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1. 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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2. 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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3. 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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4. Tortora G, Caputo R, Damiano V, Bianco R, Chen J, Agrawal S, Bianco AR, Ciardiello F: A novel MDM2 anti-sense oligonucleotide has anti-tumor activity and potentiates cytotoxic drugs acting by different mechanisms in human colon cancer. Int J Cancer; 2000 Dec 1;88(5):804-9
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  • [Title] A novel MDM2 anti-sense oligonucleotide has anti-tumor activity and potentiates cytotoxic drugs acting by different mechanisms in human colon cancer.
  • In this study, we have used a novel oligonucleotide anti-sense MDM2, with mixed-backbone structure and demonstrate that it causes inhibition of MDM2 expression, induction of both p53 and p21/WAF1 expression and a dose-dependent, growth-inhibitory effect in human GEO colon-cancer cells.
  • We also show that anti-sense MDM2 has a co-operative growth-inhibitory effect with different classes of cytotoxic drugs acting by different mechanisms.
  • Moreover, anti-sense MDM2 induces apoptosis and markedly enhances the apoptotic activity of different cytotoxic drugs.
  • Finally, we show that anti-sense MDM2 has anti-tumor activity in vivo in nude mice bearing GEO xenografts and potentiates the anti-tumor effect of cytotoxic drugs.
  • Indeed, despite the short treatment period, the combination of anti-sense MDM2 and cytotoxic drugs causes a marked delay in tumor growth and prolongation of mice survival, lasting several months after treatment cessation.
  • The anti-tumor effect is associated with inhibition of MDM2 expression in tumor specimens of animals treated with anti-sense MDM2, alone or in combination with a cytotoxic drug.
  • Our results provide the rationale for development of a novel mixed-backbone anti-sense MDM2 into a clinical setting in therapeutic combination strategies with conventional cytotoxic drugs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colonic Neoplasms / drug therapy. Nuclear Proteins. Oligonucleotides, Antisense / therapeutic use. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Division / drug effects. Disease Models, Animal. Drug Synergism. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Proto-Oncogene Proteins c-mdm2. Tumor Cells, Cultured

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 11072252.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins; 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
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5. Ogura Y, Mizumoto K, Tanaka M, Ohuchida K, Murakami M, Yamada D, Ishikawa N, Nagai E: Strategy for prevention of local recurrence of pancreatic cancer after pancreatectomy: antitumor effect of gemcitabine mixed with fibrin glue in an orthotopic nude mouse model. Surgery; 2006 Jul;140(1):66-71
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  • [Title] Strategy for prevention of local recurrence of pancreatic cancer after pancreatectomy: antitumor effect of gemcitabine mixed with fibrin glue in an orthotopic nude mouse model.
  • BACKGROUND: Pancreatic cancer frequently recurs after operative treatment, resulting in a poor prognosis.
  • Fibrin glue (FG) is a biocompatible, adherent hemostat that can deliver high concentrations of anticancer drugs to residual cancer cells.
  • Seven days later, groups of mice were treated with 80 mg/kg GEM mixed with 0.5 mL fibrin glue (GEM + FG), 0.5 mL FG alone (FG), single intraperitoneal (i.p.) injection of 80 mg/kg GEM (GEM1), i.p. injection of 80 mg/kg GEM weekly for 3 weeks (GEM1,2,3), GEM + FG followed by weekly GEM injections for 2 weeks (GEM + FG + GEM2,3), or i.p. injection of PBS weekly for 3 weeks (controls).
  • This procedure may be useful clinically to prevent the local recurrence of pancreatic cancer after pancreatectomy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Deoxycytidine / analogs & derivatives. Fibrin Tissue Adhesive / administration & dosage. Neoplasm Recurrence, Local / prevention & control. Pancreatectomy. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy. Fluorescent Dyes / administration & dosage. Fluorescent Dyes / pharmacokinetics. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Rhodamines / administration & dosage. Rhodamines / pharmacokinetics. Transplantation, Heterologous

