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


2. Taniguchi E, Nishijo K, McCleish AT, Michalek JE, Grayson MH, Infante AJ, Abboud HE, Legallo RD, Qualman SJ, Rubin BP, Keller C: PDGFR-A is a therapeutic target in alveolar rhabdomyosarcoma. Oncogene; 2008 Nov 20;27(51):6550-60
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  • [Title] PDGFR-A is a therapeutic target in alveolar rhabdomyosarcoma.
  • Alveolar rhabdomyosarcoma is an aggressive skeletal muscle cancer of childhood.
  • Our initial studies of rhabdomyosarcoma gene expression for patients enrolled in a national clinical trial suggested that platelet-derived growth factor receptor A (PDGFR-A) may be a mediator of disease progression and metastasis.
  • Using our conditional mouse tumor models that authentically recapitulate the primary mutations and metastatic progression of alveolar rhabdomyosarcomas in humans, we found by immunoblotting and immunokinase assays that PDGFR-A and its downstream effectors, mitogen-activated protein kinase and Akt, were highly activated in both primary and metastatic tumors.
  • These results establish proof-of-principal for PDGFR-A as a therapeutic target in alveolar rhabdomyosarcoma.

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  • [Cites] Kidney Int. 2000 Mar;57(3):908-17 [10720944.001]
  • [Cites] FEBS Lett. 2007 Dec 22;581(30):5831-5 [18053811.001]
  • [Cites] J Exp Med. 2001 Sep 3;194(5):581-9 [11535627.001]
  • [Cites] Nat Genet. 2001 Oct;29(2):143-52 [11544480.001]
  • [Cites] Genes Dev. 2002 Mar 15;16(6):676-80 [11914272.001]
  • [Cites] Nat Rev Cancer. 2002 Apr;2(4):251-65 [12001987.001]
  • [Cites] Nat Rev Drug Discov. 2002 Jul;1(7):493-502 [12120256.001]
  • [Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] Mod Pathol. 2004 Jun;17(6):660-9 [15098008.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Feb;80(3):731-5 [6298772.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):4118-30 [9632796.001]
  • [Cites] N Engl J Med. 1999 Jul 29;341(5):342-52 [10423470.001]
  • [Cites] Physiol Rev. 1999 Oct;79(4):1283-316 [10508235.001]
  • [Cites] Genes Dev. 2004 Nov 1;18(21):2614-26 [15489287.001]
  • [Cites] Genes Dev. 2004 Nov 1;18(21):2608-13 [15520281.001]
  • [Cites] J Cell Biochem. 2004 Nov 1;93(4):741-52 [15660418.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3206-13 [16030188.001]
  • [Cites] Curr Biol. 2005 Oct 25;15(20):1861-6 [16243034.001]
  • [Cites] Pediatr Blood Cancer. 2006 Mar;46(3):329-38 [16261596.001]
  • [Cites] Oncogene. 2006 Mar 30;25(14):2060-9 [16331269.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 23;103(21):8078-83 [16690743.001]
  • [Cites] Science. 2007 May 18;316(5827):1039-43 [17463250.001]
  • [Cites] Cancer. 2007 Nov 15;110(10):2293-303 [17896786.001]
  • [Cites] J Mol Diagn. 2001 May;3(2):55-61 [11333300.001]
  • (PMID = 18679424.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30CA54174; United States / NCI NIH HHS / CA / R01 CA133229; United States / NCI NIH HHS / CA / CA133229-01; United States / NCI NIH HHS / CA / P30 CA054174; United States / NCI NIH HHS / CA / R01 CA133229-01; United States / NCI NIH HHS / CA / R01CA133229
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS161083; NLM/ PMC2813858
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3. Hajdin K, D'Alessandro V, Niggli FK, Schäfer BW, Bernasconi M: Furin targeted drug delivery for treatment of rhabdomyosarcoma in a mouse model. PLoS One; 2010;5(5):e10445
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  • [Title] Furin targeted drug delivery for treatment of rhabdomyosarcoma in a mouse model.
  • Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children.
  • Improvement of treatment efficacy and decreased side effects through tumor-targeted drug delivery would be desirable.
  • Treatment of RMS in mice with doxorubicin coupled to the targeting peptide resulted in a two-fold increase in therapeutic efficacy compared to doxorubicin treatment alone.
  • Our findings indicate surface-furin binding as novel mechanism for therapeutic cell penetration which needs to be further investigated.
  • Furthermore, this work demonstrates that specific targeting of membrane-bound furin in tumors is possible for and suggests that RMS and other tumors might benefit from proprotein convertases targeted drug delivery.
