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  • 1
    Online Resource
    Online Resource
    Antiangiogenic Agents in Cancer Therapy (2008)
    Totowa, NJ : Humana Press
    Details Availability
    Keywords: Medicine ; Cancer research ; Pharmacology ; Oncology ; Surgical oncology ; Biomedicine ; Cancer Surgery ; Medicine ; Oncology ; Toxicology ; Neoplasms drug therapy ; Antineoplastic Agents therapeutic use ; Neovascularization, Pathologic drug therapy ; Angiogenese ; Inhibitor
    Description / Table of Contents: Antiangiogenesis remains a dynamic and evolving field in oncology. New therapeutic targets continue to emerge followed by the rapid development of new therapeutic agents to be investigated in clinical trials. Optimizing the therapeutic potential of antiangiogenic agents in combination with the other therapies in the armamentarium to fight cancer will be an on-going challenge. Antiangiogenic Agents in Cancer Therapy, Second Edition provides a current, up-dated perspective on the state of the art of angiogenesis and therapy with a compendium of scientific findings and approaches to the study of ...
    Type of Medium: Online Resource
    Pages: Online-Ressource (XVIII, 559 p, online resource)
    Edition: Second Edition
    ISBN: 9781597451840
    Series Statement: Cancer Drug Discovery and Development
    URL: https://doi.org/10.1007/978-1-59745-184-0
    URL: http://dx.doi.org/10.1007/978-1-59745-184-0
    URL: https://swbplus.bsz-bw.de/bsz301456089cov.jpg
    URL: http://www.gbv.de/dms/bowker/toc/9781588298706.pdf
    DOI: 10.1007/978-1-59745-184-0
    RVK:
    XI 7000
    Language: English
    Note: Includes bibliographical references and index , Front Matter; Vascular Endothelial Growth Factor Family and Its Receptors; The Cycle Between Angiogenesis, Perfusion, and Hypoxia in Tumors; The Role of Integrins in Tumor Angiogenesis; Tumor Endothelial Cell Abnormalities; The Extracellular Matrix and VEGF Processing; Endothelial Precursor Cells; Role of Pericytes in Angiogenesis; Newer Vascular Targets; Chemokines in Angiogenesis; Angiopoietin/Tie2 Signaling Regulates Tumor Angiogenesis; Imaging Angiogenesis; Tumor Blood Vessels; Lymphatic System in the Pathology of Cancer; VEGF in the Adult , Normalization of Tumor Vasculature and MicroenvironmentMetronomic Low-Dose Antiangiogenic Chemotherapy in Mice and Man; Small-Molecule Vascular Disrupting Agents in Cancer Therapy; Normalization of Tumor Vasculature and Improvement of Radiation Response by Antiangiogenic Agents; Challenges in Translating Antiangiogenic Therapy from the Bench to Bedside; Regulation of Angiogenesis in Cancer and Its Therapeutic Implications; Angiogenesis and Angiogenesis Inhibition in Sarcomas; Antiangiogenesis Agents in Colorectal Cancer; Antiangiogenic Therapy for Primary CNS Tumors , Angiogenesis Inhibitors for the Treatment of Lung CancerAntiangiogenic Therapy of Renal Cell Carcinoma; Antiangiogenesis Therapies in Gynecologic Malignancies; Antiangiogenic Agents in Myeloid Malignancies; Angiogenesis in Malignant and Non-Malignant Pediatric Tumors; Prognostic and Predictive Significance of Surrogate Biomarkers of Angiogenesis; Endpoints for the Determination of Efficacy of Antiangiogenic Agents in Clinical Trials; The Role of Imaging in the Clinical Development of Antiangiogenic Agents; Back Matter
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  • 2
    Online Resource
    Online Resource
    Cancer Drug Resistance (2006)
    Totowa, NJ : Humana Press Inc
    Details Availability
    Keywords: Medicine ; Oncology ; Medicine & Public Health ; Oncology ; Medicine ; Drug Resistance, Neoplasm ; Antineoplastic Agents therapeutic use ; Krebs ; Arzneimittelresistenz ; Pharmakotherapie
    Description / Table of Contents: Leading experts summarize and synthesize the latest discoveries concerning the changes that occur in tumor cells as they develop resistance to anticancer drugs, and suggest new approaches to preventing and overcoming it. The authors review physiological resistance based upon tumor architecture, cellular resistance based on drug transport, epigenetic changes that neutralize or bypass drug cytotoxicity, and genetic changes that alter drug target molecules by decreasing or eliminating drug binding and efficacy. Highlights include new insights into resistance to antiangiogenic therapies, oncogenes and tumor suppressor genes in therapeutic resistance, cancer stem cells, and the development of more effective therapies. There are also new findings on tumor immune escape mechanisms, gene amplification in drug resistance, the molecular determinants of multidrug resistance, and resistance to taxanes and Herceptin.
