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1. Poikonen P, Sjöström J, Amini RM, Villman K, Ahlgren J, Blomqvist C: Cyclin A as a marker for prognosis and chemotherapy response in advanced breast cancer. Br J Cancer; 2005 Sep 5;93(5):515-9
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  • [Title] Cyclin A as a marker for prognosis and chemotherapy response in advanced breast cancer.
  • We wanted to study cyclin A as a marker for prognosis and chemotherapy response.
  • The proportion of cells expressing cyclin A was determined by immunohistochemistry using a mouse monoclonal antibody to human cyclin A.
  • A high cyclin A correlated significantly to a shorter time to first relapse, risk ratio (RR) 1.94 (95% CI 1.24-3.03) and survival from diagnosis, RR 2.49 (95% CI 1.45-4.29), cutoff point for high/low proliferation group 10.5%.
  • Cyclin A did not correlate to chemotherapy response or survival after anthracycline, docetaxel or MF therapy.
  • In the present study, cyclin A did not predict chemotherapy response.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Breast Neoplasms / drug therapy. Cyclin A / metabolism
  • [MeSH-minor] Carcinoma, Ductal / diagnosis. Carcinoma, Ductal / drug therapy. Carcinoma, Ductal / metabolism. Carcinoma, Lobular / diagnosis. Carcinoma, Lobular / drug therapy. Carcinoma, Lobular / metabolism. Fluorouracil / administration & dosage. Humans. Immunoenzyme Techniques. Methotrexate / administration & dosage. Prognosis

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  • (PMID = 16091759.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin A; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2361595
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2. Jie JZ, Wang JW, Qu JG, Hung T: Suppression of human colon tumor growth by adenoviral vector-mediated NK4 expression in an athymic mouse model. World J Gastroenterol; 2007 Apr 7;13(13):1938-46
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  • [Title] Suppression of human colon tumor growth by adenoviral vector-mediated NK4 expression in an athymic mouse model.
  • AIM: To investigate the suppressive effects of adenoviral vector-mediated expression of NK4, an antagonist of hepatocyte growth factor (HGF), on human colon cancer in an athymic mouse model to explore the possibility of applying NK4 to cancer gene therapy.
  • METHODS: A human colon tumor model was developed by subcutaneous implantation of tumor tissue formed by LS174T cells grown in athymic mice.
  • Fifteen tumor-bearing mice were randomized into three groups (n = 5 in each group) at d 3 after tumor implantation and mice were injected intratumorally with phosphate-buffered saline (PBS) or with recombinant adenovirus expressing beta-galactosidase (Ad-LacZ) or NK4 (rvAdCMV/NK4) at a 6-d interval for total 5 injections in each mouse.
  • Tumor sizes were measured during treatment to draw a tumor growth curve.
  • At d 26 after the first treatment, all animals were sacrificed and the tumors were removed to immunohistochemically examine proliferating cell nuclear antigen (PCNA), microvessel density (represented by CD31), and apoptotic cells.
  • These mice were randomized into 3 groups (n = 5 in each group) at d 1 after injection and were treated by ip injection of PBS, or Ad-LacZ, or rvAdCMV/NK4 at a 6-d interval for total two injections in each mouse.
  • These findings indicate that NK4 gene transfer may be an effective tool for the treatment of colon cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Colonic Neoplasms / therapy. Genetic Therapy. Hepatocyte Growth Factor / genetics. Hepatocyte Growth Factor / metabolism. Xenograft Model Antitumor Assays / methods

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  • (PMID = 17461494.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HGF protein, human; 67256-21-7 / Hepatocyte Growth Factor
  • [Other-IDs] NLM/ PMC4146970
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3. Oliver TG, Mercer KL, Sayles LC, Burke JR, Mendus D, Lovejoy KS, Cheng MH, Subramanian A, Mu D, Powers S, Crowley D, Bronson RT, Whittaker CA, Bhutkar A, Lippard SJ, Golub T, Thomale J, Jacks T, Sweet-Cordero EA: Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer. Genes Dev; 2010 Apr 15;24(8):837-52
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  • [Title] Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer.
  • Chemotherapy resistance is a major obstacle in cancer treatment, yet the mechanisms of response to specific therapies have been largely unexplored in vivo.
  • Employing genetic, genomic, and imaging approaches, we examined the dynamics of response to a mainstay chemotherapeutic, cisplatin, in multiple mouse models of human non-small-cell lung cancer (NSCLC).
  • Prolonged cisplatin treatment promotes the emergence of resistant tumors with enhanced repair capacity that are cross-resistant to platinum analogs, exhibit advanced histopathology, and possess an increased frequency of genomic alterations.
  • We demonstrate a novel role for PIDD as a regulator of chemotherapy response in human lung tumor cells.

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  • (PMID = 20395368.001).
  • [ISSN] 1549-5477
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA034992; United States / NCI NIH HHS / CA / P30 CA014051; United States / NCI NIH HHS / CA / 5-UO1-CA84306; United States / NCI NIH HHS / CA / U01 CA084306; United States / NCI NIH HHS / CA / P30-CA14051; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01 CA034992; United States / NCI NIH HHS / CA / CA034992; United States / NCI NIH HHS / CA / R01 CA127547
  • [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 / Carrier Proteins; 0 / Death Domain Receptor Signaling Adaptor Proteins; 0 / Lrdd protein, mouse; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2854397
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4. Ganapathy M, Ghosh R, Jianping X, Zhang X, Bedolla R, Schoolfield J, Yeh IT, Troyer DA, Olumi AF, Kumar AP: Involvement of FLIP in 2-methoxyestradiol-induced tumor regression in transgenic adenocarcinoma of mouse prostate model. Clin Cancer Res; 2009 Mar 1;15(5):1601-11
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  • [Title] Involvement of FLIP in 2-methoxyestradiol-induced tumor regression in transgenic adenocarcinoma of mouse prostate model.
  • PURPOSE: The purpose of this study is to investigate whether Fas-associated death domain interleukin-1 converting enzyme like inhibitory protein (FLIP) inhibition is a therapeutic target associated with 2-methoxyestradiol (2-ME2)-mediated tumor regression.
  • EXPERIMENTAL DESIGN: Expression and levels of FLIP were analyzed using (a) real-time PCR and immunoblot analysis in androgen-independent PC-3 cells treated with the newly formulated 2-ME2 and (b) immunohistochemistry in different Gleason pattern human prostate tumors.
  • Involvement of FLIP in 2-ME2-induced tumor regression was evaluated in transgenic adenocarcinoma mouse prostate (TRAMP) mice.
  • 2-ME2 treatment reduced binding of Sp1 to the FLIP promoter as evidenced by ChIP.
  • Further, levels of FLIP associated with Fas or FADD decreased, whereas cleavage of caspase-8, levels of Bid, and apoptosis increased in response to 2-ME2 treatment in PC-3 cells.