  • [MeSH-major] Doxorubicin / therapeutic use. Drug Delivery Systems. Furin / metabolism. Rhabdomyosarcoma / drug therapy
  • [MeSH-minor] Amino Acid Motifs. Amino Acid Sequence. Animals. Cell Line, Tumor. Cell Membrane / drug effects. Cell Membrane / metabolism. Cell Proliferation / drug effects. Disease Models, Animal. Fluorescein-5-isothiocyanate / metabolism. Golgi Apparatus / drug effects. Golgi Apparatus / metabolism. Humans. Mice. Molecular Sequence Data. Peptide Library. Peptides / chemistry. Peptides / metabolism. Protein Binding / drug effects. Receptors, Cell Surface / metabolism. Reproducibility of Results. Xenograft Model Antitumor Assays

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  • [Cites] J Mol Endocrinol. 2000 Feb;24(1):1-22 [10656993.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2853-7 [15087403.001]
  • [Cites] Br J Cancer. 2000 Mar;82(6):1239-45 [10735512.001]
  • [Cites] Am J Pathol. 2001 Jan;158(1):305-16 [11141505.001]
  • [Cites] J Biol Chem. 2001 Aug 17;276(33):30686-93 [11402025.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10326-31 [11517338.001]
  • [Cites] Mol Carcinog. 2001 Aug;31(4):224-32 [11536372.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):1921-35 [12057895.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1740-6 [12060611.001]
  • [Cites] Nat Med. 2002 Jul;8(7):751-5 [12053175.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Oct;3(10):753-66 [12360192.001]
  • [Cites] Biopolymers. 2002;66(3):184-99 [12385037.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3578-87 [12411321.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):439-47 [12547702.001]
  • [Cites] Biochem Soc Trans. 2004 Jun;32(Pt3):397-402 [15157146.001]
  • [Cites] Nature. 2004 Jun 10;429(6992):629-35 [15190345.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5539-45 [15313887.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Aug 27;321(3):531-8 [15358140.001]
  • [Cites] J Biol Chem. 1993 Jun 25;268(18):13406-13 [8099909.001]
  • [Cites] FEBS Lett. 1993 Aug 9;328(1-2):25-9 [8344430.001]
  • [Cites] J Biol Chem. 1995 Nov 3;270(44):26565-9 [7592877.001]
  • [Cites] J Biol Chem. 1996 Nov 29;271(48):30442-50 [8940009.001]
  • [Cites] Br J Cancer. 1997;75(10):1509-14 [9166946.001]
  • [Cites] Biochem J. 1997 Nov 1;327 ( Pt 3):625-35 [9599222.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7293-8 [9636142.001]
  • [Cites] J Neurochem. 2004 Dec;91(6):1275-83 [15584904.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 Apr;54(1):11-29 [15780905.001]
  • [Cites] J R Soc Med. 2005 Apr;98(4):146-52 [15805554.001]
  • [Cites] Trends Pharmacol Sci. 2005 Jun;26(6):294-301 [15925704.001]
  • [Cites] Oncologist. 2005 Aug;10(7):518-27 [16079319.001]
  • [Cites] Nat Biotechnol. 2005 Sep;23(9):1147-57 [16151408.001]
  • [Cites] Mol Carcinog. 2005 Nov;44(3):151-61 [16167351.001]
  • [Cites] Biopolymers. 2006;84(3):241-9 [16333858.001]
  • [Cites] FASEB J. 2007 Apr;21(4):1088-98 [17242158.001]
  • [Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):780-3 [17635147.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9030-4 [17909005.001]
  • [Cites] Mol Pharm. 2007 Sep-Oct;4(5):631-51 [17880166.001]
  • [Cites] J Clin Invest. 2008 Jan;118(1):352-63 [18064302.001]
  • [Cites] J Biol Chem. 2008 Apr 25;283(17):11752-62 [18292083.001]
  • [Cites] Cancer Res. 2008 Sep 1;68(17):6922-31 [18757406.001]
  • [Cites] Cancer Res. 2008 Sep 1;68(17):7210-8 [18757437.001]
  • [Cites] Expert Opin Ther Targets. 2008 Oct;12(10):1289-300 [18781827.001]
  • [Cites] Int J Cancer. 2009 May 1;124(9):2026-32 [19123480.001]
  • [Cites] Mol Cancer. 2009;8:73 [19737405.001]
  • [Cites] J Biol Chem. 2009 Oct 2;284(40):27157-66 [19651771.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16157-62 [19805273.001]
  • [Cites] Future Oncol. 2009 Nov;5(9):1449-75 [19903072.001]
  • [Cites] PLoS One. 2009;4(11):e7700 [19956642.001]
  • [Cites] Cancer Cell. 2009 Dec 8;16(6):510-20 [19962669.001]
  • [Cites] Int J Biochem Cell Biol. 2010 Jun;42(6):987-95 [20197107.001]
  • [Cites] J Clin Invest. 2003 Jun;111(11):1723-32 [12782675.001]
  • [Cites] Biochem J. 2003 Jul 15;373(Pt 2):475-84 [12691605.001]
  • [Cites] J Control Release. 2003 Aug 28;91(1-2):183-6 [12932650.001]
  • [Cites] FEBS Lett. 2003 Nov 20;554(3):275-83 [14623079.001]
  • [Cites] J Cell Biol. 2003 Nov 24;163(4):871-8 [14638862.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):393-403 [14667506.001]
  • [Cites] Brain Res. 1999 Nov 27;848(1-2):45-62 [10701998.001]
  • (PMID = 20454619.001).