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  • (PMID = 16857444.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fibrin Tissue Adhesive; 0 / Fluorescent Dyes; 0 / Rhodamines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; K7G5SCF8IL / rhodamine B
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6. 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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7. 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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8. Tortora G, Bianco R, Damiano V, Fontanini G, De Placido S, Bianco AR, Ciardiello F: Oral antisense that targets protein kinase A cooperates with taxol and inhibits tumor growth, angiogenesis, and growth factor production. Clin Cancer Res; 2000 Jun;6(6):2506-12
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  • Protein kinase A type I (PKAI) transduces mitogenic signals from different growth factors and oncogenes and is overexpressed in the majority of human cancers.
  • In this study, we used a novel hybrid DNA/RNA mixed-backbone oligonucleotide (MBO) targeting the PKAI subunit RIalpha.
  • We demonstrated that after oral administration, the MBO antisense RIalpha inhibited the growth of human colon cancer xenografts in nude mice and showed a cooperative antitumor effect with Taxol, which outlasted treatment withdrawal and significantly prolonged survival of mice compared with untreated controls or to single-agent-treated mice.
  • In conclusion, a novel MBO that targets PKAI, administered p.o., is effective and cooperates with the anticancer drug Taxol on both tumor growth and expression of factors involved in the control of cell proliferation, cell cycle, and angiogenesis.
  • Because the MBO described has completed a phase I trial involving i.v. injection in cancer patients, these results provide the biological rationale of its activity after oral administration and may be translated into a therapeutic strategy in a clinical setting.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cell Cycle Proteins. Colonic Neoplasms / drug therapy. Cyclic AMP-Dependent Protein Kinases / genetics. Cyclic AMP-Dependent Protein Kinases / metabolism. Growth Substances / biosynthesis. Neovascularization, Pathologic. Oligonucleotides, Antisense / therapeutic use. Paclitaxel / pharmacology. Tumor Suppressor Proteins
  • [MeSH-minor] Administration, Oral. Animals. Cyclin-Dependent Kinase Inhibitor p27. Female. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Mice. Mice, Inbred BALB C. Mice, Nude. Microtubule-Associated Proteins / biosynthesis. Neoplasm Transplantation. Time Factors. Tumor Cells, Cultured

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  • (PMID = 10873106.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Cdkn1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Growth Substances; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Oligonucleotides, Antisense; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; P88XT4IS4D / Paclitaxel
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9. Yeung SC, She M, Yang H, Pan J, Sun L, Chaplin D: Combination chemotherapy including combretastatin A4 phosphate and paclitaxel is effective against anaplastic thyroid cancer in a nude mouse xenograft model. J Clin Endocrinol Metab; 2007 Aug;92(8):2902-9
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  • [Title] Combination chemotherapy including combretastatin A4 phosphate and paclitaxel is effective against anaplastic thyroid cancer in a nude mouse xenograft model.
  • CONTEXT: Anaplastic thyroid cancer (ATC) is extremely aggressive, and no effective treatment is available.
  • OBJECTIVE: We hypothesized that a triple-drug combination including CA4P and paclitaxel would improve efficacy against ATC.
  • SETTING: We used a nude mouse xenograft model with ARO and KAT-4 cells.
  • RESULTS: Tumor growth curve analysis (linear mixed models, P < 0.05) and xenograft weight analysis (Kruskal-Wallis one-way ANOVA on ranks, post hoc pairwise comparison, Dunn's test, P < 0.05) demonstrated that both triple-drug combinations were significantly better than placebo for both cell lines.
  • CONCLUSIONS: Both triple-drug combinations demonstrated excellent antineoplastic activity against ATC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / metabolism. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Phytogenic / administration & dosage. Bromodeoxyuridine / metabolism. Carboplatin / therapeutic use. Cell Line, Tumor. Cell Shape. Endothelial Cells / pathology. Endothelial Cells / ultrastructure. Humans. Immunohistochemistry. Mice. Mice, Nude. Microscopy, Electron, Transmission. Neoplasm Transplantation. Paclitaxel / administration & dosage. Polyenes / therapeutic use. Polyunsaturated Alkamides / therapeutic use. Stilbenes / administration & dosage. Transplantation, Heterologous