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  • (PMID = 19223508.001).
  • [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 / P30 CA54174; United States / NCI NIH HHS / CA / R01 CA135451; United States / NCI NIH HHS / CA / R01 CA135451-01; United States / NCI NIH HHS / CA / CA135451-01; United States / NCI NIH HHS / CA / P30 CA054174
  • [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 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Fas-Associated Death Domain Protein; 0 / Sp1 Transcription Factor; 0 / Tubulin Modulators; 148710-94-5 / Sp3 Transcription Factor; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
  • [Other-IDs] NLM/ NIHMS104982; NLM/ PMC2714369
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5. Mandir N, Goodlad RA: Conjugated linoleic acids differentially alter polyp number and diameter in the Apc(min/+) mouse model of intestinal cancer. Cell Prolif; 2008 Apr;41(2):279-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conjugated linoleic acids differentially alter polyp number and diameter in the Apc(min/+) mouse model of intestinal cancer.
  • MATERIALS AND METHODS: The effects of the predominant forms of CLA, namely the c9t11 and t10c12 isomers, or a mixture of these on polyp development, were investigated in the Apc(Min/+) mouse.
  • CLAs have also been linked to altered rates of cell renewal and cell proliferation so this was also studied, as was a further means of increasing tissue mass, namely crypt fission.
  • The t10c12 and the mixture significantly reduced polyp number in the proximal small intestine but they increased polyp diameter in the middle and distal small intestine, to an extent that the polyp burden was significantly increased at these sites.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Intestinal Neoplasms / prevention & control. Intestinal Polyps / drug therapy. Linoleic Acids, Conjugated / administration & dosage
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Chemoprevention. Dietary Supplements. Disease Models, Animal. Female. Isomerism. Male. Mice. Mice, Inbred C57BL. Mitosis / drug effects. beta Catenin / metabolism

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  • (PMID = 18336472.001).
  • [ISSN] 1365-2184
  • [Journal-full-title] Cell proliferation
  • [ISO-abbreviation] Cell Prolif.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Linoleic Acids, Conjugated; 0 / beta Catenin; 0 / cis-9, trans-11-conjugated linoleic acid; 0 / trans-10,cis-12-conjugated linoleic acid
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6. Klinakis A, Szabolcs M, Chen G, Xuan S, Hibshoosh H, Efstratiadis A: Igf1r as a therapeutic target in a mouse model of basal-like breast cancer. Proc Natl Acad Sci U S A; 2009 Feb 17;106(7):2359-64
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  • [Title] Igf1r as a therapeutic target in a mouse model of basal-like breast cancer.
  • Considering the strong association between dysregulated insulin-like growth factor (IGF) signaling and various human cancers, we have used an expedient combination of genetic analysis and pharmacological treatment to evaluate the potential of the type 1 IGF receptor (Igf1r) for targeted anticancer therapy in a mouse model of mammary tumorigenesis.
  • In this particular strain of genetically modified animals, histopathologically heterogeneous invasive carcinomas exhibiting up-regulation of the Igf1r gene developed extremely rapidly by mammary gland-specific overexpression of constitutively active oncogenic Kras* (mutant Kras(G12D)).
  • Immunophenotyping data and expression profiling analyses showed that, except for a minor luminal component, these mouse tumors resembled basal-like human breast cancers.
  • This is a group of aggressive tumors of poor prognosis for which there is no targeted therapy currently available, and it includes a subtype correlating with KRAS locus amplification.
  • Conditional ablation of Igf1r in the mouse mammary epithelium increased the latency of Kras*-induced tumors very significantly (approximately 11-fold in comparison with the intact model), whereas treatment of tumor-bearing animals by administration of picropodophyllin (PPP), a specific Igf1r inhibitor, resulted in a dramatic decrease in tumor mass of the main forms of basal-like carcinomas.

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  • (PMID = 19174523.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA097403; United States / NCI NIH HHS / CA / 1 P01 CA97403
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0F35AOI227 / picropodophyllin; EC 2.7.10.1 / Receptor, IGF Type 1; EC 3.6.5.2 / ras Proteins; L36H50F353 / Podophyllotoxin
  • [Other-IDs] NLM/ PMC2650161
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7. Starkey JR, Rebane AK, Drobizhev MA, Meng F, Gong A, Elliott A, McInnerney K, Spangler CW: New two-photon activated photodynamic therapy sensitizers induce xenograft tumor regressions after near-IR laser treatment through the body of the host mouse. Clin Cancer Res; 2008 Oct 15;14(20):6564-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New two-photon activated photodynamic therapy sensitizers induce xenograft tumor regressions after near-IR laser treatment through the body of the host mouse.
  • PURPOSE: The aim of this study was to show that novel photodynamic therapy (PDT) sensitizers can be activated by two-photon absorption in the near-IR region of the spectrum and to show, for the first time, that such activation can lead to tumor regressions at significant tissue depth.
  • These experiments also evaluated effects of high-energy femtosecond pulsed laser irradiation on normal tissues and characterized the response of xenograft tumors to our PDT protocols.
  • Irradiation of sensitized tumors was undertaken through the bodies of tumor-bearing mice to give a treatment depth of 2 cm.
  • Posttreatment tumor regressions and histopathology were carried out to determine the nature of the response to these new PDT agents.
  • RESULTS: Regressions of all tumor types tested were seen.
  • Histopathology was consistent with known PDT effects, and no, or minimal, changes were noted in irradiated normal tissues.
  • Experiments in larger animals are warranted to determine the maximal achievable depth of treatment.
  • [MeSH-major] Hematoporphyrins / therapeutic use. Neoplasms / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 18927297.001).
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hematoporphyrins; 0 / MPA79; 0 / Photosensitizing Agents; S88TT14065 / Oxygen
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8. Nielsen LL, Gurnani M, Shi B, Terracina G, Johnson RC, Carroll J, Mathis JM, Hajian G: Derivation and initial characterization of a mouse mammary tumor cell line carrying the polyomavirus middle T antigen: utility in the development of novel cancer therapeutics. Cancer Res; 2000 Dec 15;60(24):7066-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Derivation and initial characterization of a mouse mammary tumor cell line carrying the polyomavirus middle T antigen: utility in the development of novel cancer therapeutics.
  • Here we describe the derivation of novel cell lines from spontaneous mammary tumors that arose in mouse mammary tumor virus-polyomavirus (MMTV-PyV) Middle T (MidT) transgenic mice.
  • Clonal cell lines from four mixed cell populations were tested for adenovirus transducibility and sensitivity to p53 tumor suppressor gene therapy mediated by SCH58500, a replication-deficient adenovirus that expresses human p53.
  • This cell line carried the PyV MidT antigen, had wild-type p53 DNA, and was sensitive to suppression of proliferation by MMAC/PTEN tumor suppressor gene therapy.
  • The histopathology of MidT2-1 tumors closely resembled the histopathology of the primary transgenic tumors.
  • Tumor growth in vivo was inhibited by p53 gene therapy or by MMAC gene therapy.
  • In addition, combination therapy with a number of anticancer agents had synergistic or additive efficacy in vitro.
  • In particular, MMAC gene therapy synergized with SCH58500 or paclitaxel. In the i.p.
  • MidT2-1 tumor model p53 gene therapy enhanced the survival benefits of paclitaxel/cisplatin chemotherapy.
  • Combination therapy has become a mainstay in cancer treatment.
  • In this report, we use a novel transgenic mouse tumor cell line to suggest new combinations that might be explored in clinical cancer care.
  • These include gene therapy using the tumor suppressors MMAC and p53, chemotherapy using farnesyl transferase inhibitors, the microtubule stabilizing taxanes, and the DNA synthesis disruptors gemcitabine and cisplatin.
  • The precise biological mechanisms by which these therapies induce their antitumor effects are not fully elucidated.
  • However, the work presented here suggests that many of these therapeutic approaches have synergistic antitumor activity when used in combination.
  • [MeSH-major] Antigens, Polyomavirus Transforming / metabolism. Mammary Neoplasms, Animal / immunology. Mammary Neoplasms, Animal / therapy. Protein-Serine-Threonine Kinases. Taxoids. Tumor Cells, Cultured. Tumor Suppressor Proteins
  • [MeSH-minor] Adenoviridae / genetics. Alkyl and Aryl Transferases / antagonists & inhibitors. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Bridged Compounds / pharmacology. Cell Division. Cisplatin / pharmacology. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Dose-Response Relationship, Drug. Farnesyltranstransferase. Female. Gene Transfer Techniques. Genes, p53 / genetics. Mice. Mice, Transgenic. Nucleic Acid Synthesis Inhibitors / pharmacology. PTEN Phosphohydrolase. Paclitaxel / pharmacology. Phosphoric Monoester Hydrolases / metabolism. Polymerase Chain Reaction. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Sequence Analysis, DNA. Time Factors. Transduction, Genetic. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 11156413.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Bridged Compounds; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Taxoids; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0W860991D6 / Deoxycytidine; 1605-68-1 / taxane; B76N6SBZ8R / gemcitabine; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.67 / PTEN Phosphohydrolase; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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9. Zhang L, Zeng D, Huang H, Wang J, Tao Q, Pan C, Xu J, Zhang B, Wang A: Tissue inhibitor of metalloproteinase-2 inhibits ameloblastoma growth in a new mouse xenograft disease model. J Oral Pathol Med; 2010 Jan;39(1):94-102
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  • [Title] Tissue inhibitor of metalloproteinase-2 inhibits ameloblastoma growth in a new mouse xenograft disease model.
  • BACKGROUND: Ameloblastomas are odontogenic neoplasms characterized by local invasiveness.
  • This study was conducted to develop a new animal model of ameloblastoma and to address the role of tissue inhibitor of metalloproteinase-2 (TIMP-2) and matrix metalloproteinase-2 (MMP-2) in the growth and invasiveness of ameloblastomas.
  • METHOD: Donated fresh human ameloblastoma tissue was finely minced, screened, and subcutaneously implanted in three locations on each of 10 BALB/c-nu/nu nude mice.
  • Newly established tumors on each mouse were injected with: (i) transfection reagent;.
  • Tumors were monitored for 5 weeks and excised for histopathology, RNA, and protein analyses.
  • [MeSH-major] Ameloblastoma / drug therapy. Neoplasm Transplantation. Soft Tissue Neoplasms / drug therapy. Tissue Inhibitor of Metalloproteinase-2 / therapeutic use. Transplantation, Heterologous
  • [MeSH-minor] Adult. Animals. Blotting, Western. Disease Models, Animal. Female. Genetic Vectors / therapeutic use. Humans. Matrix Metalloproteinase 2. Matrix Metalloproteinase Inhibitors. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Invasiveness. Plasmids / therapeutic use. Reverse Transcriptase Polymerase Chain Reaction. Subcutaneous Tissue / surgery. Transfection. Tumor Cells, Cultured