  • [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 / Peptide Library; 0 / Peptides; 0 / Receptors, Cell Surface; 80168379AG / Doxorubicin; EC 3.4.21.75 / Furin; I223NX31W9 / Fluorescein-5-isothiocyanate
  • [Other-IDs] NLM/ PMC2862740
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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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5. Wan X, Shen N, Mendoza A, Khanna C, Helman LJ: CCI-779 inhibits rhabdomyosarcoma xenograft growth by an antiangiogenic mechanism linked to the targeting of mTOR/Hif-1alpha/VEGF signaling. Neoplasia; 2006 May;8(5):394-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CCI-779 inhibits rhabdomyosarcoma xenograft growth by an antiangiogenic mechanism linked to the targeting of mTOR/Hif-1alpha/VEGF signaling.
  • The goal of this study was to evaluate whether the antitumor activity of CCI-779 is related to antiangiogenic effects in vivo in tumors of mice bearing human rhabdomyosarcoma (RMS) xenografts.
  • We now demonstrate that CCI-779 rapidly inhibits mTOR activity, as indicated by S6 reduction and eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) phosphorylation in two xenograft models of RMS within 24 hours of treatment.
  • Treatment with a single 20-mg/kg dose of CCI-779 suppressed S6 phosphorylation for more than 72 hours and 4E-BP1 phosphorylation for more than 96 hours.
  • Based on these data, an intermittent treatment schedule (every 3 days for 30 days) was chosen and displayed a significant suppression of both tumor growth and mTOR signaling.

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  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2803-7 [10914727.001]
  • [Cites] Oncologist. 1999;4(1):34-44 [10337369.001]
  • [Cites] Cell. 2001 May 4;105(3):345-55 [11348591.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1758-64 [11410517.001]
  • [Cites] Oncogene. 2000 Dec 27;19(56):6680-6 [11426655.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5731-5 [11479208.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10320-5 [11504907.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2406-11 [15781656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10314-9 [11504908.001]
  • [Cites] Nat Med. 2002 Feb;8(2):128-35 [11821896.001]
  • [Cites] Curr Opin Oncol. 2002 May;14(3):273-9 [11981271.001]
  • [Cites] Curr Opin Investig Drugs. 2002 Feb;3(2):295-304 [12020063.001]
  • [Cites] FASEB J. 2002 Jun;16(8):771-80 [12039858.001]
  • [Cites] Pancreas. 2002 Aug;25(2):122-9 [12142733.001]
  • [Cites] Neoplasia. 2002 Sep-Oct;4(5):400-8 [12192598.001]
  • [Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):505-15 [10688871.001]
  • [Cites] Curr Opin Oncol. 2000 Jul;12(4):337-44 [10888419.001]
  • [Cites] Nat Cell Biol. 2002 Sep;4(9):648-57 [12172553.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):727-39 [12360276.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3767-75 [12393646.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034.001]
  • [Cites] Nat Cell Biol. 2003 Jun;5(6):559-65 [12766775.001]
  • [Cites] Nat Cell Biol. 2003 Jun;5(6):566-71 [12766776.001]
  • [Cites] Cancer Biol Ther. 2003 May-Jun;2(3):222-32 [12878853.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303.001]
  • [Cites] Nat Rev Drug Discov. 2003 Oct;2(10):803-11 [14526383.001]
  • [Cites] Oncogene. 2003 Nov 6;22(50):8205-11 [14603261.001]
  • [Cites] Trends Biochem Sci. 2003 Nov;28(11):573-6 [14607085.001]
  • [Cites] Trends Biochem Sci. 2004 Jan;29(1):32-8 [14729330.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):909-18 [14990647.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):335-48 [15122205.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2336-47 [15136596.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6993-7000 [15501979.001]
  • [Cites] Cell. 1992 Jun 26;69(7):1227-36 [1377606.001]
  • [Cites] Med Res Rev. 1994 Jan;14(1):1-22 [8309312.001]
  • [Cites] Cell. 1994 Oct 21;79(2):185-8 [7525076.001]
  • [Cites] Semin Pediatr Surg. 1994 Aug;3(3):203-6 [7987636.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):610-30 [7884423.001]
  • [Cites] Cell Growth Differ. 1995 Mar;6(3):263-9 [7794794.001]
  • [Cites] Nature. 1995 Oct 5;377(6548):441-6 [7566123.001]
  • [Cites] Mol Cell Biol. 1996 Sep;16(9):4604-13 [8756616.001]
  • [Cites] Cell. 1996 Aug 23;86(4):517-20 [8752206.001]
  • [Cites] Curr Opin Oncol. 1996 Jul;8(4):311-6 [8869806.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8104-9 [9223322.001]
  • [Cites] Med Pediatr Oncol. 1998 May;30(5):269-75 [9544222.001]
  • [Cites] Clin Cancer Res. 1996 Oct;2(10):1679-84 [9816116.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1527-32 [11245461.001]
  • (PMID = 16790088.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1592447
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6. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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7. Xu J, Timares L, Heilpern C, Weng Z, Li C, Xu H, Pressey JG, Elmets CA, Kopelovich L, Athar M: Targeting wild-type and mutant p53 with small molecule CP-31398 blocks the growth of rhabdomyosarcoma by inducing reactive oxygen species-dependent apoptosis. Cancer Res; 2010 Aug 15;70(16):6566-76
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  • [Title] Targeting wild-type and mutant p53 with small molecule CP-31398 blocks the growth of rhabdomyosarcoma by inducing reactive oxygen species-dependent apoptosis.