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  • (PMID = 17550961.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Stilbenes; 52665-74-4 / manumycin; BG3F62OND5 / Carboplatin; G34N38R2N1 / Bromodeoxyuridine; I5590ES2QZ / fosbretabulin; P88XT4IS4D / Paclitaxel
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10. 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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  • [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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11. 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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12. van der Burg SH, Bijker MS, Welters MJ, Offringa R, Melief CJ: Improved peptide vaccine strategies, creating synthetic artificial infections to maximize immune efficacy. Adv Drug Deliv Rev; 2006 Oct 1;58(8):916-30
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  • Human testing of such vaccines, although protective in mouse models, has produced mixed results.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Neoplasms / therapy. Peptides / therapeutic use. Vaccines, Synthetic / therapeutic use
  • [MeSH-minor] Animals. Antigens, Neoplasm / immunology. Epitopes, T-Lymphocyte / immunology. Humans. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Helper-Inducer / immunology

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  • (PMID = 16979788.001).
  • [ISSN] 0169-409X
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Epitopes, T-Lymphocyte; 0 / Peptides; 0 / Vaccines, Synthetic
  • [Number-of-references] 117
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13. 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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14. 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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15. Nishihara T, Sawada T, Yamamoto A, Yamashita Y, Ho JJ, Kim YS, Chung KH: Antibody-dependent cytotoxicity mediated by chimeric monoclonal antibody Nd2 and experimental immunotherapy for pancreatic cancer. Jpn J Cancer Res; 2000 Aug;91(8):817-24
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  • In a previous study, mouse monoclonal antibody (MoAb) Nd2 (m-Nd2, mouse IgG1) labeled with (131)I exhibited efficacy in in vivo radioimmunotherapy against pancreatic cancer.
  • In this study we prepared mouse / human chimeric antibody Nd2 (c-Nd2, human IgG1) for clinical use and examined whether c-Nd2 induced antibody-dependent cell-mediated cytotoxicity (ADCC).
  • Cytotoxicity to pancreatic cancer (PC) cell lines, including Nd2 antigen-positive (SW1990, RWP-1, Capan-1) and Nd2 antigen-negative (Panc-1, MiaPaca-2, Capan-2) lines, was evaluated by mixed human leukocyte and tumor cell culture (MLTC) at an effector cell to target cell (E / T) ratio of 50 with or without Nd2.
  • Cytotoxic capacity during MLTC with c-Nd2 was significantly higher than during MLTC with m-Nd2 or with no antibody.
  • These findings suggested that, because of its ability to induce ADCC, c-Nd2 may be clinically useful for the immunotherapeutic treatment of pancreatic cancer.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Pancreatic Neoplasms / therapy. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Animals. Antibody Affinity. Antibody-Dependent Cell Cytotoxicity. Disease Models, Animal. Humans. Immunotherapy. Leukocytes, Mononuclear / drug effects. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 10965023.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA24321
  • [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] JAPAN
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins
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16. 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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17. 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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18. Hoffmann J, Bohlmann R, Heinrich N, Hofmeister H, Kroll J, Künzer H, Lichtner RB, Nishino Y, Parczyk K, Sauer G, Gieschen H, Ulbrich HF, Schneider MR: Characterization of new estrogen receptor destabilizing compounds: effects on estrogen-sensitive and tamoxifen-resistant breast cancer. J Natl Cancer Inst; 2004 Feb 4;96(3):210-8
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  • BACKGROUND: Antiestrogens of the selective estrogen receptor modulator (SERM) type, such as tamoxifen, have two major limitations: their mixed agonist and antagonist profile and the development of tumor resistance.
  • METHODS: Effects of antiestrogens on the growth of estrogen-dependent breast tumors in vivo were determined using several mouse xenograft models (including the tamoxifen-sensitive tumors MCF7, T47D, and MV3366 and the tamoxifen-resistant tumors ZR75-1 and MCF7/TAM) and chemically induced (nitrosomethyl urea [NMU] and dimethylbenzanthracene [DMBA]) rat breast cancer models (groups of 10 animals).
  • We determined the initial response and effects on hormone receptor levels and the time to relapse after treatment (i.e., time to reach a predetermined tumor size threshold).
  • ER levels were dramatically reduced in MCF7 tumors after 5 weeks of ZK-703 treatment compared with ER levels in vehicle-treated tumors; by contrast, ER levels in tamoxifen-treated tumors were higher than those in control tumors.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Breast Neoplasms / drug therapy. Estradiol / pharmacology. Estrogen Receptor Modulators / pharmacology. Neoplasms, Hormone-Dependent / drug therapy. Receptors, Estrogen / drug effects. Selective Estrogen Receptor Modulators / pharmacology
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Administration, Oral. Animals. Disease Models, Animal. Disease Progression. Drug Resistance, Neoplasm. Estrogens / blood. Female. Humans. Injections, Subcutaneous. Methylnitrosourea. Mice. Tamoxifen / pharmacology. Transplantation, Heterologous

