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1. Suetsugu A, Osawa Y, Nagaki M, Moriwaki H, Saji S, Bouvet M, Hoffman RM: Simultaneous color-coded imaging to distinguish cancer "stem-like" and non-stem cells in the same tumor. J Cell Biochem; 2010 Nov 1;111(4):1035-41
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  • In this study, we demonstrate that the differential behavior, including malignancy and chemosensitivity, of cancer stem-like and non-stem cells can be simultaneously distinguished in the same tumor in real time by color-coded imaging.
  • The same number of GFP CSCs and the RFP NSCCs were mixed and injected subcutaneously or in the spleen of nude mice.
  • CSCs were highly tumorigenic and metastatic as well as highly resistant to chemotherapy in vivo compared to NSCCs.
  • The ability to specifically distinguish stem-like cancer cells in vivo in real time provides a visual target for prevention of metastasis and drug resistance.

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20672309.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA132971; United States / NCI NIH HHS / CA / CA132971
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Luminescent Proteins; 0 / Peptides; 0 / red fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
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2. Demeter K, Zádori A, Agoston VA, Madarász E: Studies on the use of NE-4C embryonic neuroectodermal stem cells for targeting brain tumour. Neurosci Res; 2005 Nov;53(3):331-42
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  • In chimera-aggregates, all types of glioma cells co-aggregated with astrocytes, but most of them segregated from stem cells.
  • If mixed suspensions of NE-4C and Gl261 cells were injected into the brain, stem cells survived and grew inside the tumour mass.
  • NE-4C stem cells, however, did not migrate towards the tumour, if implanted near to Gl261 tumours established in the adult mouse forebrain.
  • The observations indicate that not all types of stem cells could be used for targeting all sorts of brain tumours.
  • [MeSH-major] Brain Neoplasms / therapy. Brain Tissue Transplantation / methods. Ectoderm / transplantation. Stem Cell Transplantation / methods. Stem Cells / physiology
  • [MeSH-minor] Animals. Astrocytes / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation / drug effects. Coculture Techniques. Glioblastoma / physiopathology. Glioblastoma / therapy. Graft Survival / physiology. Growth Substances / metabolism. Growth Substances / pharmacology. Humans. Mice. Neoplasm Invasiveness / physiopathology. Rats

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  • (PMID = 16183159.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Growth Substances
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3. Wang H, Nan L, Yu D, Agrawal S, Zhang R: Antisense anti-MDM2 oligonucleotides as a novel therapeutic approach to human breast cancer: in vitro and in vivo activities and mechanisms. Clin Cancer Res; 2001 Nov;7(11):3613-24
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  • [Title] Antisense anti-MDM2 oligonucleotides as a novel therapeutic approach to human breast cancer: in vitro and in vivo activities and mechanisms.
  • The mouse double minute 2 (MDM2) oncogene has been suggested as a target for cancer therapy.
  • In the present study, we investigated the functions of MDM2 oncogene in the growth of breast cancer and the potential value of MDM2 as a drug target for cancer therapy by inhibiting MDM2 expression with a specific antisense antihuman-MDM2 oligonucleotide (oligo).
  • The selected antisense mixed-backbone oligo was evaluated for its in vitro and in vivo antitumor activity in human breast cancer models: MCF-7 cell line containing wild-type p53 and MDA-MB-468 cell line containing mutant p53.
  • In both models, in vivo synergistically or additive therapeutic effects of MDM2 inhibition and the clinically used cancer chemotherapeutic agents irinotecan, 5-fluorouracil, and paclitaxel (Taxol) were observed.
  • This study should provide a basis for future development of anti-MDM2 ASs as cancer therapeutic agents used alone or in combination with conventional chemotherapeutics.
  • [MeSH-major] Breast Neoplasms / drug therapy. Camptothecin / analogs & derivatives. DNA, Antisense / therapeutic use. Nuclear Proteins. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / drug effects. Cyclins / metabolism. Dose-Response Relationship, Drug. Doxorubicin / therapeutic use. Drug Synergism. Drug Therapy, Combination. Female. Fluorouracil / therapeutic use. Humans. Mice. Mice, Nude. Mutation. Neoplasm Transplantation. Proto-Oncogene Proteins c-mdm2. Time Factors. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 11705884.001).