  • Rhabdomyosarcoma (RMS) is a common soft-tissue sarcoma of childhood in need of more effective therapeutic options.
  • The expression of p53 in RMS is heterogeneous such that some tumors are wild-type whereas others are p53 mutant.
  • The small molecule CP-31398 modulates both the wild-type and the mutant p53 proteins.
  • Here, we show that CP-31398 blocks the growth of RMS cells that have either wild-type or mutant p53 status.
  • In wild-type A204 cells, CP-31398 increased the expression of p53 and its downstream transcriptional targets, p21 and mdm2; enhanced the expression of apoptosis-related proteins; and reduced proliferation biomarkers.
  • In vivo, CP-31398 decreased the growth of tumor xenografts composed of wild-type or mutant p53 tumor cells, increasing tumor-free host survival.
  • Our findings indicate that the ability of CP-31398 to modulate wild-type and mutant p53 results in the inhibition of RMS growth and invasiveness.

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  • [Copyright] (c)2010 AACR.
  • [Cites] Cancer Biol Ther. 2002 Jan-Feb;1(1):47-55 [12174820.001]
  • [Cites] Int J Oncol. 2009 Nov;35(5):1015-23 [19787255.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):2171-81 [12612087.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):577-90 [12667443.001]
  • [Cites] Hematol J. 2003;4(4):233-47 [12872148.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(15):6728-41 [15254240.001]
  • [Cites] J Natl Cancer Inst. 1969 Dec;43(6):1365-73 [5396222.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3671-5 [2023917.001]
  • [Cites] Nature. 1991 Jun 6;351(6326):453-6 [2046748.001]
  • [Cites] Cancer Res. 1992 Apr 15;52(8):2243-7 [1559227.001]
  • [Cites] Nucleic Acids Res. 1994 Sep;22(17):3551-5 [7937055.001]
  • [Cites] J Physiol. 1995 Jul 1;486 ( Pt 1):1-13 [7562625.001]
  • [Cites] N Engl J Med. 1999 Jul 29;341(5):342-52 [10423470.001]
  • [Cites] Anticancer Res. 1999 May-Jun;19(3A):1827-32 [10470122.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23):4787-94 [15570080.001]
  • [Cites] Free Radic Biol Med. 2005 Oct 1;39(7):949-59 [16140214.001]
  • [Cites] J Negat Results Biomed. 2004;3:5 [15548325.001]
  • [Cites] Cell Biol Int. 2006 Mar;30(3):197-204 [16376584.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3844-51 [16921036.001]
  • [Cites] Pediatr Blood Cancer. 2006 Nov;47(6):773-84 [16283617.001]
  • [Cites] Science. 2007 Mar 2;315(5816):1211-3 [17332387.001]
  • [Cites] Science. 1999 Dec 24;286(5449):2507-10 [10617466.001]
  • [Cites] Cell Growth Differ. 2000 May;11(5):239-46 [10845424.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(16):6008-18 [10913183.001]
  • [Cites] Med Pediatr Oncol. 2000 Aug;35(2):96-103 [10918230.001]
  • [Cites] Apoptosis. 2000 Nov;5(5):415-8 [11256882.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):68-76 [11900253.001]
  • [Cites] Oncogene. 2002 Mar 28;21(14):2119-29 [11948395.001]
  • [Cites] Exp Cell Res. 2002 Jun 10;276(2):214-22 [12027451.001]
  • [Cites] J Clin Invest. 2007 Dec;117(12):3753-64 [18060030.001]
  • [Cites] Cancer Metastasis Rev. 2008 Mar;27(1):85-94 [18175071.001]
  • [Cites] J Pharmacol Sci. 2008 Aug;107(4):370-9 [18719315.001]
  • [Cites] Cell Oncol. 2008;30(5):411-8 [18791272.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6376-86 [18927276.001]
  • [Cites] J Clin Invest. 2009 Apr;119(4):954-63 [19273910.001]
  • [Cites] DNA Repair (Amst). 2009 Apr 5;8(4):483-90 [19217357.001]
  • [Cites] Nat Cell Biol. 2009 Jun;11(6):694-704 [19448627.001]
  • [Cites] Clin Cancer Res. 2009 Jun 15;15(12):4077-84 [19509161.001]
  • [Cites] Anticancer Drugs. 2009 Jul;20(6):416-24 [19579266.001]
  • [Cites] Stem Cells. 2009 Sep;27(9):2059-68 [19544473.001]
  • [Cites] J Cell Sci. 2003 Feb 1;116(Pt 3):499-511 [12508111.001]
  • (PMID = 20682800.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES015323-03; United States / NCI NIH HHS / CA / N01CN43300; United States / NIEHS NIH HHS / ES / ES015323-02; United States / NIEHS NIH HHS / ES / R01 ES015323-02; United States / NIEHS NIH HHS / ES / ES015323-05; United States / NIEHS NIH HHS / ES / ES015323-03; United States / NIEHS NIH HHS / ES / ES015323-04; United States / NCI NIH HHS / CN / N01-CN-43300; United States / NIEHS NIH HHS / ES / R01 ES015323; United States / NIEHS NIH HHS / ES / R01 ES015323-05; United States / NIEHS NIH HHS / ES / R01 ES015323-01; United States / NIAMS NIH HHS / AR / P30 AR050948; United States / NIEHS NIH HHS / ES / ES015323-01; United States / NIEHS NIH HHS / ES / R01 ES015323-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CP 31398; 0 / Pyrimidines; 0 / Reactive Oxygen Species; 0 / SOX9 Transcription Factor; 0 / Sox9 protein, mouse; 0 / Tumor Suppressor Protein p53; 83HN0GTJ6D / Cyclosporine; 9007-43-6 / Cytochromes c
  • [Other-IDs] NLM/ NIHMS220402; NLM/ PMC2922473
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8. 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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9. 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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  • [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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10. 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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11. Rahbeeni F, Hendrikse AS, Smuts CM, Gelderblom WC, Abel S, Blekkenhorst GH: The effect of evening primrose oil on the radiation response and blood flow of mouse normal and tumour tissue. Int J Radiat Biol; 2000 Jun;76(6):871-7

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  • [Title] The effect of evening primrose oil on the radiation response and blood flow of mouse normal and tumour tissue.