    Type of Medium: Online Resource
    Pages: Online-Ressource (digital)
    ISBN: 9781597450355
    Series Statement: Cancer Drug Discovery and Development
    URL: https://doi.org/10.1007/978-1-59745-035-5
    URL: http://dx.doi.org/10.1007/978-1-59745-035-5
    URL: https://swbplus.bsz-bw.de/bsz280691459kap.htm
    URL: https://swbplus.bsz-bw.de/bsz280691459vor.htm
    URL: https://swbplus.bsz-bw.de/bsz280691459inh.htm
    URL: https://swbplus.bsz-bw.de/bsz280691459cov.jpg
    URL: http://www.gbv.de/dms/bowker/toc/9781588295309.pdf
    DOI: 10.1007/978-1-59745-035-5
    RVK:
    XH 3200
    RVK:
    XI 7020
    Language: English
    Note: Includes bibliographical references and index , Front Matter; The Cycle Between Angiogenesis, Perfusion, and Hypoxia in Tumors; Influence of Tumor pH on Therapeutic Response; Tumor Oxygenation and Treatment Response; Oncogenes and Tumor Suppressor Genes in Therapeutic Resistance; PET Imaging of Response and Resistance to Cancer Therapy; Cancer Stem Cells Implications for Development of More Effective Therapies; Therapeutic Resistance in Leukemia; Tumor Site Implantation and Animal Model Selection in Oncology; In Vivo Resistance; Characteristics of the Metastatic Phenotype; The Microenvironment and Drug Resistance , Glutathione and Glutathione S -Transferases in Drug ResistanceMetallothioneins in Drug Resistance; Molecular Determinants of Intrinsic Multidrug Resistance in Cancer Cells and Tumors; New and Revised Concepts in Multidrug Resistance; Cisplatin Resistance; Regulation of the Cellular Pharmacology and Cytotoxicity of Cisplatin by Copper Transporters; Resistance To Taxanes; CpG Island Methylation and Drug Resistance; De Novo and Acquired Resistance to Antitumor Alkylating Agents; Resistance to Antiangiogenic Agents; Resistance to Antiestrogens , Mechanisms of Glucocorticoid Actions and Resistance in Multiple MyelomaHerceptin Resistance; Role of TGF-ß in Tumor Progression and Metastasis; p53-Based Immunotherapy of Cancer; Response and Resistance to Ionizing Radiation; Amplification in DNA Copy Numbers as a Mechanism of Acquired Drug Resistance; Cancer Chemotherapy; Molecular Profiling in Breast Cancer; Tumor Immune Escape Mechanisms; Back Matter
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  • 3
    Online Resource
    Online Resource
    Cancer Chemoprevention : Volume 2: Strategies for Cancer Chemoprevention (2005)
    Totowa, NJ : Humana Press Inc
    Details Availability
    Keywords: Medicine ; Oncology ; Medicine & Public Health ; Oncology ; Medicine ; Anticarcinogenic Agents therapeutic use ; Neoplasms prevention & control ; Chemoprevention methods
    Type of Medium: Online Resource
    Pages: Online-Ressource (digital)
    ISBN: 9781592597680
    Series Statement: Cancer Drug Discovery and Development
    URL: https://doi.org/10.1007/978-1-59259-768-0
    URL: http://dx.doi.org/10.1007/978-1-59259-768-0
    URL: https://swbplus.bsz-bw.de/bsz286094037vor.htm
    URL: https://swbplus.bsz-bw.de/bsz286094037cov.jpg
    URL: https://swbplus.bsz-bw.de/bsz286094037kap.htm
    URL: https://swbplus.bsz-bw.de/bsz286094037inh.htm
    URL: http://www.gbv.de/dms/bowker/toc/9781588290779.pdf
    DOI: 10.1007/978-1-59259-768-0
    Language: English
    Note: Includes bibliographical references and index
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  • 4
    Electronic Resource
    Electronic Resource
    Nitrobenzyl halides and carbamates as prototype bioreductive alkylating agents (1980)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 23 (1980), S. 955-960 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00182a027
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  • 5
    Electronic Resource
    Electronic Resource
    Imaging radio frequency electron-spin-resonance spectrometer with high resolution and sensitivity for in vivo measurements (1989)
    [S.l.] : American Institute of Physics (AIP)
    Review of Scientific Instruments 60 (1989), S. 1040-1050 
    Details
    ISSN: 1089-7623
    Source: AIP Digital Archive
    Topics: Physics , Electrical Engineering, Measurement and Control Technology