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  • (PMID = 19895658.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Matrix Metalloproteinase Inhibitors; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.24 / Mmp2 protein, mouse
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10. Roth DR, Roman D, Cozens R, Brandt R, Seewald W, Greiner B, Wenger F, Mamom T, Germann PG: Effects of epithelial growth factor receptor (EGFR) kinase inhibitors on genetically reconstituted mouse mammary glands. Exp Toxicol Pathol; 2003 Nov;55(4):237-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of epithelial growth factor receptor (EGFR) kinase inhibitors on genetically reconstituted mouse mammary glands.
  • NeuT-transfected immortalized HC11 epithelial cells and primary mouse mammary epithelial cells have been transplanted into the gland-free mammary fat pad of female BALB/c mice.
  • Mammary tumors developed after a latency period of three to four weeks.
  • RESULTS: Oral Treatment with EGFR-KI in this transgenic organ model showed clear antitumor efficacy in a dose-dependent manner in the range between 38 and 75 mg/kg b.w.
  • For all treatments a strong correlation between the biological behavior of the tumor, histopathology and cell proliferation could be established.
  • In contrast, treatment with Taxol showed no significant reduction of tumor growth or cell proliferation in this model.
  • This new transgenic organ model comprising histopathological evaluation and cell proliferation analysis appears to be a suitable test system for drug candidates that affect specific biochemical pathways.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Mammary Glands, Animal / transplantation. Mammary Neoplasms, Experimental / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Transformed. Cell Line, Tumor. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor / methods. Female. Image Cytometry. Injections, Intravenous. Ki-67 Antigen / metabolism. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Paclitaxel / administration & dosage. Paclitaxel / therapeutic use. Treatment Outcome

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  • (PMID = 14703768.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; P88XT4IS4D / Paclitaxel
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11. Di Nicolantonio F, Knight LA, Glaysher S, Whitehouse PA, Mercer SJ, Sharma S, Mills L, Prin A, Johnson P, Charlton PA, Norris D, Cree IA: Ex vivo reversal of chemoresistance by tariquidar (XR9576). Anticancer Drugs; 2004 Oct;15(9):861-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The expression of P-glycoprotein (P-gp) has been demonstrated to confer resistance to several anticancer drugs, including anthracyclines, taxanes and vinca alkaloids.
  • Tariquidar is a novel inhibitor of P-gp that has been shown to reverse resistance to cytotoxic drugs in tumor cell lines and mouse xenografts.
  • We have used an ATP-based chemosensitivity assay (ATP-TCA) to compare the activity of cytotoxic drugs in combination with tariquidar against a variety of solid tumors (n = 37).
  • The results show that tariquidar is able to decrease resistance in a number of solid tumors resistant to cytotoxic drugs known to be P-gp substrates.
  • These data support the introduction of tariquidar in combination with chemotherapy to clinical trials of patients expressing P-gp.
  • [MeSH-major] Drug Resistance, Neoplasm / drug effects. Quinolines / pharmacology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Female. Humans. Male. Middle Aged. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. P-Glycoprotein / metabolism. Skin Neoplasms / drug therapy. Skin Neoplasms / metabolism. Skin Neoplasms / pathology. Tumor Cells, Cultured

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  • (PMID = 15457126.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / Quinolines; J58862DTVD / tariquidar
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12. Macor P, Secco E, Zorzet S, Tripodo C, Celeghini C, Tedesco F: An update on the xenograft and mouse models suitable for investigating new therapeutic compounds for the treatment of B-cell malignancies. Curr Pharm Des; 2008;14(21):2023-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An update on the xenograft and mouse models suitable for investigating new therapeutic compounds for the treatment of B-cell malignancies.
  • B-cell malignancies account for over the 90% of all lymphoid neoplasms.
  • The clonal proliferations of B-cells show a high degree of variation in terms of clinical and presenting features, histopathology, immunophenotype, and genetics.
  • The disadvantages of these models include the differences between rodent and human stroma and that they can not be used to characterise anti-tumor activity of many immunotherapeutic drugs.
  • These models can be used to study the molecular processes critical for the development, proliferation and survival of hematological malignancies and to characterise potential therapeutic targets.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Neoplasms, Experimental / metabolism. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Drug Delivery Systems. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / metabolism. Mice. Multiple Myeloma / drug therapy. Multiple Myeloma / metabolism. Species Specificity