  • PURPOSE: To investigate the effect of the oral administration of evening primrose oil on the radiation response and the blood flow of normal tissue and a tumour in BALB/c mice.
  • Tumour radiosensitivity was investigated by determining the growth delay caused by irradiation of a transplantable rhabdomyosarcoma.
  • The 86RbCl uptake technique was used to determine the blood flow in normal foot and tumour tissue.
  • The fatty-acid content of red blood cells, plasma and tumour tissue was measured using gas chromatography.
  • RESULTS: Daily evening primrose oil dietary supplementation reduced the sensitivity of skin to radiation-induced moist desquamation and prevented the radiation-associated increase in blood flow that was observed in this tissue.
  • There were no changes in tumour fatty-acid levels as a result of evening primrose oil treatment.
  • [MeSH-major] Fatty Acids, Essential / pharmacology. Radiation Tolerance / drug effects. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / radiotherapy
  • [MeSH-minor] Administration, Oral. Animals. Blood Flow Velocity / drug effects. Blood Flow Velocity / radiation effects. Erythrocytes / drug effects. Erythrocytes / metabolism. Fatty Acids / blood. Fatty Acids / metabolism. Female. Linoleic Acids. Mice. Mice, Inbred BALB C. Plant Oils. Radiation-Sensitizing Agents / administration & dosage. Radiation-Sensitizing Agents / pharmacology. Vasodilation / drug effects. Vasodilation / radiation effects. gamma-Linolenic Acid

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  • (PMID = 10902742.001).
  • [ISSN] 0955-3002
  • [Journal-full-title] International journal of radiation biology
  • [ISO-abbreviation] Int. J. Radiat. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Fatty Acids, Essential; 0 / Linoleic Acids; 0 / Plant Oils; 0 / Radiation-Sensitizing Agents; 65546-85-2 / Efamol; 78YC2MAX4O / gamma-Linolenic Acid
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12. 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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  • [Cites] FEBS Lett. 1997 Jun 23;410(1):78-82 [9247127.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3693-704 [9218810.001]
  • [Cites] Mutat Res. 1997 Nov 19;381(1):67-75 [9403032.001]
  • [Cites] Curr Opin Cell Biol. 1997 Dec;9(6):782-7 [9425342.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7 [9465032.001]
  • [Cites] Oncogene. 1998 Jan 29;16(4):533-40 [9484843.001]
  • [Cites] Biochem Cell Biol. 1997;75(4):315-25 [9493954.001]
  • [Cites] Curr Biol. 1998 Mar 26;8(7):R248-50 [9545190.001]
  • [Cites] Curr Opin Cell Biol. 1998 Apr;10(2):268-75 [9561852.001]
  • [Cites] Cell. 1999 Jan 22;96(2):235-44 [9988218.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):886-94 [10029080.001]
  • [Cites] J Biol Chem. 1999 May 7;274(19):13118-26 [10224065.001]
  • [Cites] Oncogene. 2000 Jun 15;19(26):3021-31 [10871854.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24776-80 [10811643.001]
  • [Cites] Ann Intern Med. 1984 May;100(5):704-13 [6370067.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Nature. 1985 Sep 19-25;317(6034):258-60 [2995817.001]
  • [Cites] EMBO J. 1986 Oct;5(10):2503-12 [2877871.001]
  • [Cites] Cell Growth Differ. 1990 Jul;1(7):325-31 [2177632.001]
  • [Cites] J Clin Invest. 1991 Feb;87(2):648-57 [1991849.001]
  • [Cites] Cancer Res. 1992 Apr 15;52(8):2243-7 [1559227.001]
  • [Cites] Curr Probl Cancer. 1992 Mar-Apr;16(2):61-126 [1617996.001]
  • [Cites] Annu Rev Biochem. 1992;61:441-70 [1497317.001]
  • [Cites] Prog Growth Factor Res. 1992;4(3):257-90 [1307492.001]
  • [Cites] Nature. 1994 Jun 2;369(6479):414-8 [7910953.001]
  • [Cites] Endocr Rev. 1995 Feb;16(1):3-34 [7758431.001]
  • [Cites] Cell Growth Differ. 1995 Mar;6(3):263-9 [7794794.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):358-62 [7566093.001]
  • [Cites] Trends Biochem Sci. 1995 Oct;20(10):435-9 [8533159.001]
  • [Cites] EMBO J. 1995 Nov 1;14(21):5279-87 [7489717.001]
  • [Cites] EMBO J. 1996 Feb 1;15(3):658-64 [8599949.001]
  • [Cites] Curr Opin Cell Biol. 1995 Dec;7(6):806-14 [8608011.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4076-80 [8633019.001]
  • [Cites] J Endocrinol. 1996 Jun;149(3):367-72 [8691094.001]
  • [Cites] Trends Biochem Sci. 1996 May;21(5):181-5 [8871403.001]
  • [Cites] Physiol Rev. 1996 Oct;76(4):1005-26 [8874492.001]
  • [Cites] Endocrinol Metab Clin North Am. 1996 Sep;25(3):591-614 [8879988.001]
  • [Cites] Oncogene. 1996 Dec 5;13(11):2415-20 [8957083.001]
  • [Cites] Oncogene. 1997 May 8;14(18):2127-36 [9174048.001]
  • [Cites] Eur J Cancer. 1997 Apr;33(4):638-44 [9274448.001]