    Notes: We report the development of a novel radio frequency electron-spin-resonance spectrometer designed to provide measurements with high molar sensitivity and resolution in vivo. Radio frequency (250 MHz) is chosen to obtain good penetration in animal tissue and large aqueous samples with modest sacrifice of sensitivity. The spectrometer has a lumped component resonator and operates in continuous-wave mode. The spectrometer is capable of two-dimensional imaging, and with a modest addition should be capable of three-dimensional imaging. We demonstrate 3-mm spatial resolution for DPPH samples. For 10-ml samples of aqueous nitroxide, we demonstrate sensitivity (normalized to spectral width of 1 G) to 3×10−8-M concentrations and spectral resolution of 0.1 G. Spectra from nitroxide spin label injected into a live mouse are shown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1140314
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  • 6
    Electronic Resource
    Electronic Resource
    Synthesis and evaluation of the antitumor activity of 4,5-diamino-substituted 1,2-benzoquinones (1993)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 36 (1993), S. 1797-1801 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00065a001
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  • 7
    Electronic Resource
    Electronic Resource
    Influence of scheduling on two-drug combinations of alkylating agents in vivo (1989)
    Springer
    Cancer chemotherapy and pharmacology 25 (1989), S. 161-166 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of schedule and sequence on the survival of EMT6 tumor cell and bone marrow (CFU-GM) obtained after treatment using combinations of cyclophosphamide (CTX) and thiotEPA or melphalan (l-PAM) were examined and analyzed by isobologram methodology. On a single-injection schedule, when CTX and thiotEPA were given simultaneously or thiotEPA was given prior to CTX, the result was slightly greater than additive tumor-cell kill. However, when CTX preceded thiotEPA by 4 h, there was less than additive cell kill. When the interval between the administration of the two drugs was 8 h, both sequences of the drugs produced greater than additive tumor-cell kill. Simultaneous administration of CTX and thiotEPA on a multiple-injection schedule resulted in sub-additive tumor-cell kill. On the multiple-injection schedule, extending the interval between injections of CTX and thiotEPA to 4 and 8 h resulted in increasing tumor-cell kill. With the 4- and 8-h intervals, no significant sequence-dependent difference in tumor-cell kill was obtained. The results of CTX andl-PAM combinations paralleled those of CTX and thiotEPA. Bone marrow (CFU-GM) survival was used as a representative normal tissue with which to compare tumor-cell survival after each treatment to obtain a measure of therapeutic effect. The trends for the ratios of bone marrow: tumor cell survival were the same for the treatment sequences of CTX with thiotEPA orl-PAM; however, greater magnitudes of differential tumor-cell kill were obtained with CTXl-PAM combinations. Using this measure, the greatest therapeutic effectiveness was seen with single-dosel-PAM or thiotEPA followed 4 h later by CTX and with CTX given as a single or as multiple doses followed 8 h later byl-PAM or thiotEPA. Such data from tumor-model systems may be useful in the development of more effective alkylating agent regimens for use in the clinic.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689576
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  • 8
    Electronic Resource
    Electronic Resource
    β-Cyclodextrin tetradecasulfate/tetrahydrocortisol±minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma (1993)
    Springer
    Cancer chemotherapy and pharmacology 33 (1993), S. 229-238 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μM, 24 h) and β-cyclodextrin tetradecasulfate (100 μM, 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μM, 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686221
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  • 9
    Electronic Resource
    Electronic Resource
    In vivo modulation of several anticancer agents by β-carotene (1994)