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  • (PMID = 18691113.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 195
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13. Isayeva T, Ren C, Ponnazhagan S: Intraperitoneal gene therapy by rAAV provides long-term survival against epithelial ovarian cancer independently of survivin pathway. Gene Ther; 2007 Jan;14(2):138-46
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  • [Title] Intraperitoneal gene therapy by rAAV provides long-term survival against epithelial ovarian cancer independently of survivin pathway.
  • Despite improvements from cytoreductive surgery and chemotherapy, recurrent disease remains a formidable challenge.
  • In the present study, we demonstrate for the first time that stable intra-abdominal genetic transfer of endostatin and angiostatin (E+A) by recombinant adeno-associated virus (rAAV) provides sustained antitumor effects on the growth and dissemination of epithelial ovarian cancer in a mouse model.
  • Further, when combined with paclitaxel (taxol), the effect of this therapy was dramatically increased and resulted in long-term tumor-free survival overcoming prior limitations of chemotherapy and gene therapy.
  • The combined effects of angiosuppressive therapy and chemotherapy were found to be independently of survivin pathway.
  • Evidence for the superior effects of the combination therapy was indicated by significantly lower ascites volume with less hemorrhage and tumor conglomerates, lower ascites vascular endothelial growth factor, higher tumor cell apoptosis and decreased blood vasculature, and long-term disease-free survival.
  • Histopathology of visceral organs and liver enzyme assays indicated no toxicity or pathology.
  • [MeSH-major] Angiogenesis Inhibitors / genetics. Dependovirus / genetics. Genetic Therapy / methods. Genetic Vectors / administration & dosage. Neoplasm Recurrence, Local / therapy. Ovarian Neoplasms / therapy
  • [MeSH-minor] Angiostatins / genetics. Angiostatins / therapeutic use. Animals. Antineoplastic Agents / therapeutic use. Ascitic Fluid / drug effects. Combined Modality Therapy. Drug Resistance, Neoplasm. Endostatins / genetics. Endostatins / therapeutic use. Female. Gene Expression. Inhibitor of Apoptosis Proteins. Injections, Intraperitoneal. Mice. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Paclitaxel / therapeutic use. Signal Transduction / physiology. Survival Rate. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16943851.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA90850; United States / NCI NIH HHS / CA / R01CA98817
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Endostatins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Vascular Endothelial Growth Factor A; 86090-08-6 / Angiostatins; P88XT4IS4D / Paclitaxel
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14. Schurigt U, Sevenich L, Vannier C, Gajda M, Schwinde A, Werner F, Stahl A, von Elverfeldt D, Becker AK, Bogyo M, Peters C, Reinheckel T: Trial of the cysteine cathepsin inhibitor JPM-OEt on early and advanced mammary cancer stages in the MMTV-PyMT-transgenic mouse model. Biol Chem; 2008 Aug;389(8):1067-74
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  • [Title] Trial of the cysteine cathepsin inhibitor JPM-OEt on early and advanced mammary cancer stages in the MMTV-PyMT-transgenic mouse model.
  • Recent data suggest proteases of the papain-like cysteine cathepsin family as molecular targets for cancer therapy.
  • Here, we report the treatment of polyoma middle T oncogene-induced breast cancers in mice with the cell-permeable broad-spectrum cysteine cathepsin inhibitor JPM-OEt.
  • However, at the endpoint of both experiments no significant differences in tumour weights, histopathology and lung metastasis were found between the inhibitor and the control group.
  • Measurement of cysteine cathepsin activities in tissue extracts after intraperitoneal injection of JPM-OEt revealed effective inhibition of cysteine cathepsins in pancreas, kidneys and liver, while activities in mammary cancers and in lungs were not significantly affected.
  • We conclude that the pharmacokinetic properties of JPM-OEt, which result in poor bioavailability, may prohibit its use for stand-alone treatment of solid mammary cancers and their lung metastases.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Cathepsins / antagonists & inhibitors. Cysteine Proteinase Inhibitors / therapeutic use. Leucine / analogs & derivatives. Mammary Tumor Virus, Mouse / physiology

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  • (PMID = 18710344.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB005011
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cysteine Proteinase Inhibitors; 0 / JPM 565; EC 3.4.- / Cathepsins; GMW67QNF9C / Leucine
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15. Bandapalli OR, Kahlert C, Hellstern V, Galindo L, Schirmacher P, Weitz J, Brand K: Cross-species comparison of biological themes and underlying genes on a global gene expression scale in a mouse model of colorectal liver metastasis and in clinical specimens. BMC Genomics; 2008;9:448
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  • [Title] Cross-species comparison of biological themes and underlying genes on a global gene expression scale in a mouse model of colorectal liver metastasis and in clinical specimens.
  • BACKGROUND: Invasion-related genes over-expressed by tumor cells as well as by reacting host cells represent promising drug targets for anti-cancer therapy.
  • Generally, histopathology and gene expression correlated well as the highest single gene overlap was found to be 44% in syn-compartmental comparisons (liver versus liver) whereas cross-compartmental overlaps were much lower (e.g. liver versus tumor: 9.7%).
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Liver Neoplasms / genetics. Liver Neoplasms / secondary

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  • (PMID = 18823562.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2573898
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16. McDougal A, Sethi Gupta M, Ramamoorthy K, Sun G, Safe SH: Inhibition of carcinogen-induced rat mammary tumor growth and other estrogen-dependent responses by symmetrical dihalo-substituted analogs of diindolylmethane. Cancer Lett; 2000 Apr 14;151(2):169-79
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  • DihaloDIMs (100 mg/kg/dayx3) were not estrogenic in the immature female B6C3F1 mouse uterus; however, in animals co-treated with E2 (0.02 microg/mouse), 5,5'-dichloro- and 6,6'-dichloroDIM inhibited uterine progesterone receptor (PR) binding and uterine peroxidase activity, whereas 5,5'-dichloro- and 5,5'-dichloro-2,2'-dimethylDIM inhibited only the latter response.
  • 4,4'-Dichloro-, 5,5'-dibromo- and 6,6'-dichloroDIM, significantly inhibited mammary tumor growth at doses of 1 mg/kg every second day, and no significant changes in organ weights or liver and kidney histopathology were observed.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Carcinogens / toxicity. Estradiol / pharmacology. Indoles / pharmacology. Mammary Neoplasms, Animal / chemically induced. Mammary Neoplasms, Animal / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Division / drug effects. Dose-Response Relationship, Drug. Estrogen Antagonists / chemistry. Estrogen Antagonists / pharmacology. Estrogen Antagonists / therapeutic use. Female. Halogens / metabolism. Humans. Mice. Organ Size / drug effects. Peroxidase / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Progesterone / metabolism. Tumor Cells, Cultured. Uterus / drug effects. Uterus / enzymology. Uterus / growth & development. Uterus / metabolism

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  • (PMID = 10738111.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES09106
  • [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] IRELAND
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Estrogen Antagonists; 0 / Halogens; 0 / Indoles; 0 / Receptors, Progesterone; 4TI98Z838E / Estradiol; EC 1.11.1.7 / Peroxidase; SSZ9HQT61Z / 3,3'-diindolylmethane
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17. Li Z, Mahesh SP, Shen DF, Liu B, Siu WO, Hwang FS, Wang QC, Chan CC, Pastan I, Nussenblatt RB: Eradication of tumor colonization and invasion by a B cell-specific immunotoxin in a murine model for human primary intraocular lymphoma. Cancer Res; 2006 Nov 1;66(21):10586-93
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  • Human primary intraocular lymphoma (PIOL) is predominantly a B cell-originated malignant disease with no appropriate animal models and effective therapies available.
  • This study aimed to establish a mouse model to closely mimic human B-cell PIOL and to test the therapeutic potential of a recently developed immunotoxin targeting human B-cell lymphomas.
  • The resemblance of this tumor model to human PIOL was examined by fundoscopy, histopathology, immunohistochemistry, and evaluated for molecular markers.
  • The therapeutic effectiveness of immunotoxin HA22 was tested by injecting the drug intravitreally.
  • This model may be a valuable tool in understanding the molecular pathogenesis of human PIOL and for the evaluation of new therapeutic approaches.
  • The results of B cell-specific immunotoxin therapy may have clinical implications in treating human PIOL.
  • [MeSH-major] B-Lymphocytes / drug effects. Eye Neoplasms / therapy. Immunotoxins / therapeutic use. Lymphoma, B-Cell / therapy