  • (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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13. Amstutz R, Wachtel M, Troxler H, Kleinert P, Ebauer M, Haneke T, Oehler-Jänne C, Fabbro D, Niggli FK, Schäfer BW: Phosphorylation regulates transcriptional activity of PAX3/FKHR and reveals novel therapeutic possibilities. Cancer Res; 2008 May 15;68(10):3767-76
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  • [Title] Phosphorylation regulates transcriptional activity of PAX3/FKHR and reveals novel therapeutic possibilities.
  • Inhibition of constitutive active signaling pathways, which are a characteristic phenomenon for many tumors, can be an effective therapeutic strategy.
  • In contrast, oncogenic transcription factors, often activated by mutational events, are in general less amenable to small-molecule inhibition despite their obvious importance as therapeutic targets.
  • One example of this is alveolar rhabdomyosarcoma (aRMS), in which specific translocations lead to the formation of the chimeric transcription factor PAX3/FKHR.
  • Consequently, we show that PKC412 exerts a potent antitumorigenic potential for aRMS treatment both in vitro and in vivo.
  • Our study suggests that posttranscriptional modifications of oncogenic transcription factors can be explored as a promising avenue for targeted cancer therapy.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. Gene Expression Regulation, Neoplastic. Paired Box Transcription Factors / metabolism. Rhabdomyosarcoma / drug therapy. Staurosporine / analogs & derivatives

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  • (PMID = 18483260.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxo1 protein, mouse; 0 / PAX3 protein, human; 0 / Paired Box Transcription Factors; 120685-11-2 / 4'-N-benzoylstaurosporine; 138016-91-8 / Pax3 protein, mouse; H88EPA0A3N / Staurosporine
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14. 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
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] 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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  • [Cites] J Virol. 2000 Feb;74(3):1364-72 [10627547.001]
  • [Cites] J Clin Invest. 2004 Sep;114(5):623-33 [15343380.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2961-78 [10898340.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4311-4 [10969766.001]
  • [Cites] Br J Cancer. 2002 Jul 1;87(1):106-12 [12085265.001]
  • [Cites] Immunity. 2002 Aug;17(2):211-20 [12196292.001]
  • [Cites] Nat Immunol. 2002 Nov;3(11):999-1005 [12407407.001]
  • [Cites] Curr Mol Med. 2003 Nov;3(7):643-51 [14601638.001]
  • [Cites] Cell Tissue Res. 2003 Oct;314(1):167-77 [12883995.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):71-8 [14708027.001]
  • [Cites] Health Technol Assess. 2004;8(4):1-176 [14960258.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):423-36 [15170445.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2224-34 [15231578.001]
  • [Cites] J Immunol Methods. 1985 Mar 18;77(2):305-19 [3981007.001]
  • [Cites] Eur J Immunol. 1997 Oct;27(10):2626-33 [9368619.001]
  • [Cites] Trends Cell Biol. 2004 Nov;14(11):628-38 [15519852.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1383-95 [15471951.001]
  • [Cites] J Clin Oncol. 2005 Feb 10;23(5):953-64 [15598976.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1294-305 [15735015.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):263-74 [15776005.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2964-71 [15805300.001]
  • [Cites] Br J Cancer. 2005 Apr 11;92(7):1182-7 [15785750.001]
  • [Cites] J Immunol. 2005 Apr 15;174(8):4880-91 [15814715.001]
  • [Cites] Cancer Cell. 2005 Jun;7(6):513-20 [15950901.001]
  • [Cites] Springer Semin Immunopathol. 2005 Jun;27(1):19-35 [15965711.001]
  • [Cites] J Clin Invest. 2005 Sep;115(9):2363-72 [16138190.001]
  • [Cites] Nat Med. 2005 Nov;11(11):1180-7 [16208318.001]
  • [Cites] J Biol Chem. 1998 Aug 21;273(34):21769-76 [9705314.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):540-50 [15229479.001]
  • [Cites] Cell Mol Life Sci. 2004 Jul;61(14):1785-94 [15241554.001]
  • [Cites] Eur J Cancer. 2004 Jul;40(11):1660-7 [15251154.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5378-84 [15289345.001]
  • [Cites] Biol Chem. 1999 Dec;380(12):1449-54 [10661874.001]
  • (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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15. Dudkin L, Dilling MB, Cheshire PJ, Harwood FC, Hollingshead M, Arbuck SG, Travis R, Sausville EA, Houghton PJ: Biochemical correlates of mTOR inhibition by the rapamycin ester CCI-779 and tumor growth inhibition. Clin Cancer Res; 2001 Jun;7(6):1758-64
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  • To further understand the relationship between plasma systemic exposure and inhibition of the target Ser/Thr kinase, mTOR/FRAP, two assays have been developed.
