdhary RK, Sharif I, Chansarkar N, Dolphin D, Ratkay L, Delaney S, Meadows H: Correlation of photosensitizer delivery to lipoproteins and efficacy in tumor and arthritis mouse models; comparison of lipid-based and Pluronic P123 formulations. J Pharm Pharm Sci; 2003 May-Aug;6(2):198-204
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  • [Title] Correlation of photosensitizer delivery to lipoproteins and efficacy in tumor and arthritis mouse models; comparison of lipid-based and Pluronic P123 formulations.
  • PURPOSE: The purpose of this study was the use of animal models to demonstrate the importance of drug delivery (verteporfin) to plasma lipoproteins in order to attain efficacy of photodynamic therapy (PDT) in vivo.
  • METHODS: Photosensitizers appropriately formulated in various vehicles such as pluronics and lipid-based systems were compared to delivery of the drug in DMSO in two in vivo systems.
  • The first was a tumor model using male DBA/2 mice inoculated intradermally with M1 rhabdomyosarcoma cells and in the second, arthritis in the MRL -lpr mouse strain was enhanced by two intradermal injections of complete Freunds adjunct.
  • RESULTS: Those formulations in which the drug was in a monomeric form were better able to transfer drug to lipoproteins, which in turn led to superior PDT in vivo.
  • CONCLUSIONS: The ability to introduce drug in monomeric form into the circulation correlates well with efficacy of photosensitizer formulations in mouse arthritis and tumor models.
  • [MeSH-major] Chemistry, Pharmaceutical. Drug Delivery Systems. Lipoproteins / metabolism. Photochemotherapy. Photosensitizing Agents / administration & dosage

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  • (PMID = 12935430.001).
  • [ISSN] 1482-1826
  • [Journal-full-title] Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Société canadienne des sciences pharmaceutiques
  • [ISO-abbreviation] J Pharm Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Lipoproteins; 0 / Photosensitizing Agents
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15. Huang S, Liu LN, Hosoi H, Dilling MB, Shikata T, Houghton PJ: p53/p21(CIP1) cooperate in enforcing rapamycin-induced G(1) arrest and determine the cellular response to rapamycin. Cancer Res; 2001 Apr 15;61(8):3373-81
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  • The relationship between G(1) checkpoint function and rapamycininduced apoptosis was examined using two human rhabdomyosarcoma cell lines, Rh1 and Rh30, that express mutated p53 alleles.
  • Exposure to rapamycin (100 ng/ml) for 24 h significantly increased the proportion of Rh1 and Rh30 cells in G(1) phase, although there were no significant changes in expression of cyclins D1, E, or A in drug-treated cells.
  • The response to rapamycin was next examined in wild-type or murine embryo fibroblasts nullizygous for p53or p21(CIP1).
  • Under serum-free conditions, rapamycin-treated wild-type MEFs showed no increase in apoptosis compared to controls.
  • Under serum-containing conditions, rapamycin inhibited incorporation of BrdUrd significantly more in wild-type murine embryo fibroblasts (MEFs) than in those lacking p53 or p21(CIP1).
  • In contrast, only 19% of wild-type cells incorporated BrdUrd in the presence of rapamycin.
  • However, cyclin A was reduced to very low levels by rapamycin in wild-type cells, but remained high in cells lacking p53 or p21(CIP1).
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Cyclins / physiology. G1 Phase / drug effects. Protein Kinases. Sirolimus / pharmacology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Adenoviridae / genetics. Animals. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cyclin-Dependent Kinase Inhibitor p21. Fibroblasts / cytology. Fibroblasts / drug effects. Humans. Mice. Phosphotransferases (Alcohol Group Acceptor) / antagonists & inhibitors. Phosphotransferases (Alcohol Group Acceptor) / biosynthesis. Phosphotransferases (Alcohol Group Acceptor) / physiology. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / pathology. TOR Serine-Threonine Kinases

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  • (PMID = 11309295.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5T32CA09346; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA23099; United States / NCI NIH HHS / CA / CA77776
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Tumor Suppressor Protein p53; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
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16. Tan M, Fang HB, Tian GL, Houghton PJ: Repeated-measures models with constrained parameters for incomplete data in tumour xenograft experiments. Stat Med; 2005 Jan 15;24(1):109-19
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  • In cancer drug development, xenograft experiments (models) where mice are grafted with human cancer cells are used to elucidate the mechanism of action and/or to assess efficacy of a promising compound.
  • A key outcome variable in these experiments is tumour volumes measured over a period of time, while mice are treated with an anticancer agent following certain schedules.
  • However, a mouse may die during the experiment or may be sacrificed when its tumour volume quadruples and then incomplete repeated measurements arise.
  • In addition, if no treatment were given to the tumour-bearing mice, the tumours would keep growing until the mice die or are sacrificed.
  • This intrinsic growth of tumour in the absence of treatment constrains the parameters in the regression and causes further difficulties in statistical analysis.
  • [MeSH-minor] Algorithms. Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Female. Humans. Longitudinal Studies. Mice. Mice, SCID. Neoplasms, Experimental / drug therapy. Rhabdomyosarcoma / drug therapy

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  • [Copyright] 2004 John Wiley & Sons, Ltd.
  • (PMID = 15523707.001).
  • [ISSN] 0277-6715
  • [Journal-full-title] Statistics in medicine
  • [ISO-abbreviation] Stat Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA023099; United States / NCI NIH HHS / CA / CA106767
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; XT3Z54Z28A / Camptothecin
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