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  • (PMID = 17079483.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 EY000222-22
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CD22 protein, human; 0 / CXCR5 protein, human; 0 / Immunotoxins; 0 / Receptors, CXCR4; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Sialic Acid Binding Ig-like Lectin 2
  • [Other-IDs] NLM/ NIHMS22190; NLM/ PMC1931503
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18. Okaro AC, Fennell DA, Corbo M, Davidson BR, Cotter FE: Pk11195, a mitochondrial benzodiazepine receptor antagonist, reduces apoptosis threshold in Bcl-X(L) and Mcl-1 expressing human cholangiocarcinoma cells. Gut; 2002 Oct;51(4):556-61
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  • MATERIALS AND METHODS: Cells growing in culture were used to perform in vitro experiments over 48-96 hours following treatment.
  • The cytotoxic agents used were 5 fluorouracil 10 microM and etoposide (Vp16) 10 microM, together with ultraviolet and 0.5-1 Gy x ray irradiation with or without 75 microM Pk11195.
  • Severe combined immunodeficient non-obese diabetic (SCID-NOD) mice with subcutaneous xenografts using the Egi-1 and Tfk-1 cell lines were treated with etoposide with or without addition of Pk11195 over a 72 hour period during which time the xenograft growth patterns were monitored.
  • RESULTS: In vitro, the effect of Pk11195 on induction of apoptosis in cholangiocarcinoma cells following stimulation by chemotherapy or radiotherapy was found to be both time and dose dependent, with Pk11195 increasing rates of apoptosis by 50-95%.
  • Intraperitoneal administration of Pk11195 in combination with Vp16 was found to increase the growth inhibiting effects of Vp16 on xenografts during the treatment phase.
  • CONCLUSION: This is the first study to demonstrate that functional antagonism of coexpressed Bcl-X(L) and Mcl-1 proteins using the mBzR antagonist Pk11195 can facilitate apoptosis in cholangiocarcinoma following chemotherapy and radiotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Bile Duct Neoplasms / drug therapy. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy. Isoquinolines / pharmacology

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  • (PMID = 12235080.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BCL2L1 protein, human; 0 / GABA-A Receptor Antagonists; 0 / Isoquinolines; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 85340-56-3 / PK 11195
  • [Other-IDs] NLM/ PMC1773378
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19. Subramanian IV, Bui Nguyen TM, Truskinovsky AM, Tolar J, Blazar BR, Ramakrishnan S: Adeno-associated virus-mediated delivery of a mutant endostatin in combination with carboplatin treatment inhibits orthotopic growth of ovarian cancer and improves long-term survival. Cancer Res; 2006 Apr 15;66(8):4319-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adeno-associated virus-mediated delivery of a mutant endostatin in combination with carboplatin treatment inhibits orthotopic growth of ovarian cancer and improves long-term survival.
  • A human ovarian cancer cell line, which migrates to mouse ovaries and establishes peritoneal carcinomatosis, was used to evaluate the cooperative effect of an antiangiogenic gene therapy combined with chemotherapy.
  • Both external and internal imaging, along with histopathology, showed migration of i.p. injected human ovarian cancer cell line to mouse ovaries.
  • Using this model, we evaluated the effect of adeno-associated virus (AAV)-mediated expression of a mutant endostatin either alone or in combination with carboplatin treatment.
  • Antiangiogenic gene therapy inhibited orthotopic growth of ovarian cancer and resulted in 33% long-term tumor-free survival.
  • A single cycle of carboplatin treatment combined with mutant endostatin gene therapy resulted in 60% of the animals remaining tumor free for >200 days, which was significantly better than rAAV-LacZ and/or carboplatin.
  • Combination treatment delayed tumor appearance in 40% of the animals, wherein the residual tumors were smaller in size with limited or no peritoneal metastasis.
  • These studies suggest that AAV-mediated gene therapy of P125A-endostatin in combination with carboplatin is a useful method to inhibit peritoneal dissemination of ovarian carcinoma.

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  • (PMID = 16618757.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114340; United States / NIDA NIH HHS / DA / DA 11806
  • [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 / Endostatins; BG3F62OND5 / Carboplatin
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20. Wicha MS: Development of 'synthetic lethal' strategies to target BRCA1-deficient breast cancer. Breast Cancer Res; 2009;11(5):108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent clinical trials demonstrating the efficacy of poly(ADP-ribose) polymerase (PARP) inhibitors for the treatment of BRCA1-deficient breast cancer have provided support for the 'synthetic lethal' concept of targeted cancer therapeutics.
  • A new study provides further preclinical validation of this concept by demonstrating that BRCA1-deficient mouse mammary tumor cells are selectively sensitive to an inhibitor of the polycomb gene EZH2.
  • [MeSH-major] BRCA1 Protein / deficiency. Breast Neoplasms / drug therapy. Poly(ADP-ribose) Polymerase Inhibitors
  • [MeSH-minor] Animals. DNA-Binding Proteins / antagonists & inhibitors. Female. Histone-Lysine N-Methyltransferase / antagonists & inhibitors. Humans. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / enzymology. Mammary Neoplasms, Experimental / genetics. Mice. Polycomb Repressive Complex 2. Transcription Factors / antagonists & inhibitors

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  • (PMID = 19804613.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / DNA-Binding Proteins; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Ezh2 protein, mouse; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Polycomb Repressive Complex 2
  • [Other-IDs] NLM/ PMC2790845
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21. McCallum M, Baker C, Gillespie K, Cohen B, Stewart H, Leonard R, Cameron D, Leake R, Paxton J, Robertson A, Purdie C, Gould A, Steel M: A prognostic index for operable, node-negative breast cancer. Br J Cancer; 2004 May 17;90(10):1933-41
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • In the case of molecular assays, sensitivity and reliability were compromised by the age of the tissue specimens and the variability of fixation protocols.
  • In selecting patients for adjuvant systemic chemotherapy, the proposed index improves considerably on current international guidelines and matches the performance reported for 'gene-expression signature' analysis.
  • [MeSH-major] Biomarkers, Tumor / analysis. Breast Neoplasms / pathology. Breast Neoplasms / surgery. Lymphatic Metastasis. Muscle Proteins. Neoplasm Staging

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  • (PMID = 15138474.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Tagln protein, mouse; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC2409476
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22. Banerjee S, Choi M, Aboukameel A, Wang Z, Mohammad M, Chen J, Yang D, Sarkar FH, Mohammad RM: Preclinical studies of apogossypolone, a novel pan inhibitor of bcl-2 and mcl-1, synergistically potentiates cytotoxic effect of gemcitabine in pancreatic cancer cells. Pancreas; 2010 Apr;39(3):323-31
Hazardous Substances Data Bank. Gossypol .

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  • OBJECTIVE: Overexpression of antiapoptotic Bcl-2 family proteins confers resistance to conventional therapy in pancreatic cancer patients.
  • In vivo efficacy of ApoG2 was evaluated in a xenograft model to confirm its therapeutic benefit with gemcitabine.
  • Furthermore, administration of ApoG2 with gemcitabine resulted in a statistically higher antitumor activity compared with either ApoG2 or gemcitabine alone in a severe combined immunodeficiency mouse xenograft model.
  • CONCLUSIONS: Apogossypolone, which functions as a potent pan-Bcl-2 family inhibitor, seems therapeutically promising for future translational studies including the treatment of pancreatic cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Deoxycytidine / analogs & derivatives. Gossypol / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis Regulatory Proteins / antagonists & inhibitors. Cell Line, Tumor. Drug Resistance, Neoplasm. Drug Synergism. Female. Humans. Membrane Proteins / antagonists & inhibitors. Mice. Mice, SCID. Myeloid Cell Leukemia Sequence 1 Protein. Proto-Oncogene Proteins / antagonists & inhibitors. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / antagonists & inhibitors

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  • (PMID = 19823097.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109389; United States / NCI NIH HHS / CA / R01 CA109389
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Mcl1 protein, mouse; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / apogossypolone; 0 / bcl-2-Associated X Protein; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; KAV15B369O / Gossypol
  • [Other-IDs] NLM/ NIHMS512774; NLM/ PMC3807128
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23. Li J, Chigurupati S, Agarwal R, Mughal MR, Mattson MP, Becker KG, Wood WH 3rd, Zhang Y, Morin PJ: Possible angiogenic roles for claudin-4 in ovarian cancer. Cancer Biol Ther; 2009 Oct;8(19):1806-14
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  • In addition, an in vivo mouse dorsal skinfold assay confirms that cells expressing claudin-4 secrete factors that can mediate angiogenesis in the dorsal skin of mice.
  • [MeSH-major] Membrane Proteins / biosynthesis. Ovarian Neoplasms / blood supply

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  • (PMID = 19657234.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000395-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLDN4 protein, human; 0 / Claudin-4; 0 / Cldn4 protein, mouse; 0 / Membrane Proteins
  • [Other-IDs] NLM/ NIHMS137709; NLM/ PMC2795001
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24. Kline RP, Wu EX, Petrylak DP, Szabolcs M, Alderson PO, Weisfeldt ML, Cannon P, Katz J: Rapid in vivo monitoring of chemotherapeutic response using weighted sodium magnetic resonance imaging. Clin Cancer Res; 2000 Jun;6(6):2146-56
Hazardous Substances Data Bank. SODIUM CHLORIDE .