  • In mice, administration of rapamycin (5 or 20 mg/kg) caused rapid association of 4E-BP1 with eIF4E within 4 h in both human colon adenocarcinoma GC(3) and rhabdomyosarcoma Rh30 xenografts.
  • Using phospho-specific antibody against Thr(70) of 4E-BP1, rapid and persistent dephosphorylation within 30 min of exposure to rapamycin was detected in Rh18 rhabdomyosarcoma cells.
  • Because immunoblotting may be more suitable for assaying tumor biopsy tissue, a "blinded" comparison between the effect of CCI-779 on Thr(70) phosphorylation and growth inhibition of human tumor xenografts was undertaken.
  • Mice were treated daily for 5 days with CCI-779 (20 mg/kg/day) or with drug vehicle, and tumor diameters were measured.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Neoplasms / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenocarcinoma / metabolism. Animals. Blotting, Western. Carrier Proteins / metabolism. Cell Division. Eukaryotic Initiation Factor-4E. Humans. Immunoblotting. Mice. Mice, Inbred CBA. Neoplasm Transplantation. Peptide Initiation Factors / metabolism. Phosphoproteins / metabolism. Phosphorylation. Protein Binding. Rhabdomyosarcoma / metabolism. Time Factors. Tumor Cells, Cultured

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  • (PMID = 11410517.001).
  • [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 / CA21765; United States / NCI NIH HHS / CA / CA23099; United States / NCI NIH HHS / CA / CA77776; United States / NCI NIH HHS / CO / N01-CO-56000
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Antibiotics, Antineoplastic; 0 / Carrier Proteins; 0 / EIF4EBP1 protein, human; 0 / Eif4ebp1 protein, mouse; 0 / Eukaryotic Initiation Factor-4E; 0 / Peptide Initiation Factors; 0 / Phosphoproteins; 624KN6GM2T / temsirolimus; W36ZG6FT64 / Sirolimus
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16. 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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17. 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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18. 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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19. 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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20. 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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21. 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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22. Houghton PJ, Morton CL, Gorlick R, Kolb EA, Keir ST, Reynolds CP, Kang MH, Maris JM, Wu J, Smith MA: Initial testing of a monoclonal antibody (IMC-A12) against IGF-1R by the Pediatric Preclinical Testing Program. Pediatr Blood Cancer; 2010 Jul 1;54(7):921-6
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  • BACKGROUND: Many childhood malignancies including sarcomas, neuroblastoma, and Wilms tumor show the presence of both, active, type-1-insulin-like growth factor receptor (IGF-1R), and the autocrine production of its ligands IGF-1/IGF-2.
  • IMC-A12 was tested in vivo at a dose of 1 mg/mouse administered intraperitoneally twice weekly for 6 weeks.
  • RESULTS: In vitro, IMC-A12-induced T/C values <50% in only three cell lines, a rhabdomyosarcoma cell line (Rh41) and two Ewing sarcoma cell lines (TC-71 and CHLA-9).
  • Using the PPTP "time to event" activity measure, IMC-A12 induced intermediate (n = 13) or high (n = 1) activity in 33 xenografts evaluable for this activity measure, including 6 of 6 rhabdomyosarcoma xenografts, 3 of 5 osteosarcoma xenografts, 2 of 5 neuroblastoma xenografts, and 1 of 5 Ewing sarcoma xenografts.
  • The only objective response observed was observed in a rhabdomyosarcoma xenograft (Rh28) that achieved a maintained complete response.
  • IMC-A12 showed its greatest activity in vivo against the PPTP's rhabdomyosarcoma xenografts.