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  • (PMID = 14759988.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Receptor Modulators; 0 / Estrogens; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 0 / ZK253; 0 / ZK703; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 684-93-5 / Methylnitrosourea
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19. Robey IF, Baggett BK, Kirkpatrick ND, Roe DJ, Dosescu J, Sloane BF, Hashim AI, Morse DL, Raghunand N, Gatenby RA, Gillies RJ: Bicarbonate increases tumor pH and inhibits spontaneous metastases. Cancer Res; 2009 Mar 15;69(6):2260-8
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  • Here, we show that oral NaHCO(3) selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer.
  • This treatment regimen was shown to significantly increase the extracellular pH, but not the intracellular pH, of tumors by (31)P magnetic resonance spectroscopy and the export of acid from growing tumors by fluorescence microscopy of tumors grown in window chambers.
  • NaHCO(3) therapy also reduced the rate of lymph node involvement, yet did not affect the levels of circulating tumor cells, suggesting that reduced organ metastases were not due to increased intravasation.
  • In contrast, NaHCO(3) therapy significantly reduced the formation of hepatic metastases following intrasplenic injection, suggesting that it did inhibit extravasation and colonization.
  • In tail vein injections of alternative cancer models, bicarbonate had mixed results, inhibiting the formation of metastases from PC3M prostate cancer cells, but not those of B16 melanoma.
  • Although the mechanism of this therapy is not known with certainty, low pH was shown to increase the release of active cathepsin B, an important matrix remodeling protease.