  • [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 CA 80698
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA, Antisense; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 67656-30-8 / 10-hydroxycamptothecin; 80168379AG / Doxorubicin; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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4. Volz J, Volz-Köster S, Kanis S, Klee D, Ahlert C, Melchert F: Modulation of tumor-induced lethality after pneumoperitoneum in a mouse model. Cancer; 2000 Jul 15;89(2):262-6
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  • [Title] Modulation of tumor-induced lethality after pneumoperitoneum in a mouse model.
  • The effect of this procedure on tumor-induced lethality and the therapeutic effect of mitoxantrone and taurolidin mixed with heparin and sodium chloride was investigated.
  • The different drugs were added immediately after the release of the pneumoperitoneum and after 48 hours.
  • The 78 control animals received the drugs at the same time without preexisting pneumoperitoneum.
  • Survival time was registered.
  • RESULTS: The survival time was reduced significantly in all pneumoperitoneum groups compared with the corresponding control group without pneumoperitoneum.
  • The effect of mitoxantrone on survival time (mean, 62.08 days) was diminished significantly by the application of a pneumoperitoneum (mean, 34.27 days).
  • Taurolidine/heparin appeared to have a positive effect on survival time only in the case of a previous pneumoperitoneum (mean of 21.12 days vs. mean of 16.04 days in the pneumoperitoneum control group; P < 0.001).
  • CONCLUSIONS: The induction of a pneumoperitoneum appears to decrease survival time by increasing tumor cell growth and decreases the efficacy of intraperitoneal chemotherapy.
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cell Division / drug effects. Cell Division / physiology. Disease Models, Animal. Female. Heparin / administration & dosage. Mice. Mitoxantrone / administration & dosage. Neoplasm Transplantation. Pilot Projects. Survival Analysis. Taurine / administration & dosage. Taurine / analogs & derivatives. Thiadiazines / administration & dosage. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 10918154.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Thiadiazines; 1EQV5MLY3D / Taurine; 8OBZ1M4V3V / taurolidine; 9005-49-6 / Heparin; BZ114NVM5P / Mitoxantrone
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5. Wang H, Hang J, Shi Z, Li M, Yu D, Kandimalla ER, Agrawal S, Zhang R: Antisense oligonucleotide targeted to RIalpha subunit of cAMP-dependent protein kinase (GEM231) enhances therapeutic effectiveness of cancer chemotherapeutic agent irinotecan in nude mice bearing human cancer xenografts: in vivo synergistic activity, pharmacokinetics and host toxicity. Int J Oncol; 2002 Jul;21(1):73-80
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  • [Title] Antisense oligonucleotide targeted to RIalpha subunit of cAMP-dependent protein kinase (GEM231) enhances therapeutic effectiveness of cancer chemotherapeutic agent irinotecan in nude mice bearing human cancer xenografts: in vivo synergistic activity, pharmacokinetics and host toxicity.
  • The RIalpha-subunit of cAMP-dependent protein kinase (PKA) is overexpressed in various human cancers and PKA has been suggested to be a potential target for cancer therapy.
  • We have shown an antisense oligonucleotide with advanced chemistry (mixed-backbone oligonucleotide) targeted to PKA RIalpha-subunit (GEM231) to have anti-tumor activity in vitro and in vivo.
  • In the present study, we demonstrated synergistic effects between the anti-PKA antisense oligonucleotide and the clinically used anticancer agent irinotecan, using nude mouse models of human cancers of colon (LS174T and DLD-1), breast (MCF-7), prostate (DU-145 and PC-3) and lung (H1299).
  • To elucidate the underlying mechanisms, in vivo pharmacokinetics of irinotecan was determined following pre-treatment of oligo GEM 231 in CD-1 mice and nude mice bearing LS174T xenografts.
  • GEM 231 increased tissue uptake of irinotecan.
  • However, no significant change in host toxicity was observed following combination treatment of irinotecan and GEM231 compared with irinotecan alone.