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  • A novel pulse sequence strategy uses sodium magnetic resonance imaging to monitor the response to chemotherapy of mouse xenograft tumors propagated from human prostate cancer cell lines.
  • An inversion pulse suppresses sodium with long longitudinal relaxation times, weighting the image toward intracellular sodium nuclei.
  • Experiments with these same drugs and cells, treated in culture, detected a significant intracellular sodium elevation (10-20 mM) using a ratiometric fluorescent dye.
  • Histopathology on formalin-fixed sections of explanted tumors confirmed that drug administration reduces proliferation (2.2 versus 8.6 mitotic figures per high power field; P < 0.0001), an effect that inversely correlates with the sodium magnetic resonance image response on a tumor-to-tumor basis (P < 0.02; n = 10).
  • Advantages of this sodium imaging technique include rapid determination of drug efficacy, improved diagnosis of lesions, ease of coregistration with high resolution proton magnetic resonance imaging, and absence of costly or toxic reagents.
  • [MeSH-major] Magnetic Resonance Imaging / methods. Paclitaxel / analogs & derivatives. Prostatic Neoplasms / drug therapy. Sodium. Taxoids
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. Cell Nucleus / metabolism. Etoposide / pharmacology. Flow Cytometry. Fluorescent Antibody Technique. Fluorescent Dyes / pharmacology. Humans. Male. Mice. Neoplasm Transplantation / pathology. Phantoms, Imaging. Sodium Chloride / chemistry. Time Factors. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 10873063.001).
  • [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 / Annexin A5; 0 / Antineoplastic Agents, Phytogenic; 0 / Fluorescent Dyes; 0 / Taxoids; 15H5577CQD / docetaxel; 451W47IQ8X / Sodium Chloride; 6PLQ3CP4P3 / Etoposide; 9NEZ333N27 / Sodium; P88XT4IS4D / Paclitaxel
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25. You S, Zuo L, Li W: Optimizing the time of Doxil injection to increase the drug retention in transplanted murine mammary tumors. Int J Nanomedicine; 2010;5:221-9
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  • [Title] Optimizing the time of Doxil injection to increase the drug retention in transplanted murine mammary tumors.
  • It has been proposed that the liposomal formulated doxorubicin (ie, Doxil), given at the menstrual/estrous stage with the predicted highest tumor vascular permeability, allows significantly increased drug retention in the breast tumor.
  • In the current study, syngeneic murine 4T1 mammary tumors were established on the backs of female BALB/c mice and Doxil was administered at particular mouse estrous cycle stages.
  • The results indicated that Doxil administration during certain times in the mouse estrous cycle was crucial for drug retention in 4T1 tumor tissues.
  • Significantly higher drug concentrations were detected in the tumor tissues when Doxil was administered during the diestrus stage, as compared to when the drug injection was given at all other estrous stages.
  • Our study also showed that the tumor-bearing mice exhibited nearly normal rhythmicity of the estrous cycle post drug injection, indicating the feasibility of continual injection of Doxil at the same estrous cycle stage.
  • Some of these factors have been shown to be vascular modulators in diverse tissues.
  • In this report, we demonstrated that the concentration of P4 in the plasma and/or estrous cycle stage of 4T1 tumor-bearing mice can be used to select the best time for administrating the liposomal anticancer drugs.
  • [MeSH-major] Doxorubicin / administration & dosage. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Dose-Response Relationship, Drug. Female. Injections, Intralesional / methods. Mice. Mice, Inbred BALB C. Treatment Outcome

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  • (PMID = 20463938.001).
  • [ISSN] 1178-2013
  • [Journal-full-title] International journal of nanomedicine
  • [ISO-abbreviation] Int J Nanomedicine
  • [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] New Zealand
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2865017
  • [Keywords] NOTNLM ; Doxil / breast cancer therapy / menstrual cycle / mouse mammary tumor / progesterone
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26. Farinelle S, Malonne H, Chaboteaux C, Decaestecker C, Dedecker R, Gras T, Darro F, Fontaine J, Atassi G, Kiss R: Characterization of TNP-470-induced modifications to cell functions in HUVEC and cancer cells. J Pharmacol Toxicol Methods; 2000 Jan-Feb;43(1):15-24
Hazardous Substances Data Bank. TAXOL .

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  • The in vitro effects were characterized on the mouse mammary MXT adenocarcinoma, on which we also characterized the influence of three clinically active anti-tumor compounds (as cytotoxic references).
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antibiotics, Antineoplastic / pharmacology. Endothelium, Vascular / drug effects. Mammary Neoplasms, Experimental / blood supply. Mammary Neoplasms, Experimental / drug therapy. Sesquiterpenes / pharmacology
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Biocompatible Materials. Cell Division / drug effects. Cell Movement / drug effects. Collagen. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Cyclohexanes. Drug Combinations. Glioblastoma / drug therapy. Glioblastoma / pathology. Growth Inhibitors / pharmacology. Growth Inhibitors / toxicity. Humans. Laminin. Mice. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Paclitaxel / pharmacology. Paclitaxel / toxicity. Proteoglycans. Tumor Cells, Cultured / drug effects

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  • (PMID = 11091126.001).
  • [ISSN] 1056-8719
  • [Journal-full-title] Journal of pharmacological and toxicological methods
  • [ISO-abbreviation] J Pharmacol Toxicol Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Biocompatible Materials; 0 / Cyclohexanes; 0 / Drug Combinations; 0 / Growth Inhibitors; 0 / Laminin; 0 / Proteoglycans; 0 / Sesquiterpenes; 119978-18-6 / matrigel; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; 9007-34-5 / Collagen; P88XT4IS4D / Paclitaxel
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27. Thewes V, Orso F, Jäger R, Eckert D, Schäfer S, Kirfel G, Garbe S, Taverna D, Schorle H: Interference with activator protein-2 transcription factors leads to induction of apoptosis and an increase in chemo- and radiation-sensitivity in breast cancer cells. BMC Cancer; 2010;10:192
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  • By using information obtained from Ingenuity Pathway Analysis Systems we were able to present proven or potential connections between AP-2 regulated genes involved in cell death and response to chemo- and radiation therapy, (i.e.
  • Therefore, interference with AP-2 function could increase the sensitivity of tumor cells towards therapeutic intervention.
  • [MeSH-major] Apoptosis. Drug Resistance, Neoplasm. Mammary Neoplasms, Experimental / metabolism. Radiation Tolerance. Transcription Factor AP-2 / metabolism

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  • (PMID = 20459791.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Isoforms; 0 / Transcription Factor AP-2; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2890516
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28. Zhang M, Yao Z, Zhang Z, Garmestani K, Goldman CK, Ravetch JV, Janik J, Brechbiel MW, Waldmann TA: Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors. Blood; 2006 Jul 15;108(2):705-10
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  • [Title] Effective therapy for a murine model of human anaplastic large-cell lymphoma with the anti-CD30 monoclonal antibody, HeFi-1, does not require activating Fc receptors.
  • Overexpression of CD30 on some neoplasms versus its limited expression on normal tissues makes this receptor a promising target for antibody-based therapy.
  • We investigated the therapeutic efficacy of HeFi-1, a mouse IgG1 monoclonal antibody, which recognizes the ligand-binding site on CD30, and humanized anti-Tac antibody (daclizumab), which recognizes CD25, in a murine model of human ALCL.
  • The ALCL model was established by intravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID/NOD) wild-type or SCID/NOD Fc receptor common gamma chain-deficient (FcRgamma(-/-)) mice.
  • HeFi-1, given at a dose of 100 microg weekly for 4 weeks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRgamma(-/-) mice (P < .01) as compared with the control groups.