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  • [Cites] Biochem Pharmacol. 1999 May 1;57(9):1047-58 [10796075.001]
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  • (PMID = 19276390.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA077575-09; United States / NCI NIH HHS / CA / R01 CA077575; United States / NCI NIH HHS / CA / CA 077575; United States / NCI NIH HHS / CA / R01 CA077575-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 8MDF5V39QO / Sodium Bicarbonate; EC 3.4.22.1 / Cathepsin B
  • [Other-IDs] NLM/ NIHMS179466; NLM/ PMC2834485
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20. Lee HJ, Lee HS, Hur K, Kim WH, Yanagihara K, Becker KF, Lee KU, Yang HK: Tumor specificity and in vivo targeting of an antibody against exon 9 deleted E-cadherin in gastric cancer. J Cancer Res Clin Oncol; 2007 Dec;133(12):987-94
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.
  • METHODS: Among nine human diffuse-type gastric cancer cell lines, we selected a cell line expressing exon 9 deleted E-cadherin (HSC-45M2) by direct sequencing.
  • Tumor specificity and tumor specific in vivo targeting of E-cad delta 9-1 were evaluated in nude mouse bearing a tumor derived from HSC-45M2 cell line by immunohistochemical staining.
  • RESULTS: Immunohistochemical staining of various tissues from nude mice showed that only tumor tissue reacted with E-cad delta 9-1.
  • However, immunohistochemical staining of the same tissues after systemic injection of E-cad delta 9-1 showed that reticuloendothelial and hypervascular organs reacted with E-cad delta 9-1, but tumor tissue showed only a slight reaction.
  • Evaluation of the reactivity of 299 gastric cancer patients to E-cad delta 9-1 showed that 4.8% (9/187) of patients, who all had diffuse- or mixed-type gastric cancers, reacted positively, but none of the 112 intestinal-type gastric cancer patients reacted positively.
  • CONCLUSION: Considering that E-cad delta 9-1 showed good tumor specificity and that some diffuse-type gastric cancers were immunopositive to it, this antibody could be a candidate therapeutic antibody against gastric cancers that express mutant E-cadherin.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Cadherins / genetics. Cadherins / immunology. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibody Specificity. Cell Line, Tumor. Exons. Female. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Neoplasm Transplantation. Sensitivity and Specificity. Sequence Deletion. Xenograft Model Antitumor Assays

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  • (PMID = 17576594.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cadherins
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21. Zbar AP, Thomas H, Wilkinson RW, Wadhwa M, Syrigos KN, Ross EL, Dilger P, Allen-Mersh TG, Kmiot WA, Epenetos AA, Snary D, Bodmer WF: Immune responses in advanced colorectal cancer following repeated intradermal vaccination with the anti-CEA murine monoclonal antibody, PR1A3: results of a phase I study. Int J Colorectal Dis; 2005 Sep;20(5):403-14
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Fifteen patients with advanced colorectal cancer received either 0.5-, 1.0- or 5.0-mg doses of PR1A3 mixed with 10% w/v Alum adjuvant (Superfos Biosector, Denmark) intradermally at 4-week intervals for 3 months.
  • Patient serum was assessed for anti-idiotypic (Ab2), anti-anti-idiotypic (Ab3) and human anti-mouse antibody (HAMA) reactivity.
  • Delayed-type hypersensitivity (DTH) responses developed in 12 of the 15 patients.
  • Pre-treatment PBMC proliferation with PHA was subnormal in each patient compared with controls, becoming normal (or supranormal) in all patients during immunisation (P<0.001).
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoembryonic Antigen / drug effects. Carcinoembryonic Antigen / immunology. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / immunology
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Anti-Idiotypic / blood. Antibodies, Anti-Idiotypic / drug effects. Antibodies, Anti-Idiotypic / immunology. Antibodies, Neoplasm / blood. Antibodies, Neoplasm / drug effects. Antibodies, Neoplasm / immunology. Antigens, Neoplasm / blood. Antigens, Neoplasm / drug effects. Antigens, Neoplasm / immunology. Case-Control Studies. Cell Proliferation / drug effects. Cytokines / blood. Cytokines / drug effects. Cytokines / immunology. Dose-Response Relationship, Immunologic. Female. Humans. Hypersensitivity, Delayed / immunology. Immune Sera / drug effects. Immune Sera / immunology. Immunity, Mucosal / drug effects. Injections, Intradermal. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Male. Middle Aged. Receptors, Interleukin-2 / blood. Receptors, Interleukin-2 / drug effects. Receptors, Interleukin-2 / immunology. Treatment Outcome

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  • (PMID = 15864608.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Carcinoembryonic Antigen; 0 / Cytokines; 0 / Immune Sera; 0 / PR1A3 monoclonal antibody; 0 / Receptors, Interleukin-2
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