  • These results suggest that GEM231 have a role in irinotecan metabolism and its antitumor activity, providing a basis for future development of this oligonucleotide as a chemosensitizer for irinotecan-based therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / toxicity. Camptothecin / analogs & derivatives. Neoplasms, Experimental / metabolism. Oligonucleotides, Antisense / therapeutic use
  • [MeSH-minor] Animals. Body Weight / drug effects. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Colonic Neoplasms / drug therapy. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / genetics. Dose-Response Relationship, Drug. Drug Synergism. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Male. Mice. Mice, Nude. Neoplasm Transplantation. Oligonucleotides / administration & dosage. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / genetics. Prostatic Neoplasms / metabolism. Survival Rate. Tissue Distribution. Treatment Outcome

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  • (PMID = 12063552.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 80698
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GEM231; 0 / Oligonucleotides; 0 / Oligonucleotides, Antisense; 7673326042 / irinotecan; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; XT3Z54Z28A / Camptothecin
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6. Ramesh R, Mhashilkar AM, Tanaka F, Saito Y, Branch CD, Sieger K, Mumm JB, Stewart AL, Boquoi A, Dumoutier L, Grimm EA, Renauld JC, Kotenko S, Chada S: Melanoma differentiation-associated gene 7/interleukin (IL)-24 is a novel ligand that regulates angiogenesis via the IL-22 receptor. Cancer Res; 2003 Aug 15;63(16):5105-13
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  • The sMDA-7/IL-24-mediated inhibitory effect was 10-50 times more potent than endostatin, IFN-gamma, and IFN-inducible protein 10 in vitro.
  • In vivo, the growth of human lung tumor cells was significantly inhibited, and vascularization was reduced when the cells were mixed with 293 cells stably expressing sMDA-7/IL-24.
  • Systemic administration of sMDA-7/IL-24 inhibited lung tumor growth in a mouse xenograft model.
  • These data demonstrate that sMDA-7/IL-24 is a novel and potent antiangiogenic effector and support the development of MDA-7/IL-24-based therapeutics.
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Division / drug effects. Cell Movement / drug effects. Chemokine CXCL10. Chemokines, CXC / physiology. Collagen / pharmacology. DNA-Binding Proteins / metabolism. Endostatins. Endothelium, Vascular / cytology. Female. Genes, Tumor Suppressor. Humans. Interferon-gamma / physiology. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Peptide Fragments / pharmacology. STAT3 Transcription Factor. Trans-Activators / metabolism. Transplantation, Heterologous. Tumor Cells, Cultured

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  • [ErratumIn] Cancer Res. 2004 Feb 15;64(4):1559. Boquio Amelia [corrected to Boquoi Amelie]
  • (PMID = 12941841.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 897598; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P50 CA70907; United States / NCI NIH HHS / CA / R43 CA86587
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Chemokine CXCL10; 0 / Chemokines, CXC; 0 / DNA-Binding Proteins; 0 / Endostatins; 0 / Interleukins; 0 / Peptide Fragments; 0 / Receptors, Interleukin; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Stat3 protein, mouse; 0 / Trans-Activators; 0 / interleukin-22 receptor; 0 / interleukin-24; 82115-62-6 / Interferon-gamma; 9007-34-5 / Collagen
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7. Kawakami K, Kawakami M, Husain SR, Puri RK: Effect of interleukin (IL)-4 cytotoxin on breast tumor growth after in vivo gene transfer of IL-4 receptor alpha chain. Clin Cancer Res; 2003 May;9(5):1826-36
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  • To assess whether overexpression of IL-4Ralpha chain in vivo by plasmid-mediated gene transfer can enhance antitumor activity of IL-4 cytotoxin in mouse models of breast tumor, we injected MDA-MB-231 human breast cancer cells in both flanks of athymic nude mice.
  • Animals then received three intratumoral (i.t.) injections of either IL-4Ralpha encoding vector (left flank) or vector only (right flank) mixed with liposome followed by IL-4 cytotoxin administration.
  • IL-4 cytotoxin administration may be a useful strategy for the treatment of breast cancer.