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  • (PMID = 16551968.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD30; 0 / Antigens, Neoplasm; 0 / Immunoglobulin G; 0 / Receptors, Fc; CUJ2MVI71Y / daclizumab
  • [Other-IDs] NLM/ PMC1895489
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29. Mattheolabakis G, Taoufik E, Haralambous S, Roberts ML, Avgoustakis K: In vivo investigation of tolerance and antitumor activity of cisplatin-loaded PLGA-mPEG nanoparticles. Eur J Pharm Biopharm; 2009 Feb;71(2):190-5
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  • Normal BALB/c mice tolerated three weekly intravenous injections of a relatively high dose of blank PLGA-mPEG nanoparticles (500 mg/kg, equivalent to about 10mg nanoparticles/mouse) and three weekly intravenous injections of a high dose of nanoparticle-entrapped cisplatin (10 mg/kg).
  • Also, histopathology examination indicated that there were no differences in the kidneys or spleens from animals treated with cisplatin-loaded nanoparticles or blank nanoparticles compared to the untreated control group.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Colorectal Neoplasms / drug therapy. Nanoparticles
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Dose-Response Relationship, Drug. Drug Carriers / chemistry. Female. HT29 Cells. Humans. Injections, Intravenous. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Polyethylene Glycols / chemistry. Polyglactin 910 / chemistry. Survival Rate. Xenograft Model Antitumor Assays

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  • (PMID = 18929649.001).
  • [ISSN] 1873-3441
  • [Journal-full-title] European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft für Pharmazeutische Verfahrenstechnik e.V
  • [ISO-abbreviation] Eur J Pharm Biopharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / poly(D,L-lactic-co-glycolic acid)-methoxy-poly(ethyleneglycol) copolymer; 30IQX730WE / Polyethylene Glycols; 34346-01-5 / Polyglactin 910; Q20Q21Q62J / Cisplatin
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30. Hosotani R, Miyamoto Y, Fujimoto K, Doi R, Otaka A, Fujii N, Imamura M: Trojan p16 peptide suppresses pancreatic cancer growth and prolongs survival in mice. Clin Cancer Res; 2002 Apr;8(4):1271-6
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  • PURPOSE: The tumor suppressor gene p16INK4A is inactivated frequently in a large number of human cancers, and many investigators have attempted to restore the function of p16 using the p16 wild-type gene and viral vectors.
  • EXPERIMENTAL DESIGN: Injections (i.p.) of the Trojan p16 peptide (100 microg/mouse/day) were given for 3 weeks in the AsPC-1 and BxPC-3 s.c. tumor models.
  • Tumor growth, histopathology, and TUNEL staining of the tumor and toxicity of the animals were evaluated.
  • RESULTS: In the AsPC-1 s.c. tumor model, a significant growth inhibition was obtained by the Trojan p16 treatment when compared with the three control treatments, i.e., vehicle, unconjugated form of p16, or Trojan peptide alone.
  • Histopathology of the BxPC-3 s.c. tumor in the Trojan p16 treatment group revealed marked vacuole formation and apoptotic death of cancer cells.
  • CONCLUSIONS: These results provide evidence that the Trojan p16 peptide system, a gene-oriented peptide coupled with a peptide vector, functions for experimental pancreatic cancer therapy.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / genetics. Pancreatic Neoplasms / drug therapy. Peptide Fragments / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Animals. Blood Cell Count. Body Weight / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Molecular Sequence Data. Neoplasm Transplantation. Survival Analysis. Survival Rate. Tumor Cells, Cultured / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 11948142.001).
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Peptide Fragments
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31. Choedon T, Shukla SK, Kumar V: Chemopreventive and anti-cancer properties of the aqueous extract of flowers of Butea monosperma. J Ethnopharmacol; 2010 May 27;129(2):208-13
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  • ) (Fabaceae) popularly known as 'flame of the forest' has been widely used in the traditional Indian medical system of 'Ayurveda' for the treatment of a variety of ailments including liver disorders.
  • The chemopreventive and anti-angiogenic effects of the extract were evaluated by its daily oral administration in a HBV-related X15-myc mouse model of hepatocellular carcinoma (HCC).
  • RESULTS: Treatment with the aqueous extract inhibited cell proliferation and accumulation of cells in G1 phase.
  • Oral administration of the extract in transgenic mice conferred hepatoprotection as is evident from normal serum ALT levels and improved liver histopathology and lowered serum VEGF level.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Butea. Carcinoma, Hepatocellular / drug therapy. Cell Proliferation / drug effects. Liver Neoplasms / drug therapy. Phytotherapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Administration, Oral. Alanine Transaminase / blood. Animals. Anti-Inflammatory Agents / pharmacology. Anti-Inflammatory Agents / therapeutic use. Antioxidants / pharmacology. Antioxidants / therapeutic use. Apoptosis / drug effects. Cell Death / drug effects. Cell Line, Tumor. Flowers. Humans. Liver / drug effects. Liver / metabolism. Liver / pathology. Mice. Mice, Transgenic. Mitogen-Activated Protein Kinases / metabolism. Vascular Endothelial Growth Factor A / blood

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20307637.001).
  • [ISSN] 1872-7573
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Plant Extracts; 0 / Vascular Endothelial Growth Factor A; EC 2.6.1.2 / Alanine Transaminase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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32. Shanker A, Brooks AD, Tristan CA, Wine JW, Elliott PJ, Yagita H, Takeda K, Smyth MJ, Murphy WJ, Sayers TJ: Treating metastatic solid tumors with bortezomib and a tumor necrosis factor-related apoptosis-inducing ligand receptor agonist antibody. J Natl Cancer Inst; 2008 May 7;100(9):649-62
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  • We explored the therapeutic potential and in vivo toxicity of a combination of bortezomib, a proteasome inhibitor, and MD5-1, a tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor (DR5) agonist monoclonal antibody, in mouse carcinomas.
  • Toxicity was assessed by histopathology and hematology.
  • Treatment with bortezomib and MD5-1 reduced lung metastases in mice carrying Renca and 4T1 tumors (mean number of metastases, bortezomib + MD5-1 vs MD5-1: Renca-FLAG, 1 vs 8, difference = 7, 95% CI = 5 to 9, P < .001; 4T1, 1 vs 12, difference = 11, 95% CI = 9 to 12, P < .001) and increased median survival of mice bearing Renca-FLAG tumors (bortezomib + MD5-1 vs bortezomib + control isotype antibody: 22 of 30 [73%] were still alive at day 180 vs median survival of 42 days [95% CI = 41 to 44 days, P < .001]) in the absence of obvious toxicity.
  • CONCLUSION: Bortezomib combined with DR5 agonist monoclonal antibody may be a useful treatment for metastatic solid tumors.

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  • (PMID = 18445820.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CO / N01 CO012400; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 69G8BD63PP / Bortezomib; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8
  • [Other-IDs] NLM/ NIHMS118537; NLM/ PMC2753966
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33. Quang PN, Schmidt BL: Endothelin-A receptor antagonism attenuates carcinoma-induced pain through opioids in mice. J Pain; 2010 Jul;11(7):663-71
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.
  • We previously reported that endothelin A (ET-A) receptor antagonism attenuates carcinoma-induced pain in a cancer pain mouse model.
  • PERSPECTIVE: This article proposes a novel mechanism for ET-A receptor antagonist drugs in managing cancer-induced pain.
  • An improved understanding of the role of innate opioid analgesia in ET-A receptor-mediated antinociception might provide novel alternatives to morphine therapy for the treatment of cancer pain.