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6950-8 [16203787.001]
  • [Cites] Mol Cancer Ther. 2005 Aug;4(8):1214-21 [16093437.001]
  • [Cites] Biochim Biophys Acta. 2006 Aug;1766(1):1-22 [16844299.001]
  • [Cites] Drug News Perspect. 2006 Jun;19(5):261-72 [16941048.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2006 Jan;11(1):27-39 [16947084.001]
  • [Cites] Mol Cancer Ther. 2007 Jan;6(1):1-12 [17237261.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):886-97 [17363483.001]
  • [Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 2):5549s-5555s [17875788.001]
  • [Cites] Pediatr Blood Cancer. 2007 Dec;49(7):928-40 [17066459.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):37-45 [17420992.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jun;50(6):1190-7 [18260118.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1735-45 [12365022.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] Mol Cell Biol. 1990 Feb;10(2):464-73 [2153917.001]
  • [Cites] Cell Growth Differ. 1990 Jul;1(7):325-31 [2177632.001]
  • [Cites] Am J Clin Pathol. 1994 Feb;101(2):198-203 [8116575.001]
  • [Cites] J Clin Invest. 1994 Jul;94(1):445-8 [8040287.001]
  • [Cites] Cancer Res. 1994 Nov 1;54(21):5531-4 [7923191.001]
  • [Cites] Ann Intern Med. 1995 Jan 1;122(1):54-9 [7619109.001]
  • [Cites] Physiol Rev. 1996 Oct;76(4):1005-26 [8874492.001]
  • [Cites] Breast Cancer Res Treat. 1998 Feb;47(3):235-53 [9516079.001]
  • [Cites] Clin Cancer Res. 2005 Mar 1;11(5):2063-73 [15756033.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):223-34 [16397046.001]
  • (PMID = 20166202.001).
  • [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 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ NIHMS155711; NLM/ PMC3003867
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23. 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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24. 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.
  • The ALL cell lines were more sensitive and the rhabdomyosarcoma cell lines less sensitive than the remaining PPTP cell lines.
  • 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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  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):886-97 [17363483.001]
  • [Cites] Nat Rev Cancer. 2007 Feb;7(2):107-17 [17251917.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):37-45 [17420992.001]
  • [Cites] Oncol Res. 2008;17(3):115-25 [18669163.001]
  • [Cites] Nature. 2008 Sep 4;455(7209):119-23 [18615013.001]
  • [Cites] Biochim Biophys Acta. 2008 Sep;1786(1):60-72 [18662747.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8998-9004 [18974145.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):5-6 [19111875.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):67-78 [19111882.001]
  • [Cites] Mol Cancer Ther. 2009 Jan;8(1):36-44 [19139111.001]
  • [Cites] Mol Cell Biol. 2009 Feb;29(4):1059-71 [19075002.001]
  • [Cites] Cell Cycle. 2009 Mar 15;8(6):876-88 [19221504.001]
  • [Cites] Head Neck. 2009 May;31(5):625-34 [19107951.001]
  • [Cites] Curr Med Chem. 2009;16(16):1949-63 [19519375.001]
  • [Cites] Clin Cancer Res. 2008 Mar 15;14(6):1639-48 [18347165.001]
  • [Cites] Pediatr Blood Cancer. 2007 Dec;49(7):928-40 [17066459.001]
  • [Cites] J Natl Cancer Inst. 2002 Sep 4;94(17):1320-9 [12208897.001]
  • [Cites] Cancer Cell. 2003 Jan;3(1):51-62 [12559175.001]
  • [Cites] Cancer Metastasis Rev. 2003 Dec;22(4):451-64 [12884918.001]
  • [Cites] Nat Genet. 2003 Aug;34(4):403-12 [12881723.001]
  • [Cites] Cell. 2003 Sep 5;114(5):585-98 [13678582.001]
  • [Cites] Oncogene. 2003 Nov 13;22(51):8293-301 [14614453.001]
  • [Cites] Blood. 2004 May 15;103(10):3905-14 [14764536.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1589-94 [15466974.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):3052-65 [9606188.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2149-53 [15271853.001]
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6950-8 [16203787.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):223-34 [16397046.001]
  • [Cites] Semin Oncol. 2006 Aug;33(4):436-48 [16890798.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):32-40 [17210681.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):237-45 [17210704.001]
  • [CommentIn] Pediatr Blood Cancer. 2010 Jul 15;55(1):3-4 [20486161.001]
  • (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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25. Neale G, Su X, Morton CL, Phelps D, Gorlick R, Lock RB, Reynolds CP, Maris JM, Friedman HS, Dome J, Khoury J, Triche TJ, Seeger RC, Gilbertson R, Khan J, Smith MA, Houghton PJ: Molecular characterization of the pediatric preclinical testing panel. Clin Cancer Res; 2008 Jul 15;14(14):4572-83
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Identifying novel therapeutic agents for the treatment of childhood cancers requires preclinical models that recapitulate the molecular characteristics of their respective clinical histotypes.
  • Profiling led to exclusion of two tumor lines that were of mouse origin and five osteosarcoma lines that did not cluster with human or xenograft osteosarcoma samples.
  • Several consistent copy number changes not reported previously were found (e.g., gain at 22q11.21 that was observed in 5 of 7 glioblastoma samples, loss at 16q22.3 that was observed in 5 of 9 Ewing's sarcoma and 4 of 12 rhabdomyosarcoma models, and amplification of 21q22.3 that was observed in 5 of 7 osteosarcoma models).
  • CONCLUSIONS: These data indicate that the preclinical models accurately recapitulate expression profiles and genetic alterations common to childhood cancer, supporting their value in drug development.

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  • (PMID = 18628472.001).
  • [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 CA082830; United States / NCI NIH HHS / CM / N01-CM-37027-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ NIHMS634910; NLM/ PMC4209898
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