  • [MeSH-major] Genetic Therapy / methods. Immunotoxins / pharmacology. Interleukin-4 / pharmacology. Mammary Neoplasms, Experimental / therapy. Receptors, Interleukin-4 / genetics
  • [MeSH-minor] Animals. Antigens, Neoplasm. Antineoplastic Agents / immunology. Antineoplastic Agents / pharmacology. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Gene Transfer Techniques. Humans. Injections, Intralesional. Macrophage Activation. Mice. Mice, Nude. Radioligand Assay. Tumor Cells, Cultured / transplantation

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  • (PMID = 12738741.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Immunotoxins; 0 / Receptors, Interleukin-4; 207137-56-2 / Interleukin-4
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8. De Luca A, Arra C, D'Antonio A, Casamassimi A, Losito S, Ferraro P, Ciardiello F, Salomon DS, Normanno N: Simultaneous blockage of different EGF-like growth factors results in efficient growth inhibition of human colon carcinoma xenografts. Oncogene; 2000 Nov 30;19(51):5863-71
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  • We have synthesized novel, antisense mixed backbone oligonucleotides (AS MBOs) directed against TGFalpha, AR and CR.
  • A more significant tumor growth inhibition was observed when mice were treated with a combination of the three AS MBOs as compared to treatment with a single AS MBO.
  • These data suggest that combinations of AS oligonucleotides directed against different growth factors might represent a novel, experimental therapy approach of colon carcinomas.
  • [MeSH-major] Colonic Neoplasms / pathology. Epidermal Growth Factor. Glycoproteins / antagonists & inhibitors. Intercellular Signaling Peptides and Proteins. Membrane Glycoproteins. Neoplasm Proteins / antagonists & inhibitors. Oligonucleotides, Antisense / pharmacology. Thionucleotides / pharmacology. Transforming Growth Factor alpha / antagonists & inhibitors
  • [MeSH-minor] Amphiregulin. Animals. EGF Family of Proteins. GPI-Linked Proteins. Growth Inhibitors / genetics. Growth Inhibitors / pharmacology. Growth Substances / biosynthesis. Growth Substances / genetics. Humans. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 11127817.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Areg protein, mouse; 0 / EGF Family of Proteins; 0 / GPI-Linked Proteins; 0 / Glycoproteins; 0 / Growth Inhibitors; 0 / Growth Substances; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / TDGF1 protein, human; 0 / Tdgf1 protein, mouse; 0 / Thionucleotides; 0 / Transforming Growth Factor alpha; 62229-50-9 / Epidermal Growth Factor
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9. Wang H, Nan L, Yu D, Lindsey JR, Agrawal S, Zhang R: Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms. Mol Med; 2002 Apr;8(4):185-99
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  • [Title] Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms.
  • This study investigates the functions of the MDM2 oncogene in colon cancer growth and the potential value of MDM2 as a drug target for cancer therapy, by inhibiting MDM2 expression with an antisense anti-human-MDM2 oligonucleotide.
  • MATERIALS AND METHODS: The selected antisense mixed-backbone oligonucleotide was evaluated for its in vitro and in vivo antitumor activity in human colon cancer models: LS174T cell line containing wild-type p53 and DLD-1 cell line containing mutant p53.
  • In vivo antitumor activity of the oligonucleotide occurred in a dose-dependent manner in both models and synergistically or additive therapeutic effects of MDM2 inhibition and the cancer chemotherapeutic agents 10-hydroxycamptothecin and 5-fluorouracil were also observed.
  • This study should provide a basis for future development of anti-MDM2 antisense oligonucleotides as cancer therapeutic agents used alone or in combination with conventional chemotherapeutics.

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  • (PMID = 12149568.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 80698
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 67656-30-8 / 10-hydroxycamptothecin; 80168379AG / Doxorubicin; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2039984
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10. Kawakami K, Kawakami M, Husain SR, Puri RK: Potent antitumor activity of IL-13 cytotoxin in human pancreatic tumors engineered to express IL-13 receptor alpha2 chain in vivo. Gene Ther; 2003 Jul;10(13):1116-28
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  • In this study, we have exploited IL-13Ralpha2 chain and established a novel approach for pancreatic cancer therapy.
  • For this, a plasmid encoding the IL-13Ralpha2 chain gene was mixed with liposomes and injected into subcutaneously or orthotopically xenografted human pancreatic tumors in immunodeficient mice, followed by systemic or local therapy by a recombinant IL-13 cytotoxin.