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 20071245.001).
  • [ISSN] 1528-8447
  • [Journal-full-title] The journal of pain : official journal of the American Pain Society
  • [ISO-abbreviation] J Pain
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE018561-01; United States / NIDCR NIH HHS / DE / R21 DE018561; United States / NIDCR NIH HHS / DE / R21 DE018561-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics; 0 / Antihypertensive Agents; 0 / Endothelin A Receptor Antagonists; 0 / Narcotic Antagonists; 0 / Opioid Peptides; 0 / Peptides, Cyclic; 0 / Receptors, Opioid; 136553-81-6 / cyclo(Trp-Asp-Pro-Val-Leu)
  • [Other-IDs] NLM/ NIHMS157593; NLM/ PMC2891170
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34. Marchini C, Montani M, Konstantinidou G, Orrù R, Mannucci S, Ramadori G, Gabrielli F, Baruzzi A, Berton G, Merigo F, Fin S, Iezzi M, Bisaro B, Sbarbati A, Zerani M, Galiè M, Amici A: Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies. PLoS One; 2010;5(11):e14131
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] Mesenchymal/stromal gene expression signature relates to basal-like breast cancers, identifies bone metastasis and predicts resistance to therapies.
  • BACKGROUND: Mounting clinical and experimental evidence suggests that the shift of carcinomas towards a mesenchymal phenotype is a common paradigm for both resistance to therapy and tumor recurrence.
  • METHODOLOGY/PRINCIPAL FINDINGS: By integrating in silico and in vitro studies with our epithelial and mesenchymal tumor models, we compare herein crucial molecular pathways of previously described carcinoma-derived mesenchymal tumor cells (A17) with that of both carcinomas and other mesenchymal phenotypes, such as mesenchymal stem cells (MSCs), breast stroma, and various types of sarcomas.
  • By using a recently developed computational approach with publicly available microarray data, we show that these signatures:.
  • 3) are up-regulated after hormonal treatment;.
  • 4) predict resistance to neoadjuvant therapies.
  • CONCLUSIONS/SIGNIFICANCE: Our results demonstrate that mesenchymalization is an intrinsic property of the most aggressive tumors and it relates to therapy resistance as well as bone metastasis.
  • [MeSH-major] Bone Neoplasms / genetics. Breast Neoplasms / genetics. Gene Expression Profiling. Mesoderm / metabolism. Stromal Cells / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cluster Analysis. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Drug Resistance, Neoplasm / genetics. Epithelial Cells / metabolism. Female. Humans. Mesenchymal Stromal Cells / metabolism. Mice. Neoadjuvant Therapy / methods. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction

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  • MedlinePlus Health Information. consumer health - Breast Cancer.
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  • (PMID = 21152434.001).
  • [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] EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2994727
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35. Mahasreshti PJ, Kataram M, Wang MH, Stockard CR, Grizzle WE, Carey D, Siegal GP, Haisma HJ, Alvarez RD, Curiel DT: Intravenous delivery of adenovirus-mediated soluble FLT-1 results in liver toxicity. Clin Cancer Res; 2003 Jul;9(7):2701-10
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have previously reported the locoregional (i.p.) delivery of adenovirus-mediated antiangiogenic soluble FLT-1 (sFLT-1; a naturally encoded potent VEGF antagonist) gene therapy to inhibit VEGF action in a murine ovarian carcinoma model.
  • This study was predicated on the fact that systemic delivery of sFLT-1 might allow an approach for therapy of disseminated tumor.
  • The therapeutic effect of sFLT-1 was evaluated by survival duration of the mice.
  • Systemic levels of sFLT-1 were evaluated by ELISA and the toxicity was evaluated by histopathology.
  • This localization lead to sFLT-1 overexpression, mainly in the liver, resulting in hemorrhage and tissue toxicity.
  • Tumor-specific targeting of the vectors and tumor-specific expression strategies should be used to ensure a clinically useful antiangiogenesis gene therapy.
  • [MeSH-major] Adenoviridae / genetics. Extracellular Matrix Proteins / therapeutic use. Liver / drug effects
  • [MeSH-minor] Animals. Cell Division. Cell Line, Tumor. Cell Survival. Enzyme-Linked Immunosorbent Assay. Female. Genetic Therapy / methods. Genetic Vectors. Green Fluorescent Proteins. Humans. Immunohistochemistry. Luminescent Proteins / metabolism. Mice. Mice, SCID. Microscopy, Fluorescence. Myosin Heavy Chains. Neoplasm Metastasis. Neovascularization, Pathologic. Nonmuscle Myosin Type IIB. Ovarian Neoplasms / genetics. Ovarian Neoplasms / metabolism. Time Factors. Vascular Endothelial Growth Factor Receptor-1

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  • (PMID = 12855650.001).
  • [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 CA68245; United States / NCI NIH HHS / CA / T32 CA75930
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Luminescent Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 3.6.1.- / Nonmuscle Myosin Type IIB; EC 3.6.1.- / nonmuscle myosin type IIB heavy chain; EC 3.6.4.1 / Myosin Heavy Chains
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36. Hausner SH, Abbey CK, Bold RJ, Gagnon MK, Marik J, Marshall JF, Stanecki CE, Sutcliffe JL: Targeted in vivo imaging of integrin alphavbeta6 with an improved radiotracer and its relevance in a pancreatic tumor model. Cancer Res; 2009 Jul 15;69(14):5843-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cell surface receptor alpha(v)beta(6) is epithelial specific, and its expression is tightly regulated; it is low or undetectable in adult tissues but has been shown to be increased in many different cancers, including pancreatic, cervical, lung, and colon cancers.
  • We have recently shown the feasibility of imaging alpha(v)beta(6) in vivo by positron emission tomography (PET) using the peptide [(18)F]FBA-A20FMDV2.
  • Here, we describe improved alpha(v)beta(6) imaging agents and test their efficacy in a mouse model with endogenous alpha(v)beta(6) expression.
  • Pancreatic ductal adenocarcinoma is highly metastatic and current preoperative evaluation of resectability using noninvasive imaging has limited success, with most patients having metastases at time of surgery.
  • The fact that these tumors express alpha(v)beta(6) suggests that this probe has significant potential for the in vivo detection of this malignancy, thus having important implications for patient care and therapy.

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  • (PMID = 19549907.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA107792-02; United States / NCI NIH HHS / CA / R21 CA107792; United States / NCI NIH HHS / CA / R21 CA107792-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Benzoates; 0 / Fluorine Radioisotopes; 0 / Integrins; 0 / Radiopharmaceuticals; 0 / Viral Proteins; 0 / integrin alphavbeta6; V5ROO2HOU4 / 4-fluorobenzoic acid
  • [Other-IDs] NLM/ NIHMS117292; NLM/ PMC2711989
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37. Harper CE, Patel BB, Wang J, Arabshahi A, Eltoum IA, Lamartiniere CA: Resveratrol suppresses prostate cancer progression in transgenic mice. Carcinogenesis; 2007 Sep;28(9):1946-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the current study, Transgenic Adenocarcinoma Mouse Prostate males were fed resveratrol (625 mg resveratrol per kg AIN-76A diet) or phytoestrogen-free, control diet (AIN-76A) starting at 5 weeks of age.
  • Mechanisms of action and histopathology studies were conducted at 12 and 28 weeks of age, respectively.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Prostatic Neoplasms / drug therapy. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Cell Division / drug effects. Crosses, Genetic. Disease Progression. Female. Heterozygote. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic

  • Genetic Alliance. consumer health - Prostate cancer.
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  • Hazardous Substances Data Bank. RESVERATROL .
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  • (PMID = 17675339.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 47888; United States / NCI NIH HHS / CA / P30 CA-13148-34
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; Q369O8926L / resveratrol
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