    Springer
    Cancer chemotherapy and pharmacology 34 (1994), S. 235-241 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of the collagenase inhibitor minocycline and of β-carotene to act as positive modulators of cytotoxic anticancer agents was assessed in vitro and in vivo. Cell-culture studies were conducted using the human SCC-25 squamous carcinoma cell line. Simultaneous exposure of the cells to minocycline and β-carotene or 13-cis-retinoic acid along with cisplatin (CDDP) resulted in a small decrease in the cytotoxicity of the CDDP. The addition of each of the modulator combinations for 1 h or 24 h to treatment with melphalan (L-PAM) or carmustine (BCNU) resulted in greater-than-additive cytotoxicity with each of four regimens. The modulator combinations of minocycline and β-carotene applied for 1 h or 24 h and the modulator combination of munocycline and 13-cis-retinoic acid produced greater-than-additive cytotoxicity at 50 μM 4-hydroperoxycyclophosphamide (4-HC), whereas minocycline and 13-cis-retinoic acid applied for 1 h was antagonistic with 4-HC and the other modulator treatments at low concentrations of 4-HC resulted in subadditive cytotoxicity. The effect of treatment with β-carotene alone and in combination with several different anticancer agents was examined in two murine solid tumors, the FSaII fibrosarcoma and the SCC VII carcinoma. Administration of the modulators alone or in combination did not alter the growth of either tumor. Whereas increases in tumor growth delay occurred with the antitumor alkylating agents and β-carotene and with minocycline and β-carotene, a diminution in tumor growth delay was produced by 5-fluorouracil in the presence of these modulators. The modulator combination also resulted in increased tumor growth delay with Adriamycin and etoposide. Tumor-cell survival assay showed increased killing of FSaII tumor cells with the modulator combination and melphalan or cyclophosphamide as compared with the drugs alone. These results indicate that further investigation of this modulator strategy is warranted.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685083
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  • 10
    Electronic Resource
    Electronic Resource
    CAI: effects on cytotoxic therapies in vitro and in vivo (1994)
    Springer
    Cancer chemotherapy and pharmacology 34 (1994), S. 515-521 
    Details
    ISSN: 1432-0843
    Keywords: L651582 ; CAI ; Combination therapy ; Antitumor alkylating agents
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract CAI (NSC 609974; L651582), a new agent that has demonstrated antimetastatic activity in vitro and in vivo, was not very cytotoxic toward EMT-6 mouse mammary carcinoma cells in culture or toward FSaIIC fibrosarcoma cells in vivo. Coexposure of EMT-6 cells to CAI and antitumor alkylating agents under various environmental conditions did not markedly increase the cytotoxicity of cisplatin (CDDP), melphalan, or carmustine (BCNU). However, the combination of CAI and 4-hydroperoxycyclophosphamide (4-HC) produced much greater than additive killing of EMT-6 cells. CAI also increased the sensitivity of hypoxic EMT-6 cells to X-rays. CAI increased the cytotoxicity of cyclophosphamide toward FSaIIC tumor cells when animals were treated with single doses of both drugs. The effect of CAI on tumor cell killing by cyclophosphamide was greatest at high doses of the antitumor alkylating agent. CAI administration appeared to result in increased serum levels of prostaglandin E2 and leukotriene B4 in animals bearing the Lewis lung tumor. Administration of CAI on days 4–18 did not alter the growth of the Lewis lung carcinoma but did result in an increase in the tumor-growth delay produced by treatment with CDDP, cyclophosphamide, melphalan, BCNU, and fractionated radiation. Although CAI did not reduce the number of lung metastases present in Lewis lung carcinoma-bearing mice on day 20, it did appear to reduce the number of large (vascularized) metastases present on that day.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685664
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