  • Since macrophages were found to produce nitric oxide, IL-13Ralpha2-targeted cancer therapy involved not only a direct tumor cell killing by IL-13 cytotoxin but also activation of innate immune response at the tumor site.
  • Therefore, this approach may be a new powerful tool for pancreatic cancer or other localized cancer therapy.
  • [MeSH-major] Genetic Therapy / methods. Immunotoxins / pharmacology. Interleukin-13 / pharmacology. Pancreatic Neoplasms / therapy. Receptors, Interleukin / genetics
  • [MeSH-minor] Animals. Antigens, Neoplasm. Binding Sites. Gene Expression. Humans. Injections, Intralesional. Interleukin-13 Receptor alpha1 Subunit. Macrophage Activation. Mice. Mice, Nude. Models, Animal. Neoplasm Transplantation. Nitric Oxide / biosynthesis. Radioligand Assay. Receptors, Interleukin-13. Reverse Transcriptase Polymerase Chain Reaction. Transfection / methods

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  • (PMID = 12808442.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / IL13RA1 protein, human; 0 / Il13ra1 protein, mouse; 0 / Immunotoxins; 0 / Interleukin-13; 0 / Interleukin-13 Receptor alpha1 Subunit; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-13; 31C4KY9ESH / Nitric Oxide
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11. Wang H, Wang S, Nan L, Yu D, Agrawal S, Zhang R: Antisense anti-MDM2 mixed-backbone oligonucleotides enhance therapeutic efficacy of topoisomerase I inhibitor irinotecan in nude mice bearing human cancer xenografts: In vivo activity and mechanisms. Int J Oncol; 2002 Apr;20(4):745-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antisense anti-MDM2 mixed-backbone oligonucleotides enhance therapeutic efficacy of topoisomerase I inhibitor irinotecan in nude mice bearing human cancer xenografts: In vivo activity and mechanisms.
  • In the present study, we demonstrated synergistic effects between anti-MDM2 antisense oligonucleotides and the clinically used anticancer agent irinotecan, using nude mouse models of human colon cancers (LS174T and DLD-1).
  • Both oligonucleotides increased tissue uptake of irinotecan and the conversion of irinotecan to its active metabolite SN-38.
  • These results suggest that oligonucleotides have a role in irinotecan metabolism and action, providing a basis for future development of antisense oligonucleotides as a sensitizer for irinotecan-based therapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / therapeutic use. Colonic Neoplasms / drug therapy. Nuclear Proteins. Oligonucleotides, Antisense / therapeutic use. Proto-Oncogene Proteins / genetics. Topoisomerase I Inhibitors
  • [MeSH-minor] Animals. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. Dose-Response Relationship, Drug. Drug Resistance. Drug Synergism. Female. Humans. Mice. Mice, Nude. Mutation. Neoplasm Transplantation. Proto-Oncogene Proteins c-mdm2. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 11894120.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 80698
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins; 0 / Topoisomerase I Inhibitors; 0 / Tumor Suppressor Protein p53; 7673326042 / irinotecan; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; XT3Z54Z28A / Camptothecin
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12. Zhang J, Dai J, Qi Y, Lin DL, Smith P, Strayhorn C, Mizokami A, Fu Z, Westman J, Keller ET: Osteoprotegerin inhibits prostate cancer-induced osteoclastogenesis and prevents prostate tumor growth in the bone. J Clin Invest; 2001 May;107(10):1235-44
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  • OPG completely prevented the establishment of mixed osteolytic/osteoblastic tibial tumors, as were observed in vehicle-treated animals, but it had no effect on subcutaneous tumor growth.

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  • (PMID = 11375413.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR007008; United States / NIA NIH HHS / AG / R01 AG-15904; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / P50 CA-69568; United States / NCRR NIH HHS / RR / T32 RR-07008
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Glycoproteins; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tnfrsf11a protein, mouse; 0 / Tnfrsf11b protein, mouse; 0 / Tnfsf11 protein, mouse
  • [Other-IDs] NLM/ PMC209296
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